Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This chapter reviews the pathogenesis of disordered divalent mineral and bone metabolism in alcoholism, emphasizing the role of impaired vitamin D physiology. Normally, vitamin D metabolites are derived principally from cholecalciferol, which is synthesized in the skin via the energy of sunlight. Most alcoholics have subnormal levels of 25-hydroxyvitamin D [25(OH)D]. Those with Laennec's cirrhosis also have low levels of vitamin D binding protein due to impaired hepatic protein synthesis and as a result, have low serum concentrations of total, but not free, 1,25-dihydroxyvitamin D. The causes of 25(OH)D deficiency in alcoholics include reduced hepatic 25-hydroxylase activity, lack of sun exposure, inadequate dietary intake, and malabsorption. Hypomagnesemia and hypophosphatemia, which are very common in hospitalized alcoholics, result from deficient intake, malabsorption, excessive renal losses, and cellular uptake of both ions. Hypocalcemia in alcoholics is caused primarily by hypoalbuminemia but can result also from deficient intake, malabsorption, hypomagnesemia, and renal calcium wastage. Low vitamin D activity may contribute significantly to the calcium and phosphate deficiencies. Osteoporosis is extremely common in alcoholics whereas osteomalacia is exceptional. However, both bone disorders respond well to vitamin D therapy. Thus, alcoholics should be screened periodically for vitamin D deficiency and osteopenia, and when either is detected they should receive vitamin D supplements.
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PMID:Disorders of divalent ions and vitamin D metabolism in chronic alcoholism. 375 48