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Biomedical subjects

T C Stamp

Publications and source records attributed to T C Stamp.

At least 55 records · Page 3Linked to original sources

Altered vitamin-D metabolism in pregnancy.

Low levels of plasma-25-hydroxy-vitamin-D (25-OHD) (less than 16 nmol/1) were found in 33% of a group of pregnant women studied in South London. Non-White women in the last 10 weeks of pregnancy had significantly reduced levels compared with non-pregnant controls (P less than 0.02). Plasma-25-OHD was unrelated to dietary vitamin-D intake, age, parity, social class, plasma-calcium, and plasma-albumin. Reduction of plasma-25-OHD could contribute to the fall in plasma-calcium during pregnancy, and may result from enhanced maternal metabolism or increased utilisation of vitamin D by the fetus.

Alkaline Phosphatase↗

The effect of 25-hydroxy vitamin D3 in the osteomalacia of chronic renal failure.

1. Five patients with the osteomalacia of chronic renal failure were given 50--100 nmol of 25-hydroxy vitamin D3 intravenously per day for 24--28 days. 2. In all five patients, during administration of 25-hydroxy vitamin D3 there was a substantial rise in the plasma concentration of 25-hydroxy vitamin D from initially abnormally low values. 3. Significant improvement in bone mineralization, intestinal calcium absorption and muscle strength occurred in the three patients with the greatest rise in plasma 25-hydroxy vitamin D.

Aged↗

Vitamin-D deficiency in the osteomalacia of chronic renal failure.

The plasma level of 25-hydroxy-vitamin D (25-OHD) has been measured and the histological appearances of bone examined in 22 patients with stable chronic renal failure. The results show that osteomalacia occurred only in those patients with relatively low levels of 25-OHD. It is concluded that the osteomalacia of chronic renal failure results from a lack of 25-hydroxy-vitamin D3 superimposed on an existing deficiency of 1,25-dihydroxy-vitamin D3 (1,25-(OH)2D3) rather than from lack of 1,25-(OH)2D3 alone.

Adolescent↗

Recessive hypophosphataemic rickets, and possible aetiology of the 'vitamin D-resistant' syndrome.

Two out of 3 children of a first-cousin marriage presented with severe rickets in infancy and are now adult. Their disease has shown continued activity, marked resistance to treatment with vitamin D, early fusion of cranial sutures, greatly increased bone density, nerve deafness, and life-long hypophosphataemia unaffected by treatment. Both parents and a third sib were normal clinically and biochemically. Blood grouping supported both stated paternity and parental consanguinity. Genetics of this unique disease can only be explained satisfactorily on the basis of autosomal recessive transmission, a mode not previously reported in primary hypophosphataemia. This homozygous disease resembles an exaggerated form of common X-linked rickets, though it is caused by a different gene. Although rare, it is particularly important because of the information it provides on the pathogenesis of both forms. We propose that both syndromes may result from multiple target organ unresponsiveness to 1,25-dihydroxycholecalciferol in intestine, kidney, bone, and parathyroid gland.

Adolescent↗

Treatment of osteolytic myelomatosis with mithramycin.

The treatment of rapidly progressive skeletal demineralisation in myelomatosis has been studied with the help of metabolic calcium balance in two patients; In one, osteoporosis accelerated during treatment with melphalan and prednisolone, although he remained normocalcaemic throughout, suggesting that osteoporosis was aggravated by corticosteroid therapy. In the other patient, who was initially hypercalcaemic, conventional treatment produced clinical remission before eventual relapse with more hypercalcaemia and skeletal dissolution. Both patients were then treated with mithramycin alone, and, although neither obtained haematological remission, bone pain was relieved, hypercalciuria and hypercalcaemia were abolished, and calcium balances proved that mithramycin was effective in restoring calcium equilibrium. The results indicate that mithramycin may abolish excessive bone resorption in myelomatosis and that severe bone dissolution may occur in the absence of hypercalcaemia. Regular determination of 24-hour urinary calcium excretion as well as of plasma-calcium is important in monitoring process. Mithramycin should be considered in the early treatment not only of hypercalcaemia but also of severe hypercalciuria, if these complications do not rapidly remit during the first course of conventional myeloma therapy, with or without steroids. Finally, these results add to evidence that a humoral factor may be responsible for osteoclast stimulation in myelomatosis.

Aged↗

Iatrogenic osteomalacia and myopathy due to phosphate depletion.

In a patient receiving regular dialysis prolonged hypophosphataemia due to aluminium hydroxide therapy resulted in osteomalacia and severe proximal myopathy. Both osteomalacia and myopathy responded to correction of hypophosphataemia without vitamin D therapy.

Adult↗