Lasson A, Borgström A, Ohlsson K
Scand J Gastroenterol. 1986 Dec;21(10):1275-80. doi: 10.3109/00365528608996455.
Elevated levels of immunoreactive pancreatic secretory trypsin inhibitor (PSTI) were found in serum from patients with perforated duodenal ulcer, bacterial peritonitis, urosepticemia, pneumonia, acute renal failure, and also after different surgical procedures. The extent of the trauma seemed to determine the maximal level of PSTI. The increase found paralleled the changes seen in the acute-phase protein antichymotrypsin. There was, however, almost no increase in trypsinogen, thought to be produced together with PSTI in the acinar cells of the pancreas. In conclusion, there is evidence that PSTI is probably also produced somewhere outside the pancreas, in agreement with recent immunohistochemical data. This production may be part of a general acute-phase reaction. Thus, PSTI may have a more general inhibitory function against trypsin-like protease release in tissue injury, instead of being a purely local trypsin inhibitor in the pancreatic gland.
在十二指肠溃疡穿孔、细菌性腹膜炎、尿毒症败血症、肺炎、急性肾衰竭患者的血清中，以及在不同外科手术后，均发现免疫反应性胰分泌性胰蛋白酶抑制剂（PSTI）水平升高。创伤程度似乎决定了PSTI的最高水平。所发现的升高与急性期蛋白抗胰凝乳蛋白酶的变化平行。然而，胰蛋白酶原几乎没有增加，而胰蛋白酶原被认为是在胰腺腺泡细胞中与PSTI一起产生的。总之，有证据表明PSTI可能也在胰腺外的其他部位产生，这与最近的免疫组织化学数据一致。这种产生可能是一般急性期反应的一部分。因此，PSTI可能对组织损伤中类胰蛋白酶的释放具有更广泛的抑制作用，而不是胰腺中纯粹的局部胰蛋白酶抑制剂。
