[Osteomalacia due to vitamin D deficiency. Part One: mechanisms (author's transl)].
Vitamin D deficiency is in most cases subclinical and can only be detected by blood vitamin assays or biochemical changes in phosphorus and calcium metabolism. Clinical and radiological osteomalacia is much less common. It is due to prolonged and profound hypovitaminaemia, which in turn depends upon a variety of factors, the main one being defective photosynthesis. Low vitamin D dietary intake apparently does not result in osteomalacia unless it is accompanied by insufficient exposure to sun. Malabsorption of cholecalciferol results from steatorrhoea of various origina. Disorders in hepatic 25-hydroxylation are due to drug enzymatic induction and seem to be unrelated to the state of the renal function. Disorders in renal 1,25-hydroxylation may be consecutive to reduced renal tissue, impaired stimulation, or inhibiton or even congenital lack of 1-alpha hydroxylase.
D000328:Adult; D000818:Animals; D002762:Cholecalciferol / Q000378:metabolism; D004032:Diet; D006801:Humans; D006900:Hydroxylation; D007408:Intestinal Absorption; D010018:Osteomalacia / Q000209:etiology*; D051381:Rats; D014466:Ultraviolet Rays; D014807:Vitamin D / Q000096:biosynthesis; D014808:Vitamin D Deficiency / Q000150:complications* / Q000503:physiopathology
D014807:Vitamin D; D002762:Cholecalciferol
Ostéomalacies par hypovitaminose D. 1ere partie: les mécanismes.