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Biomedical subjects

F Delwiche

Publications and source records attributed to F Delwiche.

29 records · Page 2Linked to original sources
PubMed1983

High levels of the circulating form of parathyroid hormone do not inhibit in vitro erythropoiesis.

Either primary or secondary hyperparathyroidism may be associated with anemia. The pathogenesis of this anemia remains obscure, but parathyroid hormone may directly suppress erythropoiesis or anemia may result from myelofibrosis. Previously reported in vitro studies of a direct inhibitory effect of PTH on erythroid progenitor growth were carried out with crude hormone preparations and appeared nonspecific. We have studied simultaneously the in vitro effects of pure (greater than 6000 U/mg) and crude (130 U/mg) preparations of PTH on murine and human hematopoietic progenitor growth. Increasing concentrations (2.5 to 20 U/ml) of crude PTH produced a dose-dependent inhibition of early erythroid (BFU-E) and granulocyte/macrophage progenitor (CFU-GM) growth in human and mouse marrow cell cultures. However, the biologically active N-terminal fragment containing amino acids 1-34 and the pure intact molecule of 84 amino acids failed to significantly inhibit hematopoietic colony growth. These observations demonstrate that in vitro inhibitory effects described with parathyroid gland extracts are not specific for erythropoiesis and may not be related to the circulating form of PTH.

Animals↗
PubMed1977

Polycythaemia and erythropoietin producing uterine fibromyoma.

A case of polycythaemia secondary to uterine fibromyoma is reported. Polycythaemia disappeared after hysterectomy. Erythropoietic activity was detected in the cyst fluid of the tumour. Plasma and urine contained no erythropoietic factor. Polycythaemia was related to erythropoietinlike material produced by the tumour.

Erythropoiesis↗
PubMed1976

Effect of sotalol on haemodynamics and renin-angiotensin-aldosterone system in hypertensive patients.

1. Twenty-three hypertensive patients were treated by sotalol, a pure beta-adrenergic receptor blocking agent. The drug produced a significant decrease of blood pressure in nineteen patients. 2. On average, cardiac index decreased but not significantly; heart rate decreased and stroke index increased significantly. Total peripheral resistance varied in both directions. 3. Sotalol determined a fall in plasma renin concentration (only significant in the high-renin group), a fall in plasma angiotensin II concentration and in urinary excretion rate of aldosterone accompanied by a rise in plasma potassium concentration. 4. The fall of blood pressure was not correlated with the decreases of renin and angiotensin II concentrations or excretion rate of aldosterone. However, in the placebo period plasma angiotensin II concentration was significantly correlated with total peripheral resistance; during sotalol treatment the variations of these two parameters seemed also to be correlated. 5. There was a poor correlation between decreases of cardiac output and of blood pressure; it was impossible to foresee the magnitude of the lowering of the blood pressure from the initial cardiac index. 6. The association of a diuretic with sotalol enhanced the hypotensive effect of the beta-receptor blocking drug, without significant increase of plasma renin and angiotensin II concentrations.

Adult↗
PubMedDate not supplied

The plicamycin and hydroxyurea combination chemotherapy for chronic granulocytic leukemia in myeloid transformation.

Between 1987-1988 we treated, in a cooperative study, 13 patients in blast crisis of CGL according to Koller and Miller's regimen. We observed no return to the chronic phase of the disease, while some patients suffered major drug-induced side effects. Six patients in accelerated phase were treated with the same combination therapy. All of them responded with a return to the chronic phase for a median of 4.5 months. In our hands the combination of plicamycin and hydroxyurea was ineffective in patients with CGL in blast crisis. This regimen could deserve further evaluation in patients with CGL in acceleration.

Adult↗