Lucas K J, Feldman J M
Cancer. 1986 Nov 15;58(10):2290-3. doi: 10.1002/1097-0142(19861115)58:10<2290::aid-cncr2820581022>3.0.co;2-4.
To examine the role of kallikrein in the etiology of flushing in the carcinoid syndrome, chromogenic substrates specific for kallikrein were used to measure two isoenzymes of this substance. The plasma and glandular kallikrein levels were determined in 20 carcinoid patients and in 17 controls. Kallikrein levels were not significantly different between these two groups. Twelve carcinoid patients and six controls were given alcohol and the kallikrein activity was measured before and at 2, 5, and 10 minutes after alcohol ingestion; kallikrein activity did not change significantly. Kallikrein was absent from the primary tumors of seven patients with carcinoids. These studies, therefore, indicate that kallikrein with subsequent induction of bradykinin formation is not solely responsible for the flushing in the carcinoid syndrome.
为研究激肽释放酶在类癌综合征潮红病因中的作用,使用对激肽释放酶具有特异性的发色底物来测定该物质的两种同工酶。测定了20例类癌患者和17例对照者的血浆和腺体激肽释放酶水平。两组之间激肽释放酶水平无显著差异。给12例类癌患者和6例对照者饮用酒精,并在饮酒前以及饮酒后2、5和10分钟测量激肽释放酶活性;激肽释放酶活性无显著变化。7例类癌患者的原发性肿瘤中未检测到激肽释放酶。因此,这些研究表明,激肽释放酶及其随后诱导的缓激肽形成并非类癌综合征潮红的唯一原因。