Berninger R W, DeLellis R A, Kaplan M M
Am J Clin Pathol. 1985 Apr;83(4):503-6. doi: 10.1093/ajcp/83.4.503.
The purpose of this article is to document clinical and pathologic observations concerning liver disease associated with the PI ElembergM phenotype of alpha 1-antitrypsin. Deposits of alpha 1-antitrypsin that were periodic acid-Schiff positive and stained with an antiserum to alpha 1-antitrypsin were found in the liver of a markedly jaundiced, terminally ill patient with Stage IV primary biliary cirrhosis. A biopsy performed three years earlier failed to reveal alpha 1-antitrypsin deposits. The phenotype PI ElembergM was verified by both acid starch gel electrophoresis and isoelectric focusing in agarose. The deposits of alpha 1-antitrypsin in the liver appear to be a consequence of the patient's disease and age and not due to an association with the PI*Elemberg allele. Accumulation of alpha 1-antitrypsin in the liver of this patient may be due to an accelerated synthesis of this protease inhibitor exceeding the liver's capacity for glycosylation or other steps in its secretion.
本文的目的是记录与α1-抗胰蛋白酶PI ElembergM表型相关的肝脏疾病的临床和病理观察结果。在一名患有IV期原发性胆汁性肝硬化、明显黄疸且处于终末期的患者肝脏中,发现了高碘酸-希夫染色阳性且能用抗α1-抗胰蛋白酶抗血清染色的α1-抗胰蛋白酶沉积物。三年前进行的一次活检未发现α1-抗胰蛋白酶沉积物。通过酸性淀粉凝胶电泳和琼脂糖等电聚焦法均验证了PI ElembergM表型。肝脏中α1-抗胰蛋白酶的沉积物似乎是患者疾病和年龄的结果,而非与PI*Elemberg等位基因相关。该患者肝脏中α1-抗胰蛋白酶的积累可能是由于这种蛋白酶抑制剂的合成加速,超过了肝脏进行糖基化或其分泌中其他步骤的能力。