Budd-Chiari syndrome in a patient with systemic lupus erythematosus.
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Biomedical subjects
Publications and source records attributed to J Ducobu.
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The effect of cimetidine on abnormally elevated serum levels of parathyroid hormone was studied in 21 patients with secondary hyperparathyroidism due to chronic renal failure, receiving regular dialysis treatment. The concentrations of carboxyl (-COOH) and aminoterminal (-NH2) fragments of circulating immunoreactive parathyroid hormone (iPTH) were determined before and after 2 months af treatment with cimetidine 400 mg/day. All patients had, on admission, raised levels of either hormonal fragment. The mean pre-treatment value was 17.2 mU/ml for -COOH terminus (upper normal limit 6.5 mU/ml) and 5.7 mU/ml for -NH2 terminus (upper normal limit 1.9 mU/ml). At the end of cimetidine treatment the mean values were 19.9 and 5.7 mU/ml respectively for the two forms of circulating iPTH. No changes in total serum calcium, phosphate or alkaline phosphatase activity were recorded during the study. These results do not indicate any lowering effect of cimetidine on serum iPTH in chronic uraemic patients with secondary hyperparathyroidism.
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The role played by prostaglandins in the secretion of ADH and modulation of its action was investigated by testing the effects of prostaglandin synthesis inhibition in patients with SIADH of cerebral or pulmonary origin. Three patients with SIADH of central origin and 3 with SIADH of peripheral origin were subjected to 4 successive water-loading tests. In the first and fourth tests, the patients absorbed water 20 ml/kg bodyweight; in the second test they absorbed alcohol 2.5 ml/kg followed by water 17.5 ml/kg. The third test was preceded by a 3-day inhibition of prostaglandin synthesis with indomethacin 200 mg/day and aspirin 1.5 g/day. In patients with SIADH of peripheral origin the percent water-load excreted after 4 hours was low (less than 35%) with the 4 tests, whereas it reached 80% (p less than 0.001) with the third test (prostaglandin inhibition) in those with SIADH of central origin. Alcohol did not significantly correct the antidiuretic effect in any of the patients in both groups. It is concluded that prostaglandins reduce ADH secretion in central SIADH but do not modify antidiuresis in peripheral SIADH, since ectopic secretion probably does not depend on prostaglandins. The prostaglandin inhibition test therefore seems to be more helpful than the alcohol test to differentiate between central and peripheral SIADH. Further studies, however, are required to confirm these findings.
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A retrospective study of 22 patients with hyponatraemia (less than 130 mEq/l) was conducted to find out whether hypouricaemia was useful in the diagnosis of SIADH. Serum levels of uric acid were inferior to 38 mg/l in 9 out of 12 patients with SIADH but not in the remaining 10 patients without SIADH. The mechanism of hypouricaemia in the syndrome seems to be an increase in uric acid excretion, since water restriction reduces the fractional clearance of urates. The authors conclude that hypouricaemia appears to constitute a reliable means of detecting SIADH in patients with hyponatraemia.
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The clinical and biochemical side-effects of diuretics administered without potassium supplement were monitored during one year in 58 hypertensive out-patients. The only changes observed were a moderate rise in triglycerides (correlated with weight increase) and in blood glucose. Blood urea, creatinine, potassium, calcium, uric acid and cholesterol remained unchanged. The objections raised against the use of diuretics as anti-hypertensive agents, such as the need for close surveillance of biochemical values and the fear that the beneficial effects on blood pressure would be upset by an increase in other cardiovascular risk factors (some of which are still highly controversial), therefore appear to be unfounded.