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Saeed A, Batra N, Rezgui R, Alshaghdali K, Alkhalaf I, Yadav DK, Dey P. Gut microbiota-centered risk factors and altered immunometabolism in the pathogenesis and prophylaxis of Clostridium difficile infection. JOURNAL OF KING SAUD UNIVERSITY - SCIENCE 2024; 36:103374. [DOI: 10.1016/j.jksus.2024.103374] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 03/31/2025]
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2
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Zhou R, Wu R, Wang L, Yang H. Increasing ratio of opportunistic infections associated with sunshine exposure and economic level burdening Chinese inflammatory bowel disease hospitalized patients: the first nationwide survey from 2014 to 2019. BMC Public Health 2024; 24:133. [PMID: 38195452 PMCID: PMC10777555 DOI: 10.1186/s12889-024-17635-6] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/26/2023] [Accepted: 01/01/2024] [Indexed: 01/11/2024] Open
Abstract
BACKGROUND The rising prevalence of opportunistic infections (OIs) in inflammatory bowel disease (IBD) in conjunction with the use of biologics/immunosuppressive agents has garnered attention. However, there is a dearth of research on OIs in Mainland China. This study seeks to evaluate the national ratio trend of OIs in IBD and elucidate the influence of economic and climate factors on IBD patients with OIs and their outcomes. METHODS The nationwide data was obtained from the Inpatient medical record home page via the Health Statistics and Information Reporting System (HSRS). Patients diagnosed with IBD were enlisted for participation, and their demographic and clinical information, encompassing infection type, surgical procedures, and expenses, were gathered. The National Bureau of Statistics provided data on monthly sunshine exposure hours and yearly Gross Domestic Product (GDP). RESULTS Findings indicate that between 2014 and 2019, a total of 381,752 patients with IBD were admitted to hospitals, with 364,249 patients lacking OIs and 17,503 patients presenting with OIs. The annual proportion of OIs exhibited an upward trend, rising from 3.54% in 2014 to 4.81% in 2019. There was a significant correlation observed between individuals who identified as male, those who visited hospitals in southern regions, or those originating from areas with lower GDP or shorter sunshine exposure hours, and a higher incidence of OIs. Among patients diagnosed with either Crohn's disease (CD) or ulcerative colitis (UC), Clostridium difficile was found to be the most prevalent infection, followed by Epstein-Barr virus and cytomegalovirus. Furthermore, the occurrence of OIs was found to be associated with an increased rate of surgical interventions in UC patients. CONCLUSIONS The rising prevalence of OIs among hospitalized patients with IBD necessitates heightened attention towards mitigating associated risk factors, particularly among IBD patients residing in less developed regions or experiencing limited exposure to sunlight. This approach aims to minimize hospital stays and associated costs.
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Affiliation(s)
- Runing Zhou
- Department of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100730, China
| | - Ruixian Wu
- Center for Health Statistics and Information, National Health Commission, Beijing, 100044, China
| | - Li Wang
- Department of Epidemiology and Biostatistics, School of Basic Medicine Peking Union Medical College, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, Beijing, 100005, China
| | - Hong Yang
- Department of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100730, China.
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Liu J, Liu J, Zhang J, Liu C, Qu C, Na L. Vitamin D deficiency in early life regulates gut microbiome composition and leads to impaired glucose tolerance in adult and offspring rats. Food Funct 2023. [PMID: 37285306 DOI: 10.1039/d3fo00503h] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 06/09/2023]
Abstract
Vitamin D has been found to be involved in glucose metabolism in recent years. Its deficiency is very common, especially in children. Whether vitamin D deficiency in early life affects adult diabetes risk is unknown. In this study, a rat model of early life vitamin D deficiency (F1 Early-VDD) was established by depriving it of vitamin D from the 0 to the 8th week. Further, some rats were switched to normal feeding conditions and sacrificed at the 18th week. Other rats were mated randomly to generate offspring rats (F2 Early-VDD), and F2 rats were fed under normal conditions and sacrificed at the 8th week. Serum 25(OH)D3 level decreased in F1 Early-VDD at the 8th week and returned to normal at the 18th week. Serum 25(OH)D3 level in F2 Early-VDD at the 8th week was also lower than that in control rats. Impaired glucose tolerance was observed in F1 Early-VDD at the 8th week and 18th week and also in F2 Early-VDD at the 8th week. The gut microbiota composition in F1 Early-VDD at the 8th week significantly changed. Among the top ten genera with a rich difference, Desulfovibrio, Roseburia, Ruminiclostridium, Lachnoclostridium, A2, GCA-900066575, Peptococcus, Lachnospiraceae_FCS020_ group, and Bilophila increased owing to vitamin D deficiency, whereas Blautia decreased. There were 108 significantly changed metabolites in F1 Early-VDD at the 8th week, of which 63 were enriched in known metabolic pathways. Correlations between gut microbiota and metabolites were analyzed. Blautia was positively related to 2-picolinic acid, whereas Bilophila was negatively related to indoleacetic acid. Moreover, some of the changes in microbiota, metabolites, and enriched metabolic pathways still existed in F1 Early-VDD rats at the 18th week and F2 Early-VDD rats at the 8th week. In conclusion, vitamin D deficiency in early life leads to impaired glucose tolerance in adult and offspring rats. This effect may be partly achieved by regulating gut microbiota and their co-metabolites.
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Affiliation(s)
- Jing Liu
- The College of Medical Technology, Shanghai University of Medicine and Health Sciences, Shanghai, China
- Department of Research, Shanghai University of Medicine and Health Sciences Affiliated Zhoupu Hospital, Shanghai, China
| | - Junyi Liu
- Department of Clinical Nutrition, Shanghai University of Medicine and Health Sciences Affiliated Zhoupu Hospital, Shanghai, China
| | - Jingyi Zhang
- College of Public Health, Shanghai University of Medicine and Health Sciences, Shanghai, China.
| | - Chunyan Liu
- College of Public Health, Shanghai University of Medicine and Health Sciences, Shanghai, China.
| | - Chunbo Qu
- College of Public Health, Shanghai University of Medicine and Health Sciences, Shanghai, China.
| | - Lixin Na
- College of Public Health, Shanghai University of Medicine and Health Sciences, Shanghai, China.
- Collaborative Innovation Center of Shanghai University of Medicine and Health Sciences, Shanghai, China
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Al-Khaldy NS, Al-Musharaf S, Aljazairy EA, Hussain SD, Alnaami AM, Al-Daghri N, Aljuraiban G. Serum Vitamin D Level and Gut Microbiota in Women. Healthcare (Basel) 2023; 11:healthcare11030351. [PMID: 36766926 PMCID: PMC9914434 DOI: 10.3390/healthcare11030351] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/27/2022] [Revised: 01/20/2023] [Accepted: 01/21/2023] [Indexed: 01/27/2023] Open
Abstract
Obesity and vitamin D deficiency are two major public health concerns. Evidence suggests that alteration in gut microbiota composition is a possible risk factor for obesity. Additionally, altered vitamin D status has a potential role in shaping the gut microbial community. Further, the prevalence of obesity has been rising in the Middle East, especially among women of reproductive age, which is of specific concern due to its adverse effects on the health of their offspring. To date, limited evidence is available on the association between gut microbiota composition and vitamin D levels in Arab women. This study aims to identify the associations between serum vitamin D, gut microbiota, and obesity among Saudi females. The current study is a case-control study including 92 women aged 18 to 25 years, (n = 48) with normal weight and (n = 44) with obesity. Anthropometric, biochemical, lifestyle data, and fecal samples were collected and analyzed. We used shotgun metagenomic sequencing to characterize microbial communities of stool samples. Vitamin D levels were significantly associated with alpha and beta diversities. Serum vitamin D levels were positively associated with bacteria known to regulate immunological responses; Bacteroides thetaiotaomicron in the normal weight group (r = 0.34, p = 0.03) and Bifidobacterium adolescentis in the obesity group (r = 0.33, p = 0.04). In conclusion, the findings suggest that vitamin D status may play a role in regulating the gut microbiota composition by inhibiting the growth of pathogenic bacteria while nourishing the beneficial strains.
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Affiliation(s)
- Noorah S. Al-Khaldy
- Department of Community Health Sciences, College of Applied Medical Sciences, King Saud University, Riyadh 11451, Saudi Arabia
| | - Sara Al-Musharaf
- Department of Community Health Sciences, College of Applied Medical Sciences, King Saud University, Riyadh 11451, Saudi Arabia
- Correspondence: ; Tel.: +966-55-424-3033
| | - Esra’a A. Aljazairy
- Department of Community Health Sciences, College of Applied Medical Sciences, King Saud University, Riyadh 11451, Saudi Arabia
| | - Syed Danish Hussain
- Biomarkers of Chronic Diseases, Riyadh Biochemistry Department, College of Science, King Saud University, Riyadh 11451, Saudi Arabia
| | - Abdullah M. Alnaami
- Biomarkers of Chronic Diseases, Riyadh Biochemistry Department, College of Science, King Saud University, Riyadh 11451, Saudi Arabia
| | - Nasser Al-Daghri
- Biomarkers of Chronic Diseases, Riyadh Biochemistry Department, College of Science, King Saud University, Riyadh 11451, Saudi Arabia
| | - Ghadeer Aljuraiban
- Department of Community Health Sciences, College of Applied Medical Sciences, King Saud University, Riyadh 11451, Saudi Arabia
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Treatment with butyrate alleviates dextran sulfate sodium and Clostridium difficile-induced colitis by preventing activity of Th17 cells via regulation of SIRT1/mTOR in mice. J Nutr Biochem 2023; 111:109155. [PMID: 36162566 DOI: 10.1016/j.jnutbio.2022.109155] [Citation(s) in RCA: 22] [Impact Index Per Article: 11.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/13/2021] [Revised: 04/23/2022] [Accepted: 08/09/2022] [Indexed: 11/20/2022]
Abstract
Inflammatory bowel disease (IBD) patients are particularly vulnerable to infection with Clostridium difficile infection (CDI).Available treatments of IBD with CDI have not effective. Butyrate, the metabolites of microbiota, plays a vital role in maintaining immune homeostasis and potential drugs for treatment of IBD with CDI. The aim of this study was to investigate the effect of butyrate on IBD with CDI. Mice were given dextran sulfate sodium (DSS) and were infected with C. difficile (CD). Butyrate was treated during the study period. Butyrate protected from DSS+CD induced colitis by improving weight loss, survival, colon shorten, activity index score, and suppressing the expression of proinflammatory cytokines including IL-6, IL-17, TNF-α, IL-1β as well as regulating Th17/Treg balance through activation of SIRT1/mTOR. Besides, SR1001, an inhitor of the orphan nuclear receptors retinoic acid-related receptor γt, which is a transcription factor specific to the formation of Th17 cells can suppress the Th17 development and alleviate the DSS+CD induced colitis in mice. Notably, the therapeutic effect of butyrate was revered when disease mice treated with butyrate and Ex-527, a SIRT1 inhibitor. Taken together, we demonstrate that butyrate alleviates dextran sulfate sodium and clostridium difficile induced colitis by preventing Th17 through activation of SIRT1/mTOR.
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Elkafas H, Walls M, Al-Hendy A, Ismail N. Gut and genital tract microbiomes: Dysbiosis and link to gynecological disorders. Front Cell Infect Microbiol 2022; 12:1059825. [PMID: 36590579 PMCID: PMC9800796 DOI: 10.3389/fcimb.2022.1059825] [Citation(s) in RCA: 35] [Impact Index Per Article: 11.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/02/2022] [Accepted: 11/18/2022] [Indexed: 12/23/2022] Open
Abstract
Every year, millions of women are affected by genital tract disorders, such as bacterial vaginosis (BV), endometrial cancer, polycystic ovary syndrome (PCOS), endometriosis, and uterine fibroids (UFs). These disorders pose a significant economic burden on healthcare systems and have serious implications for health and fertility outcomes. This review explores the relationships between gut, vaginal, and uterine dysbiosis and the pathogenesis of various diseases of the female genital tract. In recent years, reproductive health clinicians and scientists have focused on the microbiome to investigate its role in the pathogenesis and prevention of such diseases. Recent studies of the gut, vaginal, and uterine microbiomes have identified patterns in bacterial composition and changes across individuals' lives associated with specific healthy and diseased states, particularly regarding the effects of the estrogen-gut microbiome axis on estrogen-driven disorders (such as endometrial cancer, endometriosis, and UFs) and disorders associated with estrogen deficiency (such as PCOS). Furthermore, this review discusses the contribution of vitamin D deficiency to gut dysbiosis and altered estrogen metabolism as well as how these changes play key roles in the pathogenesis of UFs. More research on the microbiome influences on reproductive health and fertility is vital.
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Affiliation(s)
- Hoda Elkafas
- Department of Pharmacology and Toxicology, Egyptian Drug Authority [EDA; formerly The National Organization for Drug Control and Research (NODCAR)], Cairo, Egypt
| | - Melinique Walls
- Pritzker School of Medicine, University of Chicago, Chicago, IL, United States
| | - Ayman Al-Hendy
- Department of Obstetrics and Gynecology, University of Chicago, Chicago, IL, United States
| | - Nahed Ismail
- Department of Pathology, University of Illinois at Chicago, Chicago, IL, United States
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Interactions between Dietary Micronutrients, Composition of the Microbiome and Efficacy of Immunotherapy in Cancer Patients. Cancers (Basel) 2022; 14:cancers14225577. [PMID: 36428677 PMCID: PMC9688200 DOI: 10.3390/cancers14225577] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/17/2022] [Revised: 11/07/2022] [Accepted: 11/11/2022] [Indexed: 11/16/2022] Open
Abstract
The effectiveness of immunotherapy in cancer patients depends on the activity of the host's immune system. The intestinal microbiome is a proven immune system modulator, which plays an important role in the development of many cancers and may affect the effectiveness of anti-cancer therapy. The richness of certain bacteria in the gut microbiome (e.g., Bifidobacterium spp., Akkermanisa muciniphila and Enterococcus hire) improves anti-tumor specific immunity and the response to anti-PD-1 or anti-PD-L1 immunotherapy by activating antigen-presenting cells and cytotoxic T cells within the tumor. Moreover, micronutrients affect directly the activities of the immune system or regulate their function by influencing the composition of the microbiome. Therefore, micronutrients can significantly influence the effectiveness of immunotherapy and the development of immunorelated adverse events. In this review, we describe the relationship between the supply of microelements and the abundance of various bacteria in the intestinal microbiome and the effectiveness of immunotherapy in cancer patients. We also point to the function of the immune system in the case of shifts in the composition of the microbiome and disturbances in the supply of microelements. This may in the future become a therapeutic target supporting the effects of immunotherapy in cancer patients.
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Loureiro AV, Barbosa MLL, Morais MLGS, Souza IP, Terceiro LS, Martins CS, Sousa APR, Leitão RFC, Shin JH, Warren CA, Costa DVS, Brito GAC. Host and Clostridioides difficile-Response Modulated by Micronutrients and Glutamine: An Overview. Front Nutr 2022; 9:849301. [PMID: 35795588 PMCID: PMC9251358 DOI: 10.3389/fnut.2022.849301] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/05/2022] [Accepted: 05/16/2022] [Indexed: 11/17/2022] Open
Abstract
Changes in intestinal microbiota are integral to development of Clostridioides difficile (C. difficile)—associated nosocomial diarrhea. Certain diets, especially Western diets, increase susceptibility to C. difficile infection (CDI). Here, we discuss recent findings regarding how nutrients modulate response of the host and C. difficile during infection. Calcium has a role in the sporulation and germination process. Selenium is effective in reducing the total amount of C. difficile toxin A (TcdA) and toxin B (TcdB) and in decreasing its cytotoxicity. In addition, selenium phosphate synthetase deficiency reduces C. difficile growth and spore production. On the other hand, iron has a dual role in C. difficile growth. For instance, high intracellular levels can generate reactive hydroxyl radicals, whereas low levels can reduce its growth. In humans, zinc deficiency appears to be related to the recurrence of CDI, in contrast, in the CDI model in mice a diet rich in zinc increased the toxin's activity. Low vitamin D levels contribute to C. difficile colonization, toxin production, and inflammation. Furthermore, glutamine appears to protect intestinal epithelial cells from the deleterious effects of TcdA and TcdB. In conclusion, nutrients play an important role in modulating host and pathogen response. However, further studies are needed to better understand the mechanisms and address some controversies.
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Affiliation(s)
- Andréa V. Loureiro
- Department of Medical Sciences, Faculty of Medicine, Federal University of Ceará, Fortaleza, Brazil
| | - Maria L. L. Barbosa
- Department of Morphology, Faculty of Medicine, Federal University of Ceará, Fortaleza, Brazil
| | - Maria L. G. S. Morais
- Department of Morphology, Faculty of Medicine, Federal University of Ceará, Fortaleza, Brazil
| | - Ismael P. Souza
- Department of Morphology, Faculty of Medicine, Federal University of Ceará, Fortaleza, Brazil
| | - Letícia S. Terceiro
- Department of Medical Sciences, Faculty of Medicine, Federal University of Ceará, Fortaleza, Brazil
| | - Conceição S. Martins
- Department of Morphology, Faculty of Medicine, Federal University of Ceará, Fortaleza, Brazil
| | - Arkila P. R. Sousa
- Department of Pharmacology and Physiology, Faculty of Medicine, Federal University of Ceará, Fortaleza, Brazil
| | - Renata F. C. Leitão
- Department of Morphology, Faculty of Medicine, Federal University of Ceará, Fortaleza, Brazil
| | - Jae H. Shin
- Division of Infectious Diseases and International Health, University of Virginia, Charlottesville, Virginia, VA, United States
| | - Cirle A. Warren
- Division of Infectious Diseases and International Health, University of Virginia, Charlottesville, Virginia, VA, United States
| | - Deiziane V. S. Costa
- Division of Infectious Diseases and International Health, University of Virginia, Charlottesville, Virginia, VA, United States
| | - Gerly A. C. Brito
- Department of Medical Sciences, Faculty of Medicine, Federal University of Ceará, Fortaleza, Brazil
- Department of Morphology, Faculty of Medicine, Federal University of Ceará, Fortaleza, Brazil
- Department of Pharmacology and Physiology, Faculty of Medicine, Federal University of Ceará, Fortaleza, Brazil
- *Correspondence: Gerly A. C. Brito
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9
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Chan H, Li Q, Wang X, Liu WY, Hu W, Zeng J, Xie C, Kwong TNY, Ho IHT, Liu X, Chen H, Yu J, Ko H, Chan RCY, Ip M, Gin T, Cheng ASL, Zhang L, Chan MTV, Wong SH, Wu WKK. Vitamin D 3 and carbamazepine protect against Clostridioides difficile infection in mice by restoring macrophage lysosome acidification. Autophagy 2022; 18:2050-2067. [PMID: 34989311 PMCID: PMC9466624 DOI: 10.1080/15548627.2021.2016004] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/18/2023] Open
Abstract
Clostridioides difficile infection (CDI) is a common cause of nosocomial diarrhea. TcdB is a major C. difficile exotoxin that activates macrophages to promote inflammation and epithelial damage. Lysosome impairment is a known trigger for inflammation. Herein, we hypothesize that TcdB could impair macrophage lysosomal function to mediate inflammation during CDI. Effects of TcdB on lysosomal function and the downstream pro-inflammatory SQSTM1/p62-NFKB (nuclear factor kappa B) signaling were assessed in cultured macrophages and in a murine CDI model. Protective effects of two lysosome activators (i.e., vitamin D3 and carbamazepine) were assessed. Results showed that TcdB inhibited CTNNB1/β-catenin activity to downregulate MITF (melanocyte inducing transcription factor) and its direct target genes encoding components of lysosomal membrane vacuolar-type ATPase, thereby suppressing lysosome acidification in macrophages. The resulting lysosomal dysfunction then impaired autophagic flux and activated SQSTM1-NFKB signaling to drive the expression of IL1B/IL-1β (interleukin 1 beta), IL8 and CXCL2 (chemokine (C-X-C motif) ligand 2). Restoring MITF function by enforced MITF expression or restoring lysosome acidification with 1α,25-dihydroxyvitamin D3 or carbamazepine suppressed pro-inflammatory cytokine expression in vitro. In mice, gavage with TcdB-hyperproducing C. difficile or injection of TcdB into ligated colon segments caused prominent MITF downregulation in macrophages. Vitamin D3 and carbamazepine lessened TcdB-induced lysosomal dysfunction, inflammation and histological damage. In conclusion, TcdB inhibits the CTNNB1-MITF axis to suppress lysosome acidification and activates the downstream SQSTM1-NFKB signaling in macrophages during CDI. Vitamin D3 and carbamazepine protect against CDI by restoring MITF expression and lysosomal function in mice.
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Affiliation(s)
- Hung Chan
- Department of Anaesthesia and Intensive Care, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China
| | - Qing Li
- Department of Anaesthesia and Intensive Care, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,State Key Laboratory of Digestive Diseases, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China
| | - Xiansong Wang
- Department of Anaesthesia and Intensive Care, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China
| | - Wing Yingzhi Liu
- Department of Anaesthesia and Intensive Care, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China
| | - Wei Hu
- Department of Anaesthesia and Intensive Care, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China
| | - Judeng Zeng
- Department of Anaesthesia and Intensive Care, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China
| | - Chuan Xie
- Department of Anaesthesia and Intensive Care, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China
| | - Thomas Ngai Yeung Kwong
- Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,State Key Laboratory of Digestive Diseases, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China
| | - Idy Hiu Ting Ho
- Department of Anaesthesia and Intensive Care, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China
| | - Xiaodong Liu
- Department of Anaesthesia and Intensive Care, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China
| | - Huarong Chen
- Department of Anaesthesia and Intensive Care, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,State Key Laboratory of Digestive Diseases, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China
| | - Jun Yu
- Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,State Key Laboratory of Digestive Diseases, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Centre for Gut Microbiota Research, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China
| | - Ho Ko
- Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China
| | - Raphael Chiu Yeung Chan
- Department of Microbiology, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China
| | - Margaret Ip
- Centre for Gut Microbiota Research, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Department of Microbiology, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China
| | - Tony Gin
- Department of Anaesthesia and Intensive Care, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China
| | - Alfred Sze Lok Cheng
- State Key Laboratory of Digestive Diseases, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China
| | - Lin Zhang
- Department of Anaesthesia and Intensive Care, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,State Key Laboratory of Digestive Diseases, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China
| | - Matthew Tak Vai Chan
- Department of Anaesthesia and Intensive Care, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China
| | - Sunny Hei Wong
- Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,State Key Laboratory of Digestive Diseases, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Centre for Gut Microbiota Research, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore
| | - William Ka Kei Wu
- Department of Anaesthesia and Intensive Care, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,State Key Laboratory of Digestive Diseases, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.,Centre for Gut Microbiota Research, The Chinese University of Hong Kong, Hong Kong Special Administrative Region, China
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10
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Russell LA, Balart MT, Serrano P, Armstrong D, Pinto-Sanchez MI. The complexities of approaching nutrition in inflammatory bowel disease: current recommendations and future directions. Nutr Rev 2021; 80:215-229. [PMID: 34131736 DOI: 10.1093/nutrit/nuab015] [Citation(s) in RCA: 9] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/08/2020] [Revised: 02/03/2021] [Accepted: 02/23/2021] [Indexed: 12/18/2022] Open
Abstract
Inflammatory bowel diseases (IBDs), including Crohn's disease and ulcerative colitis predispose patients to malnutrition due to a combination of increased basal metabolic rate, decreased oral intake, and increased nutritional losses and malabsorption. Malnutrition is common, affecting up to 75% of patients with Crohn's disease and 62% of patients with ulcerative colitis, and is associated with worse disease prognosis, higher complication rates, decreased quality of life, and increased mortality risk. It is imperative to screen patients with IBD for malnutrition to assess those at increased risk and treat accordingly to prevent progression and complications. This literature review provides an overall approach to optimizing nutrition in IBD, focusing on the assessment for the diagnosis of malnutrition, management of macro- and micronutrient deficiencies, and identification of areas for future study.
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Affiliation(s)
- Lindsey A Russell
- L.A. Russell, M.T. Balart, D. Armstrong, and M.I. Pinto-Sanchez are with Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, Ontario, Canada; L.A. Russell, M.T. Balart, P. Serrano, D. Armstrong, and M.I. Pinto-Sanchez are with McMaster University, Hamilton, Ontario, Canada
| | - Maria Teresa Balart
- L.A. Russell, M.T. Balart, D. Armstrong, and M.I. Pinto-Sanchez are with Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, Ontario, Canada; L.A. Russell, M.T. Balart, P. Serrano, D. Armstrong, and M.I. Pinto-Sanchez are with McMaster University, Hamilton, Ontario, Canada
| | - Pablo Serrano
- L.A. Russell, M.T. Balart, D. Armstrong, and M.I. Pinto-Sanchez are with Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, Ontario, Canada; L.A. Russell, M.T. Balart, P. Serrano, D. Armstrong, and M.I. Pinto-Sanchez are with McMaster University, Hamilton, Ontario, Canada
| | - David Armstrong
- L.A. Russell, M.T. Balart, D. Armstrong, and M.I. Pinto-Sanchez are with Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, Ontario, Canada; L.A. Russell, M.T. Balart, P. Serrano, D. Armstrong, and M.I. Pinto-Sanchez are with McMaster University, Hamilton, Ontario, Canada
| | - Maria Ines Pinto-Sanchez
- L.A. Russell, M.T. Balart, D. Armstrong, and M.I. Pinto-Sanchez are with Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, Ontario, Canada; L.A. Russell, M.T. Balart, P. Serrano, D. Armstrong, and M.I. Pinto-Sanchez are with McMaster University, Hamilton, Ontario, Canada
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Ham NS, Hwang SW, Oh EH, Kim J, Lee HS, Park SH, Yang DH, Ye BD, Byeon JS, Myung SJ, Yang SK. Influence of Severe Vitamin D Deficiency on the Clinical Course of Inflammatory Bowel Disease. Dig Dis Sci 2021; 66:587-596. [PMID: 32219610 DOI: 10.1007/s10620-020-06207-4] [Citation(s) in RCA: 17] [Impact Index Per Article: 4.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/25/2019] [Accepted: 03/10/2020] [Indexed: 12/11/2022]
Abstract
BACKGROUND Previous studies have shown vitamin D status to be associated with disease activity in patients with inflammatory bowel disease (IBD), but its influence on the clinical course of IBD has not been established. AIMS We aimed to analyze whether the serum 25-hydroxyvitamin D3 [25(OH)D] status is associated with clinical characteristics and affects the risk of surgery in patients with IBD. METHODS From the IBD registry of the Asan Medical Center, we identified all patients who had at least one 25(OH)D measurement; we then analyzed the association between clinical factors and 25(OH)D status. 25(OH)D was considered borderline deficient, deficient, and severely deficient at levels of < 30, < 20, and < 10 ng/mL, respectively. RESULTS We included 711 Crohn's disease (CD) and 764 ulcerative colitis (UC) patients who had not undergone surgery before 25(OH)D was measured. Both in CD and in UC patients, reduced 25(OH)D was associated with higher disease activity scores and CRP levels (p < 0.001). Severe 25(OH)D deficiency was associated with ileocolonic disease and complicated behavior in CD (p < 0.05) and was relevant to the disease extent in UC (p < 0.001). Additionally, severe 25(OH)D deficiency was associated with CMV colitis in patients with UC (p < 0.001). In multivariable analysis, severe deficiency of 25(OH)D was an independent risk factor for surgery in both CD (HR 1.93, 95% confidence interval [CI] 1.38-2.70) and UC (HR 2.77, 95% CI 1.14-6.74). CONCLUSION Severe 25(OH)D deficiency may be a marker of a more aggressive clinical course of IBD.
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Affiliation(s)
- Nam Seok Ham
- Department of Gastroenterology, University of Ulsan College of Medicine, Asan Medical Center, 88 Olympic-ro 43-gil, Songpa-gu, Seoul, 05505, Korea
| | - Sung Wook Hwang
- Department of Gastroenterology, University of Ulsan College of Medicine, Asan Medical Center, 88 Olympic-ro 43-gil, Songpa-gu, Seoul, 05505, Korea.
- Inflammatory Bowel Disease Center, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea.
| | - Eun Hye Oh
- Department of Gastroenterology, University of Ulsan College of Medicine, Asan Medical Center, 88 Olympic-ro 43-gil, Songpa-gu, Seoul, 05505, Korea
| | - Jeongseok Kim
- Department of Gastroenterology, University of Ulsan College of Medicine, Asan Medical Center, 88 Olympic-ro 43-gil, Songpa-gu, Seoul, 05505, Korea
| | - Ho-Su Lee
- Department of Biochemistry and Molecular Biology, University of Ulsan College of Medicine, Seoul, Korea
| | - Sang Hyoung Park
- Department of Gastroenterology, University of Ulsan College of Medicine, Asan Medical Center, 88 Olympic-ro 43-gil, Songpa-gu, Seoul, 05505, Korea
- Inflammatory Bowel Disease Center, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea
| | - Dong-Hoon Yang
- Department of Gastroenterology, University of Ulsan College of Medicine, Asan Medical Center, 88 Olympic-ro 43-gil, Songpa-gu, Seoul, 05505, Korea
| | - Byong Duk Ye
- Department of Gastroenterology, University of Ulsan College of Medicine, Asan Medical Center, 88 Olympic-ro 43-gil, Songpa-gu, Seoul, 05505, Korea
- Inflammatory Bowel Disease Center, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea
| | - Jeong-Sik Byeon
- Department of Gastroenterology, University of Ulsan College of Medicine, Asan Medical Center, 88 Olympic-ro 43-gil, Songpa-gu, Seoul, 05505, Korea
| | - Seung-Jae Myung
- Department of Gastroenterology, University of Ulsan College of Medicine, Asan Medical Center, 88 Olympic-ro 43-gil, Songpa-gu, Seoul, 05505, Korea
| | - Suk-Kyun Yang
- Department of Gastroenterology, University of Ulsan College of Medicine, Asan Medical Center, 88 Olympic-ro 43-gil, Songpa-gu, Seoul, 05505, Korea
- Inflammatory Bowel Disease Center, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea
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12
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Park SW, Lee YJ, Ryoo E. Difference in Vitamin D Levels Between Children with Clostridioides difficile Enteritis and Those with Other Acute Infectious Enteritis. Pediatr Gastroenterol Hepatol Nutr 2021; 24:81-89. [PMID: 33505897 PMCID: PMC7813570 DOI: 10.5223/pghn.2021.24.1.81] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/17/2020] [Revised: 09/02/2020] [Accepted: 09/19/2020] [Indexed: 11/14/2022] Open
Abstract
PURPOSE A steady increase in Clostridioides difficile enteritis (CDE) has been reported recently. CDE is associated with intestinal dysbiosis, and vitamin D receptors are known to play an important role in this microbial imbalance as immunological regulators. We investigated the difference in vitamin D levels between children with CDE and those with other acute infectious enteritis. METHODS This retrospective study was conducted on children below 18 years of age who visited the Gil hospital, underwent investigation to assess vitamin D levels, and had confirmed gastrointestinal infection between January 2015 and December 2018. Patients were divided into two groups: the "CDE group" (n=18) and the "other infectious enteritis group" (n=88); their clinical characteristics, other laboratory results, and vitamin D levels were analyzed. RESULTS There was no difference in gender, age, and seasonal distributions between the CDE and other infectious enteritis groups. Other laboratory results were not significantly different between two groups, excluding serum albumin level (4.52±0.45 g/dL vs. 4.31±0.28 g/dL, p=0.011). The mean 25-hydroxy vitamin D level in the CDE group was higher than that in the control group (18.75±8.11 ng/mL vs. 14.50±6.79 ng/mL, p=0.021). CONCLUSION Vitamin D levels in the CDE group were lower than normal but higher than the other infectious enteritis group. These results suggested that CDE has a different mechanism or susceptibility associated with vitamin D in children, and even marginal changes in vitamin D levels can act as a risk factor for infection.
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Affiliation(s)
- Sang Woo Park
- Department of Pediatrics, Gachon University Gil Medical Center, Incheon, Korea
| | - Young June Lee
- Department of Pediatrics, Gachon University Gil Medical Center, Incheon, Korea
| | - Eell Ryoo
- Department of Pediatrics, Gachon University Gil Medical Center, Incheon, Korea
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13
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Guevara MA, Lu J, Moore RE, Chambers SA, Eastman AJ, Francis JD, Noble KN, Doster RS, Osteen KG, Damo SM, Manning SD, Aronoff DM, Halasa NB, Townsend SD, Gaddy JA. Vitamin D and Streptococci: The Interface of Nutrition, Host Immune Response, and Antimicrobial Activity in Response to Infection. ACS Infect Dis 2020; 6:3131-3140. [PMID: 33170652 DOI: 10.1021/acsinfecdis.0c00666] [Citation(s) in RCA: 13] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
Streptococcus species are common causes of human infection. These Gram-positive, encapsulated bacterial pathogens infect diverse anatomic spaces, leading to infections including skin and soft tissue infection, endocarditis, pneumonia, meningitis, sinusitis, otitis media, chorioamnionitis, sepsis, and even death. Risk for streptococcal infection is highest in low- and middle-income countries where micronutrient deficiency is common. Epidemiological data reveal that vitamin D deficiency is associated with enhanced risk of streptococcal infection and cognate disease outcomes. Additionally, vitamin D improves antibacterial defenses by stimulating innate immune processes such as phagocytosis and enhancing production of reactive oxygen species (oxidative burst) and antimicrobial peptides (including cathelicidin and lactoferrin), which are important for efficient killing of bacteria. This review presents the most recent published work that studies interactions between the micronutrient vitamin D, the host immune system, and pathogenic streptococci as well as comparisons with other relevant infection models.
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Affiliation(s)
- Miriam A. Guevara
- Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee 37232, United States
| | - Jacky Lu
- Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee 37232, United States
| | - Rebecca E. Moore
- Department of Chemistry, Vanderbilt University, Nashville, Tennessee 37232, United States
| | - Schuyler A. Chambers
- Department of Chemistry, Vanderbilt University, Nashville, Tennessee 37232, United States
| | - Alison J. Eastman
- Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee 37232, United States
| | - Jamisha D. Francis
- Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee 37232, United States
| | - Kristen N. Noble
- Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee 37232, United States
| | - Ryan S. Doster
- Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee 37232, United States
| | - Kevin G. Osteen
- Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee 37232, United States
- Department of Veterans Affairs, Tennessee Valley Healthcare Systems, Nashville, Tennessee 37212, United States
- Department of Obstetrics and Gynecology, Vanderbilt University Medical Center, Nashville, Tennessee 37232, United States
| | - Steven M. Damo
- Department of Chemistry, Fisk University, Nashville, Tennessee 37208, United States
- Department of Biochemistry, Vanderbilt University, Nashville, Tennessee 37232, United States
| | - Shannon D. Manning
- Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan 48824, United States
| | - David M. Aronoff
- Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee 37232, United States
- Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee 37232, United States
- Department of Obstetrics and Gynecology, Vanderbilt University Medical Center, Nashville, Tennessee 37232, United States
| | - Natasha B. Halasa
- Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee 37232, United States
- Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee 37232, United States
- Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee 37232, United States
| | - Steven D. Townsend
- Department of Chemistry, Vanderbilt University, Nashville, Tennessee 37232, United States
| | - Jennifer A. Gaddy
- Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee 37232, United States
- Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee 37232, United States
- Department of Veterans Affairs, Tennessee Valley Healthcare Systems, Nashville, Tennessee 37212, United States
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Mishima Y, Ishihara S. Molecular Mechanisms of Microbiota-Mediated Pathology in Irritable Bowel Syndrome. Int J Mol Sci 2020; 21:ijms21228664. [PMID: 33212919 PMCID: PMC7698457 DOI: 10.3390/ijms21228664] [Citation(s) in RCA: 48] [Impact Index Per Article: 9.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/01/2020] [Revised: 11/12/2020] [Accepted: 11/13/2020] [Indexed: 02/07/2023] Open
Abstract
Irritable bowel syndrome (IBS) is one of the most prevalent functional gastrointestinal disorders, and accumulating evidence gained in both preclinical and clinical studies indicate the involvement of enteric microbiota in its pathogenesis. Gut resident microbiota appear to influence brain activity through the enteric nervous system, while their composition and function are affected by the central nervous system. Based on these results, the term “brain–gut–microbiome axis” has been proposed and enteric microbiota have become a potential therapeutic target in IBS cases. However, details regarding the microbe-related pathophysiology of IBS remain elusive. This review summarizes the existing knowledge of molecular mechanisms in the pathogenesis of IBS as well as recent progress related to microbiome-derived neurotransmitters, compounds, metabolites, neuroendocrine factors, and enzymes.
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Gayam V, Mandal AK, Ditah CM, Sidhu J, Konala VM, Adapa S, Naramala S, Garlapati P. Outcomes of Clostridioides difficile in Patients with Vitamin D Deficiency: A Propensity-Matched National Inpatient Sample Analysis. South Med J 2020; 113:593-599. [PMID: 33140114 DOI: 10.14423/smj.0000000000001168] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/23/2022]
Abstract
OBJECTIVES We aimed to determine in-hospital outcomes, length of hospital stay, and resource utilization in a contemporary cohort of Clostridioides difficile infection (CDI) and vitamin D deficiency (VDD). METHODS The National Inpatient Sample database for 2016 and 2017 was used for data analysis using International Classification of Diseases, Tenth Revision, Clinical Modification/Procedure Coding System (ICD-10-CM/PCS) codes to identify the patients with the principal diagnosis of CDI and VDD. We assessed the all-cause in-hospital mortality, morbidity, length of hospital stay (LOS), and total costs between propensity-matched groups of CDI without VDD versus CDI with VDD. RESULTS We identified 202,234 patients with CDI, 4515 of whom were patients with VDD and 197,719 of whom were without VDD. After propensity matching, there was no difference in the in-hospital mortality between the two groups (odds ratio [OR] 1.5, 95% confidence interval [CI] 0.58-4.3; P = 0.90). CDI with VDD has a higher odds of sepsis (OR 1.6, 95% CI 1.3-1.9; P = 0.0), and peritonitis (OR 1.6, 95% CI 1.4-3.8; P = 0.01). Mean LOS (5.9 ± 1.8 vs 5.4 ± 2, P < 0.01) and mean total charges ($11,500 vs $9971, P < 0.04) were higher in CDI with VDD. The factors affecting the LOS were acute coronary syndrome (P = 0.04), mechanical ventilation (P = 0.03), obesity (P = 0.004), acute kidney injury (P = 0.04), and sepsis (P = 0.05). CONCLUSIONS In this large cohort in a propensity-matched analysis, VDD does not increase the in-hospital mortality in CDI. VDD increases the odds of complications with a higher LOS and resource utilization. These findings may be clinically relevant to guide clinicians to routinely monitor vitamin D status and supplement in patients at risk of CDI.
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Affiliation(s)
- Vijay Gayam
- From the Department of Internal Medicine, Interfaith Medical Center, Brooklyn, New York, the Department of Internal Medicine, Division of Medical Oncology, Ashland Bellefonte Cancer Center, Ashland, Kentucky, the Division of Nephrology, The Nephrology Group, Fresno, California, and the Department of Internal Medicine, Division of Rheumatology, Adventist Medical Center, Hanford, California
| | - Amrendra Kumar Mandal
- From the Department of Internal Medicine, Interfaith Medical Center, Brooklyn, New York, the Department of Internal Medicine, Division of Medical Oncology, Ashland Bellefonte Cancer Center, Ashland, Kentucky, the Division of Nephrology, The Nephrology Group, Fresno, California, and the Department of Internal Medicine, Division of Rheumatology, Adventist Medical Center, Hanford, California
| | - Chobufo Muchi Ditah
- From the Department of Internal Medicine, Interfaith Medical Center, Brooklyn, New York, the Department of Internal Medicine, Division of Medical Oncology, Ashland Bellefonte Cancer Center, Ashland, Kentucky, the Division of Nephrology, The Nephrology Group, Fresno, California, and the Department of Internal Medicine, Division of Rheumatology, Adventist Medical Center, Hanford, California
| | - Jasdeep Sidhu
- From the Department of Internal Medicine, Interfaith Medical Center, Brooklyn, New York, the Department of Internal Medicine, Division of Medical Oncology, Ashland Bellefonte Cancer Center, Ashland, Kentucky, the Division of Nephrology, The Nephrology Group, Fresno, California, and the Department of Internal Medicine, Division of Rheumatology, Adventist Medical Center, Hanford, California
| | - Venu Madhav Konala
- From the Department of Internal Medicine, Interfaith Medical Center, Brooklyn, New York, the Department of Internal Medicine, Division of Medical Oncology, Ashland Bellefonte Cancer Center, Ashland, Kentucky, the Division of Nephrology, The Nephrology Group, Fresno, California, and the Department of Internal Medicine, Division of Rheumatology, Adventist Medical Center, Hanford, California
| | - Sreedhar Adapa
- From the Department of Internal Medicine, Interfaith Medical Center, Brooklyn, New York, the Department of Internal Medicine, Division of Medical Oncology, Ashland Bellefonte Cancer Center, Ashland, Kentucky, the Division of Nephrology, The Nephrology Group, Fresno, California, and the Department of Internal Medicine, Division of Rheumatology, Adventist Medical Center, Hanford, California
| | - Srikanth Naramala
- From the Department of Internal Medicine, Interfaith Medical Center, Brooklyn, New York, the Department of Internal Medicine, Division of Medical Oncology, Ashland Bellefonte Cancer Center, Ashland, Kentucky, the Division of Nephrology, The Nephrology Group, Fresno, California, and the Department of Internal Medicine, Division of Rheumatology, Adventist Medical Center, Hanford, California
| | - Pavani Garlapati
- From the Department of Internal Medicine, Interfaith Medical Center, Brooklyn, New York, the Department of Internal Medicine, Division of Medical Oncology, Ashland Bellefonte Cancer Center, Ashland, Kentucky, the Division of Nephrology, The Nephrology Group, Fresno, California, and the Department of Internal Medicine, Division of Rheumatology, Adventist Medical Center, Hanford, California
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16
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Chandrakumar A, Zohni H, El-Matary W. Clostridioides difficile Infection in Children With Inflammatory Bowel Disease. Inflamm Bowel Dis 2020; 26:1700-1706. [PMID: 31765471 DOI: 10.1093/ibd/izz285] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/08/2019] [Indexed: 12/17/2022]
Abstract
BACKGROUND The study's objective was to investigate the incidence and risk factors associated with Clostridioides difficile (previously known as Clostridium) infection (CDI) in children with inflammatory bowel disease (IBD) in the province of Manitoba. METHODS Our longitudinal population-based cohort was comprised of all children and young adults aged <17 years diagnosed with IBD in the Canadian province of Manitoba between 2011 and 2019. The diagnosis of CDI was confirmed based on the Triage C. difficile immunoassay and polymerase chain reaction assay to detect the presence of toxigenic C. difficile. The Fisher exact test was used to examine the relationship between categorical variables. A Cox regression model was used to estimate the risk of CDI development in IBD patients. RESULTS Among 261 children with IBD, 20 (7.7%) developed CDI with an incidence rate of 5.04 cases per 1000 person-years, and the median age at diagnosis (interquartile range) was 12.96 (9.33-15.81) years. The incidence rates of CDI among UC and CD patients were 4.16 cases per 1000 person-years and 5.88 cases per 1000 person-years, respectively (P = 0.46). Compared with children without CDI, those who had CDI were at increased risk of future exposure to systemic corticosteroids (adjusted hazard ratio [aHR], 4.38; 95% confidence interval [CI], 1.46-13.10) and anti-tumor necrosis factor (anti-TNF) biologics (aHR, 3.31; 95% CI, 1.11-9.90). The recurrence rate of CDI in our pediatric IBD population was 25%. CONCLUSIONS Our findings confirm that children with IBD are at high risk of developing CDI, which may predict future escalation of IBD therapy.
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Affiliation(s)
- Abin Chandrakumar
- Clinical Research Unit, Children's Hospital Research Institute of Manitoba, Winnipeg, MB, Canada
- Section of Pediatric Gastroenterology, Winnipeg Children's Hospital, Max Rady College of Medicine, Rady Faculty of Health Sciences and Children's Hospital Research Institute, Winnipeg, MB, Canada
| | - Hussein Zohni
- Section of Pediatric Gastroenterology, Winnipeg Children's Hospital, Max Rady College of Medicine, Rady Faculty of Health Sciences and Children's Hospital Research Institute, Winnipeg, MB, Canada
| | - Wael El-Matary
- Section of Pediatric Gastroenterology, Winnipeg Children's Hospital, Max Rady College of Medicine, Rady Faculty of Health Sciences and Children's Hospital Research Institute, Winnipeg, MB, Canada
- Max Rady College of Medicine, Rady Faculty of Health Sciences, Winnipeg, MB, Canada
- §Department of Pediatrics and Child Health, Max Rady College of Medicine, Rady Faculty of Health Sciences and Children's Hospital Research Institute, Winnipeg, MB, Canada
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17
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Palchaudhuri S, Albenberg L, Lewis JD. Diet Recommendations for Hospitalized Patients With Inflammatory Bowel Disease: Better Options Than Nil Per Os. CROHN'S & COLITIS 360 2020; 2:otaa059. [PMID: 33954288 PMCID: PMC8096188 DOI: 10.1093/crocol/otaa059] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
Hospitalizations are a time when providers often have uncertainty about what to feed patients with inflammatory bowel disease (IBD). While there are many trials evaluating the role of diet in the management of IBD, the role of diet for the hospitalized patient is less clear. The hospitalization may serve as an opportunity to educate patients about the role of diet, try different diets, and develop dietary recommendations for after discharge. Here, we review the literature for dietary considerations during hospitalizations and acute settings, as well as upon discharge. Patients with IBD benefit from screening and nutritional support for malnutrition and nutritional deficiencies. Enteral nutrition and exclusion diets are promising as induction and maintenance therapies, but no specific recommendations during hospitalization for adult patients are available currently. There are very few reasons to enforce bowel rest or clear liquids other than bowel obstruction, uncontrolled sepsis, or need for urgent or emergent surgery; most patients - including many with penetrating or stricturing disease - benefit from feeding in whichever capacity is tolerated, with enteral and parenteral nutrition used as needed to reach nutritional goals. Future studies are needed to define how the use of different diets can influence the outcomes of patients hospitalized for IBD.
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Affiliation(s)
- Sonali Palchaudhuri
- Division of Gastroenterology and Hepatology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA,Address correspondence to: Sonali Palchaudhuri, MD, Division of Gastroenterology, Perelman School of Medicine at the University of Pennsylvania, 3400 Civic Center Boulevard, Philadelphia, PA 19104 ()
| | - Lindsey Albenberg
- Division of Pediatric Gastroenterology, Hepatology, and Nutrition, The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania, USA
| | - James D Lewis
- Division of Gastroenterology and Hepatology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA
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18
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Garcia PM, Moore J, Kahan D, Hong MY. Effects of Vitamin D Supplementation on Inflammation, Colonic Cell Kinetics, and Microbiota in Colitis: A Review. Molecules 2020; 25:molecules25102300. [PMID: 32422882 PMCID: PMC7288056 DOI: 10.3390/molecules25102300] [Citation(s) in RCA: 12] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/16/2020] [Revised: 05/06/2020] [Accepted: 05/12/2020] [Indexed: 02/06/2023] Open
Abstract
Vitamin D is widely known to regulate bone health, but there is increasing evidence that it may also ameliorate colitis through inflammation, cell proliferation and apoptosis, and the microbiota. The purpose of this review is to systematically examine the mechanisms by which vitamin D reduces colitis. PubMed and Web of Science were searched for articles published between 2008 and 2019 using key words such as "vitamin D," "colitis," "inflammatory bowel disease," "inflammation," "apoptosis," "cell proliferation," and "gut bacteria". Retrieved articles were further narrowed and it was determined whether their title and abstracts contained terminology pertaining to vitamin D in relation to colitis in human clinical trials, animal studies, and cell culture/biopsy studies, as well as selecting the best match sorting option in relation to the research question. In total, 30 studies met the established criteria. Studies consistently reported results showing that vitamin D supplementation can downregulate inflammatory pathways of COX-2, TNF-α, NF-κB, and MAPK, modify cell kinetics, and alter gut microbiome, all of which contribute to an improved state of colitis. Although vitamin D and vitamin D analogs have demonstrated positive effects against colitis, more randomized, controlled human clinical trials are needed to determine the value of vitamin D as a therapeutic agent in the treatment of colitis.
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Abstract
PURPOSE OF REVIEW This article provides an updated review on the role of diet in the risk of developing Crohn's disease (CD) and CD management, areas of ongoing study. RECENT FINDINGS Higher intake of dietary fiber (fruit fiber) has been associated with a reduced risk for CD. The exclusive enteral nutrition (EEN) diet remains the most validated nutritional recommendation for inducing remission in CD. The specific carbohydrate diet (SCD) has demonstrated reductions in CD severity scores in conjunction with medical therapies, and larger trials on its efficacy are ongoing. Several new exclusion diets modeled after EEN and SCD have shown potential efficacy in smaller studies that warrant replication. There is a paucity of clear dietary recommendations for the reduction in risk of CD clinical relapse. There are various components of diet that likely impact risk for CD development and contribute to its disease course; however, studies are often limited in their size or ability to demonstrate mechanistic causation. Further studies including diets that aim to expand on the restrictive nature of EEN may lead to stronger evidence for a diet-based approach to CD management.
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Affiliation(s)
- Donald Goens
- Department of Internal Medicine, University of Chicago, Chicago, IL, USA
| | - Dejan Micic
- Department of Internal Medicine, Section of Gastroenterology, Hepatology and Nutrition, University of Chicago, Chicago, IL, 60637, USA.
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20
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Olmedo-Martín RV, González-Molero I, Olveira G, Amo-Trillo V, Jiménez-Pérez M. Vitamin D in Inflammatory Bowel Disease: Biological, Clinical and Therapeutic Aspects. Curr Drug Metab 2019; 20:390-398. [PMID: 31109269 DOI: 10.2174/1389200220666190520112003] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/17/2019] [Revised: 04/13/2019] [Accepted: 04/25/2019] [Indexed: 12/15/2022]
Abstract
BACKGROUND Vitamin D has an immunoregulatory action in Inflammatory Bowel Disease (IBD) as well as other immune-mediated disorders. Its influence on intestinal permeability, innate and adaptive immunity, and the composition and diversity of the microbiota contribute to the maintenance of intestinal homeostasis. Patients with IBD have a greater prevalence of vitamin D deficiency than the general population, and a possible association between this deficit and a worse course of the disease. However, intervention studies in patients with IBD have proved inconclusive. OBJECTIVE To review all the evidence concerning the role of vitamin D as an important factor in the pathophysiology of IBD, review the associations found between its deficiency and the prognosis of the disease, and draw conclusions for the practical application from the main intervention studies undertaken. METHODS Structured search and review of basic, epidemiological, clinical and intervention studies evaluating the influence of vitamin D in IBD, following the basic principles of scientific data. RESULTS Vitamin D deficiency is associated with disease activity, quality of life, the consumption of social and healthcare resources, and the durability of anti-TNFα biological treatment. Determination of new metabolites of vitamin D, measurement of its absorption capacity and questionnaires about sun exposure could help identify groups of IBD patients with a special risk of vitamin D deficiency. CONCLUSION Well-designed intervention studies are needed in IBD, with probably higher objective plasma doses of vitamin D to establish its efficacy as a therapeutic agent with immunomodulatory properties. Meanwhile, vitamin D deficiency should be screened for and corrected in affected patients in order to achieve adequate bone and phosphocalcic metabolism.
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Affiliation(s)
- Raúl Vicente Olmedo-Martín
- Clinical Management Unit of Digestive Diseases, Regional University Hospital of Malaga, Malaga, Spain; Faculty of Medicine, University of Malaga, Malaga, Spain.,Institute of Biomedical Research in Malaga (IBIMA), Malaga, Spain
| | - Inmaculada González-Molero
- Clinical Management Unit of Endocrinology and Nutrition, Regional University Hospital of Malaga; Institute of Biomedical Research in Malaga (IBIMA), Malaga, Spain; Faculty of Medicine, University of Malaga; CIBERDEM, Malaga, Spain
| | - Gabriel Olveira
- Clinical Management Unit of Endocrinology and Nutrition, Regional University Hospital of Malaga; Institute of Biomedical Research in Malaga (IBIMA), Malaga, Spain; Faculty of Medicine, University of Malaga; CIBERDEM, Malaga, Spain
| | - Víctor Amo-Trillo
- Clinical Management Unit of Digestive Diseases, Regional University Hospital of Malaga, Malaga, Spain; Faculty of Medicine, University of Malaga, Malaga, Spain.,Institute of Biomedical Research in Malaga (IBIMA), Malaga, Spain
| | - Miguel Jiménez-Pérez
- Clinical Management Unit of Digestive Diseases, Regional University Hospital of Malaga, Malaga, Spain; Faculty of Medicine, University of Malaga, Malaga, Spain.,Institute of Biomedical Research in Malaga (IBIMA), Malaga, Spain
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21
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Naderpoor N, Mousa A, Fernanda Gomez Arango L, Barrett HL, Dekker Nitert M, de Courten B. Effect of Vitamin D Supplementation on Faecal Microbiota: A Randomised Clinical Trial. Nutrients 2019; 11:nu11122888. [PMID: 31783602 PMCID: PMC6950585 DOI: 10.3390/nu11122888] [Citation(s) in RCA: 50] [Impact Index Per Article: 8.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/20/2019] [Revised: 11/20/2019] [Accepted: 11/25/2019] [Indexed: 12/14/2022] Open
Abstract
In animal studies, vitamin D supplementation has been shown to improve gut microbiota and intestinal inflammation. However, limited evidence exists on the effect of vitamin D supplementation on the human gut microbiota. We examined the effect of vitamin D supplementation on faecal microbiota in 26 vitamin D-deficient (25-hydroxyvitamin D (25(OH)D) ≤50 nmol/L), overweight or obese (BMI ≥25 kg/m2) otherwise healthy adults. Our study was ancillary to a community based double-blind randomised clinical trial, conducted between 2014 and 2016. The participants provided stool samples at baseline and after 100,000 international units (IU) loading dose of cholecalciferol followed by 4000 IU daily or matching placebo for 16 weeks. Faecal microbiota was analysed using 16S rRNA sequencing; V6-8 region. There was no significant difference in microbiome α-diversity between vitamin D and placebo groups at baseline and follow-up (all p > 0.05). In addition, no clustering was found based on vitamin D supplementation at follow-up (p = 0.3). However, there was a significant association between community composition and vitamin D supplementation at the genus level (p = 0.04). The vitamin D group had a higher abundance of genus Lachnospira, and lower abundance of genus Blautia (linear discriminate analysis >3.0). Moreover, individuals with 25(OH)D >75 nmol/L had a higher abundance of genus Coprococcus and lower abundance of genus Ruminococcus compared to those with 25(OH)D <50 nmol/L. Our findings suggest that vitamin D supplementation has some distinct effects on faecal microbiota. Future studies need to explore whether these effects would translate into improved clinical outcomes.
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Affiliation(s)
- Negar Naderpoor
- Monash Centre for Health Research and Implementation, School of Public Health and Preventive Medicine, Monash University, Clayton, VIC 3168 Australia
- Diabetes and Vascular Medicine Unit, Monash Health, Clayton, VIC 3168, Australia
| | - Aya Mousa
- Monash Centre for Health Research and Implementation, School of Public Health and Preventive Medicine, Monash University, Clayton, VIC 3168 Australia
| | | | - Helen L. Barrett
- Mater Research Institute, The University of Queensland, South Brisbane, QLD 4101, Australia
- Department of Endocrinology, Mater Health, South Brisbane, QLD 4101, Australia
| | - Marloes Dekker Nitert
- School of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, QLD 4101, Australia
- Mater Research Institute, The University of Queensland, South Brisbane, QLD 4101, Australia
| | - Barbora de Courten
- Monash Centre for Health Research and Implementation, School of Public Health and Preventive Medicine, Monash University, Clayton, VIC 3168 Australia
- Diabetes and Vascular Medicine Unit, Monash Health, Clayton, VIC 3168, Australia
- Correspondence: ; Tel.: +61-3-857-22651; Fax: +61-3-9594-7554
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22
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Sood A, Ahuja V, Kedia S, Midha V, Mahajan R, Mehta V, Sudhakar R, Singh A, Kumar A, Puri AS, Tantry BV, Thapa BR, Goswami B, Behera BN, Ye BD, Bansal D, Desai D, Pai G, Yattoo GN, Makharia G, Wijewantha HS, Venkataraman J, Shenoy KT, Dwivedi M, Sahu MK, Bajaj M, Abdullah M, Singh N, Singh N, Abraham P, Khosla R, Tandon R, Misra SP, Nijhawan S, Sinha SK, Bopana S, Krishnaswamy S, Joshi S, Singh SP, Bhatia S, Gupta S, Bhatia S, Ghoshal UC. Diet and inflammatory bowel disease: The Asian Working Group guidelines. Indian J Gastroenterol 2019; 38:220-246. [PMID: 31352652 PMCID: PMC6675761 DOI: 10.1007/s12664-019-00976-1] [Citation(s) in RCA: 31] [Impact Index Per Article: 5.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/08/2019] [Accepted: 05/17/2019] [Indexed: 02/06/2023]
Abstract
INTRODUCTION These Asian Working Group guidelines on diet in inflammatory bowel disease (IBD) present a multidisciplinary focus on clinical nutrition in IBD in Asian countries. METHODOLOGY The guidelines are based on evidence from existing published literature; however, if objective data were lacking or inconclusive, expert opinion was considered. The conclusions and 38 recommendations have been subject to full peer review and a Delphi process in which uniformly positive responses (agree or strongly agree) were required. RESULTS Diet has an important role in IBD pathogenesis, and an increase in the incidence of IBD in Asian countries has paralleled changes in the dietary patterns. The present consensus endeavors to address the following topics in relation to IBD: (i) role of diet in the pathogenesis; (ii) diet as a therapy; (iii) malnutrition and nutritional assessment of the patients; (iv) dietary recommendations; (v) nutritional rehabilitation; and (vi) nutrition in special situations like surgery, pregnancy, and lactation. CONCLUSIONS Available objective data to guide nutritional support and primary nutritional therapy in IBD are presented as 38 recommendations.
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Affiliation(s)
- Ajit Sood
- Department of Gastroenterology, Dayanand Medical College and Hospital, Ludhiana, 141 001, India.
| | - Vineet Ahuja
- Department of Gastroenterology, All India Institute of Medical Sciences, New Delhi, 110 023, India
| | - Saurabh Kedia
- Department of Gastroenterology, All India Institute of Medical Sciences, New Delhi, 110 023, India
| | - Vandana Midha
- Department of Internal Medicine, Dayanand Medical College and Hospital, Ludhiana, 141 001, India
| | - Ramit Mahajan
- Department of Gastroenterology, Dayanand Medical College and Hospital, Ludhiana, 141 001, India
| | - Varun Mehta
- Department of Gastroenterology, Dayanand Medical College and Hospital, Ludhiana, 141 001, India
| | - Ritu Sudhakar
- Department of Dietetics, Dayanand Medical College and Hospital, Ludhiana, 141 001, India
| | - Arshdeep Singh
- Department of Gastroenterology, Dayanand Medical College and Hospital, Ludhiana, 141 001, India
| | - Ajay Kumar
- BLK Super Speciality Hospital, New Delhi, 110 005, India
| | | | | | - Babu Ram Thapa
- Department of Gastroenterology Postgraduate Institute of Medical Education and Research, Chandigarh, 160 012, India
| | - Bhabhadev Goswami
- Department of Gastroenterology, Gauhati Medical College, Guwahati, 781 032, India
| | - Banchha Nidhi Behera
- Department of Dietetics, Postgraduate Institute of Medical Education and Research, Chandigarh, 160 012, India
| | - Byong Duk Ye
- Department of Gastroenterology, Asan Medical Center, Seoul, South Korea
| | - Deepak Bansal
- Consultant Gastroenterology, Bathinda, 151 001, India
| | - Devendra Desai
- P. D. Hinduja Hospital and Medical Research Centre, Mumbai, 400 016, India
| | - Ganesh Pai
- Department of Gastroenterology, Kasturba Medical College, Manipal, 576 104, India
| | | | - Govind Makharia
- Department of Gastroenterology, All India Institute of Medical Sciences, New Delhi, 110 023, India
| | | | | | - K T Shenoy
- Department of Gastroenterology, Sree Gokulum Medical College and Research Foundation, Trivandrum, 695 011, India
| | - Manisha Dwivedi
- Department of Gastroenterology, Moti Lal Nehru Medical College, Allahabad, 211 001, India
| | - Manoj Kumar Sahu
- Department of Gastroenterology, IMS and Sum Hospital, Bhubaneswar, 756 001, India
| | | | - Murdani Abdullah
- Department of Internal Medicine, Faculty of Medicine Universitas Indonesia, Dr. Cipto Mangunkusumo General Hospital, Jakarta, Indonesia
| | - Namrata Singh
- Department of Gastroenterology and Human Nutrition, All India Institute of Medical Sciences, New Delhi, 110 023, India
| | - Neelanjana Singh
- Dietician, Pushpawati Singhania Research Institute, New Delhi, 110 001, India
| | - Philip Abraham
- P D Hinduja Hospital and Medical Research Centre, Veer Savarkar Marg, Cadel Road, Mahim, Mumbai, 400 016, India
| | - Rajiv Khosla
- Max Super Speciality Hospital, Saket, New Delhi, 110 017, India
| | - Rakesh Tandon
- Pushpawati Singhania Research Institute, New Delhi, 110 001, India
| | - S P Misra
- Department of Gastroenterology, Moti Lal Nehru Medical College, Allahabad, 211 001, India
| | - Sandeep Nijhawan
- Department of Gastroenterology, SMS Medical College, Jaipur, 302 004, India
| | - Saroj Kant Sinha
- Department of Gastroenterology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160 012, India
| | - Sawan Bopana
- Fortis Hospital, Vasant Kunj, New Delhi, 110 070, India
| | | | - Shilpa Joshi
- Dietician, Mumbai Diet and Health Centre, Mumbai, 400 001, India
| | - Shivram Prasad Singh
- Department of Gastroenterology, Sriram Chandra Bhanj Medical College and Hospital, Cuttack, 753 001, India
| | - Shobna Bhatia
- Department of Gastroenterology, King Edward Memorial Hospital, Mumbai, 400 012, India
| | - Sudhir Gupta
- Shubham Gastroenterology Centre, Nagpur, 440 001, India
| | - Sumit Bhatia
- Consultant Gastroenterology, Medanta The Medicity, Gurgaon, 122 001, India
| | - Uday Chand Ghoshal
- Department of Gastroenterology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, 226 014, India
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23
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Balram B, Battat R, Al-Khoury A, D'Aoust J, Afif W, Bitton A, Lakatos PL, Bessissow T. Risk Factors Associated with Clostridium difficile Infection in Inflammatory Bowel Disease: A Systematic Review and Meta-Analysis. J Crohns Colitis 2019; 13:27-38. [PMID: 30247650 DOI: 10.1093/ecco-jcc/jjy143] [Citation(s) in RCA: 42] [Impact Index Per Article: 7.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
BACKGROUND AND AIM Clostridium difficile infection [CDI] is a significant concern in inflammatory bowel disease [IBD]. Risk factors and consequences associated with CDI in inflammatory bowel disease [IBD] patients are important to characterize. The aim of this research was to perform a systematic review and meta-analysis on risk factors and outcomes associated with CDI in IBD patients. METHODS Multiple databases were searched for studies investigating risk factors, colectomy and mortality risk in IBD patients with and without CDI. This was stratified by short [<3 months] and long-term [>1 year] outcomes. Summary estimates were calculated using a random-effects model. Quality assessment used the Newcastle-Ottawa scale. RESULTS Twenty-two studies met inclusion criteria. Antibiotics use within 30 days of diagnosis was associated with CDIs (odds ratio [OR]: 1.85, 95% confidence interval [CI]:1.36, 2.52). Colonic involvement in Crohn's disease patients was associated with significantly higher CDI rates [OR: 2.76, 95% CI: 1.75, 4.35]. There was a significant association between biologic medication use and CDI [OR: 1.65, 95% CI: 1.18, 2.30], with minimal heterogeneity [I2 = 4.0%]. The long-term colectomy risk was significantly higher for IBD patients with CDI compared with that for IBD patients without CDI [OR: 2.22, 95% CI: 1.17, 4.18]. Significantly higher mortality was found for CDI in IBD patients both short-term [OR: 3.84, 95% CI: 2.62, 5.61] and long-term [OR: 3.65, 95% CI: 1.58, 8.44]. Substantial heterogeneity existed. Most studies were of moderate quality. CONCLUSION Colonic involvement, and biologic and antibiotic use appear to be risk factors associated with CDI among IBD patients. CDI is associated with increased short- and long-term mortality.
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Affiliation(s)
- Bhairavi Balram
- Department of Internal Medicine, McGill University Health Center, Montreal, QC, Canada
| | - Robert Battat
- Division of Gastroenterology, Montreal General Hospital, McGill University Health Center, Montreal, QC, Canada.,Division of Gastroenterology, Jewish General Hospital, Ch. de la Côte-Sainte-Catherine, Montreal, QC, Canada
| | - Alex Al-Khoury
- Department of Internal Medicine, McGill University Health Center, Montreal, QC, Canada
| | - Julie D'Aoust
- Department of Internal Medicine, McGill University Health Center, Montreal, QC, Canada
| | - Waqqas Afif
- Division of Gastroenterology, Montreal General Hospital, McGill University Health Center, Montreal, QC, Canada
| | - Alain Bitton
- Division of Gastroenterology, Montreal General Hospital, McGill University Health Center, Montreal, QC, Canada
| | - Peter L Lakatos
- Division of Gastroenterology, Montreal General Hospital, McGill University Health Center, Montreal, QC, Canada.,First Department of Medicine, Semmelweis University, Budapest, Hungary
| | - Talat Bessissow
- Division of Gastroenterology, Montreal General Hospital, McGill University Health Center, Montreal, QC, Canada
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24
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Vitamin D: Nutrient, Hormone, and Immunomodulator. Nutrients 2018; 10:nu10111656. [PMID: 30400332 PMCID: PMC6266123 DOI: 10.3390/nu10111656] [Citation(s) in RCA: 465] [Impact Index Per Article: 66.4] [Reference Citation Analysis] [Abstract] [Key Words] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/24/2018] [Revised: 10/24/2018] [Accepted: 10/31/2018] [Indexed: 12/15/2022] Open
Abstract
The classical functions of vitamin D are to regulate calcium-phosphorus homeostasis and control bone metabolism. However, vitamin D deficiency has been reported in several chronic conditions associated with increased inflammation and deregulation of the immune system, such as diabetes, asthma, and rheumatoid arthritis. These observations, together with experimental studies, suggest a critical role for vitamin D in the modulation of immune function. This leads to the hypothesis of a disease-specific alteration of vitamin D metabolism and reinforces the role of vitamin D in maintaining a healthy immune system. Two key observations validate this important non-classical action of vitamin D: first, vitamin D receptor (VDR) is expressed by the majority of immune cells, including B and T lymphocytes, monocytes, macrophages, and dendritic cells; second, there is an active vitamin D metabolism by immune cells that is able to locally convert 25(OH)D3 into 1,25(OH)2D3, its active form. Vitamin D and VDR signaling together have a suppressive role on autoimmunity and an anti-inflammatory effect, promoting dendritic cell and regulatory T-cell differentiation and reducing T helper Th 17 cell response and inflammatory cytokines secretion. This review summarizes experimental data and clinical observations on the potential immunomodulating properties of vitamin D.
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25
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Abstract
Inflammatory bowel disease [IBD], including ulcerative colitis and Crohn's disease, is a chronic and unpredictable condition characterised by alternating periods of remission interspersed with relapses. In recent years, accumulating support for an immunomodulating effect of vitamin D on both the innate and the adaptive immune systems has been presented. Through the vitamin D receptor, the active form of vitamin D, 1,25[OH]2D, induces antimicrobial peptide secretion, decreases dendritic cell activity, and promotes Th2 and regulatory T cell development and activity. In addition, vitamin D promotes an increased ratio of anti-inflammatory cytokines to pro-inflammatory cytokines. Studies in IBD point to a role for vitamin D in ameliorating disease outcome. Suboptimal circulating levels of 25-hydroxyvitamin D are common in IBD and appear to be associated with an increased risk of flares, IBD-related hospitalisations and surgeries, an inadequate response to tumour necrosis factor [TNF] inhibitors, a deterioration in quality of life, and low bone mineral density. With only few available randomised double-blind, placebo-controlled studies investigating therapeutic effects of vitamin D related to IBD, further research is necessary to determine the true therapeutic potential of vitamin D, as well as to define its optimal range in serum to achieve and maintain quiescence of disease. This review aims to summarise the latest knowledge on the extraskeletal effects of vitamin D in IBD, and outlines the potential deleterious consequences of vitamin D deficiency in this patient cohort.
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Affiliation(s)
- Ole Haagen Nielsen
- Department of Gastroenterology, Herlev Hospital, University of Copenhagen, Copenhagen, Denmark
| | - Lars Rejnmark
- Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark
| | - Alan C Moss
- Department of Medicine, Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard University, Boston, MA, USA
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26
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Jain M, Venkataraman J. Vitamin D levels in ulcerative colitis at first diagnosis: Does it "bell the cat"? Indian J Gastroenterol 2018; 37:276-277. [PMID: 29855855 DOI: 10.1007/s12664-018-0853-x] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/04/2023]
Affiliation(s)
- Mayank Jain
- Department of Gastroenterology, Gleneagles Global Health City, 439, Cheran Nagar, Chennai, 600 100, India.
| | - Jayanthi Venkataraman
- Department of Gastroenterology, Gleneagles Global Health City, 439, Cheran Nagar, Chennai, 600 100, India
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27
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Li Y, Xu H, Xu T, Xiao M, Tang H, Wu D, Tan B, Li J, Yang H, Lv H, Xu Y, Qian J. Case-Control Study of Inflammatory Bowel Disease Patients with and without Clostridium difficile Infection and Poor Outcomes in Patients Coinfected with C. difficile and Cytomegalovirus. Dig Dis Sci 2018; 63:3074-3083. [PMID: 30094621 PMCID: PMC6182452 DOI: 10.1007/s10620-018-5230-1] [Citation(s) in RCA: 17] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/04/2018] [Accepted: 07/30/2018] [Indexed: 12/18/2022]
Abstract
BACKGROUND AND AIMS Clostridium difficile infection (CDI) incidence and risk factors in patients with inflammatory bowel disease (IBD) have been extensively studied. However, data describing CDI in Chinese patients with IBD are limited. We investigated the cumulative incidence, risk factors, and outcomes of CDI in Chinese IBD patients. METHODS We conducted a retrospective, case-control study of patients hospitalized with IBD and CDI at Peking Union Medical College Hospital from January 2010 to December 2015. CDI was diagnosed based on the presence of active symptoms and positive enzyme immunoassay-based stool test results for C. difficile toxin A or B (CDAB). Controls were selected from CDAB-negative patients with IBD and matched by age, gender, phenotypes of IBD and the same time period of CDAB testing at a 1:2 or 1:3 ratio. RESULTS We identified 60 (7.41%) cases of CDI among 810 patients with IBD, and 137 control cases were selected. Univariate analysis revealed that IBD patients with CDI had higher rates of concurrent corticosteroid use, proton pump inhibitor, antibiotic use, recent hospitalization, parenteral nutrition support, and cytomegalovirus (CMV) coinfection (P < 0.05). Multivariate analysis revealed that concurrent corticosteroid use (odds ratio [OR] = 6.803, 95% confidence interval [CI] = 2.901-15.954, P < 0.001) and hospitalization within 1 month (OR = 3.028, 95% CI = 1.225-7.480, P = 0.016) were associated with CDI. CMV and C. difficile coinfection (hazard ratio [HR] = 4.185, 95% CI = 1.492-11.736, P = 0.007) as well as disease severity (HR 2.070, 95% CI = 1.006-4.261, P = 0.048) were independently associated with colectomy following CDI. CONCLUSIONS IBD patients with concurrent corticosteroid use and recent hospitalization are at a higher risk of CDI. CMV and C. difficile coinfection is associated with poorer outcomes.
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Affiliation(s)
- Yue Li
- 0000 0001 0662 3178grid.12527.33Department of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, No. 1 Shuaifuyuan, Dongcheng District, Beijing, 100730 China
| | - Hui Xu
- 0000 0001 0662 3178grid.12527.33Department of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, No. 1 Shuaifuyuan, Dongcheng District, Beijing, 100730 China
| | - Tao Xu
- 0000 0001 0662 3178grid.12527.33Department of Epidemiology and Biostatistics, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China
| | - Meng Xiao
- 0000 0001 0662 3178grid.12527.33Department of Clinical Laboratory, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China
| | - Hao Tang
- 0000 0001 0662 3178grid.12527.33Department of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, No. 1 Shuaifuyuan, Dongcheng District, Beijing, 100730 China
| | - Dong Wu
- 0000 0001 0662 3178grid.12527.33Department of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, No. 1 Shuaifuyuan, Dongcheng District, Beijing, 100730 China
| | - Bei Tan
- 0000 0001 0662 3178grid.12527.33Department of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, No. 1 Shuaifuyuan, Dongcheng District, Beijing, 100730 China
| | - Ji Li
- 0000 0001 0662 3178grid.12527.33Department of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, No. 1 Shuaifuyuan, Dongcheng District, Beijing, 100730 China
| | - Hong Yang
- 0000 0001 0662 3178grid.12527.33Department of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, No. 1 Shuaifuyuan, Dongcheng District, Beijing, 100730 China
| | - Hong Lv
- 0000 0001 0662 3178grid.12527.33Department of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, No. 1 Shuaifuyuan, Dongcheng District, Beijing, 100730 China
| | - Yingchun Xu
- 0000 0001 0662 3178grid.12527.33Department of Clinical Laboratory, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China
| | - Jiaming Qian
- 0000 0001 0662 3178grid.12527.33Department of Gastroenterology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, No. 1 Shuaifuyuan, Dongcheng District, Beijing, 100730 China
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Abstract
There are many mechanisms to explain how food may drive and ameliorate inflammation. Although there are no consistent macronutrient associations inflammatory bowel disease (IBD) development, many exclusion diets have been described: IgG-4 guided exclusion diet; semivegetarian diet; low-fat, fiber-limited exclusion diet; Paleolithic diet; Maker's diet; vegan diet; Life without Bread diet; exclusive enteral nutrition (EEN), the Specific Carbohydrate Diet (SCD) and the low FODMAP diet. The literature on diet and IBD is reviewed with a particular focus on EEN, SCD, and low FODMAP diets. Lessons learned from the existing observations and strengths and shortcomings of existing data are presented.
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29
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Lasting Impact of Clostridium difficile Infection in Inflammatory Bowel Disease: A Propensity Score Matched Analysis. Inflamm Bowel Dis 2017; 23:2180-2188. [PMID: 29084081 PMCID: PMC5685936 DOI: 10.1097/mib.0000000000001251] [Citation(s) in RCA: 17] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]
Abstract
BACKGROUND Patients with inflammatory bowel disease are at an increased risk of Clostridium difficile infection (CDI), but the impact of CDI on disease severity is unclear. The aim of this study was to determine the effect of CDI on long-term disease outcome in a matched cohort of patients with inflammatory bowel disease. METHODS Patients who tested positive for infection formed the CDI-positive group. We generated a 1:2 propensity matched case to control cohort based on risk factors for CDI in the year before infection. Health care utilization data (emergency department use, hospitalizations, and telephone encounters), medications, laboratories, disease activity, and quality-of-life metrics were compared by CDI status. RESULTS A total of 198 patients (66 CDI and 132 matched controls) were included (56.6% women; 60.1% Crohn's disease, and 39.9% ulcerative colitis). In the year of infection, having CDI was significantly associated with more steroid and antibiotic exposure, elevated C-reactive protein or erythrocyte sedimentation rate, low vitamin D, increased disease activity, worse quality of life, and increased health care utilization (all P < 0.01). During the next year after infection, patients with CDI continued to have increased exposure to CDI-targeted antibiotics (P < 0.001) and other antibiotics (P = 0.02). They also continued to have more clinic visits (P = 0.02), telephone encounters (P = 0.001), and increased health care financial charges (P = 0.001). CONCLUSIONS CDI in inflammatory bowel disease is significantly associated with markers of disease severity, increased health care utilization and poor quality of life during the year of infection, and a 5-fold increase in health care charges in the year after infection (see Video Abstract, Supplemental Digital Content, http://links.lww.com/IBD/B658).
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30
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D’Aoust J, Battat R, Bessissow T. Management of inflammatory bowel disease with Clostridium difficile infection. World J Gastroenterol 2017; 23:4986-5003. [PMID: 28785153 PMCID: PMC5526769 DOI: 10.3748/wjg.v23.i27.4986] [Citation(s) in RCA: 54] [Impact Index Per Article: 6.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/24/2017] [Revised: 05/16/2017] [Accepted: 06/19/2017] [Indexed: 02/06/2023] Open
Abstract
AIM To address the management of Clostridium difficile (C. difficile) infection (CDI) in the setting of suspected inflammatory bowel disease (IBD)-flare.
METHODS A systematic search of the Ovid MEDLINE and EMBASE databases by independent reviewers identified 70 articles including a total of 932141 IBD patients or IBD-related hospitalizations.
RESULTS In those with IBD, CDI is associated with increased morbidity, including subsequent escalation in IBD medical therapy, urgent colectomy and increased hospitalization, as well as excess mortality. Vancomycin-containing regimens are effective first-line therapies for CDI in IBD inpatients. No prospective data exists with regards to the safety or efficacy of initiating or maintaining corticosteroid, immunomodulator, or biologic therapy to treat IBD in the setting of CDI. Corticosteroid use is a risk factor for the development of CDI, while immunomodulators and biologics are not.
CONCLUSION Strong recommendations regarding when to initiate IBD specific therapy in those with CDI are precluded by a lack of evidence. However, based on expert opinion and observational data, initiation or resumption of immunosuppressive therapy after 48-72 h of targeted antibiotic treatment for CDI may be considered.
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31
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Burke KE, Boumitri C, Ananthakrishnan AN. Modifiable Environmental Factors in Inflammatory Bowel Disease. Curr Gastroenterol Rep 2017; 19:21. [PMID: 28397132 PMCID: PMC5651146 DOI: 10.1007/s11894-017-0562-0] [Citation(s) in RCA: 23] [Impact Index Per Article: 2.9] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 04/11/2023]
Abstract
PURPOSE OF REVIEW Environmental factors may influence predisposition to develop inflammatory bowel diseases (Crohn's disease, ulcerative colitis) or alter its natural history by modification of both the host immune response and intestinal microbial composition. The purpose of this review is to translate such evidence into clinical practice by a focus on interventional studies that have modified such environmental influences to improve disease outcomes. RECENT FINDINGS Several environmental influences have been identified in the recent literature including tobacco use, diet, antibiotics, vitamin D deficiency, stress, appendectomy, and oral contraceptive use. Some risk factors have similar influences on both Crohn's disease and ulcerative colitis while others are disease-specific or have divergent effects. Emerging epidemiologic evidence has confirmed the association of many of these factors with incident disease using prospective data. In addition, laboratory data has supported their mechanistic plausibility and relevance to intestinal inflammation.
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Affiliation(s)
- Kristin E Burke
- Division of Gastroenterology, Massachusetts General Hospital, Boston, USA
| | - Christine Boumitri
- Division of Gastroenterology, University of Missouri-Columbia, Columbia, USA
| | - Ashwin N Ananthakrishnan
- Division of Gastroenterology, Massachusetts General Hospital, Boston, USA.
- Massachusetts General Hospital Crohn's and Colitis Center, 165 Cambridge Street, 9th Floor, Boston, MA, 02114, USA.
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Law CCY, Tariq R, Khanna S, Murthy S, McCurdy JD. Systematic review with meta-analysis: the impact of Clostridium difficile infection on the short- and long-term risks of colectomy in inflammatory bowel disease. Aliment Pharmacol Ther 2017; 45:1011-1020. [PMID: 28206678 DOI: 10.1111/apt.13972] [Citation(s) in RCA: 20] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/07/2016] [Revised: 10/18/2016] [Accepted: 01/16/2017] [Indexed: 12/12/2022]
Abstract
BACKGROUND Clostridium difficile infection (CDI) is associated with increased mortality in inflammatory bowel disease (IBD), but the risk of colectomy is variable and has not been adequately studied. AIM To perform a systematic review and meta-analysis to assess the impact of CDI on colectomy risk in IBD. METHODS Multiple databases were searched systematically for observational studies reporting colectomy risk in IBD, stratified by the presence of CDI, and the duration of follow-up (short term 3 months, and long term at least 1 year). Weighted summary estimates were calculated using generalised inverse variance with random-effects model. Study quality was assessed using the Newcastle-Ottawa scale. RESULTS Twelve observational studies were identified and included 35 057 IBD patients with CDI, and 929 259 without CDI. CDI did not increase the short-term colectomy risk in IBD patients overall (10 studies) (OR: 1.35; 95% CI: 0.68-2.67), or in patients with ulcerative colitis (nine studies) (OR: 1.20; 95% CI: 0.39-3.76). In contrast, CDI was associated with higher long-term colectomy risk in patients with IBD overall (five studies) (OR: 2.23; 95% CI: 1.18-4.21), and in patients with ulcerative colitis (four studies) (OR: 2.96; 95% CI: 1.19-7.34). The results were stable in subgroups stratified by recruitment period, hospitalisation status and geographical location. All studies were at least of moderate quality. The results were limited in the ability to compare IBD severity and the type of anti-microbial therapy. CONCLUSION Based on 12 observational studies with at least moderate quality, Clostridium difficile infection appears to increase colectomy risk in IBD in the long- but not short- term.
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Affiliation(s)
- C C Y Law
- Division of Gastroenterology and Hepatology, The Ottawa Hospital, Ottawa, ON, Canada
| | - R Tariq
- Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN, USA
| | - S Khanna
- Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN, USA
| | - S Murthy
- Division of Gastroenterology and Hepatology, The Ottawa Hospital, Ottawa, ON, Canada
| | - J D McCurdy
- Division of Gastroenterology and Hepatology, The Ottawa Hospital, Ottawa, ON, Canada
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Vitamin D Levels and Outcomes in Inflammatory Bowel Disease-Which is the Chicken and Which is the Egg? Clin Gastroenterol Hepatol 2017; 15:247-248. [PMID: 27825894 DOI: 10.1016/j.cgh.2016.11.001] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/31/2016] [Accepted: 11/01/2016] [Indexed: 02/07/2023]
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Forbes A, Escher J, Hébuterne X, Kłęk S, Krznaric Z, Schneider S, Shamir R, Stardelova K, Wierdsma N, Wiskin AE, Bischoff SC. ESPEN guideline: Clinical nutrition in inflammatory bowel disease. Clin Nutr 2016; 36:321-347. [PMID: 28131521 DOI: 10.1016/j.clnu.2016.12.027] [Citation(s) in RCA: 414] [Impact Index Per Article: 46.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/21/2016] [Accepted: 12/28/2016] [Indexed: 12/14/2022]
Abstract
INTRODUCTION The ESPEN guideline presents a multidisciplinary focus on clinical nutrition in inflammatory bowel disease (IBD). METHODOLOGY The guideline is based on extensive systematic review of the literature, but relies on expert opinion when objective data were lacking or inconclusive. The conclusions and 64 recommendations have been subject to full peer review and a Delphi process in which uniformly positive responses (agree or strongly agree) were required. RESULTS IBD is increasingly common and potential dietary factors in its aetiology are briefly reviewed. Malnutrition is highly prevalent in IBD - especially in Crohn's disease. Increased energy and protein requirements are observed in some patients. The management of malnutrition in IBD is considered within the general context of support for malnourished patients. Treatment of iron deficiency (parenterally if necessary) is strongly recommended. Routine provision of a special diet in IBD is not however supported. Parenteral nutrition is indicated only when enteral nutrition has failed or is impossible. The recommended perioperative management of patients with IBD undergoing surgery accords with general ESPEN guidance for patients having abdominal surgery. Probiotics may be helpful in UC but not Crohn's disease. Primary therapy using nutrition to treat IBD is not supported in ulcerative colitis, but is moderately well supported in Crohn's disease, especially in children where the adverse consequences of steroid therapy are proportionally greater. However, exclusion diets are generally not recommended and there is little evidence to support any particular formula feed when nutritional regimens are constructed. CONCLUSIONS Available objective data to guide nutritional support and primary nutritional therapy in IBD are presented as 64 recommendations, of which 9 are very strong recommendations (grade A), 22 are strong recommendations (grade B) and 12 are based only on sparse evidence (grade 0); 21 recommendations are good practice points (GPP).
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Affiliation(s)
- Alastair Forbes
- Norwich Medical School, University of East Anglia, Bob Champion Building, James Watson Road, Norwich, NR4 7UQ, United Kingdom.
| | - Johanna Escher
- Erasmus Medical Center - Sophia Children's Hospital, Office Sp-3460, Wytemaweg 80, 3015 CN, Rotterdam, The Netherlands.
| | - Xavier Hébuterne
- Gastroentérologie et Nutrition Clinique, CHU de Nice, Université Côte d'Azur, Nice, France.
| | - Stanisław Kłęk
- General and Oncology Surgery Unit, Stanley Dudrick's Memorial Hospital, 15 Tyniecka Street, 32-050, Skawina, Krakau, Poland.
| | - Zeljko Krznaric
- Clinical Hospital Centre Zagreb, University of Zagreb, Kispaticeva 12, 10000, Zagreb, Croatia.
| | - Stéphane Schneider
- Gastroentérologie et Nutrition Clinique, CHU de Nice, Université Côte d'Azur, Nice, France.
| | - Raanan Shamir
- Tel-Aviv University, Schneider Children's Medical Center of Israel, 14 Kaplan St., Petach-Tikva, 49202, Israel.
| | - Kalina Stardelova
- University Clinic for Gastroenterohepatology, Clinical Centre "Mother Therese", Mother Therese Str No 18, Skopje, Republic of Macedonia.
| | - Nicolette Wierdsma
- VU University Medical Center, Department of Nutrition and Dietetics, De Boelelaan 1117, 1081 HV, Amsterdam, The Netherlands.
| | - Anthony E Wiskin
- Paediatric Gastroenterology & Nutrition Unit, Bristol Royal Hospital for Children, Upper Maudlin Street, Bristol, BS2 8BJ, United Kingdom.
| | - Stephan C Bischoff
- Institut für Ernährungsmedizin (180) Universität Hohenheim, Fruwirthstr. 12, 70593 Stuttgart, Germany.
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Clark A, Mach N. Role of Vitamin D in the Hygiene Hypothesis: The Interplay between Vitamin D, Vitamin D Receptors, Gut Microbiota, and Immune Response. Front Immunol 2016; 7:627. [PMID: 28066436 PMCID: PMC5179549 DOI: 10.3389/fimmu.2016.00627] [Citation(s) in RCA: 102] [Impact Index Per Article: 11.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/22/2016] [Accepted: 12/08/2016] [Indexed: 01/13/2023] Open
Abstract
The hygiene hypothesis postulates that higher levels of cleanliness and improper exposure to microorganisms early in childhood could disturb the intestinal microbiome resulting in abnormal immune responses. Recently, more attention has been put on how a lack of sun exposure and consequently vitamin D deficiency could lead to less immune tolerance and aberrant immune responses. Moreover, vitamin D receptor (VDR) function has been positioned to be a critical aspect of immune response and gut homeostasis. Therefore, this review focuses on the role that the interaction between vitamin D, VDR function, and gut microbiome might have on autoimmune diseases in the context of the hygiene hypothesis. Literature shows that there is a high correlation between vitamin D deficiency, VDR dysfunction, gut microbiota composition, and autoimmune diseases. The biologically active form of vitamin D, 1,25(OH)2D3, serves as the primary ligand for VDRs, which have been shown to play a fundamental role in reducing autoimmune disease symptoms. Although the biological functions of VDR, the effects of its genetic variants, and the effects of epigenetic profiles in its promoter region are largely unknown in humans, studies in murine models are increasingly demonstrating that VDRs play a crucial role in attenuating autoimmune disease symptoms by regulating autophagy and the production of antimicrobial peptides, such cathelicidin and β-defensin, which are responsible for modifying the intestinal microbiota to a healthier composition. Remarkably, evidence shows that hormonal compounds and byproducts of the microbiota such as secondary bile acids might also activate VDR. Therefore, understanding the interaction between VDR and gut microbiota is of the utmost importance toward understanding the rise in autoimmune diseases in Western countries. We have gained insights on how the VDR functions affects inflammation, autophagy, and microbiota composition that could lead to the development of pathogenesis of autoimmune diseases, while confirming the role vitamin D and VDRs have in the context of hygiene hypothesis.
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Affiliation(s)
- Allison Clark
- Health Science Department, International Graduate Institute of the Open University of Catalonia (UOC) , Barcelona , Spain
| | - Núria Mach
- Health Science Department, International Graduate Institute of the Open University of Catalonia (UOC), Barcelona, Spain; Animal Genetics and Integrative Biology Unit (GABI), INRA, AgroParisTech, Université Paris-Saclay, Jouy-en-Josas, France
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Simsek Y, Cakır I, Yetmis M, Dizdar OS, Baspinar O, Gokay F. Effects of Vitamin D treatment on thyroid autoimmunity. JOURNAL OF RESEARCH IN MEDICAL SCIENCES 2016; 21:85. [PMID: 28163731 PMCID: PMC5244647 DOI: 10.4103/1735-1995.192501] [Citation(s) in RCA: 35] [Impact Index Per Article: 3.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 02/18/2016] [Revised: 05/14/2016] [Accepted: 06/15/2016] [Indexed: 11/22/2022]
Abstract
Background: Vitamin D was shown to be related to autoimmune thyroid diseases (AITDs) in the previous studies. We aimed to investigate the relationship between Vitamin D and thyroid autoimmunity. Materials and Methods: Eighty-two patients, diagnosed with AITD by the endocrinology outpatient clinic, were included in this prospective study. All of the patients had both AITD and Vitamin D deficiency, defined as serum values <20 ng/mL. They were randomly assigned into two groups. The first group included 46 patients and the second one included 36 patients. The first group was treated with Vitamin D for 1 month at 1000 IU/day. The second group served as the control group and was not treated with Vitamin D replacement. Serum thyroid-stimulating hormone, free T4 (fT4), thyroid peroxidase antibody (TPO-Ab), thyroglobulin antibody (TgAb), and Vitamin D levels were measured at the initiation of the study and again at 1 month in all patients. Results: Two groups were similar with regard to age, sex, and type of thyroid disease. Whereas TPO-Ab (before; 278.3 ± 218.4 IU/ml and after; 267.9 ± 200.7 IU/ml) and TgAb (before; 331.9 ± 268.1 IU/ml and after; 275.4 ± 187.3 IU/ml) levels were significantly decreased by the Vitamin D replacement therapy in group 1 (P = 0.02, P = 0.03, respectively), the evaluated parameters in the control group did not significantly change (P = 0.869, P = 0.530, respectively). In addition, thyroid function tests did not significantly change with Vitamin D replacement in two groups. Conclusion: Vitamin D deficiency may contribute to the pathogenesis of AITDs. Since supplementation of the Vitamin D decreased thyroid antibody titers in this study in Vitamin D deficient subjects, in the future Vitamin D may become a part of AITDs' treatment, especially in those with Vitamin D insufficiency. Further clinical and experimental studies are required to understand the effect of Vitamin D on AITD.
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Affiliation(s)
- Yasin Simsek
- Department of Endocrinology and Metabolism, Kayseri Training and Research Hospital, Kayseri, Turkey
| | - Ilkay Cakır
- Department of Internal Medicine, Bagcilar Training and Research Hospital, Istanbul, Turkey
| | - Mikail Yetmis
- Department of Internal Medicine, Bagcilar Training and Research Hospital, Istanbul, Turkey
| | - Oguzhan Sitki Dizdar
- Department of Internal Medicine, Kayseri Training and Research Hospital, Kayseri, Turkey
| | - Osman Baspinar
- Department of Internal Medicine, Kayseri Training and Research Hospital, Kayseri, Turkey
| | - Ferhat Gokay
- Department of Endocrinology and Metabolism, Kayseri Training and Research Hospital, Kayseri, Turkey
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Abstract
Ulcerative colitis (UC) is a chronic inflammatory bowel disease whose pathogenesis is multifactorial and includes influences from genes, the environment, and the gut microbiome. Recent advances in diagnosis and treatment have led to significant improvement in managing the disease. Disease monitoring with the use of therapeutic drug monitoring, stool markers, and assessment of mucosal healing have garnered much attention. The recent approval of vedolizumab for treatment of moderate to severe UC has been a welcome addition. Newer biologics, including those targeting the Janus tyrosine kinase (JAK) pathway, are on the horizon to add to the current armamentarium of anti-TNF alpha and anti-integrin therapies. The recent publication of the SCENIC consensus statement on surveillance and management of dysplasia in UC patients supports the use of chromoendoscopy over random biopsies in detecting dysplasia. This review highlights these recent advances along with others that have been made with ulcerative colitis.
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Abstract
Vitamin D deficiency is common in patients with inflammatory bowel diseases and may even precede the disease onset contributing to an increased risk. Using comprehensive data from a large, referral IBD cohort, Kabbani et al. establish that low vitamin D levels are associated with greater disease activity, increased risk of surgery and hospitalizations, and lower health-related quality of life in patients with IBD. This expands the evidence base supporting such an association. However, there is a need for this field to evolve to interventional studies with vitamin D supplementation to confirm that vitamin D has a true therapeutic role for treating disease activity in IBD.
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Microbiome-Epigenome Interactions and the Environmental Origins of Inflammatory Bowel Diseases. J Pediatr Gastroenterol Nutr 2016; 62:208-19. [PMID: 26308318 PMCID: PMC4724338 DOI: 10.1097/mpg.0000000000000950] [Citation(s) in RCA: 38] [Impact Index Per Article: 4.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/17/2022]
Abstract
The incidence of pediatric inflammatory bowel disease (IBD), which includes Crohn disease and ulcerative colitis, has risen alarmingly in the Western and developing world in recent decades. Epidemiologic (including monozygotic twin and migrant) studies highlight the substantial role of environment and nutrition in IBD etiology. Here we review the literature supporting the developmental and environmental origins hypothesis of IBD. We also provide a detailed exploration of how the human microbiome and epigenome (primarily through DNA methylation) may be important elements in the developmental origins of IBD in both children and adults.
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Konijeti GG, Arora P, Boylan MR, Song Y, Huang S, Harrell F, Newton-Cheh C, O'Neill D, Korzenik J, Wang TJ, Chan AT. Vitamin D Supplementation Modulates T Cell-Mediated Immunity in Humans: Results from a Randomized Control Trial. J Clin Endocrinol Metab 2016; 101:533-8. [PMID: 26653112 PMCID: PMC4880125 DOI: 10.1210/jc.2015-3599] [Citation(s) in RCA: 37] [Impact Index Per Article: 4.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
Abstract
CONTEXT Although studies have linked vitamin D deficiency with immune-mediated diseases, data demonstrating a direct effect on T-cell function are sparse. OBJECTIVE Our objective was to determine whether oral vitamin D3 influences T-cell activation in humans with vitamin D deficiency. DESIGN This was a single-center ancillary study within Vitamin D Therapy in Individuals at High Risk of Hypertension, a double-blind, multicenter, randomized controlled trial. SETTING This study was undertaken in a single academic medical center. PARTICIPANTS Adults with vitamin D deficiency and untreated pre- or early stage I hypertension were included. INTERVENTION In Vitamin D Therapy in Individuals at High Risk of Hypertension, participants were randomized to either low- (400 IU daily) or high- (4000 IU daily) dose oral vitamin D3 for 6 months. In this ancillary study of 38 patients, we measured CD4+ T-cell activation estimated by intracellular ATP release after stimulation of whole blood with plant lectin phytohemagglutinin collected at baseline (pretreatment) and 2-month follow-up. MAIN OUTCOME MEASURE Determining whether ATP level changes were significantly different between treatment groups was the main outcome measure. RESULTS Treatment with 4000 IU of vitamin D3 decreased intracellular CD4+ ATP release by 95.5 ng/ml (interquartile range, -219.5 to 105.8). In contrast, 400 IU of vitamin D3 decreased intracellular CD4+ ATP release by 0.5 ng/ml (interquartile range, -69.2 to 148.5). In a proportional odds model, high-dose vitamin D3 was more likely than low-dose vitamin D3 to decrease CD4+ ATP release (odds ratio, 3.43; 95% confidence interval, 1.06-1.11). CONCLUSIONS In this ancillary study of a randomized controlled trial, we found that high-dose vitamin D3 significantly reduced CD4+ T-cell activation compared to low-dose vitamin D3, providing human evidence that vitamin D can influence cell-mediated immunity.
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Affiliation(s)
- Gauree Gupta Konijeti
- Division of Gastroenterology (G.G.K.), Scripps Clinic, La Jolla, California; Scripps Translational Science Institute (G.G.K.), La Jolla, California 92037; Division of Gastroenterology (G.G.K., M.R.B., A.T.C.), Massachusetts General Hospital, Boston, Massachusetts; Division of Cardiology (P.A.), University of Alabama, Birmingham, Alabama 35210; Department of Biostatistics (Y.S., S.H., F.H., D.O., T.J.W.), Vanderbilt University, Nashville, Tennessee 37232; Division of Cardiology (T.J.W.), Vanderbilt University, Nashville, Tennessee 37232; Division of Cardiology (C.N.-C.), Massachusetts General Hospital, Boston, Massachusetts; Division of Gastroenterology (J.K.), Brigham and Women's Hospital, Boston, Massachusetts 02115; and Clinical and Translational Epidemiology Unit (A.T.C.), Massachusetts General Hospital, Boston, Massachusetts 02114
| | - Pankaj Arora
- Division of Gastroenterology (G.G.K.), Scripps Clinic, La Jolla, California; Scripps Translational Science Institute (G.G.K.), La Jolla, California 92037; Division of Gastroenterology (G.G.K., M.R.B., A.T.C.), Massachusetts General Hospital, Boston, Massachusetts; Division of Cardiology (P.A.), University of Alabama, Birmingham, Alabama 35210; Department of Biostatistics (Y.S., S.H., F.H., D.O., T.J.W.), Vanderbilt University, Nashville, Tennessee 37232; Division of Cardiology (T.J.W.), Vanderbilt University, Nashville, Tennessee 37232; Division of Cardiology (C.N.-C.), Massachusetts General Hospital, Boston, Massachusetts; Division of Gastroenterology (J.K.), Brigham and Women's Hospital, Boston, Massachusetts 02115; and Clinical and Translational Epidemiology Unit (A.T.C.), Massachusetts General Hospital, Boston, Massachusetts 02114
| | - Matthew R Boylan
- Division of Gastroenterology (G.G.K.), Scripps Clinic, La Jolla, California; Scripps Translational Science Institute (G.G.K.), La Jolla, California 92037; Division of Gastroenterology (G.G.K., M.R.B., A.T.C.), Massachusetts General Hospital, Boston, Massachusetts; Division of Cardiology (P.A.), University of Alabama, Birmingham, Alabama 35210; Department of Biostatistics (Y.S., S.H., F.H., D.O., T.J.W.), Vanderbilt University, Nashville, Tennessee 37232; Division of Cardiology (T.J.W.), Vanderbilt University, Nashville, Tennessee 37232; Division of Cardiology (C.N.-C.), Massachusetts General Hospital, Boston, Massachusetts; Division of Gastroenterology (J.K.), Brigham and Women's Hospital, Boston, Massachusetts 02115; and Clinical and Translational Epidemiology Unit (A.T.C.), Massachusetts General Hospital, Boston, Massachusetts 02114
| | - Yanna Song
- Division of Gastroenterology (G.G.K.), Scripps Clinic, La Jolla, California; Scripps Translational Science Institute (G.G.K.), La Jolla, California 92037; Division of Gastroenterology (G.G.K., M.R.B., A.T.C.), Massachusetts General Hospital, Boston, Massachusetts; Division of Cardiology (P.A.), University of Alabama, Birmingham, Alabama 35210; Department of Biostatistics (Y.S., S.H., F.H., D.O., T.J.W.), Vanderbilt University, Nashville, Tennessee 37232; Division of Cardiology (T.J.W.), Vanderbilt University, Nashville, Tennessee 37232; Division of Cardiology (C.N.-C.), Massachusetts General Hospital, Boston, Massachusetts; Division of Gastroenterology (J.K.), Brigham and Women's Hospital, Boston, Massachusetts 02115; and Clinical and Translational Epidemiology Unit (A.T.C.), Massachusetts General Hospital, Boston, Massachusetts 02114
| | - Shi Huang
- Division of Gastroenterology (G.G.K.), Scripps Clinic, La Jolla, California; Scripps Translational Science Institute (G.G.K.), La Jolla, California 92037; Division of Gastroenterology (G.G.K., M.R.B., A.T.C.), Massachusetts General Hospital, Boston, Massachusetts; Division of Cardiology (P.A.), University of Alabama, Birmingham, Alabama 35210; Department of Biostatistics (Y.S., S.H., F.H., D.O., T.J.W.), Vanderbilt University, Nashville, Tennessee 37232; Division of Cardiology (T.J.W.), Vanderbilt University, Nashville, Tennessee 37232; Division of Cardiology (C.N.-C.), Massachusetts General Hospital, Boston, Massachusetts; Division of Gastroenterology (J.K.), Brigham and Women's Hospital, Boston, Massachusetts 02115; and Clinical and Translational Epidemiology Unit (A.T.C.), Massachusetts General Hospital, Boston, Massachusetts 02114
| | - Frank Harrell
- Division of Gastroenterology (G.G.K.), Scripps Clinic, La Jolla, California; Scripps Translational Science Institute (G.G.K.), La Jolla, California 92037; Division of Gastroenterology (G.G.K., M.R.B., A.T.C.), Massachusetts General Hospital, Boston, Massachusetts; Division of Cardiology (P.A.), University of Alabama, Birmingham, Alabama 35210; Department of Biostatistics (Y.S., S.H., F.H., D.O., T.J.W.), Vanderbilt University, Nashville, Tennessee 37232; Division of Cardiology (T.J.W.), Vanderbilt University, Nashville, Tennessee 37232; Division of Cardiology (C.N.-C.), Massachusetts General Hospital, Boston, Massachusetts; Division of Gastroenterology (J.K.), Brigham and Women's Hospital, Boston, Massachusetts 02115; and Clinical and Translational Epidemiology Unit (A.T.C.), Massachusetts General Hospital, Boston, Massachusetts 02114
| | - Christopher Newton-Cheh
- Division of Gastroenterology (G.G.K.), Scripps Clinic, La Jolla, California; Scripps Translational Science Institute (G.G.K.), La Jolla, California 92037; Division of Gastroenterology (G.G.K., M.R.B., A.T.C.), Massachusetts General Hospital, Boston, Massachusetts; Division of Cardiology (P.A.), University of Alabama, Birmingham, Alabama 35210; Department of Biostatistics (Y.S., S.H., F.H., D.O., T.J.W.), Vanderbilt University, Nashville, Tennessee 37232; Division of Cardiology (T.J.W.), Vanderbilt University, Nashville, Tennessee 37232; Division of Cardiology (C.N.-C.), Massachusetts General Hospital, Boston, Massachusetts; Division of Gastroenterology (J.K.), Brigham and Women's Hospital, Boston, Massachusetts 02115; and Clinical and Translational Epidemiology Unit (A.T.C.), Massachusetts General Hospital, Boston, Massachusetts 02114
| | - Dillon O'Neill
- Division of Gastroenterology (G.G.K.), Scripps Clinic, La Jolla, California; Scripps Translational Science Institute (G.G.K.), La Jolla, California 92037; Division of Gastroenterology (G.G.K., M.R.B., A.T.C.), Massachusetts General Hospital, Boston, Massachusetts; Division of Cardiology (P.A.), University of Alabama, Birmingham, Alabama 35210; Department of Biostatistics (Y.S., S.H., F.H., D.O., T.J.W.), Vanderbilt University, Nashville, Tennessee 37232; Division of Cardiology (T.J.W.), Vanderbilt University, Nashville, Tennessee 37232; Division of Cardiology (C.N.-C.), Massachusetts General Hospital, Boston, Massachusetts; Division of Gastroenterology (J.K.), Brigham and Women's Hospital, Boston, Massachusetts 02115; and Clinical and Translational Epidemiology Unit (A.T.C.), Massachusetts General Hospital, Boston, Massachusetts 02114
| | - Joshua Korzenik
- Division of Gastroenterology (G.G.K.), Scripps Clinic, La Jolla, California; Scripps Translational Science Institute (G.G.K.), La Jolla, California 92037; Division of Gastroenterology (G.G.K., M.R.B., A.T.C.), Massachusetts General Hospital, Boston, Massachusetts; Division of Cardiology (P.A.), University of Alabama, Birmingham, Alabama 35210; Department of Biostatistics (Y.S., S.H., F.H., D.O., T.J.W.), Vanderbilt University, Nashville, Tennessee 37232; Division of Cardiology (T.J.W.), Vanderbilt University, Nashville, Tennessee 37232; Division of Cardiology (C.N.-C.), Massachusetts General Hospital, Boston, Massachusetts; Division of Gastroenterology (J.K.), Brigham and Women's Hospital, Boston, Massachusetts 02115; and Clinical and Translational Epidemiology Unit (A.T.C.), Massachusetts General Hospital, Boston, Massachusetts 02114
| | - Thomas J Wang
- Division of Gastroenterology (G.G.K.), Scripps Clinic, La Jolla, California; Scripps Translational Science Institute (G.G.K.), La Jolla, California 92037; Division of Gastroenterology (G.G.K., M.R.B., A.T.C.), Massachusetts General Hospital, Boston, Massachusetts; Division of Cardiology (P.A.), University of Alabama, Birmingham, Alabama 35210; Department of Biostatistics (Y.S., S.H., F.H., D.O., T.J.W.), Vanderbilt University, Nashville, Tennessee 37232; Division of Cardiology (T.J.W.), Vanderbilt University, Nashville, Tennessee 37232; Division of Cardiology (C.N.-C.), Massachusetts General Hospital, Boston, Massachusetts; Division of Gastroenterology (J.K.), Brigham and Women's Hospital, Boston, Massachusetts 02115; and Clinical and Translational Epidemiology Unit (A.T.C.), Massachusetts General Hospital, Boston, Massachusetts 02114
| | - Andrew T Chan
- Division of Gastroenterology (G.G.K.), Scripps Clinic, La Jolla, California; Scripps Translational Science Institute (G.G.K.), La Jolla, California 92037; Division of Gastroenterology (G.G.K., M.R.B., A.T.C.), Massachusetts General Hospital, Boston, Massachusetts; Division of Cardiology (P.A.), University of Alabama, Birmingham, Alabama 35210; Department of Biostatistics (Y.S., S.H., F.H., D.O., T.J.W.), Vanderbilt University, Nashville, Tennessee 37232; Division of Cardiology (T.J.W.), Vanderbilt University, Nashville, Tennessee 37232; Division of Cardiology (C.N.-C.), Massachusetts General Hospital, Boston, Massachusetts; Division of Gastroenterology (J.K.), Brigham and Women's Hospital, Boston, Massachusetts 02115; and Clinical and Translational Epidemiology Unit (A.T.C.), Massachusetts General Hospital, Boston, Massachusetts 02114
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Owczarek D, Rodacki T, Domagała-Rodacka R, Cibor D, Mach T. Diet and nutritional factors in inflammatory bowel diseases. World J Gastroenterol 2016; 22:895-905. [PMID: 26811635 PMCID: PMC4716043 DOI: 10.3748/wjg.v22.i3.895] [Citation(s) in RCA: 168] [Impact Index Per Article: 18.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/26/2015] [Accepted: 11/13/2015] [Indexed: 02/06/2023] Open
Abstract
Inflammatory bowel disease (IBD) development is affected by complex interactions between environmental factors, changes in intestinal flora, various predisposing genetic properties and changes in the immune system. Dietary factors seem to play an underestimated role in the etiopathogenesis and course of the disease. However, research about food and IBD is conflicting. An excessive consumption of sugar, animal fat and linoleic acid is considered a risk factor for IBD development, whereas a high fiber diet and citrus fruit consumption may play a protective role. Also, appropriate nutrition in particular periods of the disease may facilitate achieving or prolonging remissions and most of all, improve the quality of life for patients. During disease exacerbation, a low fiber diet is recommended for most patients. In the remission time, an excessive consumption of alcohol and sulfur products may have a negative effect on the disease course. Attempts are also made at employing diets composed in detail in order to supplement IBD therapy. A diet with a modified carbohydrate composition, a semi-vegetarian diet and a diet low in fermentable oligosaccharides, disaccharides, monosaccharides and polyols are under investigation. Due to chronic inflammation as well as side effects of chronically used medications, patients with IBD are also at increased risk of nutritional factor deficiencies, including iron, calcium, vitamin D, vitamin B12, folic acid, zinc, magnesium and vitamin A. It should also be remembered that there is no single common diet suitable for all IBD patients; each of them is unique and dietary recommendations must be individually developed for each patient, depending on the course of the disease, past surgical procedures and type of pharmacotherapy.
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Furuya-Kanamori L, Wangdi K, Yakob L, McKenzie SJ, Doi SAR, Clark J, Paterson DL, Riley TV, Clements ACA. 25-Hydroxyvitamin D Concentrations and Clostridium difficile Infection: A Meta-Analysis. JPEN J Parenter Enteral Nutr 2015; 41:890-895. [PMID: 26701764 DOI: 10.1177/0148607115623457] [Citation(s) in RCA: 11] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/15/2022]
Abstract
BACKGROUND Well-known risk factors for Clostridium difficile infection (CDI) are exposure to antibiotics and gastric acid suppressants. Recent studies have provided some evidence of an association between hypovitaminosis D and the risk of CDI. Therefore, this meta-analysis aimed to pool all the existing evidence to investigate the association between 25-hydroxyvitamin D (25[OH]D) and CDI. METHODS A systematic search was conducted in 3 databases (PubMed, Embase, and Web of Sciences) for epidemiological studies that examined the association between mean 25(OH)D concentrations and CDI as well as between 25(OH)D status and CDI severity or recurrence. 25(OH)D status was defined as "lower" or "higher" at a threshold concentration of <20 or ≥20 ng/mL, respectively. Pooled effect sizes were computed using the inverse variance heterogeneity model of meta-analysis. RESULTS Eight publications (n = 4479 patients) were included in the meta-analysis. The mean concentration of 25(OH)D in patients with CDI was 3.54 ng/mL (95% confidence interval [CI], 0.39-6.89 ng/mL) lower than in patients without CDI. Patients with lower 25(OH)D status had a higher odds (odds ratio [OR], 1.61; 95% CI, 1.02-2.53) of developing severe CDI compared with those with a higher 25(OH)D status. No significant association was found between 25(OH)D status and CDI recurrence. CONCLUSION The results of this meta-analysis suggest that lower mean concentrations of 25(OH)D were associated with CDI. A lower 25(OH)D status increased the odds of severe CDI but not of CDI recurrence.
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Affiliation(s)
- Luis Furuya-Kanamori
- 1 Research School of Population Health, The Australian National University, Canberra, Australian Capital Territory, Australia
| | - Kinley Wangdi
- 1 Research School of Population Health, The Australian National University, Canberra, Australian Capital Territory, Australia
| | - Laith Yakob
- 2 London School of Hygiene and Tropical Medicine, Department of Disease Control, London, UK
| | - Samantha J McKenzie
- 3 Institute for Teaching and Learning Innovation, The University of Queensland, St Lucia, Queensland, Australia
| | - Suhail A R Doi
- 1 Research School of Population Health, The Australian National University, Canberra, Australian Capital Territory, Australia
| | - Justin Clark
- 4 Faculty of Health Sciences and Medicine, Bond University, Gold Coast, Queensland, Australia
| | - David L Paterson
- 5 The University of Queensland, UQ Centre for Clinical Research, Herston, Queensland, Australia
| | - Thomas V Riley
- 6 Microbiology & Immunology, The University of Western Australia and Department of Microbiology, PathWest Laboratory Medicine, Queen Elizabeth II Medical Centre, Nedlands, Western Australia, Australia
| | - Archie C A Clements
- 1 Research School of Population Health, The Australian National University, Canberra, Australian Capital Territory, Australia
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Ryz NR, Lochner A, Bhullar K, Ma C, Huang T, Bhinder G, Bosman E, Wu X, Innis SM, Jacobson K, Vallance BA. Dietary vitamin D3 deficiency alters intestinal mucosal defense and increases susceptibility to Citrobacter rodentium-induced colitis. Am J Physiol Gastrointest Liver Physiol 2015; 309:G730-42. [PMID: 26336925 PMCID: PMC4628967 DOI: 10.1152/ajpgi.00006.2015] [Citation(s) in RCA: 34] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/08/2015] [Accepted: 08/27/2015] [Indexed: 01/31/2023]
Abstract
Vitamin D deficiency affects more that 1 billion people worldwide. Although thought to increase risk of bacterial infections, the importance of vitamin D on host defense against intestinal bacterial pathogens is currently unclear since injection of the active form of vitamin D, 1,25(OH)2D3, increased susceptibility to the enteric bacterial pathogen Citrobacter rodentium by suppressing key immune/inflammatory factors. To further characterize the role of vitamin D during bacteria-induced colitis, we fed weanling mice either vitamin D3-deficient or vitamin D3-sufficient diets for 5 wk and then challenged them with C. rodentium. Vitamin D3-deficient mice lost significantly more body weight, carried higher C. rodentium burdens, and developed worsened histological damage. Vitamin D3-deficient mice also suffered greater bacterial translocation to extra-intestinal tissues, including mesenteric lymph nodes, spleen, and liver. Intestinal tissues of infected vitamin D3-deficient mice displayed increased inflammatory cell infiltrates as well as significantly higher gene transcript levels of inflammatory mediators TNF-α, IL-1β, IL-6, TGF-β, IL-17A, and IL-17F as well as the antimicrobial peptide REG3γ. Notably, these exaggerated inflammatory responses accelerated the loss of commensal microbes and were associated with an impaired ability to detoxify bacterial lipopolysaccharide. Overall, these studies show that dietary-induced vitamin D deficiency exacerbates intestinal inflammatory responses to infection, also impairing host defense.
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Affiliation(s)
- Natasha R. Ryz
- 1Division of Gastroenterology, Department of Pediatrics, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada; and
| | - Arion Lochner
- 1Division of Gastroenterology, Department of Pediatrics, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada; and
| | - Kirandeep Bhullar
- 1Division of Gastroenterology, Department of Pediatrics, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada; and
| | - Caixia Ma
- 1Division of Gastroenterology, Department of Pediatrics, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada; and
| | - Tina Huang
- 1Division of Gastroenterology, Department of Pediatrics, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada; and
| | - Ganive Bhinder
- 1Division of Gastroenterology, Department of Pediatrics, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada; and
| | - Else Bosman
- 1Division of Gastroenterology, Department of Pediatrics, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada; and
| | - Xiujuan Wu
- 1Division of Gastroenterology, Department of Pediatrics, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada; and
| | - Sheila M. Innis
- 2Division of Neonatology, Department of Pediatrics, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada
| | - Kevan Jacobson
- 1Division of Gastroenterology, Department of Pediatrics, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada; and
| | - Bruce A. Vallance
- 1Division of Gastroenterology, Department of Pediatrics, Child and Family Research Institute, University of British Columbia, Vancouver, British Columbia, Canada; and
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Ferguson LR. Nutritional Modulation of Gene Expression: Might This be of Benefit to Individuals with Crohn's Disease? Front Immunol 2015; 6:467. [PMID: 26441972 PMCID: PMC4566049 DOI: 10.3389/fimmu.2015.00467] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/17/2015] [Accepted: 08/27/2015] [Indexed: 12/18/2022] Open
Abstract
The incidence of inflammatory bowel diseases (IBD), including Crohn's disease (CD), is increasing worldwide, especially in young children and adolescents. Although hospitalized patients are usually provided with enteral or parenteral support, continuing care typically requires a trial-and-error approach to suppressing symptoms and maintaining disease remission. Current nutritional advice does not differ from general population guidelines. International collaborative studies have revealed 163 distinct genetic loci affecting susceptibility to IBD, in some of which host-microbe interactions can be seen to play an important role. The nature of these loci enables a rationale for predicting nutritional requirements that may not be evident through standard therapeutic approaches. Certain recognized nutrients, such as vitamin D and long-chain omega-3 polyunsaturated fatty acids, may be required at higher than anticipated levels. Various phytochemicals, not usually considered in the same class as classic nutrients, could play an important role. Prebiotics and probiotics may also be beneficial. Genomic approaches enable proof of principle of nutrient optimization rather than waiting for disease symptoms to appear and/or progress. We suggest a paradigm shift in diagnostic tools and nutritional therapy for CD, involving a systems biology approach for implementation.
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Affiliation(s)
- Lynnette R Ferguson
- Discipline of Nutrition and Dietetics, Faculty of Medical and Health Sciences, The University of Auckland , Auckland , New Zealand ; Auckland Cancer Society Research Centre, Faculty of Medical and Health Sciences, The University of Auckland , Auckland , New Zealand
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Lu C, Yang J, Yu W, Li D, Xiang Z, Lin Y, Yu C. Association between 25(OH)D Level, Ultraviolet Exposure, Geographical Location, and Inflammatory Bowel Disease Activity: A Systematic Review and Meta-Analysis. PLoS One 2015; 10:e0132036. [PMID: 26172950 PMCID: PMC4501705 DOI: 10.1371/journal.pone.0132036] [Citation(s) in RCA: 41] [Impact Index Per Article: 4.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/25/2015] [Accepted: 06/09/2015] [Indexed: 12/20/2022] Open
Abstract
Background There is no consensus on the vitamin D levels and inflammatory bowel disease (IBD). Aim To conduct a systematic review and meta-analysis to analyze the relationship between IBD and 25(OH)D, sun exposure, and latitude, and to determine whether vitamin D deficiency affects the severity of IBD. Methods We searched the PubMed, EBSCO, and ClinicalTrials.gov databases to identify all studies that assessed the association between 25(OH)D, sun exposure, latitude, and IBD through November 1, 2014, without language restrictions. Studies that compared 25(OH)D levels between IBD patients and controls were selected for inclusion in the meta-analysis. We calculated pooled standardized mean differences (SMDs) and odds ratios (ORs). Results Thirteen case-control studies investigating CD and 25(OH)D levels were included, and eight studies part of above studies also investigated the relationship between UC and 25(OH)D. Both CD patients (SMD: 0.26 nmol/L, 95% confidence interval [CI]: 0.09–0.42 nmol/L) and UC patients (SMD: 0.5 nmol/L, 95% CI: 0.15–0.85 nmol/L) had lower levels of 25(OH)D than controls. In addition, CD patients and UC patients were 1.95 times (OR, 1.95; 95% CI, 1.48–2.57) and 2.02 times (OR, 2.02; 95% CI, 1.13–3.60) more likely to be 25(OH)D deficient than controls. We also included 10 studies investigating the relationship between CD activity and vitamin D. Results showed that patients with active CD (CD Activity Index≥150) were more likely to have low vitamin D levels. In addition, whether low sun exposure and high latitude were related to a high morbidity of CD need to be provided more evidence. Conclusion Our study shows that IBD patients have lower vitamin D levels. For active CD patients, vitamin D levels were low. These findings suggest that vitamin D may play an important role in the development of IBD, although a direct association could not be determined in our study.
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Affiliation(s)
- Chao Lu
- Department of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, China
| | - Jun Yang
- Department of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, China
| | - Weilai Yu
- Department of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, China
| | - Dejian Li
- Department of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, China
| | - Zun Xiang
- Department of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, China
| | - Yiming Lin
- Department of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, China
| | - Chaohui Yu
- Department of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, China
- * E-mail:
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Bashir M, Prietl B, Tauschmann M, Mautner SI, Kump PK, Treiber G, Wurm P, Gorkiewicz G, Högenauer C, Pieber TR. Effects of high doses of vitamin D3 on mucosa-associated gut microbiome vary between regions of the human gastrointestinal tract. Eur J Nutr 2015; 55:1479-89. [PMID: 26130323 PMCID: PMC4875045 DOI: 10.1007/s00394-015-0966-2] [Citation(s) in RCA: 161] [Impact Index Per Article: 16.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/01/2015] [Accepted: 06/16/2015] [Indexed: 12/12/2022]
Abstract
PURPOSE Vitamin D is well known for its effects on bone mineralisation but has also been attributed immunomodulatory properties. It positively influences human health, but in vivo data describing vitamin D effects on the human gut microbiome are missing. We aimed to investigate the effects of oral vitamin D3 supplementation on the human mucosa-associated and stool microbiome as well as CD8(+) T cells in healthy volunteers. METHODS This was an interventional, open-label, pilot study. Sixteen healthy volunteers (7 females, 9 males) were endoscopically examined to access a total of 7 sites. We sampled stomach, small bowel, colon, and stools before and after 8 weeks of vitamin D3 supplementation. Bacterial composition was assessed by pyrosequencing the 16S rRNA gene (V1-2), and CD8(+) T cell counts were determined by flow cytometry. RESULTS Vitamin D3 supplementation changed the gut microbiome in the upper GI tract (gastric corpus, antrum, and duodenum). We found a decreased relative abundance of Gammaproteobacteria including Pseudomonas spp. and Escherichia/Shigella spp. and increased bacterial richness. No major changes occurred in the terminal ileum, appendiceal orifice, ascending colon, and sigmoid colon or in stools, but the CD8(+) T cell fraction was significantly increased in the terminal ileum. CONCLUSION Vitamin D3 modulates the gut microbiome of the upper GI tract which might explain its positive influence on gastrointestinal diseases, such as inflammatory bowel disease or bacterial infections. The local effects of vitamin D demonstrate pronounced regional differences in the response of the GI microbiome to external factors, which should be considered in future studies investigating the human microbiome.
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Affiliation(s)
- Mina Bashir
- Division of Endocrinology and Metabolism, Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 15, 8036, Graz, Austria
| | - Barbara Prietl
- Division of Endocrinology and Metabolism, Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 15, 8036, Graz, Austria
| | - Martin Tauschmann
- Division of Endocrinology and Metabolism, Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 15, 8036, Graz, Austria
| | - Selma I Mautner
- Division of Endocrinology and Metabolism, Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 15, 8036, Graz, Austria
| | - Patrizia K Kump
- Division of Gastroenterology and Hepatology, Department of Internal Medicine, Medical University of Graz, Graz, Austria
| | - Gerlies Treiber
- Division of Endocrinology and Metabolism, Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 15, 8036, Graz, Austria
| | - Philipp Wurm
- Institute of Pathology, Medical University of Graz, Graz, Austria
| | | | - Christoph Högenauer
- Division of Gastroenterology and Hepatology, Department of Internal Medicine, Medical University of Graz, Graz, Austria.
| | - Thomas R Pieber
- Division of Endocrinology and Metabolism, Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 15, 8036, Graz, Austria.
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Vitamin D and inflammatory bowel disease. BIOMED RESEARCH INTERNATIONAL 2015; 2015:470805. [PMID: 26000293 PMCID: PMC4427008 DOI: 10.1155/2015/470805] [Citation(s) in RCA: 68] [Impact Index Per Article: 6.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 11/27/2014] [Revised: 02/02/2015] [Accepted: 02/13/2015] [Indexed: 12/11/2022]
Abstract
Vitamin D deficiency has been recognized as an environmental risk factor for Crohn's disease since the early 80s. Initially, this finding was correlated with metabolic bone disease. Low serum 25-hydroxyvitamin D levels have been repeatedly reported in inflammatory bowel diseases together with a relationship between vitamin D status and disease activity. Subsequently, low serum vitamin D levels have been reported in various immune-related diseases pointing to an immunoregulatory role. Indeed, vitamin D and its receptor (VDR) are known to interact with different players of the immune homeostasis by controlling cell proliferation, antigen receptor signalling, and intestinal barrier function. Moreover, 1,25-dihydroxyvitamin D is implicated in NOD2-mediated expression of defensin-β2, the latter known to play a crucial role in the pathogenesis of Crohn's disease (IBD1 gene), and several genetic variants of the vitamin D receptor have been identified as Crohn's disease candidate susceptibility genes. From animal models we have learned that deletion of the VDR gene was associated with a more severe disease. There is a growing body of evidence concerning the therapeutic role of vitamin D/synthetic vitamin D receptor agonists in clinical and experimental models of inflammatory bowel disease far beyond the role of calcium homeostasis and bone metabolism.
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Meta-analysis of the association between vitamin D and autoimmune thyroid disease. Nutrients 2015; 7:2485-98. [PMID: 25854833 PMCID: PMC4425156 DOI: 10.3390/nu7042485] [Citation(s) in RCA: 125] [Impact Index Per Article: 12.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/15/2015] [Revised: 02/10/2015] [Accepted: 03/16/2015] [Indexed: 01/13/2023] Open
Abstract
Although emerging evidence suggests that low levels of vitamin D may contribute to the development of autoimmune disease, the relationship between vitamin D reduction and autoimmune thyroid disease (AITD), which includes Graves’ disease (GD) and Hashimoto thyroiditis (HT), is still controversial. The aim was to evaluate the association between vitamin D levels and AITD through systematic literature review. We identified all studies that assessed the association between vitamin D and AITD from PubMed, Embase, CENTRAL, and China National Knowledge Infrastructure (CNKI) databases. We included studies that compared vitamin D levels between AITD cases and controls as well as those that measured the odds of vitamin D deficiency by AITD status. We combined the standardized mean differences (SMD) or the odds ratios (OR) in a random effects model. Twenty case-control studies provided data for a quantitative meta-analysis. Compared to controls, AITD patients had lower levels of 25(OH)D (SMD: −0.99, 95% CI: −1.31, −0.66) and were more likely to be deficient in 25(OH)D (OR 2.99, 95% CI: 1.88, 4.74). Furthermore, subgroup analyses result showed that GD and HT patients also had lower 25(OH)D levels and were more likely to have a 25(OH)D deficiency, suggesting that low levels of serum 25(OH)D was related to AITD.
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Ananthakrishnan AN, Greer JB, Schraut WH, Regueiro MD, Davis PL, Hartman DJ, Siegel CA, Herfarth HH, Williams ED, Schwartz MB. Environmental risk factors for inflammatory bowel diseases: a review. Dig Dis Sci 2015; 60:290-8. [PMID: 25204669 PMCID: PMC4304948 DOI: 10.1007/s10620-014-3350-9] [Citation(s) in RCA: 118] [Impact Index Per Article: 11.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/24/2014] [Accepted: 09/01/2014] [Indexed: 12/23/2022]
Abstract
Inflammatory bowel diseases comprising Crohn's disease (CD) and ulcerative colitis (UC) are chronic immunologically mediated diseases. The key mechanism underlying the pathogenesis of these diseases is a dysregulated immune response to commensal flora in a genetically susceptible host. Thus intestinal microbial dysbiosis, host genetics, and the external environment all play an important role in the development of incident disease and in determining subsequent disease behavior and outcomes. There are several well-defined or putative environmental risk factors including cigarette smoking, appendectomy, diet, stress and depression, vitamin D as well as hormonal influence. The effect of some of the risk factors appears to differ between CD and UC suggesting that despite shared genetic and immunologic mechanisms, distinct pathways of pathogenesis exist. There is a growing body of literature identifying risk factors for incident disease. There is less rigorous literature defining triggers of relapse, and few controlled clinical trials examining if modification of such risk factors results in an improvement in patient outcomes. This is an area of considerable patient, physician, and scientific interest, and there is an important unmet need for rigorous studies of the external environment in disease pathogenesis and subsequent course.
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Affiliation(s)
- Ashwin N Ananthakrishnan
- Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, MA
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Wong KK, Lee R, Watkins RR, Haller N. Prolonged Clostridium difficile Infection May Be Associated With Vitamin D Deficiency. JPEN J Parenter Enteral Nutr 2015; 40:682-7. [DOI: 10.1177/0148607114568121] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/10/2014] [Accepted: 12/16/2014] [Indexed: 11/16/2022]
Affiliation(s)
- Ken Koon Wong
- Department of Internal Medicine, Akron General Medical Center, Akron, Ohio
| | - Rebecca Lee
- Department of Medicine, Northeast Ohio Medical University, Rootstown, Ohio
| | - Richard R. Watkins
- Department of Internal Medicine, Akron General Medical Center, Akron, Ohio
- Department of Medicine, Northeast Ohio Medical University, Rootstown, Ohio
- Division of Infectious Disease, Akron General Medical Center, Akron, Ohio
| | - Nairmeen Haller
- Department of Internal Medicine, Akron General Medical Center, Akron, Ohio
- Department of Medicine, Northeast Ohio Medical University, Rootstown, Ohio
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