Eun Bae Suh, Hoon Lee Jeong, Soo Park Young, Ok Kim Seon, Young Choi Ji, Yong Ahn Ji, Hoon Kim Do, Don Choi Kee, June Song Ho, Hyug Lee Gin, Choe Jaewon, Jin Jang Se, Jung Hwoon-Yong
a Health Screening and Promotion Center , University of Ulsan College of Medicine, Asan Medical Center , Seoul , South Korea .
b Department of Internal Medicine .
Scand J Gastroenterol. 2016;51(2):137-44. doi: 10.3109/00365521.2015.1083049.
Ghrelin is mainly secreted by the gastric oxyntic mucosa and its production is impaired in chronic atrophic gastritis. This study aimed at evaluating how serum total ghrelin correlates with the extent of atrophy, and to compare its performance as a serologic marker with that of pepsinogen (PG).
Data were collected from 154 patients with atrophic gastritis. The histological extent of atrophy was assessed by three paired biopsies from the antrum, corpus lesser curvature (CLC), and corpus greater curvature (CGC). Fasting serum concentrations of total ghrelin, pepsinogen I and II were measured. Regression analysis was performed to evaluate the factors associated with serum total ghrelin. The serologic performance was compared with that of pepsinogen using receiver-operating characteristic (ROC) curves.
The Helicobacter pylori infection rate was 85%, and extensive atrophic gastritis involving CGC was found in 24%. Serum total ghrelin was significantly decreased in patients with extensive CGC atrophy (median: 170.4 pg/mL, vs 201.1 pg/mL in patients without atrophy; p < 0.001), and its levels correlated with those of pepsinogen I and I/II ratio. The decrease of serum total ghrelin was independent of age, gender, body mass index (BMI), and H. pylori infection status. The sensitivity and specificity of serum total ghrelin in predicting extensive atrophy were 57% and 79%, respectively. The discriminatory ability was similar to that of pepsinogen I/II ratio (p = 0.612), and lower than that of pepsinogen I (p = 0.040).
Serum total ghrelin is decreased during extensive atrophy involving CGC. The serologic performance is lower than that of pepsinogen I.
胃饥饿素主要由胃泌酸黏膜分泌，其分泌在慢性萎缩性胃炎中受损。本研究旨在评估血清总胃饥饿素与萎缩程度的相关性，并将其作为血清学标志物的性能与胃蛋白酶原（PG）进行比较。
收集154例萎缩性胃炎患者的数据。通过取自胃窦、胃体小弯（CLC）和胃体大弯（CGC）的三对活检组织评估萎缩的组织学程度。测定空腹血清总胃饥饿素、胃蛋白酶原I和II的浓度。进行回归分析以评估与血清总胃饥饿素相关的因素。使用受试者工作特征（ROC）曲线将血清学性能与胃蛋白酶原进行比较。
幽门螺杆菌感染率为85%，24%的患者存在累及CGC的广泛性萎缩性胃炎。在累及CGC广泛性萎缩的患者中，血清总胃饥饿素显著降低（中位数：170.4 pg/mL，无萎缩患者为201.1 pg/mL；p < 0.001），其水平与胃蛋白酶原I及I/II比值相关。血清总胃饥饿素的降低与年龄、性别、体重指数（BMI）和幽门螺杆菌感染状态无关。血清总胃饥饿素预测广泛性萎缩的敏感性和特异性分别为57%和79%。其鉴别能力与胃蛋白酶原I/II比值相似（p = 0.612），低于胃蛋白酶原I（p = 0.040）。
在累及CGC的广泛性萎缩过程中血清总胃饥饿素降低。血清学性能低于胃蛋白酶原I。
