[Value of almitrine dimesylate in the long-term treatment of chronic obstructive bronchitis].
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Biomedical subjects
Publications and source records attributed to C Seignalet.
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The role of the complement system in human allergic asthma has been studied by serum complement evaluation by radial immuno-hemolysis. Various groups were tested: 50 normal subjects, 49 allergic patients, 6 pollen sensible patients during and after pollinic season. Complement was evaluated during and after allergen challenge (11 patients). No significative variations were established neither during the challenge nor after (15 mn, 45 mn, 1 h).
A double-blind study was conducted to evaluate the effects of almitrine, administered orally as 3.5 mg/kg/day for one month, when compared with placebo in 20 patients with chronic obstructive pneumopathies from smoking, currently in the stage of chronic hypercapnic respiratory insufficiency. Clinical improvement was obtained, with a reduction in dyspnea and a more comfortable respiration. Objective signs of improvement where enhanced adaptation to assisted ventilation (3 cases out of 5), and less secondary infection in the almitrine group (0/10) than the placebo group (4/10). A statistically significant improvement (p less than 0.01) was recorded in blood oxygen and bicarbonates levels, and to a lesser degree, in blood CO2 levels (p less than 0.05) and without any increase in overall ventilation. As tolerance was good (8/10), almitrine appears to occupy a place of choice in the field of respiratory analeptic therapy. Its efficacy and convenience in use for daily practice require confirmation in long-term studies (more than 6 months).
In one family of twenty-four members hereditary angio-oedema was present in the family for six generations. The protein C1 esterase inactivator found in nine patients proved to be non-active in a functional test. Another anomaly found in the complementary system was labelled C3 nephritic factor without any renal, or other clinical symptoms. Study of HL-A haplotypes did not show any linkage with the loci A, B and C. Hereditary angio-oedema is a disease arising from a specific defect in the inactivator of the C1 esterase (C1 INA) which is a regulating component of the complement system (Donaldson & Evans, 1963). This system is of current interest because of its interaction with other mechanisms of inflammation. Moreover, some links have been discovered recently between HL-A and hereditary defects of complement. This paper reports new findings in a family with hereditary angio-oedema.
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