Abstract
Clinical observations suggest that some aneurysms may be manifestations of intrinsic tissue abnormalities or systemic disease. Several investigators have reported reduced elastin content and increased elastase activity in infrarenal aortic aneurysms. Alpha1-antitrypsin is the primary serum protease inhibitor modulating elastase activity. Elevated elastase activity caused by reduced alpha1-antitrypsin inhibition, theoretically, could contribute to aneurysm formation. We report a case of ruptured middle colic artery aneurysm in a patient with multiple visceral artery aneurysms and profound alpha1-antitrypsin deficiency. Reported middle colic artery aneurysms are reviewed, and etiologic implications are discussed.
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