Analgesic intolerance with or without bronchial asthma: Is there a marker?


Kalyoncu A., Karakaya G., Yilmaz E., Balci B., Karaduman A., Yasavul U.

JOURNAL OF INVESTIGATIONAL ALLERGOLOGY AND CLINICAL IMMUNOLOGY, cilt.13, sa.3, ss.162-169, 2003 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 13 Konu: 3
  • Basım Tarihi: 2003
  • Dergi Adı: JOURNAL OF INVESTIGATIONAL ALLERGOLOGY AND CLINICAL IMMUNOLOGY
  • Sayfa Sayıları: ss.162-169

Özet

Background: The prevalence of analgesic intolerance (AI) is less than 1% in the general population and about 10% in adult asthmatics, in whom the disease tends to be more severe. Objective: A possible clinical-laboratory marker was sought that would differentiate patients who have AI with/without asthma, AI with asthma, and AI without asthma from the healthy subjects. Methods: In the survey, 66 analgesic-intolerant patients (36 having asthma) were compared with 50 healthy subjects using a nickel patch-test, 65 patients (39 having asthma) with 55 healthy subjects for the presence of a genetic marker (A38G and A444C SNPs in CC16 and LTC4S genes), and 32 patients (14 having asthma) with 118 healthy subjects for presence and frequency of human leukocyte antigens (HLA). Results: The mean age of the patients with At with/without asthma and the healthy subjects for the nickel patch-test group, genetic marker group, and the 14LA group was 39.8 +/- 10.5 and 33.3 +/- 11.1, 41.5 +/- 11.6 and 38.1 +/- 13.4, and 39.4 +/- 12.5 and 41 +/- 2.6, respectively. The frequency of the females in the same groups, in the same order, was 72.7% and 54%, 81.5% and 62%, and 71.9% and 59.3%, respectively. The frequency of positive nickel patch-test results and the A38G and A444C frequency in CC 16 and LTC4S genes were not significantly different (p > 0.05). The frequency of HLA antigens HLA-A3, -B52, -DR16, -DQ5, -DQ8 and -DQ9 were significantly higher; and -A24, -B35, -B44, -DQ6 and -DQ7 were significantly lower in the AI group with/without asthma compared to the control group (p < 0.05). Conclusion: As a result, nickel patch-test positivity and the genes which we have studied do not seem to be markers for AI with/without asthma. However, there might be a relation between At with/without asthma and the types of the HLA system. Further surveys are needed with other genes and possible markers.