Metastatic emphysema: a mechanism for acquiring inguinal herniation.
Since our previous work had indicated that veterans with inguinal herniation demonstrated qualitative and quantitative changes in connective tissue, we tested the hypothesis that a possible mechanism for the defect was chronic exposure to circulating proteases generated in the lung by cigarette smoke. We investigated 59 men (average age: 60 years) with eigher primary direct of indirect hernias. Most of the patients smoked. Circulating serum elastolytic activity was significantly greater in patients with direct hernias who smoked when compared with controls (p less than 0.001). In addition, the serum alpha-1-antitrypsin inhibitory capacity was significantly lower in this category than controls (p less than 0.001). Patients with indirect defects who smoked also had significantly higher elastolytic values but to a lesser degree (p less than 0.01). Serum antiprotease and protein concentrations were within the normal range in all categories. Our results indicate that an imbalance between blood protease and antiproteases, resulting from chronic smoking can damage connective tissue in the groin as well as the lung.
D005260:Female; D006552:Hernia, Inguinal / Q000209:etiology*; D006801:Humans; D008875:Middle Aged; D010447:Peptide Hydrolases / Q000097:blood; D011480:Protease Inhibitors / Q000097:blood; D011656:Pulmonary Emphysema / Q000150:complications* / Q000201:enzymology; D012907:Smoking; D000515:alpha 1-Antitrypsin / Q000097:blood
D011480:Protease Inhibitors; D000515:alpha 1-Antitrypsin; D010447:Peptide Hydrolases