Calciferols vitamin deficiency

The effects of the steroid hormone calcitriol (see p. 330) in bone are complex. On the one hand, it promotes bone formation by stimulating osteoblast differentiation (top). This is particularly important in small children, in whom calcitriol deficiency can lead to mineralization disturbances (rickets see p.364). On the other hand, calcitriol increases blood Ca "" levels through increased Ca "" mobilization from bone. An overdose of vitamin D (chole-calciferol), the precursor of calcitriol, can therefore have unfavorable effects on the skeleton similar to those of vitamin deficiency (hypervitaminosis see p.364). 

VII.a.2.2. Treatment. Treatment of established vitamin D deficiency requires much larger doses of vitamin D, such as calciferol tablets of 1 mg (40,000 units) daily. Newer but more expensive preparations such as alfa-calcidol and calcitriol are very effective, and are particularly valuable in patients with renal failure who are unable to hydroxylate calciferol. Patients treated with pharmacological doses of vitamin D preparations must be monitored by checking serum calcium at regular intervals because of the risk of inducing hypercalcaemia. This should always be suspected if patients develop thirst, nausea or vomiting. The newer hydroxylated preparations have a shorter effective half-life, and therefore problems of overdosage are quicker to resolve once identified. 

Vitamin D (cholecalciferol ergocalciferol) has its active form as 1,25-dihydroxylchole-calciferol. It is responsible for calcium uptake, and a deficiency of the vitamin results in rickets (in children) and osteomalacia (in adults). The symptoms of both syndromes are soft, pliable bones. High levels of vitamin D are toxic. 

As a brief introductory summary, vitamin D substances perform the following fundamental physiological functions (1) promote normal growth (via bone growth) (2) enhance calcium and phosphorus absorption from the intestine (3) serve to prevent rickets (4) increase tubular phosphorus reabsorpiion (5) increase citrate blood levels (6) maintain and activate alkaline phosphatase m bone (7) maintain serum calcium and phosphorus levels. A deficiency of D substances may be manifested in the form of rickets, osteomalacia, and hypoparathyroidism. Vitamin D substances are required by vertebrates, who synthesize these substances in the skin when under ultraviolet radiation, Animals requiring exogenous sources include infant vertebrates and deficient adult vertebrates, Included there are vitamin D (calciferol ergocalciferol) and vitamin D< (activated 7-dehydrocholesterol cholecalciferol). 

Vitamin D analogs Calcifediol (Calderol) Calcitriol (Rocaltrol) Dihydrotachysterol (DHT, Hytakerol) Ergocalciferol (Calciferol, Drisdol) Generally enhance bone formation by increasing the absorption and retention of calcium and phosphate in the body useful in treating disorders caused by vitamin D deficiency, including hypocalcemia, hypophosphatemia, rickets, and osteomalacia... 

Wu F, Staykova T, Horne A, et al. Efficacy of an oral, 10-day course of high-dose calciferol in correcting vitamin D deficiency. N Z Med J 2003 116 U536. 

Miravet, L., J. R. Del, M. Carre, M. L. Queille, and P. Bordier The Biological Activity of Synthetic 25,26-Dihydroxycholecalciferol and 24,25-Dihydroxychole-calciferol in Vitamin D-Deficient Rats. Calcif. Tiss. Res. 21, 145 (1976). 

Infants with severe cholestasis due to 3jff-HSDH deficiency may have hypo-calcaemia due to malabsorption of vitamin D or severely deranged clotting due to malabsorption of vitamin K. Vitamins D and K should be given either parenterally or orally in a form that is absorbed despite intestinal bile salt deficiency (e.g. la-hydroxy-cholecalciferol or 1,25-dihydroxy-chole-calciferol). Fresh frozen plasma and intravenous calcium supplement may occasionally be required. 

Another substance, chemically related to vitamin D2 (calciferol), has an effect similar to that of parathormone. This is dihydrotochysterol (AT 10). The effect is, however, in some aspects more comparable to D-hypervitaminosis. Dihydrotachysterol is used frequently in tetany caused by a deficiency of the parathyroid hormone, because the peptide hormone is not readily available. 

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