Case Report Open Access
Copyright ©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Clin Cases. Feb 6, 2021; 9(4): 943-950
Published online Feb 6, 2021. doi: 10.12998/wjcc.v9.i4.943
Renal failure and hepatitis following ingestion of raw grass carp gallbladder: A case report
Li-Na Zhou, Shao-Shao Dong, Sheng-Ze Zhang, Department of Nephrology, Wenzhou People's Hospital, Wenzhou 325000, Zhejiang Province, China
Wen Huang, Department of Nephrology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang Province, China
ORCID number: Li-Na Zhou (0000-0002-6045-6304); Shao-Shao Dong (0000-0001-8452-6728); Sheng-Ze Zhang (0000-0002-5702-3321); Wen Huang (0000-0002-0010-3056).
Author contributions: Zhou LN wrote the article; Dong SS performed renal biopsy and conventional hemodialysis on the patient; Zhang SZ collected the data; Huang W approved the final version of the manuscript.
Informed consent statement: The Ethics Committee of Wenzhou People's Hospital approved the publication of this report. Informed consent was obtained from the patient for the publication of this report.
Conflict-of-interest statement: The authors declare that they have no conflict of interest to disclose.
CARE Checklist (2016) statement: The authors have read the CARE Checklist (2016), and the manuscript was prepared and revised according to the CARE Checklist (2016).
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Corresponding author: Wen Huang, MD, Doctor, Department of Nephrology, The Second Affiliated Hospital of Wenzhou Medical University, No. 108 College Road, Wenzhou 325000, Zhejiang Province, China. 207071@wzhealth.com
Received: October 7, 2020
Peer-review started: October 7, 2020
First decision: November 14, 2020
Revised: November 18, 2020
Accepted: November 29, 2020
Article in press: November 29, 2020
Published online: February 6, 2021
Processing time: 103 Days and 21.7 Hours

Abstract
BACKGROUND

Fish gallbladder has long been used as a folk remedy in Asian countries. Multiple organ damage after ingestion of fish gallbladder resulting in near mortality has been known to us. Here, we describe a case of acute renal failure (ARF) and hepatitis due to grass carp gallbladder poisoning and review the literature.

CASE SUMMARY

A previously healthy, 50-year-old woman was admitted to our hospital with a 2-d history of generalized abdominal pain and repeated vomiting following ingestion of two raw grass carp gallbladders in an attempt to alleviate her cough. She developed anuria on day 4 with markedly elevated serum creatinine, urea, bilirubin, alanine aminotransferase, and aspartate aminotransferase. Based on thorough evaluation of her history and prompt biochemical investigations, we diagnosed her with ARF and hepatitis secondary to fish gallbladder poisoning. Her renal biopsy revealed acute tubular necrosis, following which she underwent six sessions of conventional hemodialysis due to renal failure. Supportive treatment with gastric mucosal protectant and liver protectant was administered for targeted organ protection. The patient’s liver function gradually recovered, and serum creatinine was 164 mmol/L at discharge on day 24. Over a follow-up period of 2 wk, her renal function completely recovered.

CONCLUSION

Physicians should be mindful of toxic complications of raw grass carp gallbladder ingestion and we should promote awareness to reduce incidences of food poisoning.

Key Words: Grass carp gallbladder; Case report; Acute renal failure; Hepatitis; Ichthyogallotoxin; Hemodialysis

Core Tip: We describe the clinical presentation of a patient who suffered acute renal and hepatic insult following ingestion of raw carp gallbladder. To our knowledge, cardiac and hematological effects of this toxicity have never been reported before. We believe that this paper will be of interest because ingestion of raw gallbladder is a common practice in rural southern and southeastern Asia, and with global travel becoming more prevalent, knowledge on this clinical scenario will benefit physicians all worldwide.



INTRODUCTION

Fish gallbladder has long been used as a folk remedy in Asian countries. In some rural areas of southeastern and southern provinces in China, including Hong Kong and Taiwan[1], the habit of swallowing fish gallbladder to cure diseases such as asthma, arthritis, and cough; enhance visual acuity; and relieve pain is prevalent. Multiple organ damage after the ingestion of fish gallbladder nearly resulting in death has been known to occur. Cases of poisoning have also been reported in Cambodia, Japan, South Korea, India, and Vietnam[2-4]. This practice poses a serious health concern from the standpoint of food safety. With improved developments in healthcare in China, we now have an effective treatment for patients with fish gallbladder poisoning. The purpose of this report is to raise awareness regarding food poisoning that may arise secondary to the ingestion of raw cyprinid fish.

CASE PRESENTATION
Chief complaints

A previously healthy, 50-year-old woman was admitted to our hospital with a 2-d history of generalized abdominal pain and repeated vomiting following ingestion of two raw grass carp gallbladders.

History of present illness

The patient consumed two raw grass carp gallbladders (approximately 4-6 mL) for alleviation of her cough 2 d prior to presenting at our hospital. She developed diffuse abdominal pain and profuse vomiting 6 h after its ingestion, accompanied by sweating, dry mouth, heaviness in the chest, and dizziness.

History of past illness

She had no history of hypertension, diabetes, cardiac disease, cerebrovascular disease, allergies, or surgical interventions.

Personal and family history

She had no relevant family history.

Physical examination

At admission, her temperature was 37.1 °C, pulse rate 46/min, respiratory rate 20/min, and blood pressure 108/74 mmHg. She had upper abdominal tenderness, with no rebound pain, hyperactive bowel sounds of 5-6/min, and no pain on renal percussion. The rest of her systemic examination was unremarkable.

Laboratory examinations

At admission, her serum creatinine was 344 μmol/L and urea was 15.88 mmol/L (normal range being 2.5-6.4 mmol/L). On day 4, her urine output decreased drastically (< 100 mL over 24 h). Serum creatinine markedly rose to 505 μmol/L. Liver function tests revealed increased alanine aminotransferase, aspartate aminotransferase, total bilirubin, and direct bilirubin, as shown in Table 1.

Table 1 Selected indicators after admission.

Day 3
Day 41
Day 5
Day 6
Day 7
Day 10
Day 122
Day 14
Day 17
Day 193
Day 22
Day 244
Day 31
Reference
Liver function
ALT2739.001674.001052.00684.00264.0086.0061.0039.007-40 U/L
AST1399.00416.00155.0076.0037.0021.0023.0021.0013-35 U/L
Glutamyl transpetidase212.00178.00162.00141.00104.0078.0089.0080.0010-60 U/L
Total bile acid32.3014.8017.00 < 9.67 mol/L
Glucocholic acid29.8513.1011.60< 5.80 mol/L
Total bilirubin49.7032.7025.3017.3012.7015.3015.7012.503.4-21.1 μmol/L
Direct bilirubin43.5026.6019.2012.708.108.308.907.40< 6.8 μmol/L
Albumin42.9038.7035.9035.2036.5036.0049.1048.5040.0-55.0 g/L
Renal function
Serum creatinine344.00505.00521.00551.00589.00590.00580.00458.00242.00164.0010446-920 μmol/L
Urea15.8819.6017.3015.0010.2011.4014.8018.3015.8012.206.542.5-6.4 mmol/L
Uric acid647.00739.80550.50500.30454.80391.30406.50427.10375.1095.2-446.3 mmol/L
Uronoscopy
Urine protein2+(1)1+(0.5)
Urine chlorine187.8110-250 mmol/24 h
Urine sodium221.940-220 mmol/24 h
Urine potassium19.8525-100 mmol/24 h
Urine uric acid0.71.5-4.4 mmol/24 h
24 h urine protein303 30-150 mg/24 h
Urine-NAG22.90.3-11.5 U/L
Urine IgG149.0< 9.6 mg/L
Urine β2-microglobulin3.44< 0.2 mg/L
Urine α1-microglobulin34.0< 12.0 mg/L
Urine transferrin55.0< 2.3 mg/L
Urine amylase542.0032-641 U/L
Routine blood test
Leukocytes5.75.607.006.906.408.506.906.405.93.5-9.5 × 109/L
Neutrophils4.74.605.505.104.907.104.804.303.92.0-7.0 × 109/L
Lymphocytes0.560.600.901.000.900.901.401.401.50.8-4.0 × 109/L
Hemoglobin125116.00114.00105.0093.0092.0089.0091.0083115-150 g/L
Platelets156128.00116.00122.0098.0084.00111.00156.00161125-350 × 109/L
Inflammatory indicators
C-reactive protein1.412.906.10< 10.0 mg/L
Procalcitionin3.310.12< 0.50 ng/mL
Serum amyloid A89.607.600-10 mg/L
Erythrocyte sedimentation rate 9< 20 mm/h
Coagulation function
Prothrombin time12.4011.2011.509.5-14.1 s
Activated partial thromboplastin time25.5027.7025.1-36.5 s
Thrombin time17.2014.6011.8-17.8 s
D-dimer7.201.694.84< 0.50 mg/L
Blood gas analysis
PH7.357.35-7.45
PaCO229.435.0-48.0 mmHg
PaO281.980.0-100.0 mmHg
Actual bicarbonate radical1622-27 mmol/L
Standard bicarbonate radical1821-25 mmol/L
Electrolytes
K+4.604.404.203.803.803.503.403.803.804.004.003.5-5.3 mmol/L
Na+138.00133.00135.00137.00137.00137.00136.00137.00139.00136.00138.00137-147 mmol/L
Cl-103.00100.0099.0099.00101.0099.0095.0090.0095.0094.0098.0099-110 mmol/L
P1.501.341.641.651.301.222.041.640.83-1.48 mmol/L
Ca2+2.292.222.182.212.102.172.102.312.492.15-2.5 mmol/L
Other indicators
Serum ferritin770.711.0-306.8 ng/mL
Transferrin saturation1815%-45%
Folic acid11.43.1-20.5 ug/L
Vitamin B12453187-883 ng/L
Erythropoietin3.84.30-29.00 mIU/mL
Parathyroid hormone75.10151.4015-65 pg/mL
Serum β2-microglobulin7.321.3-2.7 mg/L
Serum amylase159.00137.00205.0030-110 U/L
Heart functionCreatine kinase and Troponin normal range
Hepatophilic virusHAV, HBV, HCV, HEV, and TORCH were negative
Immunization indicatorsANA, anti-GBM and ANCA negative; IgE 212 IU/mL (< 100 IU/mL), C3 0.57 (0.9-1.8 g/L), C4 0.1 (0.1-0.4 g/L), C1q 101 (159-233 mg/L). IgA, IgG, and IgM were normal; Widal’s test negative
Imaging examinations

Her echocardiogram (ECG) revealed sinus bradycardia of new onset, with a heart rate (HR) of 46/min at that time.

FINAL DIAGNOSIS

The patient was diagnosed with acute renal failure (ARF) and hepatitis.

TREATMENT

The patient was started on 3-4 h sessions of hemodialysis on day 4 due to renal failure, which was then maintained every 2 d. Gastric mucosal protectant omeprazole 40 mg iv daily for 4 d and reduced glutathione 1.2 g iv daily for 14 d were administered.

OUTCOME AND FOLLOW-UP

The patient’s urine output increased to 1400 mL/24 h on day 12, liver function improved, and dialysis was withdrawn on day 19. After the exclusion of contraindications, she consented to undergo renal biopsy to identify the cause of her ARF on day 13; the biopsy revealed acute tubular necrosis. She was discharged on day 24, with serum creatinine level having decreased to 164 μmol/L. After discharge, she was followed with weekly serum biochemical tests at the nephrology outpatient department and her renal function recovered completely after 2 wk.

Repeat ECG revealed persistence of sinus bradycardia (HR 52 bpm). Test results are shown in Table 1. Cardiac ultrasound and pulmonary and abdominal computed tomography findings were normal.

DISCUSSION

Wu et al[2] have reviewed fish with poisonous gallbladders in China. There are currently 12 known species of fish with poisonous bile in China, all of which belong to the freshwater fish family Cyprinidae. Poisoning caused by grass carp gallbladder accounts for > 80% of all cases because the grass carp has a relatively big gallbladder.

Ichthyogallotoxin has been studied extensively in grass carp bile[5]. The compound 5α-cyprinol sulfate (5α-cholestane-3α, 7α, 12α, 26, 27-pentol-26-sulfate) has the molecular formula C27H48O8S. Mohri et al[6] reported that essentially all bile toxicity could be explained by the properties of cyprinol sulfate, based on the LD50 values. Toxicity is dose-dependent, depending on the quantity of bile and size of the ingested fish gallbladder[7].

After the ingestion of fish gallbladder, damage to multiple organs, such as the gastrointestinal, renal, hepatic, cardiac, and neurological systems, has been reported previously[8]. The initial symptoms[8] were similar to those of gastroenteritis, occurring 0.5-4 h after the consumption of the offending agent. Edema, oliguria, or anuria may occur within 2-3 d after poisoning, sometimes even as late as 3-6 d, as reported previously[8]. A remarkable increase in urea, serum creatinine, and urine N-acetyl-beta-D-glucosaminidase (NAG) with non-glomerular proteinuria was observed in our patient. ARF caused by the ingestion of fish gallbladder has been reported in several case series[9,10], with a morbidity rate of 55%-100% and overall mortality rate of 91.7% in all gallbladder consumers. Although some reports have shown improvement of renal function within 2-3 wk[11], the recovery time was 5 wk in our patient. Elevation of liver enzymes or jaundice occurs in 75%-87% of patients[9]. Liver and kidney damages often occur simultaneously[12], and mild hepatitis caused by carp gallbladder is usually self-limited. Our patient’s liver function recovered on day 19, which was consistent with the findings of previous reports. These patients can also die of fulminant hepatic failure[3]. Other manifestations include cardiac complications (palpitations, hypertension, and myocardial damage) and neurological involvement (convulsion and coma), which vary individually.

The exact mechanisms of the toxic effects are not clear. However, necrosis of the renal proximal tubules (PT) may play an important role in the development of ARF[13]. The pathological severity correlated with clinical symptoms of sudden oliguria or anuria as well as increased urine NAG, a marker of tubular injury[14]. In an animal study[13], glomerular filtration rate decreased 24 h after the ingestion of 0.3 mL of grass carp bile, suggesting that nephrotoxic substances cause cellular damages by inhibiting the cytochrome oxidase, promoting calcium influx, and inducing lysosome membrane instability[9]. In a porcine study, Choi et al[15] suggested that nitric oxide generation and the phospholipase C pathway affect the release of renal dipeptidase from the PT, which may be involved in the development of ARF in vivo after the ingestion of carp bile. The significance of interstitial edema and inflammation characterized by infiltration of lymphocytes and monocytes observed on renal biopsy can be explained by the serious inflammatory response to cell necrosis induced by increased cell membrane permeability and the resultant enzyme release. In addition to renal toxicity, fish bile may cause a series of inflammatory responses evidenced by increased inflammatory mediators and cytokines, eventually leading to pathological changes of cell degeneration and necrosis. Another study[16] showed that plasma endothelin levels correlated with the severity of carp gallbladder poisoning. In our patient, C-reactive protein, procalcitionin, and serum amyloid A levels were increased. However, the role of inflammation in carp gallbladder toxicity requires further elucidation.

Moreover, in our patient, we found decreased leukocytes, neutrophils, lymphocytes, hemoglobin, and platelets and sinus bradycardia in the ECG, which, to our knowledge, have not been previously reported. In 1993, Lim et al[17] reported a case of sinus bradycardia that persisted for 2 d even after atropine was administered for symptomatic relief. A previous study has demonstrated experimentally that bile acids can affect the cardiovascular functions of animals both in vivo and in vitro, inducing bradycardia and systemic hypotension[18]. Further, it was found that the bile salts cause potent hemolysis in vitro[18]. In our patient, decreased counts of leukocytes, neutrophils, lymphocytes, and platelets resolved spontaneously, although anemia lasted for > 3 wk. Sinus bradycardia persisted for 2 d. We hypothesized that there may be an undiscovered hematotoxin or cardiotoxin in fish gallbladder, which needs further investigations.

There is no specific antidote for carp gallbladder poisoning. However, gastric lavage using 1%-5% soda or warm water is necessary in the first 72 h. Protecting the gastric mucosa by administering raw eggs or cattle milk may be effective[11]. Conventional hemodialysis is an effective temporary treatment for anuria or oliguria. Liu et al[19] revealed that continuous venovenous hemodiafiltration could effectively remove inflammatory mediators, metabolites, bilirubin, and toxins in severe cases while maintaining homeostasis. Our patient did not receive gastric lavage with 1%-5% soda or warm water due to the earlier misdiagnosis of gastroenteritis and delayed presentation at our center after poisoning. Supportive treatments, including gastric mucosal protectant and liver protectant, were provided appropriately and were tolerated in our patient, which aided her clinical recovery.

CONCLUSION

In summary, the diagnosis of this disease is primarily clinical and dependent on the history, as there are no special laboratory tests to confirm the disease. General practitioners, emergency physicians, and gastroenterologists should be mindful of the toxic complications of raw grass carp gallbladder. Educating the public regarding the toxic effects of raw gallbladder injection could be helpful in reducing the incidence of its toxicity, especially in the rural areas.

ACKNOWLEDGEMENTS

This case report was supported by ward doctors, especially in collection of specimens, treatment, analysis, and interpretation of data. We also extend our gratitude to the patient for providing the necessary medical history information, and to Dr. Huang for assistance in editing the final manuscript.

Footnotes

Manuscript source: Unsolicited manuscript

Specialty type: Medicine, research and experimental

Country/Territory of origin: China

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P-Reviewer: Barzilay J, Dumitrascu D S-Editor: Huang P L-Editor: Wang TQ P-Editor: Wang LYT

References
1.  Asakawa M, Noguchi T. Food poisonings by ingestion of cyprinid fish. Toxins (Basel). 2014;6:539-555.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 10]  [Cited by in F6Publishing: 11]  [Article Influence: 1.1]  [Reference Citation Analysis (0)]
2.  Wu HL, Chen YH, Chong DH, Mou Y. Study on the gallbladder poisonous fishes in China. Shanghai Haiyang Daxue Xuebao. 2001;10:102-108.  [PubMed]  [DOI]  [Cited in This Article: ]
3.  Krishna A, Singh PP, Vardhan H, Kumar O, Prasad G. Acute kidney injury with consumption of raw gall bladder of Indian carp fish (Labeo rohita): A single center study from India. Nephrology (Carlton). 2019;24:47-49.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 3]  [Cited by in F6Publishing: 4]  [Article Influence: 0.8]  [Reference Citation Analysis (0)]
4.  Xuan BH, Thi TX, Nguyen ST, Goldfarb DS, Stokes MB, Rabenou RA. Ichthyotoxic ARF after fish gallbladder ingestion: a large case series from Vietnam. Am J Kidney Dis. 2003;41:220-224.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 27]  [Cited by in F6Publishing: 29]  [Article Influence: 1.4]  [Reference Citation Analysis (0)]
5.  Goto T, Holzinger F, Hagey LR, Cerrè C, Ton-Nu HT, Schteingart CD, Steinbach JH, Shneider BL, Hofmann AF. Physicochemical and physiological properties of 5alpha-cyprinol sulfate, the toxic bile salt of cyprinid fish. J Lipid Res. 2003;44:1643-1651.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 41]  [Cited by in F6Publishing: 43]  [Article Influence: 2.0]  [Reference Citation Analysis (0)]
6.  Mohri T, Tanaka Y, Fukamachi K, Horikawa K, Takahashi K, Inada Y, Yasumoto T. Cyprinol as watersoluble poisoning component of carp. J Food Hyg Soc. 1992;33:133-143.  [PubMed]  [DOI]  [Cited in This Article: ]
7.  Park SK, Kim DG, Kang SK, Han JS, Kim SG, Lee JS, Kim MC. Toxic acute renal failure and hepatitis after ingestion of raw carp bile. Nephron. 1990;56:188-193.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 31]  [Cited by in F6Publishing: 33]  [Article Influence: 1.0]  [Reference Citation Analysis (0)]
8.  Deng Y, Xiao G, Jin Y, Luo X, Meng X, Li J, Ao Z, Xiao J, Zhou L. Multiple organ dysfunction syndrome due to ingestion of fish gall bladder. Chin Med J (Engl). 2002;115:1020-1022.  [PubMed]  [DOI]  [Cited in This Article: ]
9.  Kung SW, Chan YC, Tse ML, Lau FL, Chau TL, Tam MK. Acute renal failure and hepatitis following ingestion of carp gallbladder. Clin Toxicol (Phila). 2008;46:753-757.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 18]  [Cited by in F6Publishing: 16]  [Article Influence: 1.1]  [Reference Citation Analysis (0)]
10.  Owada A, Shinohara S, Fukumoto Y, Nishimura M, Matsui N, Fujiwara H. Two cases of acute renal failure induced by raw carp gallbladder. Saishin Igaku. 1990;45:605-609.  [PubMed]  [DOI]  [Cited in This Article: ]
11.  Hu XR, Lu L, Wang YS, Shang J, Wang BW, Huang LF. Clinical analysis of 86 cases of acute fish bile poisoning. Zhonghua Neike Zazhi. 2000;39:273-274.  [PubMed]  [DOI]  [Cited in This Article: ]
12.  Lin YF, Lin SH. Simultaneous acute renal and hepatic failure after ingesting raw carp gall bladder. Nephrol Dial Transplant. 1999;14:2011-2012.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 21]  [Cited by in F6Publishing: 24]  [Article Influence: 1.0]  [Reference Citation Analysis (0)]
13.  Chen CF, Chen WY, Yen TS. The effect of raw grass carp (Ctenopharyngodon idellus) bile on renal function in the conscious rat. Taiwan Yi Xue Hui Za Zhi. 1983;82:1203-1209.  [PubMed]  [DOI]  [Cited in This Article: ]
14.  Zhou Y, Vaidya VS, Brown RP, Zhang J, Rosenzweig BA, Thompson KL, Miller TJ, Bonventre JV, Goering PL. Comparison of kidney injury molecule-1 and other nephrotoxicity biomarkers in urine and kidney following acute exposure to gentamicin, mercury, and chromium. Toxicol Sci. 2008;101:159-170.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 212]  [Cited by in F6Publishing: 222]  [Article Influence: 13.1]  [Reference Citation Analysis (0)]
15.  Choi K, Park SW, Lee KJ, Lee HB, Han HJ, Park SK, Park HS. Grass carp (Ctenopharyngodon idellus) bile may inhibit the release of renal dipeptidase from the proximal tubules by nitric oxide generation. Kidney Blood Press Res. 2000;23:113-118.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 4]  [Cited by in F6Publishing: 5]  [Article Influence: 0.2]  [Reference Citation Analysis (0)]
16.  Xia CY, Zhou JG, Xie JP, Zhang GY, Zhang L, Wu SP. [Plasma endothelin levels in patients with multiple organ dysfunction syndrome caused by fish gall bladder poisoning]. Zhonghua Neike Zazhi. 2004;43:205-208.  [PubMed]  [DOI]  [Cited in This Article: ]
17.  Lim PS, Lin JL, Hu SA, Huang CC. Acute renal failure due to ingestion of the gallbladder of grass carp: report of 3 cases with review of literature. Ren Fail. 1993;15:639-644.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 12]  [Cited by in F6Publishing: 12]  [Article Influence: 0.4]  [Reference Citation Analysis (0)]
18.  Chen CF, Yen TS, Chen WY, Chapman BJ, Munday KA. The renal, cardiovascular and hemolytic actions in the rat of a toxic extract from the bile of the grass carp (Ctenopharyngodon idellus). Toxicon. 1984;22:433-439.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 16]  [Cited by in F6Publishing: 16]  [Article Influence: 0.4]  [Reference Citation Analysis (0)]
19.  Liu Z, Zhao M. Continuous Renal Replacement Therapy for Multiple Organ Injury Induced by Raw Fish Gallbladder Poisoning. Am J Ther. 2017;24:e773-e774.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2]  [Cited by in F6Publishing: 2]  [Article Influence: 0.4]  [Reference Citation Analysis (0)]