Konturek S J, Gonciarz M, Gonciarz Z, Bielanski W, Mazur W, Mularczyk A, Konturek P C, Goetze J P, Rehfeld J F
Dept. of Physiology, Medical College, Jagiellonian University, Kraków, Poland.
Scand J Gastroenterol. 2003 Jun;38(6):643-7. doi: 10.1080/00365520310002472.
Gastrin and its precursor, progastrin, are synthesized in the stomach, particularly when infected with Helicobacter pylori, and they are metabolized, at least in part, in the liver. However, little is known about their levels in various hepatic diseases.
This study was carried out on 147 patients including chronic hepatitis B (n = 35), hepatitis C (n = 52) and liver cirrhosis (n = 60) of class A (n = 38), class B (n = 15) and class C (n = 7) (Child-Pugh classification) and age- and sex-matched healthy controls (n = 65). The diagnosis of chronic hepatitis was confirmed by liver biopsy in all patients, whereas the diagnosis of liver cirrhosis was based on clinical and laboratory findings. Liver biopsy was done in 38 out of 60 patients. Blood samples were collected under basal conditions and separated plasma samples were kept frozen at -70 degrees C until radioimmunoassay of progastrin and its products, including bioactive amidated gastrins.
Median (range) plasma concentrations of total progastrin product and amidated gastrin in control subjects were 147.5 (73-345) pM and 33 (15-65), respectively. These concentrations in hepatitis B and C were not significantly different from those in controls. In cirrhosis (classes A, B and C), the concentrations of the progastrin and of gastrin were significantly (P < 0.05) higher than in controls reaching, respectively, 253.5 (135-683 pM) and 47.5 (17-385) pM. Both progastrin and gastrin levels were significantly higher in H. pylori-positive than in negative cirrhotic patients. Antibodies against H. pylori were present in about 50% of controls, 68% of hepatitis B, 57% of hepatitis C and in 83% in cirrhosis patients. The difference in H. pylori prevalence between cirrhosis and controls was statistically significant.
Plasma levels of progastrin and gastrin are significantly increased in cirrhotic patients and this could be attributed to reduced metabolism of these peptides in liver cirrhosis and to their increased release due to H. pylori infection rate in this disease.
胃泌素及其前体，即前胃泌素，在胃中合成，尤其是在感染幽门螺杆菌时，并且它们至少部分地在肝脏中代谢。然而，关于它们在各种肝脏疾病中的水平知之甚少。
本研究对147例患者进行，包括慢性乙型肝炎（n = 35）、丙型肝炎（n = 52）以及A类（n = 38）、B类（n = 15）和C类（n = 7）（Child-Pugh分级）的肝硬化患者（n = 60），以及年龄和性别匹配的健康对照者（n = 65）。所有患者的慢性肝炎诊断均通过肝活检确诊，而肝硬化诊断基于临床和实验室检查结果。60例患者中有38例进行了肝活检。在基础条件下采集血样，分离后的血浆样本保存在-70℃直至进行前胃泌素及其产物（包括生物活性酰胺化胃泌素）的放射免疫测定。
对照者中总前胃泌素产物和酰胺化胃泌素的血浆浓度中位数（范围）分别为147.5（73 - 345）pM和33（15 - 65）pM。乙型和丙型肝炎患者的这些浓度与对照者无显著差异。在肝硬化患者（A、B和C类）中，前胃泌素和胃泌素的浓度显著高于对照者（P < 0.05），分别达到253.5（135 - 683 pM）和47.5（17 - 385）pM。幽门螺杆菌阳性的肝硬化患者的前胃泌素和胃泌素水平均显著高于阴性患者。约50%的对照者、68%的乙型肝炎患者、57%的丙型肝炎患者以及83%的肝硬化患者存在抗幽门螺杆菌抗体。肝硬化患者与对照者之间幽门螺杆菌感染率的差异具有统计学意义。
肝硬化患者血浆前胃泌素和胃泌素水平显著升高，这可能归因于肝硬化中这些肽的代谢减少以及由于该疾病中幽门螺杆菌感染率增加导致其释放增加。
