Protease inhibitor profile of black Americans with and without chronic cardiopulmonary disease.
An epidemiologic study of protease inhibitor (alpha(1)-antitrypsin) was undertaken among 599 ambulatory and hospitalized black American patients with chronic cardiopulmonary disease referred for pulmonary function testing, and 115 ethnically matched, healthy control subjects. Clinical evaluation consisted of respiratory questionnaire completion, physical examination, chest radiograph, and spirography. Protease inhibitor evaluation consisted of measurement of serum trypsin inhibitory capacity in all subjects corrected by comparison with control sera, while 200 of these subjects were phenotyped for alpha(1)-antitrypsin electrophoretic variants.Results showed mean serum trypsin inhibitory capacity for all subjects was 1.56, SD ± 0.47 mg/ml, while corrected values were 111.2, SD ± 30.5 percent of control. Acute phase reactivity was present for patients with heart disease, pulmonary malignancy, p<0.01 for both, and pulmonary fibrosis, p<0.05, when compared with controls. Prevalence of protease inhibitor variants in 29 controls was two heterozygotes for the Z variant (seven percent), and one homozygote for the S variant. Among 94 patients with chronic obstructive pulmonary disease, prevalence was 1.1 percent each for ZZ and SZ phenotypes, and 2.1 percent for MZ. Suprprisingly, the sole ZZ patient had asthmatic bronchitis rather than emphysema.Computed allele frequencies for Pi M and Z were comparable to those for a random sample of black Americans in St. Louis, but differed from a sample of black infants in Brooklyn, NY.These results indicate that protease inhibitor deficiency variants are not as uncommon among black Americans as the literature suggests. Furthermore, the heterozygous state is not necessarily a risk factor in development of chronic obstructive pulmonary disease. Protease inhibitor deficiency states therefore appear to play less important a role in etiology of chronic cardiopulmonary disease in black Americans than among their Caucasian counterparts.Preliminary work was published in abstract form.(1)
D000293:Adolescent; D000328:Adult; D044383:Black People; D004812:Epidemiologic Methods; D005260:Female; D006331:Heart Diseases / Q000209:etiology* / Q000235:genetics; D006801:Humans; D008171:Lung Diseases / Q000209:etiology* / Q000235:genetics; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D012907:Smoking / Q000150:complications; D000515:alpha 1-Antitrypsin / Q000235:genetics; D019896:alpha 1-Antitrypsin Deficiency; D001741:Black or African American
D000515:alpha 1-Antitrypsin