الفهرس 
The effect of U1-antitrypsin deficiency and bacterial loads on the efficacy of chronic obstructive pulmonary disease pharmacotherapy in Egyptian patients
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Abstract
Chronic obstructive pulmonary disease (COPD) is associated with slowly progressive airflow obstruction. chronic obstructive pulmonary disease (COPD) is caused by the combination of smoking, genetic susceptibility and exacerbated by infection. The genetic cause of COPD is {uF061}1-antitrypsin (AAT) deficiency where the gene encoding this protein shows genetic polymorphisms increasing the complexity of COPD predisposing factors. In addition, the development of pulmonary infections with different bacterial species is associated with exacerbation of COPD. How the different genotypes when combined with different types and loads of bacterial infections could affect the outcome of COPD and its responsiveness to therapy remain unclear. This is especially true regarding Egyptian patients where COPD is widespread and at the same time genotyping of these patients is almost absent. Screen for the AAT deficiency alleles phenotypically and genotypically and hence assess the contribution of two of the most common deficiencies (Pi*S and Pi*Z) and two of the rare deficiencies alleles that were predicted to be prevalent in Egypt (Pi*Mmalton and Pi*Q0Cairo) in the development of COPD in Egypt. Compare this study results to the results collected in North African countries to study the mutation pattern in North Africa. Determine the effects of AATD on the efficacy of COPD conventional pharmacotherapy. Fifty-nine subjects (29 controls and 30 COPD patients) were tested for genetic AATD and respiratory function. The bacterial loads were determined to the patients{u2019} group who were then given a long acting beta-agonist and corticosteroid inhaler for 6 months