Search PubMed⌕ Search

Biomedical subjects

J Rozniecki

Publications and source records attributed to J Rozniecki.

196 records · Page 11Linked to original sources
PubMedDate not supplied

[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↗
PubMedDate not supplied

Complement in allergen-induced bronchospasm in house-dust RAST negative asthmatic patients.

We studied a group of asthmatic patients with aspirin intolerance who were RAST-negative for house-dust and Dermatophagoides-pteronyssinus despite having positive skin tests and positive inhalation tests to these allergens. Total haemolytic activity (CH50), C3, C4 and C3PA were measured after allergen-induced bronchospasm in these patients and also in a group of RAST-positive asthmatic patients taken as a control group. We did not find any change in complement level after allergen-induced bronchospasm in both groups of patients.

Allergens↗
PubMedDate not supplied

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↗
PubMedDate not supplied

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↗
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↗