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Biomedical subjects

M Szmidt

Publications and source records attributed to M Szmidt.

At least 37 records · Page 2Linked to original sources
PubMed1993

[Chemotactic activity of serum granulocytes after aspirin in patients with aspirin-sensitive urticaria who find themselves in a state of tolerance for this drug].

The increase in neutrophil chemotactic activity (NCA) is related to degranulation of mast cells. The study included 10 patients in whom aspirin-induced urticaria was related to NCA increase. Tolerance state to ASA was achieved by administering this drug in incremental doses. In none of the examined patients after 600 mg of ASA given during induced tolerance state, the increase of NCA was observed. The authors conclude that in patients with ASA-urticaria, after ASA desensitization, mast cells degranulation does not occur.

Adult↗
PubMed1993

[Aspirin-sensitive urticaria; a clinical study].

In the paper clinical characteristics of patients with aspirin-induced urticaria were performed. The group of 71 patients, 49 women (69%) and 22 men (31%), mean age of sensitivity symptoms demonstration--32.5 years, underwent allergological, laryngological and histamine dihydrochloride inhalatory tests. Nasal polyps were found in 2 persons (2.8%), atopic diseases in 23 persons (32.3%) and at least one feature of atopy in 37 persons (51.9%). 49 subjects (69%) suffered from urticaria which was not associated with ingestion of aspirin. In 22 patients urticaria developed solely due to aspirin. Urticaria not associated with aspirin had been presents for 2 weeks to 30 years before the onset of sensitivity to aspirin. The authors conclude that aspirin-sensitive urticaria results from concomitance of two different phenomena in one person, i.e. sensitivity to aspirin and urticaria not associated with ingestion of the drug.

Adolescent↗
PubMed1993

[Urticaria-angioedema type of sensitivity to aspirin and other nonsteroidal anti-inflammatory drugs; diagnostic value of anamnesis and challenge tests with acetylsalicylic acid in detecting this sensitivity].

The aim of the paper was to estimate the value of challenge tests with acetylsalicylic acid in diagnosis of ASA-induced urticaria. The study was performed in 71 persons with suspected urticaria/angioedema type of sensitivity to ASA. The anamnesis confirmed sensitivity in 67 examined patients (94.4%) and showed that the sensitive patients usually suffered from extensive urticaria (37 persons, i.e. 55.5%) after ingestion of ASA. Eight persons (12%) reacted with loss of consciousness and 4 (6.0%) with oedema of the larynx. Oral challenge test with acetylsalicylic acid was performed in 53 examined persons, in 49 (92.4%) of which it was positive. Threshold doses of acetylsalicylic acid ranged from 40 to 300 mg. In 11 persons the test was repeated and in 8 performed three times. It was observed that both the threshold acetylsalicylic acid doses and the time of appearance of the sensitivity symptoms were changeable. All ASA-sensitive reacted to indomethacin in the similar way as to ASA. Paracetamol, on the other hand, was well tolerated by all 25 tested patients with urticaria/angioedema type of sensitivity to ASA.

Adolescent↗
PubMed1991

[Neutrophil chemotactic activity after administration of aspirin during aspirin tolerance in patients with asthma and aspirin hypersensitivity].

The increase of neutrophil chemotactic activity (NCA) is related to degranulation of mast cells. In aspirin asthma following aspirin bronchial provocation NCA increases in 50% to 100% of the studied patients. The authors studied NCA after aspirin in patients with aspirin asthma during a state of induced tolerance. If NCA would not increase that would imply that in the state of induced tolerance degranulation of mast cells does not occur. Out of 22 subjects NCA was increased in 11. In these patients tolerance to aspirin was induced and NCA was once more studied. The authors found that in these patients after a dose of 600 mg of aspirin NCA was not increased. This could impose that in patients with aspirin asthma that developed tolerance to aspirin degranulation of mast cells does not occur.

Adult↗
PubMed1991

[Alpha 1-antitrypsin and its phenotype in patients with asthma and aspirin hypersensitivity].

Alpha-1 antitrypsin (A-1-AT) levels were determined in 46 patients with aspirin sensitive asthma using the Eriksson method. The control group was made up of 17 asthmatics without aspirin sensitivity and 78 healthy volunteers. In 30 patients with aspirin asthma the phenotype of A-1-AT was determined using the Laurell method. The serum A-1-AT level was significantly higher in asthmatics in comparison with the healthy subjects. In the 30 subjects in whom the phenotype of A-1-AT was determined none of the phenotypes characteristic for lowered A-1-AT level were found more frequently than in groups without sensitivity to aspirin.

Adult↗
PubMed1991

[Effect of aspirin on FMLP (formyl-meth-leu-phe)-stimulated leukocytes in patients with asthma and hypersensitivity to aspirin].

In order to determine if aspirin sensitivity effects leukocyte reaction in aspirin sensitive asthma patients the authors studied the influence of aspirin on chemiluminescence in 12 aspirin sensitive asthmatics and 13 non-aspirin asthmatics. Leukocyte suspension were carried out according to Böyum. Chemiluminescence was determined using the LKB--Wallac counter. No statistical differences in leukocyte chemiluminescence was found in both groups.

Adult↗
PubMed1987

Tolerance to acetylsalicylic acid (ASA) induced in ASA-sensitive asthmatics does not depend on initial adverse reaction.

A state of tolerance to aspirin (ASA) was induced in 10 aspirin-sensitive patients by daily administration of incremental doses of ASA. No adverse reactions were reported. The initial dose (from 5 to 60 mg) was gradually increased each day up to 300 mg and then doubled. 50 mg indomethacin given the day after administration of 600 mg ASA did not elicit any symptom of intolerance. The authors discuss a possible mechanism of tolerance to aspirin in ASA-sensitive asthmatics after ASA administration, suggesting that it might be connected either with inhibition of the lipooxygenetic pathway of arachidonic acid metabolism or with blockade of the cyclooxygenase supplementary binding site by salicylic acid, a product of acetylsalicylic acid hydrolysis. This would prevent aspirin from binding with the catalytic cyclooxygenase site.

Adult↗
PubMed1987

Fibrinolysis, blood coagulation, and platelet function during aspirin-induced bronchoconstriction in aspirin-intolerant asthmatics.

Nineteen asthmatic patients, 11 with and eight without aspirin (ASA) intolerance were studied in order to test possible platelet and coagulation system involvement in the pathogenesis of aspirin-induced bronchoconstriction (AIB). Aspirin-intolerant asthmatics were challenged with a previously established ASA threshold dose and, in nine of them, a positive asthmatic reaction occurred (mean fall in FEV1 39.4%). Seven out of nine patients with a positive reaction had a significant decrease in euglobulin lysis time (P less than .01) during AIB. A positive reaction after ASA was accompanied by an increase in the plasma recalcification time in five of these patients. There were no concomitant statistically significant changes in the platelet count, circulating platelet aggregates, and platelet factor 4 activity. In a control group of ASA-tolerant asthmatics, aspirin at a 200-mg dose did not evoke any respiratory reaction and, during two hours after ASA, no significant variation was found in any of the laboratory parameters studied. We conclude that activation of fibrinolysis accompanying AIB results from intrinsic pharmacologic properties of aspirin, and may contribute to the pathogenesis of aspirin intolerance through a more generalized activation of plasma proteolytic activity.

Adult↗
PubMed1986

Clinical efficacy of aspirin in "desensitised" aspirin-sensitive asthmatics.

The effect of daily aspirin (ASA) administration after "desensitisation" was studied in 16 aspirin-sensitive asthmatics. Fourteen patients completed the trial; 12 of them also had perennial rhinitis and eight in addition suffered from chronic headache. During 4 weeks of daily treatment with 600 mg of ASA a marked reduction of the nasal symptoms score was noticed in 8/12 patients and head pain score was significantly decreased in 6/8 patients when compared with the 4-week non-ASA period. Daily aspirin resulted in decreases in both the mean asthma score and in daily beta-agonist usage in 7/14 patients, and 10/13 patients showed a decrease in bronchial responsiveness to inhaled histamine (geometric mean of provocative concentration of histamine 1.8 and 5.8 mg/ml, respectively. In four patients we noticed untoward epigastric symptoms. A decrease in thrombocyte counts was observed during ASA treatment. Our study suggests that daily aspirin administration after "desensitisation" may be helpful in the management of some ASA-sensitive asthmatics.

Adult↗
PubMed1985

The effect of aspirin during aspirin "desensitisation" on compound 48/80 and histamine-induced skin responses in aspirin-sensitive asthmatics.

In a group of aspirin-sensitive asthmatics we studied skin weal and flare responses to intradermal injections of compound 48/80 and histamine during oral aspirin (ASA) provocation and after ASA "desensitisation". During provocation (bronchospasm accompanied by naso-ocular symptoms) the mean weal area after compound 48/80 increased to about 42.4% (P less than 0.05). Neither the threshold (provocative) doses of ASA nor 600 mg ASA, when given after ASA-desensitisation, significantly influenced the weal reactions to compound 48/80 (mean changes of area were -1.8% and -16.5% respectively). Aspirin did not change flare reactions to compound 48/80 and weal and flare reactions to histamine on any of the three study occasions. Initial (pre-aspirin) weal reactions to compound 48/80 after desensitisation to the threshold ASA doses were significantly reduced, but after desensitisation to 600 mg ASA were significantly increased as compared with the reactions before. These data suggest that ASA-"desensitisation" may influence the skin reactivity to non-specific mast cell degranulating stimulus in ASA-sensitive asthmatics.

Adult↗
PubMed1985

Bronchial hyperreactivity to histamine in aspirin sensitive asthmatics: relationship to aspirin threshold and effect of aspirin desensitisation.

Twenty seven aspirin sensitive asthmatic patients were studied to determine the relationship between non-specific bronchial responsiveness to inhaled histamine and the degree of sensitivity to aspirin (aspirin threshold dose). No correlation was found between provocative concentration of histamine (PC20H) and aspirin threshold dose. In 11 patients the influence of aspirin desensitisation on bronchial reactivity to inhaled histamine was examined. Mean PC20H measured the day after the patients were desensitised to 600 mg of aspirin did not change significantly from the values before desensitisation. These observations suggest that sensitivity to aspirin and non-specific bronchial hyperreactivity in asthmatic patients are independent phenomena.

Adult↗