Curable malabsorption in a 67-year-old man.
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Biomedical subjects
Publications and source records attributed to R R Ghose.
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Aminoglutethimide, a drug which inhibits adrenal hormone synthesis, may alleviate pain in metastatic breast carcinoma. A case is reported in which severe hyperkalaemia supervened two years after commencing treatment with aminoglutethimide; a constant dose was used in conjunction with cortisone supplements. This indicates the need for constant biochemical monitoring, or better still, prophylactic administration of fluorohydrocortisone as mineralocortical replacement. This is the first case of aminoglutethimide-induced hyperkalaemia reported, illustrating the rarity of the complication. Adrenal failure due to glucocorticoid deficiency was also present and required an increased dosage of cortisone. Maintenance of glucocorticoid and mineralcorticoid need regular review throughout therapy, to counteract intercurrent stress.
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Prospective measurements of serum thyrotrophin and thyroxine concentrations were made in six patients with primary hypothyroidism treated consecutively with an incremental regimen of oral thyroxine. A fall in thyrotrophin occurred over several months, accompanied by a concurrent slow rise in serum thyroxine. Those patients with the highest initial values for thyrotrophin showed the typical curvilinear decline in thyrotrophin, whereas the remaining patients disclosed a transient rise in thyrotrophin for the first 3 months. This paradoxical rise was not associated with depression of cardiac output or glomerular filtration rate. The significance of thyrotrophin augmentation is uncertain, but it may be more common than generally appreciated. It did not occur in those patients with the most severe degrees of thyroid deficiency. Thyroxine exerts a dual action, and augmentation of thyrotrophin may reflect a dominant effect of increased protein synthesis, in contrast to negative feedback inhibition which suppresses thyrotrophin. These opposing actions are in competition at different dose levels of thyroxine, and may contribute not only to augmentation or suppression of thyrotrophin, but also to the curvi-linear pattern of fall. Such variations impair the utility of thyrotrophin as an index of euthyroidism.
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Two middle-aged men were referred for control of severe hypertension, presumed to be 'essential'. Late-onset enuresis, a small palpable bladder, and slight prostatic enlargement were elicited in one patient; history and examination were unremarkable in the other patient, apart from moderate prostatic enlargement. Intravenous urography revealed massive bilateral hydronephrosis with hydroureters in both patients. Surgical relief of retention was associated with post-obstructive diuresis and normalization of blood pressure, although recurrence of hypertension occurred later in one patient. These patients suffered from high pressure chronic retention, a syndrome characterized by impairment of renal function and hypertension. Surgical relief of retention was accompanied by prompt correction of hypertension, and gradual, sustained recovery of renal function.
Random estimations of plasma arginine vasopressin concentration were undertaken in 6 non-oedematous patients receiving diuretic therapy for hypertension, who were admitted to hospital with severe hyponatraemia. Hyponatraemia resolved within 2 weeks of discontinuing the diuretic. Measurable amounts of plasma arginine vasopressin were detected in all 6 patients. Sequential biochemical measurements in one patient, performed when plasma sodium concentration and osmolality were returning to the normal range, disclosed that urine osmolality remained higher than plasma osmolality during the first 5 days, when urine volume and sodium excretion were low. Thus the rise in plasma sodium was not initially related to water diuresis. The ability to excrete a water load was severely limited on the fifth day, but improved progressively by the tenth and seventeenth days. Diuretic-induced hyponatraemia is associated with incomplete suppression of anti-diuretic hormone secretion arising from non-osmotic stimulation, in conjunction with transient impairment of renal diluting ability which could be due to net sodium deficit.
A longitudinal study of sequential measurement of glomerular filtration rate and effective renal plasma flow was conducted over a 5-year period of antihypertensive drug treatment, in four adult patients admitted to hospital with previously untreated malignant essential hypertension. Treatment produced a substantial and sustained lowering of systemic arterial blood pressure, compared with grossly elevated pretreatment levels. Nevertheless, glomerular filtration rate and effective renal plasma flow remained relatively stable in all four patients, at roughly the same level at which they were admitted. It was concluded that effective therapy for hypertension may not necessarily reverse the vascular changes of arteriolar fibrinoid necrosis, which characterize malignant essential hypertension. Permanent damage to the renal arterioles, and the territory of kidney supplied by these vessels, may be a feature of this condition.
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A 28-year-old man, who presented with acute cerebellar ataxia, was found to have haematological features of infectious mononucleosis. There was serological evidence of recent infection with Epstein-Barr virus. It is speculated that cerebellar dysfunction results from virus-induced inflammatory changes within the central nervous system.
An adult patient presenting in summertime with sarcoidosis and demonstrating raised levels of serum calcium and 1,25-dihydroxycholecalciferol was observed to have a serum immuno-reactive parathyroid hormone concentration in the mid-normal range. Renal function was normal. Corticosteroid administration quickly depressed serum calcium and 1,25-dihydroxycholecalciferol into the normal range; serum parathyroid hormone also fell to low levels. It was concluded that corticosteroid suppression, when incorporating measurements of serum calcium and 1,25-dihydroxycholecalciferol concentrations, can distinguish between sarcoidosis-related hypercalcaemia and primary hyperparathyroidism. The significance of the changes in parathyroid hormone concentration is obscure.