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Biomedical subjects

J Rozniecki

Publications and source records attributed to J Rozniecki.

At least 91 records · Page 5Linked 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↗
PubMed1985

A lymphocyte-derived histamine-releasing factor in asthmatic patients. III. Further studies.

Peripheral blood lymphocytes from atopic asthmatic patients cultured overnight (16 hours) produced a novel lymphokine-histamine releasing factor (HRF) in the culture supernatant. Activity of this lymphokine has been tested in the basophil histamine release test. Supernatant from unstimulated lymphocytes released 29% histamine from basophils. A short incubation of lymphocytes with skin test-positive allergens (grass, mite) enhanced the generation of HRF. Skin test-negative allergens had no effect. HRF appeared in the supernatant as early as four hours after the start of the culture and its production level remained high even at 48 hours. Gel-filtration with Sephadex G-75 revealed an apparent molecular weight for HRF in the range of 10,000 to 15,000. HRF is relatively heat stable at 56 degrees C.

Allergens↗
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↗
PubMed1984

A mononuclear cell derived histamine releasing factor (HRF) in asthmatic patients. Histamine release from basophils in vitro.

Mononuclear cells from asthmatic patients produced a histamine releasing factor (HRF). Mononuclear cells produced this factor in culture spontaneously but significantly much more following specific allergen stimulation. This factor released histamine from both sensitized and unsensitized basophils in vitro. Mononuclear cells from healthy subjects produced HRF only after nonspecific mitogen/phytohemagglutinin stimulation. Asthmatic patients on immunotherapy with essential benefits failed to produce HRF.

Adult↗
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↗