Copyright
©2014 Baishideng Publishing Group Inc.
World J Gastroenterol. Oct 28, 2014; 20(40): 14660-14671
Published online Oct 28, 2014. doi: 10.3748/wjg.v20.i40.14660
Published online Oct 28, 2014. doi: 10.3748/wjg.v20.i40.14660
Factors | Main mechanism(s) involved |
Direct effect of ethanol | Direct effect on osteoblast function (oxidative damage). Possible effect on bone resorption (cytokines) |
Liver disease | Decreased absorption of proteins, calcium, vitamin D, nutrients in general |
Altered hormonal profile (altered IGF-1, vitamin D, gonadal hormones) | |
Chronic pancreatitis | Altered absorption. Malnutrition |
Malnutrition | Decreased osteoid synthesis. Decreased IGF-1 levels. Altered nutrient intake. Altered absorption. Increased cytokine levels? |
Alcoholic hypogonadism | Altered trophic effect on bone and muscle |
Alcoholic myopathy/neuropathy | Altered trophic effect on bone (probably via Wnt β catenin pathway) |
Iron excess (increased absorption) | Interference with osteoblast function |
Zinc deficiency (malnutrition; alcohol?) | Possibly, defective protein synthesis |
Cytokines (IL-6; TNF-α) | Possibly, increased bone resorption |
Lifestyle | Trauma. Bone fractures. Impaired nutrient intake |
- Citation: González-Reimers E, Santolaria-Fernández F, Martín-González MC, Fernández-Rodríguez CM, Quintero-Platt G. Alcoholism: A systemic proinflammatory condition. World J Gastroenterol 2014; 20(40): 14660-14671
- URL: https://www.wjgnet.com/1007-9327/full/v20/i40/14660.htm
- DOI: https://dx.doi.org/10.3748/wjg.v20.i40.14660