The Effect of Polymorphysm of The f3-2 Adrenergic Receptor on The Response to f3-2 Agonist in Bronchial Asthma Patients  

Oleh:

Syamsu ; Yusuf, Irawan ; Budu ; Patellongi, Ilhamjaya

Jenis: Article from Journal - ilmiah nasional - terakreditasi DIKTI
Dalam koleksi: Acta Medica Indonesiana vol. 39 no. 01 (Jan. 2007), page 8.
Topik: polymorphism; beta-2 agonist; beta-2 receptor

Ketersediaan

Perpustakaan FK Nomor Panggil: A02.K.2004.01 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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ABSTRACT Aim: to discover the role of [32-adrenergic receptor ([32-AR) polymorphism on the response to beta-2 agonist, particularly in coding amino acid at sequences 16 and 27 as well as adjacent nucleotides. Methods: the study was conducted by nested case contra I method with consecutive samples of asthma patients aged 15-60 years at the outpatient clinic, Department of Pulmonolgy in Dt; Wahidin Sudirahusodo General Hospital, Makassar. Twenty-eight patients were found irresponsive to terbutaline nebulation (increased FEV 1 < 15%) and 56 patients were responsive (increased FEV1 L 15%). DNA extraction and amplification were peiformed by PCR as well as polymorphism detection, which was done by automatic sequencing machine. ResuLJs: the Arg 16 polymorphism did not have any effect on the response to terbutaline nebulation, but Gin 27 polymorphism did with OR 3. 18. New polymorphism was found in nucleotide at 2()h order before the start codon, it was TIC 20, which also has an effect on the response to terbutaline nebulation with OR 4.53. When the three polymorphisms were combined, the effect were greater with OR 11.11. 1t was found that age, gender, obesity, onset and etllllicity had no effect on the response to terbutaline nebulation. Conclusion: polymorphism of the novel Gin 27 and TIC -20 (newly known) have an effect on the response to beta-2 agonist. Both combinatioil and polymorphism of Arg 16 will bring greater effect on the response to beta-2 agonist.asthma in the general population is increasing and the economic costs of this disorder, i.e. morbidity, health care expenses, lost productivity and even mortality, are staggering.2 The 2-adrenergic agonists are the most potent bronchodilators presently currently available for asthma treatment. Genetic factors controlling 2-adrenergic receptor (2-AR) function may be very important determinant of response to bronchodilator therapy and thus of severity and duration of asthmatic symptoms.] Polymorphisms of ~2-AR can affect receptor regula¬tion. Smaller studies examining the effects of such polymorph isms on the response to ~2-agonist therapy have produced inconsistent results.4 Over past several years, there has been considerable controversy about the role of inhaled ~2-agonist in the asthma treatment. Studies using mutagenesis and recombinant expression in cells and transgenic mice as well as using airway smooth muscle cell, which are endogenously expressing these 2-AR variant, have shown that some forms of the ~2-AR demonstrate distinct differences in signaling and/or regulation after exposure to 2-agonist. Study by Israel et al suggested that these polymorphisms may be associated with various asthma severity.4 Furthermore, other studies have reported a relationship between these polymorphism and the degree of responsiveness or desensitization to the bronchodilator effect of 2agonist.5 In vitro studies have shown that common

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