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Biomedical subjects

T Cundy

Publications and source records attributed to T Cundy.

103 records · Page 6Linked to original sources
PubMed1981

The role of vitamin D metabolites in the osteomalacia of renal disease.

Osteomalacia is commonly found in patients with severe renal impairment. Its aetiology is multifactional and not simply due to deficient production of active metabolites of vitamin D. Decreased availability of calcium and phosphate and the accumulation of aluminium is some dialysis-treated patients are also important aetiological factors. The treatment of osteomalacia depends, in part, upon its accurate diagnosis, and identifying and reversing the underlying cause.

Calcium↗
PubMed1980

An evaluation of 1 alpha-hydroxy-and 1,25-dihydroxyvitamin D3 in the treatment of renal bone disease.

40 patients with bone disease due to chronic renal failure have been treated with 1 alpha-hydroxyvitamin D3 or 1,25-dihydroxyvitamin D3 for a total of 750 patient-months. Both compounds were very effective in relieving bone pain and muscle weakness, and in reversing the radiographic and biochemical indices of disturbed skeletal metabolism. Their effects as judged from bone biopsies were, however, less complete, and histological improvement occurred only in a few patients. Patients with the combination of osteitis fibrosa and osteomalacia responded better than patients with either abnormality alone. Factors of importance in adversely influencing the outcome of treatment included a high pre-treatment level of calcium or immunoreactive parathyroid hormone, and a failure to augment secretion of calcitonin during treatment. It is concluded that a major therapeutic advantage of 1 alpha-OHD3 and 1,25(OH)2D3 over previously available forms of vitamin D is their rapid onset and reversal of action. These drugs do not invariably reverse bone disease and may give rise to unwanted effects. They should therefore only be used with adequate clinical, biochemical and radiographic supervision. They should not be used indiscriminately in all renal patients.

Adolescent↗
PubMed1979

The relationship between disturbed metabolism of vitamin D and bone disease in chronic renal failure.

Following the discovery that the kidney is involved in the metabolism of vitamin D, a causal relationship has been sought between defective production of 1,25-dihydroxy vitamin D3 and bone disease in chronic renal failure. This paper reviews some of the clinical evidence for and against such a relationship, and considers the possible role of other vitamin D metabolites in the pathophysiology of renal bone disease.

Bone Diseases↗
PubMed1979

Treatment of renal bone disease with 1 alpha-hydroxylated derivatives of vitamin D3. Clinical, biochemical, radiographic and histological responses.

Forty patients with severe bone disease and chronic renal failure were treated with 1 alpha-hydroxycholecalciferol (1 alpha-OHD3) or 1,25-dihydroxycholecalciferol (1,25(OH)2D3) for 7--49 months (total = 738 patient months). There were symptomatic, biochemical and radiographic improvements in the majority of patients (greater than 70 per cent). Paired bone biopsies, taken before and during treatment in 26 patients, showed no change in bone matrix area, whereas matrix area decreased in a control group of 26 patients over the same period. There were small but consistent decreases in bone marrow fibrosis and in bone cell (osteoblast and osteoclast) counts in treated patients but not in controls. However, the proportion of patients who showed histological 'cure', in the sense of complete reversal of marrow fibrosis or excess osteoid was no greater in the treated than in the control group...

Adolescent↗
PubMed1978

Is 24,25-dihydroxycholecalciferol a calcium-regulating hormone in man?

Small doses (1-10 microgram daily) of 24,25-dihydroxycholecalciferol (24,25-(OH)2D3), a renal metabolite of vitamin D of uncertain function, increased intestinal absorption of calcium in normal people and in patients with various disorders or mineral metabolism, including anephric subjects. In five of six patients studied, calcium balance increased, but, unlike 1,25-dihydroxycholecalciferol, 24,25-(OH)2D3 did not increase plasma or urinary calcium concentrations. These results suggest that 24,25-(OH)2D3 may be an important regulator of skeletal metabolism in man with potential value as a therapeutic agent.

Adult↗
PubMed1978

Physiological and pharmacological aspects of 24,25-dihydroxycholecalciferol in man.

The present study describes the response to small oral doses (1--10 microgram/day) of 24,25-DHCC in man. Contrary to expectation, 24,25-DHCC was as potent as 1,25-DHCC in increasing intestinal absorption of calcium both in normal persons and in patients with a variety of disorders of calcium metabolism. Despite this increase in intestinal absorption, plasma and urine calcium did not increase after 24,25-DHCC as they did after 1,25-DHCC. Metabolic balance studies showed calcium balances to increase by 1.6 to 11.5 mmoles/day in 5 of the 6 patients studied. 24,25-DHCC increased intestinal absorption of calcium equally well in anephric patients, suggesting that conversion of 24,25-DHCC to 1,24,25-trihydroxycholecalciferol by the kidney cannot be the sole mechanism by which 24,25-DHCC expresses biological activity, even though in vitamin D deficient rats nephrectomy does abolish the ability of large doses of 24,25-DHCC to increase calcium absorption. It is concluded that 24,25-DHCC may be a calcium-regulating hormone in man. In view of the effects demonstrated here and its relatively high concentration in plasma and slow turnover rate, 24,25-DHCC has the properties that might be ideal for a long-acting stimulator of bone mineralisation. Further work is needed to explain why 24,25-DHCC has effects in man which are not readily seen in other species.

Bone Development↗
PubMed1978

Biological activity of endogenous and exogenous calcitonin in patients with osteitis fibrosa and chronic renal failure.

Successful treatment of osteitis fibrosa with 1alpha-hydroxycholecalciferol (1alpha-OHD3) in 9 patients with end-stage chronic renal failure was associated with a significant increase in plasma levels of immunoreactive calcitonin (iCT) independently of changes in plasma calcium, and a decrease in levels of parathyroid hormone (iPTH). In 9 further patients whose plasma alkaline phosphatase activity failed to suppress with 1alpha-OHD3, changes in iPTH were associated with proportionate changes in iCT. This suggests that a rise in endogenous calcitonin (CT) secretion contributes to the success of treatment with 1alpha-OHD3. In 13 further patients, injections of salmon CT induced a fall in plasma calcium and phosphate which was proportional to the prevailing level of plasma alkaline phosphatase. These data provide further evidence that bone resorption can be effectively inhibited when CT levels are raised either by exogenous CT or its endogenous stimulation.

Alkaline Phosphatase↗