Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004093 (asthenia)
 2,650 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diclofurime is a non-inotropic arterial vasodilator and an antagonist to calcium transport. We studied its antihypertensive effect in 16 hypertensive subjects. When given alone at an average dose of 240 mg/day, it induced an overall significant diminution of systolic and diastolic arterial pressure. Among the 16 subjects studied, diclofurime lowered arterial pressure below 150/90 mm Hg in seven, induced an improvement in arterial pressure in six, and showed no effect in three. When hypertension is not controlled with 450 mg diclofurime in 3 doses/day, it may be given in association with acebutolol. Diclofurime is well tolerated. The most troublesome side effects noted were headache, cardiac erethism, asthenia and edema in the lower limbs. These clinical signs were usually transient. Among these 32 patients side effects required interruption of treatment in three. Laboratory follow-up was made on day 78 and 180 after initiation of treatment. No significant change in results was noted. Renal function was studied in seven patients having normal renal function and in six chronic renal failure patients whose inulin clearance was about 30 ml min-I. It was observed that in the normal subject, the injection of a loading dose of 40 mg diclofurime followed by a maintenance dose of 80 mg during one hour induced a slight increase in glomerular filtration and a greater increase in renal blood flow; the filtered fraction was thus diminished. Diclofurime induced a clear and sustained increase in excretion of water and sodium chloride without modifying urinary excretion of potassium. In severe renal failure, no significant changes in glomerular filtration, renal blood flow or electrolyte excretion were observed with diclofurime.
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PMID:[Diclofurime: a new antihypertensive agent. Effectiveness and kidney tolerance]. 679 31

We investigated the reconstitutive potential of haematopoietic progenitor cells collected in autologous whole blood during multicycle dose-intensified chemotherapy. Forty patients with metastatic solid tumours were treated with up to six cycles of cisplatin and escalating doses of ifosfamide every 14 days. Cisplatin was administered in 3% sodium chloride over 3 h, followed by ifosfamide over 24 h and mesna over 36 h. The first cohort of patients received granulocyte colony-stimulating factor (G-CSF) days 4-14. Once dose-limiting toxicity was reached in cohort 1, the study continued with a second cohort of patients, in whom, in addition to G-CSF on days 4-14, 500 ml of G-CSF and chemotherapy-'primed' whole blood was collected on day 15, i.e. on day 1 of treatment cycles two to six, before cisplatin administration. This volume of blood was kept unprocessed at 4 degrees C and reinfused 20-24 h after the completion of ifosfamide. In cohort 1, dose-limiting toxicity (DLT) was reached at ifosfamide 6.0 g m(-2) with two out of six of the patients developing neutropenic fever. Although in cohort 2 no neutropenic fever was encountered, neither the frequency nor the duration of grade 4 neutropenia and thrombocytopenia were reduced. Cumulative asthenia resulted in DLT at 7.0 g m(-2). The median number of CD34+ cells in 500 ml of whole blood after the first cycle (i.e. at start of cycle 2) was 1.15 x 10(6) kg(-1). This number was significantly greater after the second cycle (2.06 x 10(6) kg(-1), P = 0.01) and then gradually decreased after cycles three to six. After storing whole blood, the number of CD34+ cells had not decreased (median + 10%). We conclude that the method of combined bone marrow support by G-CSF and haematopoietic progenitor cells in autologous whole blood collected before each cycle of a 2-weekly regimen of cisplatin-ifosfamide does not result in clinically measurable reduced bone marrow toxicity compared with what can be expected by the use of G-CSF alone.
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PMID:A phase I/II study of multicyclic dose-intensive chemotherapy supported with G-CSF, or G-CSF and haematopoietic progenitor cells in whole blood, in two consecutive cohorts of patients. 964 59