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Biomedical subjects

M Szmidt

Publications and source records attributed to M Szmidt.

95 records · Page 6Linked to original sources
PubMedDate not supplied

Aspirin-induced neutrophil chemotactic activity (NCA) in patients with aspirin-sensitive urticaria after desensitization to the drug.

The increase in neutrophil chemotactic activity (NCA) is related to mast cell degranulation. This study was performed in 10 patients in whom aspirin-induced urticaria was connected with increased NCA. A state of tolerance to aspirin (ASA) was achieved by administering incremental doses of acetylsalicylic acid. In none of the examined patients was an increase in NCA observed after 600 mg of ASA given after desensitization. The authors conclude that in patients with ASA-induced urticaria, mast cell degranulation does not occur after ASA desensitization.

Adult↗
PubMedDate not supplied

Tolerance to aspirin in aspirin-sensitive asthmatics. Methods of inducing the tolerance state and its influence on the course of asthma and rhinosinusitis.

Aspirin-sensitive asthma is a serious clinical problem, frequently involving dramatic exacerbation and sometimes even death after the accidental ingestion of aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs). The majority of such asthmatics usually suffer from chronic rhinosinusitis and nasal polyps as well, and almost half of them from headaches. Widal et al. in 1922, and later, Zeiss and Lockey were able to elicit tolerance to aspirin (ASA). In all the studies performed so far, tolerance to ASA was achieved by giving double threshold ASA doses every day or every few hours. This method elicited severe dyspnea and sometimes pronounced extrabronchial sensitivity symptoms. From our previous studies, it appeared that the smaller the aspirin dose, the weaker the sensitivity symptoms, and that it is possible to induce tolerance after eliciting only very slight sensitivity reactions. Based on this observation, we elaborated a new method of eliciting aspirin tolerance by the daily administration of gradually increasing doses of aspirin starting with subthreshold doses. Applying this method, we achieved tolerance to aspirin without any adverse reactions. The patients in a tolerance state to ASA also tolerated well other NSAIDs, i.e. indomethacin and diclofenac. It is possible to maintain a tolerance state for a long time by the administration of ASA at proper intervals. It was shown that such a procedure may have a beneficial influence on the course of asthma and rhinitis. In our opinion, inducing and maintaining aspirin tolerance in aspirin-sensitive asthmatics is indicated in the following situations: 1) the need to treat coexisting rheumatic diseases; 2) the need to treat coexisting intractable headaches; and 3) the need for symptomatic treatment of ASA-sensitive asthma and rhinitis.(ABSTRACT TRUNCATED AT 250 WORDS)

Aspirin↗
PubMedDate not supplied

The value of C1 esterase inhibitor in patients with aspirin-sensitive urticaria.

The aim of the study was to evaluate the concentration and activity of C1 esterase inhibitor (C1 INH) in patients with aspirin-sensitive urticaria. C1 INH deficiency is the basis of hereditary angioneurotic edema. The study was performed on 32 subjects with aspirin-sensitive urticaria. The value of C1 INH in examined patients was the same as in the control group. There seems to be no coexistence of aspirin-sensitive urticaria and C1 esterase inhibitor deficiency.

Adolescent↗
PubMedDate not supplied

The influence of misoprostol (synthetic analogue of prostaglandin E1) on aspirin-induced bronchoconstriction in aspirin-sensitive asthma.

It is believed that aspirin (ASA) and other nonsteroidal anti-inflammatory drugs elicit dyspnea in ASA-sensitive asthmatics by blocking cyclooxygenase. It is unclear whether this bronchospasm is due to the shunting of arachidonic acid into the lipoxygenase pathway or to the removal of a cyclooxygenase product which prevents bronchospasm. Diminished tissue concentration of PGE may cause bronchoconstriction. PGE also modulates mast cells, decreasing the release of anaphylaxis mediators. The authors investigated the influence of a synthetic analogue of PGE1-misoprostol (Cytotec, Searle)-on post-aspirin bronchoconstriction in seven ASA-sensitive asthmatics. On the first day, the effect of a placebo was studied. On the second day, the bronchodilatory effect of misoprostol (Cytotec, Searle) alone was examined. After a few days, a predetermined threshold dose of ASA was administered. Seven days later, at least 400 micrograms of misoprostol +200 micrograms 2 h later, together with a predetermined ASA dose, were administered. In all but one patient, the protective influence of misoprostol on ASA-induced bronchoconstriction was observed. The maximum drop in FEV1 (forced expiratory volume in one second) in % after ASA in each of the patients was 40, 25, 24, 33, 47 and 54, and after ASA with misoprostol 10, 9, 4, (+8), 10, (+2) and 45, respectively. Misoprostol given together with ASA attenuated aspirin-induced bronchoconstriction, reaching statistical significance at 3 and 3.5 h. It also diminished extrapulmonary symptoms.

Adult↗