萎缩性胃炎患者血清中酰胺化胃泌素-17和胃蛋白酶原I水平：一项观察性病例对照研究。

Serum levels of amidated gastrin-17 and pepsinogen I in atrophic gastritis: an observational case-control study.

作者信息

Sipponen P, Ranta P, Helske T, Kääriäinen I, Mäki T, Linnala A, Suovaniemi O, Alanko A, Härkönen M

机构信息

Dept of Pathology, Helsinki District University Central Hospital, Espoo, Finland.

出版信息

Scand J Gastroenterol. 2002 Jul;37(7):785-91.

PMID:12190091

Abstract

BACKGROUND

Helicobacter pylori infection is often diagnosed with non-endoscopic methods, such as serology or breath or antigen stool tests. These tests provide information on the presence or absence of the H. pylori gastritis only. We investigated whether atrophic gastritis can be diagnosed and typed non-endoscopically if the serum levels of pepsinogen I (S-PGI) and gastrin-17 (S-G-17) are assayed in connection with H. pylori testing.

METHODS

The present investigation is an observational case-control study comprising 100 selected dyspeptic outpatients with (cases) or without (controls) advanced (moderate or severe) atrophic gastritis. Before the blood tests, all patients underwent a diagnostic gastroscopy with multiple biopsies. The series of cases includes 56 patients. Eight had an advanced antrum limited atrophic gastritis, 13 had resected antrum (in two of whom the corpus mucosa in the stump was atrophic), and 30 had corpus-limited atrophic gastritis. Four patients had an advanced atrophic gastritis in both the antrum and corpus (multifocal atrophic gastritis), and the whole stomach was removed in one patient. Twenty of the 44 controls had a non-atrophic H. pylori gastritis. Both the antrum and corpus were normal and healthy in 24 patients. The S-PGI and S-G-17 were determined with EIA methods using monoclonal antibodies to PGI and amidated G-17. Postprandial S-G-17 (S-G-17prand) was measured 20 min after a protein-rich drink. The H. pylori antibodies were assayed with a polyclonal EIA method.

RESULTS

A low S-PGI (<25 microg/l; an empirical cut-off with best discrimination) was found in 31 of 37 patients (84%) with and in 3 of 63 patients (5%) without corpus atrophy in the biopsy specimens. A low S-G-17prand (<5 pmol/l) was found in all 8 patients with H. pylori-associated antral atrophy and in 11 of 14 patients (79%) with resected antrum but in 3 of 20 control patients (15%) with H. pylori-related non-atrophic gastritis. Median and mean values of both S-G-17prand and S-PGI decreased with increasing grade of antral and corpus atrophy, respectively. Among all patients with atrophic gastritis (multifocal atrophic gastritis, or atrophic gastritis limited to antrum or corpus) or resected stomach, 50 of 56 patients (89%; Cl 95%: 81%-97%) had a low S-PGI and/or a low S-G-17prand with positive H. pylori serology. Such low values werc found in 3 of the 44 control patients (7%; CI 95%: 0%-14%).

CONCLUSIONS

Low serum levels of G-17prand and PGI are conceivable biomarkers of atrophic antral and corpus gastritis, respectively. A low S-G-17prand is a sign of the multifocal or antrum-limited atrophic gastritis in patients infected with H. pylori.

摘要

背景

幽门螺杆菌感染常通过非内镜检查方法诊断，如血清学、呼气试验或抗原粪便检测。这些检测仅能提供幽门螺杆菌胃炎是否存在的信息。我们研究了在进行幽门螺杆菌检测的同时检测血清胃蛋白酶原I（S-PGI）和胃泌素-17（S-G-17）水平，是否能非内镜诊断萎缩性胃炎并进行分型。

方法

本研究为一项观察性病例对照研究，纳入100例有（病例组）或无（对照组）重度（中度或重度）萎缩性胃炎的消化不良门诊患者。在血液检测前，所有患者均接受了诊断性胃镜检查及多处活检。病例组包括56例患者。8例为重度胃窦局限性萎缩性胃炎，13例胃窦已切除（其中2例残端胃体黏膜萎缩），30例为胃体局限性萎缩性胃炎。4例患者胃窦和胃体均有重度萎缩性胃炎（多灶性萎缩性胃炎），1例患者全胃切除。44例对照组患者中，20例有非萎缩性幽门螺杆菌胃炎。24例患者胃窦和胃体均正常健康。采用针对PGI和酰胺化G-17的单克隆抗体通过酶免疫分析方法测定S-PGI和S-G-17。饮用富含蛋白质饮料20分钟后测定餐后S-G-17（S-G-17prand）。采用多克隆酶免疫分析方法检测幽门螺杆菌抗体。

结果

活检标本中胃体萎缩的37例患者中有31例（84%）S-PGI低（<25μg/l；经验性临界值，鉴别能力最佳），63例无胃体萎缩的患者中有3例（5%）S-PGI低。所有8例幽门螺杆菌相关性胃窦萎缩患者及14例胃窦切除患者中的11例（79%）餐后S-G-17（S-G-17prand）低（<5pmol/l），但20例幽门螺杆菌相关性非萎缩性胃炎对照组患者中有3例（15%）餐后S-G-17低。S-G-17prand和S-PGI的中位数和平均值分别随胃窦和胃体萎缩程度加重而降低。在所有患有萎缩性胃炎（多灶性萎缩性胃炎，或局限于胃窦或胃体的萎缩性胃炎）或胃切除的患者中，56例患者中有50例（89%；95%置信区间：81%-97%）S-PGI低和/或S-G-17prand低且幽门螺杆菌血清学阳性。44例对照组患者中有3例（7%；95%置信区间：0%-14%）出现此类低值。