Vitamin D metabolism and chronic liver disease.
In recent years, considerable developments have taken place in the understanding of the vitamin D compounds which allows them, or at least their metabolites, to be classified as hormones. The liver has, for many years, entered into any consideration of the normal control of vitamin D status and metabolism in a number of roles. The main importance of the liver in vitamin D metabolism is now recognized to be the critical role it plays in the hydroxylation pathway and consequent formation of biologically active metabolites. Because the liver plays a critical central role in vitamin D metabolism, and possibly determines the overall efficiency of utilization, it may be expected that disorders of vitamin D metabolism, with associated clinical sequelae in the form of metabolic bone disease and hypocalcemia, and clinical features of patients with chronic disorders of liver function. The serum concentration 25-hydroxyvitamin D (25-OHD) is generally accepted as reflecting total body vitamin D status in patients with normal renal function. Low serum 25-OHD concentrations have been reported in patients with a variety of hepatic disorders including: symptomatic primary biliary cirrhosis, alcoholic liver disease, chronic active liver disease, and large bile-duct obstruction owing to carcinoma or stones. The mechanisms for the low circulating serum 25-OHD concentrations in patients with chronic liver disease are complex and multifactorial. The disturbances in vitamin D metabolism in patients with chronic liver disease and biliary disease are associated with disturbances in calcium homeostasis and together they present clinically as hepatic osteodystrophy. The latter consists of osteomalacia, possibly sometimes complicated by secondary hyperparathyroidism, osteoporosis, and periosteal new bone formation.
D015650:24,25-Dihydroxyvitamin D 3; D001692:Biological Transport; D001847:Bone Diseases / Q000209:etiology; D002112:Calcifediol / Q000097:blood / Q000172:deficiency / Q000378:metabolism; D002117:Calcitriol / Q000502:physiology; D002118:Calcium / Q000378:metabolism; D002352:Carrier Proteins / Q000378:metabolism; D002762:Cholecalciferol / Q000378:metabolism; D053493:Cholestanetriol 26-Monooxygenase; D002908:Chronic Disease; D004032:Diet; D004100:Dihydroxycholecalciferols / Q000378:metabolism; D006801:Humans; D006900:Hydroxylation; D007408:Intestinal Absorption; D007668:Kidney / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008107:Liver Diseases / Q000150:complications / Q000378:metabolism*; D008286:Malabsorption Syndromes / Q000209:etiology; D012867:Skin / Q000378:metabolism / Q000528:radiation effects; D013250:Steroid Hydroxylases / Q000378:metabolism; D014466:Ultraviolet Rays; D014807:Vitamin D / Q000378:metabolism*; D014809:Vitamin D-Binding Protein
D002352:Carrier Proteins; D004100:Dihydroxycholecalciferols; D014809:Vitamin D-Binding Protein; D014807:Vitamin D; D002762:Cholecalciferol; D015650:24,25-Dihydroxyvitamin D 3; D013250:Steroid Hydroxylases; C506831:CYP27A1 protein, human; D053493:Cholestanetriol 26-Monooxygenase; D002117:Calcitriol; D002112:Calcifediol; D002118:Calcium