PubMed Health⌕ Search

Biomedical subjects

T Cundy

Publications and source records attributed to T Cundy.

At least 91 records · Page 5Linked to original sources
PubMed1985

Bone metabolism in acute parathyroid crisis.

Studies on bone metabolism described in a fatal case of acute parathyroid crisis, occurring in a 48-year-old woman in whom serum immunoreactive parathyroid hormone levels were very high, and a 5 g parathyroid adenoma was found at operation. The histological and biochemical findings suggested a massive and acute increase in bone resorption. There was, however, no evidence of any compensatory increase in bone formation, indicating that acute parathyroid crisis is characterized by a marked dissociation between bone resorption and formation. It is suggested that a sudden fall in oestrogen levels may contribute to the pathogenesis of this disorder.

Acute Disease↗
PubMed1985

Referrals to psychiatrists in a general hospital--comparison of two methods of liaison psychiatry: preliminary communication.

Patients on a general medical ward were offered a liaison psychiatric service with 'unlimited' access, in which referrals were accepted from nurses, other paramedical staff and junior doctors in addition to senior medical staff. This new service (method II) was compared with the usual liaison service (method I, referrals initiated or approved by senior medical staff only) which was continued in parallel on a comparable general medical ward. Method II resulted in a threefold increase in referral rate and led to a significant alteration in the types of problem attracting referral. Despite the much higher rate of method II referrals, however, similar percentages of referrals by both methods were offered psychiatric follow up. The results do not support the commonly held belief that it is the failure of ward staff to recognize psychiatric morbidity which accounts for the low rate of referrals to many psychiatric liaison services.

Adult↗
PubMed1985

Progression of cardiovascular disease in acromegalic patients treated by external pituitary irradiation.

Cardiovascular complications are a major cause of morbidity and mortality in acromegaly and seem to be related to the long duration of the disorder. Conventional external pituitary irradiation for acromegaly produces a consistent, but slow, fall in elevated serum growth hormone (GH) levels. It has not been established whether such treatment is effective in preventing the development of cardiovascular complications. The evolution of cardiovascular disease has therefore been studied in 11 acromegalic patients followed up for a mean 10 years (range 3-17) after external pituitary irradiation. At the final follow-up fasting serum GH were significantly (P less than 0.01) lower than pre-irradiation levels, but cardiovascular events (myocardial infarction, dysrhythmias, hypertension, major arterial disease, heart failure) increased significantly in prevalence (P less than 0.01) during this period. Electrocardiographic abnormalities also increased in prevalence. At the final follow-up 6 patients had cardiomegaly on chest X-ray and echocardiographs (10 patients) were abnormal in every case. All 11 patients had evidence of complete or partial anterior hypopituitarism. We confirm that external pituitary irradiation is effective in reducing elevated serum GH levels in acromegaly, but suggest that such a slow reduction in serum GH levels does not retard the development of cardiovascular complications.

Acromegaly↗
PubMed1985

Hyperparathyroid bone disease in chronic renal failure.

Much has been learnt over the past 80 years of the pathogenesis and management of hyperparathyroid bone disease in uraemia. Clinically it has changed from a rare disorder of childhood and adolescence to a common and difficult problem in patients maintained on dialysis programmes. Whereas effective treatments are now available for hyperparathyroid bone disease, these are not curative and there is clearly much more work to be done before a full understanding of its pathogenesis, and the best methods of treatment and prevention, can be reached.

Bone Diseases↗
PubMed1983

Vitamin A and hyperparathyroid bone disease in uremia.

The possible contribution of hypervitaminosis A to bone disease in uremia was examined in 50 dialysis-treated patients with end-stage chronic renal failure. None of the patients received dietary supplements of vitamin A. In common with previous investigations, plasma concentrations of total vitamin A and the retinol-binding protein (RBP) were increased in patients, but the molar ratio of vitamin A to RBP was significantly lower than control values. A significant correlation was noted between concentrations in plasma of vitamin A and RBP. No significant relationship was found between vitamin A or the vitamin A/RBP ratio, and the measured biochemical, radiographic, or histological indices of hyperparathyroidism and bone resorption. We conclude that the elevated plasma values of vitamin A in uremia are largely attributable to the high concentrations of RBP and do not contribute significantly to the pathogenesis of renal osteodystrophy.

Adult↗
PubMed1983

Calcium metabolism and hyperparathyroidism after renal transplantation.

Plasma calcium and albumin levels were measured serially in 100 patients for two years following successful renal transplantation. Mean plasma calcium increased during the first six months after grafting, in large part attributable to an increase in plasma albumin. The variance around the mean plasma calcium did not increase suggesting that mechanisms responsible for hypercalcaemia were common to the majority of patients. 36 per cent of patients developed hypercalcaemia within two years of grafting but the incidence fell to 11 per cent when more rigorous criteria for hypercalcaemia were used. The mechanisms maintaining plasma calcium were studied in 29 of the patients, nine of whom were hypercalcaemic and 20 of whom were normocalcaemic. Before transplantation, mean plasma calcium and phosphate levels were higher, the prevalence of subperiosteal erosions and extraskeletal calcification radiographically was greater, and the duration of haemodialysis treatment was longer in the hypercalcaemic patients than in the normocalcaemic recipients. At assessment after transplantation, hypercalcaemic patients had lower levels of plasma phosphate, higher plasma levels of alkaline phosphatase and parathyroid hormone, and higher hydroxyproline excretion. Renal function and 47Ca absorption were similar in the two groups. The major cause for apparent hypercalcaemia in transplanted patients appeared to be an increase in plasma albumin. In patients with true hypercalcaemia the major cause was pre-existing hyperparathyroidism where hypercalcaemia was mediated by increased renal tubular reabsorption of calcium.

Calcium↗
PubMed1982

An estimate of the endogenous secretion rate of calcitonin in man.

1. The metabolic clearance rate (MCR) of human calcitonin was measured in 12 normal subjects and four patients with Paget's disease by the infusion of synthetic human calcitonin (15-40 microgram/h for 2-24 h), and in 10 additional patients with Paget's disease from the disappearance rate of immunoreactive calcitonin from plasma after the intravenous injection of large doses of synthetic human calcitonin (0.5-1.0 mg). 2. The estimated MCR during the infusion studies (range 531-1224 litres/day) was similar to that calculated from the disappearance of large doses of synthetic human calcitonin injected intravenously in patients with Paget's disease (mean = 1035 litres/day; range = 593-1408 litres/day). 3. An eightfold range in the basal values of plasma immunoreactive calcitonin, in spite of the presence of a relatively constant MCR, suggests that the variation in basal plasma calcitonin was due principally to variation in the endogenous secretion rate for calcitonin. 4. The results suggest that the endogenous secretion rate for calcitonin is low in normal subjects (mean 124 +/- SEM 24 microgram/day), and give a basis for selecting the doses of calcitonin which can be considered physiological.

Adolescent↗
PubMed1982

Deterioration of renal bone disease in patients treated with salmon calcitonin.

Twelve patients with chronic renal failure and osteitis fibrosa were treated for periods of 1-9 months with thrice-weekly injections of 10-200 iu salmon calcitonin. Treatment had no significant effects on symptoms of bone disease and side effects were common. A transient fall in plasma alkaline phosphatase levels occurred in only three patients, and both plasma alkaline phosphatase and hydroxyproline levels rose in the majority of patients. Radiographic signs of hyperparathyroidism increased in seven of the nine patients treated for longer than 3 months. Paired bone biopsy specimens in nine patients showed significant increases in osteoblast counts, but no changes in the indices of resorption. These treatment-induced changes were reversed when treatment with 1,25-dihydroxyvitamin D3 was substituted for calcitonin. The use of this regimen of salmon calcitonin is not recommended in the long-term management of hyperparathyroid bone disease in chronic renal failure.

Adult↗
PubMed1982

Effect of vitamin D2 on the assay of 24,25-dihydroxyvitamin D3 in man.

Serum levels of the dihydroxylated metabolite of vitamin D3, 24,25-dihydroxycholecalciferol (24, 25(OH)2D3) were measured by competitive protein-binding assay in 2 anephric patients while undergoing therapy with 25-hydroxycholecalciferol (25(OH)D3) and, at a later date, vitamin D2, ergocalciferol. Whereas there was no increase in serum levels of 24, 25 (OH)2D3 when the patients were treated with 25 (OH)D3, a significant increase was apparently seen when vitamin D2 was given. These results suggest that a metabolite of vitamin D2, non-renal in origin, may be interfering in the assay for 24, 25 (OH)2D3. The different levels of serum 24, 25 (OH)2D3 in anephric man found by various groups of workers are explained by these results.

24,25-Dihydroxyvitamin D 3↗
PubMed1981

Effects of 24,25-dihydroxy-vitamin D3 on its plasma level in man.

Small doses of 24,25-dihydroxy-vitamin D3 (24,25(OH)2D3; 2 micrograms daily) given by mouth increased plasma levels of 24,25(OH)2D3 several-fold in normal subjects and in patients with metabolic bone disease. When oral treatment was stopped, or following the intravenous administration of 24,25(OH)2D3, plasma disappearance of 24,25(OH)2D3 was slow (t1/2 approx. 16 days). This suggests that the endogenous production rate of 24,25(OH)2D3 is similar to that of 1,25(OH)2D3 (less than 2 micrograms daily) but that its metabolic clearance is much slower. The slow metabolic clearance of 24,25(OH)2D3 may explain why plasma levels of this metabolite are about 100 times higher than those of 1,25(OH)2D3.

24,25-Dihydroxyvitamin D 3↗
PubMed1981

Responses to salmon calcitonin in chronic renal failure: relation to histological and biochemical indices of bone turnover.

Twenty-one patients with chronic renal failure and bone disease or hypercalcaemia were studied before and following single (twenty patients) or repeated (fourteen patients) intravenous injection of synthetic salmon calcitonin. Significant correlations were noted before treatment between bone surfaces occupied by osteoblasts or osteoclasts and plasma levels of immunoreactive parathyroid hormone, alkaline phosphatase and hydroxyproline. Following a single injection of 2--200 i.u. salmon calcitonin, plasma levels of calcium and phosphate fell for 6--8 h, but rose subsequently to pre-injection levels at 24 h. The magnitude and duration of the hypocalcaemic response was not clearly dose-dependent, but correlated with measured indices of bone cell activity. Repeated administration of calcitonin (10--200 i.u. thrice weekly for up to 2 months) lowered plasma calcium in the majority of patients and restored plasma calcium to normal in four previously hypercalcaemic patients. Mean levels of alkaline phosphatase increased but no significant changes in plasma phosphate, immunoreactive parathyroid hormone and calcitonin, or hydroxyproline occurred. Calcium absorption (six studies) did not change during treatment. We conclude that synthetic salmon calcitonin is an effective short-term inhibitor of bone resorption in patients with chronic renal failure. Its use as a possible treatment for hypercalcaemia and hyperparathyroid bone disease in chronic renal failure is discussed.

Adult↗
PubMed1981

Effects of vitamin D metabolites and analogues on renal function.

The long-term effects of vitamin D analogues and metabolites on renal function were assessed in 24 patients with and without chronic renal failure. Treatment for periods of 5-45 months did not adversely affect renal function in 10 of 11 patients with stable renal function, although transient hypercalcaemia did cause transient rises in plasma creatinine. Of 13 patients with progressive renal failure before treatment, vitamin D-like compounds or the vehicle used for their administration may have accelerated renal failure in 3 patients independently of changes in plasma calcium or phosphate. Particular difficulties in assessing the effects of vitamin D-like compounds in progressive renal disease are discussed.

Adolescent↗