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Biomedical subjects

M Szmidt

Publications and source records attributed to M Szmidt.

At least 91 records · Page 5Linked to original sources

Sensitivity to aspirin--methods of detection of sensitivity and inducing tolerance state to aspirin.

The paper deals with various methods of detection of bronchoconstrictor and urticaria/angioedema types of sensitivity to aspirin and other nonsteroidal anti-inflammatory drugs. The authors consider that anamnesis plays the major part in detection of sensitivity to these drugs. Oral challenge tests should be applied only with the use of acetylsalicylic acid administered at small, increasing doses at intervals not shorter than 24 h. Tolerance to aspirin is elicited using aspirin at 24 hour intervals, beginning with a threshold dose. The authors prefer, however, their own method where a subthreshold dose is the initial one. The protective role of sodium salicylate against aspirin-induced bronchoconstriction is also discussed.

Adult↗

[Aspirin tolerance in individuals with aspirin-induced urticaria-edematous lesions].

The study involved 22 individuals with aspirin-produced urticaria-edematous skin lesions. Hypersensitivity to aspirin was established with anamnesis showing such lesions on aspirin intake and oral test with aspirin. Threshold, provocative dose of aspirin was determined in all patients at the beginning of the study. Moreover, threshold provocative indomethacin dose was additionally determined in 12 patients. Tolerance to aspirin was produced by the oral administration of aspirin in increasing doses upto total dose 600 mg at a 24-hour intervals. Twelve patients were given 25 mg of indomethacin after 24 hours, and 50 mg of this drug after 48 hours. The patients tolerated indomethacin well during aspirin tolerance stage. The authors suggest that both urticaria-edematous and bronchial type of aspirin hypersensitivity are of the same pathogenetic origin.

Adult↗

Aspirin "desensitization" in patients with aspirin-induced urticaria and angioedema.

The study was performed on 22 patients with sensitivity to aspirin which manifested as urticaria and angioedema. Sensitivity to aspirin was established based on the anamnesis of urticaria and angioedema occurring after ingestion of aspirin and oral challenge tests with acetylsalicylic acid. At first, the threshold dose of aspirin in all patients and additionally of indomethacin in 12 patients was established. Aspirin "desensitization" was induced by administering increasing doses of acetylsalicylic acid every 24 hr until a good tolerance of 600 mg was obtained. The following day after the ingestion of 600 mg acetylsalicylic acid, 12 patients received 50 mg indomethacin. A good tolerance of 600 mg aspirin was achieved in all examined patients and 50 mg of indomethacin was also well tolerated. The authors assume that mechanism of urticaria and angioedema type of sensitivity to aspirin has the same pathogenic background as aspirin-induced bronchoconstriction.

Adult↗

Serum neutrophil chemotactic activity (NCA) during aspirin-induced bronchoconstriction.

In order to determine mast cell involvement in aspirin-induced bronchoconstriction, 16 aspirin-sensitive asthmatics and 18 control patients were studied for serum neutrophil chemotactic activity, using Nelsons method, before and after oral aspirin administration. A significant increase in NCA was observed in 6 aspirin-sensitive asthmatics during aspirin bronchoconstriction. In two persons the increase was lower. In the remaining 8 persons, no increase in NCA was observed during aspirin bronchoconstriction. None of the control patients exhibited an increase in NCA. The authors assume that, in some of the patients with aspirin-induced bronchoconstriction mast cells are really involved.

Adolescent↗

Sensitivity and tolerance to tartrazine in aspirin-sensitive asthmatics.

The occurrence of sensitivity to tartrazine was examined in 51 patients with asthma and aspirin sensitivity. All patients underwent oral challenge tests with aspirin and tartrazine. Sensitivity to tartrazine was found in 16 i.e. 31.4% of tested asthmatics. The symptoms of sensitivity to tartrazine were similar to those of aspirin. Tolerance to tartrazine was induced in 5 aspirin and tartrazine sensitive asthmatics. Sensitivity to both substances was manifested in these 5 persons as dyspnea but 2 of them had additional extrabronchial symptoms. A good tolerance of 40 mg tartrazine was achieved in all the challenged patients who did not refer any dyspnea and extrabronchial symptoms. It was also proven that, being in the aspirin tolerance state the patients could be given tartrazine with no sensitivity symptoms. The authors think that the possibility of inducing tartrazine and aspirin tolerance, as well as the course of sensitivity reaction to both substances, both point to a similar pathogenetic background.

Adult↗

Migraine in aspirin-sensitive asthmatics.

The aim of this study was to evaluate the occurrence of migraine in aspirin-sensitive asthmatics, and was performed in 46 aspirin-sensitive asthmatic patients (ASA). The control group consisted of 46 asthmatics without aspirin sensitivity. In all patients allergological and laryngological examinations were performed and histories concerning the occurrence of migraine were collected. Twenty one (45.7%) of aspirin-sensitive asthmatic patients suffered from migraine, 5 from classical migraine and 1 from dietary migraine. In the control group migraine was found in only 6 (13%) persons. A family history of migraine was positive in 11 (52.4%) asthmatics with aspirin-sensitivity and migraine and in only 1 (17%) patient with migraine but without aspirin-sensitivity. The authors conclude that the high incidence of migraine in aspirin-sensitive asthmatics may be related to a defect in their arachidonic acid metabolism.

Adult↗

[Effectiveness of ketotifen--a drug stabilizing mast cell membranes--in the treatment of chronic forms of Horton's headache].

The authors made an attempt at treating chronic cluster headache with ketotifen (Zaditen, Sandoz). The drug is the first known agent stabilizing the cell membrane of mast cells which may be taken orally. The treatment was administered to 15 patients giving the drug in doses of 1 mg thrice daily for 8 weeks. A very good therapeutic effect was achieved in 8 cases. Good effect was noticed in 5 cases. In 2 cases only slight improvement was obtained. Reduction in the number of headache attacks occured already in the first week of treatment and progressed gradually during 8 weeks of this treatment.

Adult↗

Lack of specific IgE against house-dust and Dermatophagoides pteronyssinus in aspirin-sensitive asthmatics with positive skin and inhalation test.

We studied 28 atopic asthmatics with aspirin intolerance, sensitive to house dust confirmed by positive skin tests and in some patients inhalatory challenge with house dust allergen. Specific IgE against house dust and Dermatophagoides pteronyssinus was determined by RAST in all patient twice, at 6-month intervals. Only one patient presented antibodies against these allergens in serum RAST class 1.

Adolescent↗

Asthma with aspirin intolerance. Clinical entity or coincidence of nonspecific bronchial hyperreactivity and aspirin intolerance.

The study was performed in 52 aspirin - sensitive asthmatics. It was possible to establish aspirin intolerance from the history in 46 persons and after aspirin challenge in 6 persons. All patients underwent allergological and laryngological examination and 41 aspirin oral challenge. A history of intolerance in the family was reported by 3 persons. In 6 persons, i.e. 11.5%, aspirin intolerance perceded the development of asthma. 36 persons, i.e. 70% exhibited at least 2 features of atopy, namely positive history and positive skin tests. Nasal and paranasal polyps were found in 77% of the group examined. The sequence of asthma, polyps and aspirin sensitivity has been analyzed. The authors conclude that aspirin - induced bronchoconstriction is the effect of the coincidence of two different phenomena in one subject, i. e. bronchial hyperreactivity and ASA - intolerance.

Adult↗

[Bronchial asthma caused by exposure to ash wood dust].

A 42-year-old man reported attacks of dyspnoea on non-professional exposure to ash wood dust. The skin prick tests with common allergens and ash pollen were positive. Inhalation of ash wood dust (challenge test) elicited a very strong, immediate bronchospastic reaction, associated with profuse watery rhinorrhea, conjunctival congestion and lacrimation. The symptoms did not occurred after inhalation of pine wood dust. A positive skin (prick test) reaction to ash wood extract was documented. When the patient remained unexposed to ash wood dust the dyspnoea subsided and 4-fold decrease in bronchial reactivity to histamine-PC20 increase from 0.53 mg/ml to 2.1 mg/ml (according to Cockroft) was observed. The authors conclude that the immediate bronchial reaction to inhaled ash wood dust and the immediate skin positive response to ash wood extract were due to IgE-allergen reaction. This is the second case of hypersensitivity to ash wood dust reported in the literature.

Adult↗