Chronic obstructive pulmonary disease is highly prevalent the world over. An estimated 7% to 10% of the global adult population is affected. In Brazil, the incidence of chronic bronchitis is 12.7% among individuals over the age of 40. Economic studies have great relevance in devising policies for dealing with diseases of such high prevalence. The majority of data related to the costs of chronic obstructive pulmonary disease is culled from national health databases. There have been only a few studies evaluating the direct public health costs of the disease. In analyzing those studies, one can conclude that a chronic obstructive pulmonary disease patient generates a direct annual expenditure of 1200 to 1800 USD. However, the cost is correlated with the severity of the disease. Patients suffering from the more severe forms can require as much as double that expenditure, and early diagnosis is therefore vital. The most cost-effective strategy is early detection of the disease, in concert with anti-smoking campaigns. In the most advanced stages of the disease, the greatest costs are incurred due to hospitalization. In such cases, correct treatment of the acute exacerbations of the disease is crucial to minimizing costs. The average cost of a hospital stay in Brazil is 2761 Brazilian reals, which is equal to that of one full year of outpatient treatment. Antibiotic therapy accounts for only a small fraction of the total cost of treating such acute exacerbations. The use of more efficacious antibiotics may represent a more cost-effective strategy for reducing the rate of treatment failure. Economic analysis should allow for the identification and implementation of the most cost-effective strategies for treating this disease.

Keywords: Smoking/adverse effects. Tobacco use cessation/methods. Pregnancy.

Alpha-1 antitrypsin deficiency is a recently identified genetic disease that occurs almost as frequently as cystic fibrosis. It is caused by various mutations in the SERPINA1 gene, and has numerous clinical implications. Alpha-1 antitrypsin is mainly produced in the liver and acts as an antiprotease. Its principal function is to inactivate neutrophil elastase, preventing tissue damage. The mutation most commonly associated with the clinical disease is the Z allele, which causes polymerization and accumulation within hepatocytes. The accumulation of and the consequent reduction in the serum levels of alpha-1 antitrypsin cause, respectively, liver and lung disease, the latter occurring mainly as early emphysema, predominantly in the lung bases. Diagnosis involves detection of low serum levels of alpha-1 antitrypsin as well as phenotypic confirmation. In addition to the standard treatment of chronic obstructive pulmonary disease, specific therapy consisting of infusion of purified alpha-1 antitrypsin is currently available. The clinical efficacy of this therapy, which appears to be safe, has yet to be definitively established, and its cost-effectiveness is also a controversial issue that is rarely addressed. Despite its importance, in Brazil, there are no epidemiological data on the prevalence of the disease or the frequency of occurrence of deficiency alleles. Underdiagnosis has also been a significant limitation to the study of the disease as well as to appropriate treatment of patients. It is hoped that the creation of the Alpha One International Registry will resolve these and other important issues.

Keywords: alpha 1-antitrypsin; Emphysema; Pulmonary disease, chronic obstructive.

Objective: To validate and develop an immunonephelometric assay for the determination of alpha-1 antitrypsin (AAT) levels in dried blood spots from COPD patients in Brazil. Methods: We determined AAT levels in serum samples and dried blood spots from 192 COPD patients. For the preparation of dried blood spots, a disk (diameter, 6 mm) was placed into a tube, eluted with 200 µL of PBS, and stored overnight at 4°C. All of the samples were analyzed by immunonephelometry in duplicate. We used the bootstrap resampling method in order to determine a cut-off point for AAT levels in dried blood spots. Results: The correlation coefficient between the AAT levels in serum samples and those in dried blood spots was r = 0.45. For dried blood spots, the cut-off value was 2.02 mg/dL (97% CI: 1.45-2.64 mg/dL), with a sensitivity, specificity, positive predictive value, and negative predictive value of 100%, 95.7%, 27.2%, and 100%, respectively. Conclusions: This method for the determination of AAT levels in dried blood spots appears to be a reliable screening tool for patients with AAT deficiency.