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Biomedical subjects

I Grzelewska-Rzymowska

Publications and source records attributed to I Grzelewska-Rzymowska.

At least 73 records · Page 4Linked to original sources
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↗
PubMed1984

Aspirin tolerance induced in aspirin-sensitive asthmatics.

Twenty-nine patients with asthma and aspirin-sensitivity were studied in an attempt to induce tolerance to aspirin (ASA). Starting with the smallest ASA doses eliciting bronchial obstruction (threshold doses) we doubled the doses on subsequent days and finally achieved good tolerance of 600 mg ASA per day in 27 patients. It was more difficult to achieve tolerance in patients with low ASA-thresholds than in patients with high ones. Daily ASA administration led to prolongation of the refractory state but when the intervals between consecutive doses were increased, aspirin hypersensitivity recurred. The pause sufficient for a recurrence of sensitivity to ASA was measured in 16 patients and ranged from 24 h to 9 days. Twelve patients challenged with indomethacin after ASA-desensitisation showed good drug tolerance.

Aspirin↗
PubMed1983

Potentiation by acetylsalicylic acid of skin weal response to compound 48/80 in ASA-sensitive asthmatics.

The influence of acetylsalicylic acid (ASA) on skin response to intradermal injection of compound 48/80 and histamine was studied in order to determine whether ASA elicits any abnormalities also in the skin of asthmatics reacting with bronchoconstriction to ingestion of this drug. The applied ASA dose (mean dose 150 mg) elicited bronchoconstriction in all 16 patients with asthma and ASA sensitivity (mean fall of FEV1 34%) and increased the weal response to compound 48/80 to about 51% (P less than 0.05) as compared with the response before the ASA-challenge. In asthmatic persons without ASA sensitivity a 150 mg ASA dose did not influence the skin response to any of the reagents. On the other hand, a 600 mg dose decreased skin response to histamine and compound 48/80 in persons without ASA intolerance, although the decrease was statistically significant only in the flare after compound 48/80 (P less than 0.05). The authors believe that additional local defect is needed to reveal sensitivity to ASA in the skin of ASA-sensitive asthmatics, just as bronchial hyperreactivity is indispensible for revealing the action of ASA in the bronchi.

Adult↗
PubMed1981

Histaminemia after aspirin challenge in aspirin-sensitive asthmatics.

To determine the role of mast cells in aspirin-induced bronchoconstriction, venous histaminemia was measured in 17 aspirin-sensitive patients before and after administration of aspirin. Ventilatory disturbances were measured spirographically. Venous histaminemia was determined according to Lorenz. In 11 patients the mean increase of histaminemia was from 39.6 ng/ml to 107.0 ng/ml. In the remaining 6 patients no change in histaminemia was observed after the challenge. In patients exhibiting the increase of histaminemia, symptoms of hypersensitivity to aspirin, other than dyspnea, were not common and stronger. The authors discuss a possible relationship of the aspirin effect, disturbances in prostaglandin synthesis and histamine release.

Adult↗
PubMedDate not supplied

Aspirin-induced urticaria--a clinical study.

This paper describes the clinical characteristics of patients with aspirin-induced urticaria. The group of 71 patients (49 women and 22 men), with a mean duration of symptoms of 32.5 years, underwent allergological, laryngological and histamine dihydrochloride inhalation tests. Nasal polyps were found in 2 patients (2.8%), atopic disease in 23 (32.3%) and at least one feature of atopy in 37 (51.9%). Forty-nine patients (69%) suffered from urticaria which was not associated with aspirin. In 22 patients, urticaria developed solely due to aspirin. Urticaria not associated with aspirin has been present from 2 weeks to 30 years before the onset of sensitivity to aspirin. The authors conclude that aspirin-induced urticaria results from two different concomitant phenomena, i.e. sensitivity to aspirin and urticaria not associated with ingestion of the drug.

Adolescent↗
PubMedDate not supplied

Urticaria/angioedema-type sensitivity to aspirin and other nonsteroidal anti-inflammatory drugs. Diagnostic value of anamnesis and challenge test with acetylsalicylic acid.

The aim of this study was to determine the value of challenge tests with acetylsalicylic acid in the diagnosis of ASA-induced urticaria. The study was performed in 71 patients with suspected urticaria/angioedema-type sensitivity to ASA. Anamnesis confirmed sensitivity in 67 patients (94.4%) and showed that sensitive patients usually suffered from extensive urticaria (37 patients, i.e 55.5%) after ingestion of ASA. Eight patients (12%) reacted with loss of consciousness and 4 (6.0%) with edema of the larynx. Oral challenge test with acetylsalicylic acid was performed in 53 patients, in 49 (92.4%) of whom it was positive. Threshold doses of acetylsalicylic acid ranged from 40 to 300 mg. In 11 patients, the test was repeated and in 8 it was performed 3 times. It was observed that both the threshold acetylsalicylic acid doses and the time of appearance of sensitivity symptoms were variable. All ASA-sensitive patients reacted to indomethacin in a similar manner as to ASA. Paracetamol, on the other hand, was well tolerated by all 25 evaluated patients with urticaria/angioedema-type sensitivity to ASA.

Acetaminophen↗
PubMedDate not supplied

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↗
PubMedDate not supplied

[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↗
PubMedDate not supplied

Serum neutrophil chemotactic activity (NCA) during aspirin-induced urticaria and angioedema.

In order to establish the role of mast cells in aspirin-induced urticaria and angioedema, neutrophil chemotactic activity (NCA) in serum was assayed using the method of Nelson before and after aspirin challenge. In 14 (82.4%) persons sensitive to aspirin an increase in NCA during aspirin-induced urticaria and angioedema was observed and in 9 of them (52.9%) it was considerable (index NCA greater than or equal to 2.0). None of the 18 persons from the control group with idiopathic urticaria and/or angioedema but without aspirin-sensitivity exhibit an increase in NCA after aspirin challenge. The author assumes that mast cell degranulation does occur in aspirin-induced urticaria and angioedema.

Adolescent↗
PubMedDate not supplied

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↗
PubMedDate not supplied

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↗