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Genetics May Explain Asthma Drug Failures LONDON, ENGLAND -- October 3, 1997 -- Beta2-adrenoreceptor agonists are the most important drugs currently available for the treatment of asthma. These drugs, often referred to as beta2 agonists, help stop asthma attacks by binding to protein receptors in the airways of the lung causing the airways to relax and dilate so air can move in and out easily. But prolonged exposure to these drugs can cause the protein receptors to stop responding to beta2 agonist stimulation, a process called desensitisation. As a result, these drugs sometimes lose their effectiveness with long-term use. In this week's The Lancet, Dr. Soong Tan and colleagues from the United Kingdom report some people may inherit airway receptors that are particularly prone to becoming desensitised to beta2 agonists. In the study, the researchers looked for common variants of the receptors in 22 asthmatics who had taken a long-acting beta2 agonist called formoterol for four weeks. Some of these patients had shown signs they had become less sensitive to the drug over time. One group of variants the researchers looked for is caused by a difference in the 16th aminoacid of the receptor protein, where one variant has an arginine (Arg 16) and the other a Glycine (Gly 16). The second group of variants they studied have different aminoacids at position 27. In this case, either a glutamine (Gln 27) or a glutamate (Glu 27). Since each person normally has two copies of the gene for these receptors, the patients in the study could either have similar copies of the gene, in which case they would be homozygotes (eg, Arg 16 / Arg 16) or different copies, in which case they would be heterozygotes (eg, Arg 16 / Gly 16). The researchers found those patients who were homozygous for Gly 16 (i.e., Gly 16 / Gly 16) developed significantly greater desensitisation to the agonist than those who were homozygous for Arg 16 (i.e., Arg 16 / Arg 16). The finding suggests long-acting beta2 agonists may be less effective in patients who are homozygous for Gly 16, and genetic inheritance may explain some cases of beta2-agonist failure. E-mail this page to a friend or colleague! To print, use this version