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目的探讨肝炎肝硬化患者外周血清胃泌素的变化特点,以及幽门螺杆菌(Hp)感染对血清胃泌素的影响及其临床意义。方法选择首都医科大学附属北京佑安医院确诊的肝炎肝硬化患者165例[男113例,女52例,平均年龄(51.9±11.4)岁]及同期健康志愿者30例[男12例,女18例,平均年龄(44.9±11.9岁)]作为研究对象。肝炎肝硬化组分为Child-Pugh A级(54例)、B级(60例)、C(51例)。抽取外周静脉血3 ml、行~(14)C-尿素呼气试验和电子胃镜检查(结果由两名以上专业人员诊断)。根据胃镜下活检病理和14C-尿素呼气试验判断是否Hp感染。双抗体夹心酶联免疫吸附实验检测血清胃泌素浓度,并根据标准曲线计算胃泌素含量。以肝炎肝硬化患者胃泌素水平为因变量,Hp感染情况、性别、年龄、病毒载量、总胆红素、肌酐、白蛋白、血氨、血浆凝血酶原时间、溃疡情况、静脉曲张情况为自变量进行多元逐步回归分析。结果 165例肝炎肝硬化患者中Hp感染率48.5%(80/165);Child-Pugh A、B、C级Hp感染率分别为40.7%(22/54)、50.0%(30/60)、54.9%(28/51),差异无统计学意义(P=0.335)。30例对照组Hp感染率20.0%(6/30),显著低于肝炎肝硬化组(P=0.004)。肝炎肝硬化组血清胃泌素的浓度为(772.9±368.3)pg/ml,高于对照组(260.3±117.6)pg/ml,差异有统计学意义(P<0.01)。肝炎肝硬化Hp感染者血清胃泌素平均浓度(957.2±318.5)pg/ml显著高于未感染者(595.1±324.2)pg/ml,差异有统计学意义(P<0.01)。进一步分组比较,Child A、B、C各亚组Hp感染者比未感染者的血清胃泌素浓度均亦显著升高[(781.3±233.8)pg/ml vs.(398.0±159.3)pg/ml,(884.2±235.9)pg/ml vs.(617.6±301.8)pg/ml,(1 205.9±316.5)pg/ml vs.(816.6±334.9)pg/ml,P均<0.01]。多元逐步回归分析,Hp感染对肝炎肝硬化患者血清胃泌素水平的影响最大,白蛋白水平与胃泌素水平呈负相关。肝炎肝硬化并发消化性溃疡50例,占30.3%。肝炎肝硬化合并消化性溃疡患者与无溃疡者相比,其外周血胃泌素浓度显著升高[(909.4±340.8)pg/ml vs.(713.5±365.4)pg/ml,P=0.002]。结论肝炎肝硬化患者外周血清胃泌素升高,Hp感染可能在其中发挥了重要作用。血清胃泌素升高可能是肝炎肝硬化患者易发生消化性溃疡的原因之一。
Objective To investigate the characteristics of peripheral serum gastrin in patients with liver cirrhosis and the influence of Helicobacter pylori (Hp) infection on serum gastrin and its clinical significance. Methods A total of 165 patients with hepatitis cirrhosis (113 males and 52 females, average age 51.9 ± 11.4 years old) and 30 healthy volunteers (12 males and 18 females) were enrolled in the Beijing You’an Hospital Affiliated to Capital Medical University. Case, mean age (44.9 ± 11.9 years)] as study subjects. Liver cirrhosis was classified as Child-Pugh class A (54 cases), class B (60 cases), and C (51 cases). Peripheral venous blood was drawn 3 ml, line ~ (14) C-urea breath test and electronic gastroscopy (results from two or more professionals diagnosed). According to endoscopy biopsy pathology and 14 C-urea breath test to determine whether Hp infection. Serum gastrin concentrations were measured by sandwich enzyme-linked immunosorbent assay (ELISA) and gastrin levels were calculated according to the standard curve. Hepatic cirrhosis patients with gastrin as the dependent variable, Hp infection, sex, age, viral load, total bilirubin, creatinine, albumin, blood ammonia, plasma prothrombin time, ulcers, varicose veins Multivariate stepwise regression analysis for independent variables. Results The Hp infection rate was 48.5% (80/165) in 165 patients with hepatitis cirrhosis and 40.7% (22/54), 50.0% (30/60) in Child-Pugh A, B and C, respectively % (28/51), the difference was not statistically significant (P = 0.335). The infection rate of Hp in 30 cases of control group was 20.0% (6/30), which was significantly lower than that of hepatitis cirrhosis group (P = 0.004). The concentration of serum gastrin in hepatitis cirrhosis group was (772.9 ± 368.3) pg / ml, which was significantly higher than that in control group (260.3 ± 117.6 pg / ml) (P <0.01). The mean serum concentration of gastrin (957.2 ± 318.5) pg / ml in Hp infected with hepatitis cirrhosis was significantly higher than that in uninfected patients (595.1 ± 324.2 pg / ml) (P <0.01). For further subgroups, serum gastrin concentrations in Child A, B and C subgroups were significantly higher than those in non-infected Hp patients [(781.3 ± 233.8) pg / ml vs. (398.0 ± 159.3) pg / ml , (884.2 ± 235.9) pg / ml vs. (617.6 ± 301.8) pg / ml, (1 205.9 ± 316.5) pg / ml vs. (816.6 ± 334.9) pg / ml, P all <0.01]. Multiple stepwise regression analysis showed that Hp infection had the most significant effect on serum gastrin level in cirrhotic patients with hepatitis B, and albumin level was negatively correlated with gastrin level. Hepatitis cirrhosis complicated by peptic ulcer in 50 cases, accounting for 30.3%. Serum gastrin levels in patients with hepatitis cirrhosis complicated with peptic ulcer were significantly higher than those without ulcer [(909.4 ± 340.8) pg / ml vs. (713.5 ± 365.4) pg / ml, P = 0.002]. Conclusions Serum gastrin is elevated in peripheral blood of patients with liver cirrhosis and Hp infection may play an important role. Serum gastrin may be one of the causes of peptic ulcer in patients with liver cirrhosis.