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Biomedical subjects

T C Stamp

Publications and source records attributed to T C Stamp.

17 recordsLinked to original sources
PubMed1991

Depressed levels of circulating menaquinones in patients with osteoporotic fractures of the spine and femoral neck.

Vitamin K1 functions in the conversion of glutamate residues, present in certain bone peptides, into the putatively active gamma-carboxyglutamate form. We have shown previously that the circulating levels of vitamin K1 are depressed in osteoporotic patients. However, it is known that menaquinones (vitamin K2:MK) may be more effective than vitamin K1 in this conversion of the inactive to active form of glutamate residues. A procedure for measuring such menaquinones has now demonstrated a marked deficiency of MK-7 and MK-8 in patients with osteoporotic fractures. It is suggested that estimates of circulating levels of K1, MK-7, and MK-8 might provide a biochemical risk marker of osteoporotic fractures.

Aged↗
PubMed1979

Vitamin D bioavailability: serum 25-hydroxyvitamin D levels in man after oral, subcutaneous, intramuscular, and intravenous vitamin D administration.

Bioavailability of vitamin D (D) was assessed by competitive protein-binding assay of serum 25-hydroxyvitamin D (25OHD) levels in normal adult volunteers after a single oral, sc, or im dose of commercially available D pharmaceuticals or after a single iv injection of ethanol-propylene glycol solution containing D. Similar increases in serum 25OHD levels were noted after either iv D2 or D3 (100 micrograms/kg), suggesting that the 25-hydroxylation of D2 and D3 is comparable in man. Absolute increases in serum 25OHD levels were similar in subjects receiving D in iv doses of 100 and 250 micrograms/kg; however, subjects receiving the larger dose had higher basal 25OHD levels. This finding suggests an inverse relationship in man between basal serum 25OHD concentrations and relative serum 25OHD increments after administration of pharmacological doses of D. Oil depot sc and im injection of D (200 micrograms/kg) resulted in delayed serum 25OHD increases compared to oral and iv dosing (100 micrograms/kg). Studies after im oil depot injection of [3H]D3 into rats showed that D administered in this manner had delayed bioavailability but remained unaltered in situ. Differences in D pharmaceutical bioavailability should be considered in treatment or prophylaxis with this sterol.

Administration, Oral↗
PubMed1978

Hereditary hypophosphataemic rickets with autosomal recessive inheritance and severe osteosclerosis. A report of two cases.

We have observed congenital hypophosphataemic rickets in two sons of a marriage between first cousins, their mother being clinically and biochemically normal. Both patients are now approaching middle age. In addition to severe childhood rickets and lifelong hypophosphataemia, their disease is characterised by gross osteosclerosis with extraskeletal ossification, clinically persistent osteomalacia in one and spinal cord compression in the other. The genetics of this disease can be satisfactorily explained only on the basis of autosomal recessive inheritance, a mode which has only once before been reported in the literature. The severity of certain features, which would be expected in a homozygous state, may help our understanding of the more usual X-linked form.

Adult↗
PubMed1977

Comparison of oral 25-hydroxycholecalciferol, vitamin D, and ultraviolet light as determinants of circulating 25-hydroxyvitamin D.

Circulating concentrations of 25-hydroxyvitamin D (25-OHD) were measured during short-term and long-term oral treatment with 25-hydroxycholecalciferol (25-OHD3), 25-H.C.C.) or with vitamin D in over 200 subjects over a period of 5 years. Ten times more vitamin D than 25-OHD3 was required to produce equivalent plasma-25-OHD concentrations. Plasma-25-OHD was a power function of dosage with both compounds. These data indirectly measure the superior therapeutic potency of 25-OHD3, show that dose-response relations with both compounds may be useful in diagnosis, and indicate that there are pronounced constraints on 25-hydroxylation of vitamin D. Together with the effects of ultraviolet light, now shown to be equivalent to oral vitamin D in doses of 8000-10 000 I.U. daily, these constraints may protect against vitamin-D deficiency in winter.

Administration, Oral↗
PubMed1977

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↗
PubMed1977

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↗
PubMed1976

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↗
PubMed1976

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↗
PubMed1975

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↗