血清胃蛋白酶原、胃泌素-17及幽门螺杆菌检测在健康体检人群胃癌筛查中的应用价值

目的:探讨血清胃蛋白酶原Ⅰ(pepsinogenⅠ,PGⅠ)、PGⅡ、PGⅠ/PGⅡ、胃泌素-17(gastrin-17,G-17)和胃幽门螺杆菌(Helicobacter pylori, H.pylori)等血清学筛查指标在健康体检人群胃癌筛查中的应用价值。方法:回顾性纳入2020年01月至2021年12月期间在我院健康管理中心进行血清PG、G-17检测及¹³C尿素呼气试验(¹³C urea breathing test,¹³C-UBT)的健康体检人群共25 387例作为研究对象,将PG(+)、G-17(+)、H.pylori(+)任意满足2项及以上或PG、G-17单独异常定义为高危组,对高危组患者行内镜检查及进一步病理活检,根据病理诊断分为胃癌前状态、胃癌前病变、早期胃癌、进展期胃癌及对照组(胃黏膜正常组),分析PG、G-17、H.pylori水平与胃黏膜各级病变发生的关系及对胃癌的筛查价值。结果:血清学筛查高危组7 592例,占29.9%;高危组男性的构成、H.pylori感染率、平均年龄高于低危组,PGⅠ、PGⅠ...     

902例胃癌临床流行病学特征分析

[目的]探讨分析近年来胃癌的临床流行病学特征。[方法]对2005～2009年中国医学科学院肿瘤医院诊疗的902例胃癌患者的临床资料进行回顾性统计分析。[结果]①902例胃癌患者中,男女性比例为3.2：1,男性平均年龄59.7岁,女性平均年龄53.6岁。②男性患者中胃底贲门癌占54.5%,胃窦癌占21.6%,胃体癌占17.4%。女性患者中胃窦癌、胃体癌和胃底贲门癌的发病比例基本相同,约30%。③912个癌灶病理组织类型：胃腺癌占88.5%,印戒细胞癌占8.9%,黏液腺癌占1.0%。④615例分期明确的患者中,0～Ⅰ期占18.9%,Ⅲ期和Ⅳ期占69.3%。[结论]收治的胃癌具有男性（51～70岁）高发,男性贲门癌高发,胃癌发生部位上移的临床流行病学特征。     

胃癌发生发展及预后与幽门螺杆菌相关性分析及幽门螺杆菌筛查的临床意义

目的 探讨幽门螺杆菌感染与胃癌的发生发展及预后的关系,以及幽门螺杆菌筛查的临床意义.方法 收集138例胃癌患者的组织石蜡标本,同时选择相应的癌旁组织40例作为对照组,应用实时荧光定量PCR法检测组织中幽门螺杆菌的相对感染量.结果 40例癌旁组织HP相对感染量为(5.32±1.96),138例胃癌组织HP相对感染量(13.07±6.11),两者相比差异具有统计学意义(P＜0.05).胃癌患者的1年、2年、3年生存率与HP相对感染率呈负相关,HP相对感染率越高,则胃癌患者生存率越低,差异具有统计学意义(P＜0.05).患者的年龄、浸润程度、淋巴结转移、TNM分期以及HP相对感染量与胃癌患者的预后呈正相关.HP感染阳性率男性患者为43.8％,女性患者为41.1％,差异不具统计学意义;年龄≤50岁HP阳性率为40.4％,年龄＞50岁HP阳性率为59.6％,差异具统计学意义(P＜0.05).结论 幽门螺杆菌感染在一定程度上影响胃癌的发生发展及预后,临床上对幽门螺杆菌筛查具有重要意义.     

血清脂联素、CEA、CA19-9、CA72-4联合检测在胃癌早期筛查中的临床价值分析

目的:探讨血清脂联素、CEA、CA19-9、CA72-4联合检测在胃癌早期筛查中的临床价值。方法:选取首次确诊的早期胃癌患者60例,胃癌患者再根据幽门螺杆菌是否感染分为感染组32例与未感染组28例;胃良性疾病组患者100例;健康对照组110例。采用化学发光法检测CEA、CA19-9、CA72-4水平,ELISA检测血清脂联素水平,幽门螺杆菌检测采用C14呼气试验,比较不同分组间各指标的差异。结果:胃癌组血清CEA、CA19-9、CA72-4水平均高于胃良性疾病组和健康对照组(P<0.01),血清脂联素水平显著低于胃良性疾病组和健康对照组(P<0.01);胃癌患者幽门螺杆菌感染时,血清CEA、CA19-9、CA72-4水平明显高于未感染组(P<0.01),感染组患者血清脂联素水平与未感染组比较,无显著性差异(P>0.05);四项联合检测胃癌灵敏度最高,达96.67,特异度为98.10%,阳性预测值为93.55%,阴性预测值为99.04%,阳性似然比为50.75、阴性似然比为0.03,约登指数达0.95,ROC曲线下面积为0.955。结论:胃癌早期患者血清脂联素水平不受幽门螺杆菌感染的影响,四项联合检测可明显提高检测的灵敏度和特异度,对胃癌患者早期筛查具有较高的临床应用价值。     

早期胃癌内镜特点与病理分析

目的:分析早期胃癌的胃镜及病理特点,以提高早期胃癌检出率。方法:总结该院1990年~2004年经胃镜活检及手术病理证实的早期胃癌78例患者临床资料。结果:78例早期胃癌均为单发病灶,Ⅱ型病变55例(70.5%),以分布胃窦居多为34例(43.6%),病变直径<1cm者38例(48.7%),病理示管状腺癌最多42例(53.8%),病灶周围示萎缩性胃炎54例(69.2%),中重度不典型增生46例(58.9%),肠上皮化生38例(48.7%),幽门螺杆菌阳性72例(92.3%)。结论:早期胃癌以单发小病灶,Ⅱ型病变多见,胃窦为好发部位,胃镜检查是早期胃癌确诊的重要手段,癌前病变和幽门螺杆菌与早期胃癌关系密切。     

胃癌高发现场高危人群综合防治研究

目的：通过对我国辽宁庄河及山东临朐胃癌高发区胃癌及其高危人群的筛选及癌前状态的干预研究。建立切实切可行的胃癌筛查方案,模索胃癌化学干预中期生物学评估指标。方法：利用血清胃蛋白酶原检测,双对比造影＋胃镜、胃粘膜活检两轮筛查法进行胃癌及其高危人群的筛选;利用限制性片断长度多态性分析方法对胃癌高危人群进行胃蛋白酶原C基因多态性检测,采用随机对照干预实验,对胃幽门螺杆菌感染者及高危人群分别实施抗幽门螺杆菌治疗、中药阻断治疗及大蒜素＋VitC治疗,并对干预效果进行评价;对全民进行以改变不良饮食习惯为主的群体行为干预。结果：庄河现场早期胃癌检出率为56．82％;现场普查中发现的胃癌患者3年生存率为7607％;作为胃癌初筛方法,血清胃蛋白酶原含量检测优于对比造影,国人血清胃蛋白酶原含量检测初筛胃癌的参考临界值（Cut-off)可以考虑由P1≤50＋P1／P2≤3;胃癌组胃蛋白酶原C基因EcorR Ⅰ稀有片断出现频率高于正常组而常见片断有缺失,对4例携带稀有片断的胃癌家系成员进行追踪随访,发现有2例分别在2．5年及5年后罹患者早期胃部,IL－8、PCNA、P53粘、粘蛋白与Hp感染呈正相关而p16与其呈负相关;细胞凋亡下Hp感染相关性胃疾病的发生发展过程相关。结论：庄河现场及监朐已成可以开展前瞻性胃癌流行病学、病因学及大规模人群筛查及随机对照干预实验的胃癌高发区研究 基地、胃癌高危人群一、二级预防一、二级预防初见成效。     

幽门螺杆菌感染对胃癌组织miR-146a表达及胃癌恶性进展的影响

目的 探讨幽门螺杆菌感染对胃癌组织miR-146a表达及胃癌恶性进展的影响.方法 选取82例胃癌患者,根据术后病理组织幽门螺杆菌感染检测结果分为阳性组(n=54例)与阴性组(n=28例).采用qRT-PCR法检测对比2组miR-146a表达情况;采用Cox比例风险回归模型分析幽门螺杆菌感染与胃癌恶性进展关系.结果 阳性...     

胃癌患者生存状况与幽门螺杆菌感染情况的关系

目的 探讨幽门螺杆菌感染与胃癌患者生存状况的关系.方法 回顾性分析98例胃癌患者的临床资料,根据是否发生幽门螺杆菌感染分为感染组(n=67)和非感染组(n=31),分析胃癌发病的危险因素及幽门螺杆菌感染情况对胃癌患者生存情况的影响.结果 感染组有消化道肿瘤家族史患者的比例高于非感染组患者,差异有统计学意义(P<0.05).随访6～36个月,感染组患者死亡36例,生存率为46.3％,中位生存时间为32个月;非感染组患者死亡10例,生存率为67.7％;非感染组患者的生存情况优于感染组,差异有统计学意义(χ2=4.119,P=0.042).Cox比例风险模型分析结果表明,年龄、幽门螺杆菌感染是影响胃癌患者生存情况的危险因素(OR>1,P<0.05);直系亲属无消化道肿瘤家族史是胃癌患者生存情况的保护因素(OR<1,P<0.01).结论 幽门螺杆菌感染且直系亲属有消化道肿瘤家族史患者患胃癌的可能性更高;年龄、幽门螺杆菌感染是影响胃癌患者生存情况的危险因素;直系亲属无消化道肿瘤家族史是胃癌患者生存情况的保护因素.幽门螺杆菌阴性胃癌患者生存情况优于幽门螺杆菌阳性胃癌患者.     

469例经支气管镜检查确诊40岁以下肺癌患者的临床分析

背景与目的近年来,青年肺癌在临床上已不少见,发病率呈逐年上升趋势,临床上易误诊,预后较差。现将我科诊治的469例40岁以下肺癌患者支气管镜及临床特点回顾性分析如下,探讨40岁以下肺癌患者的肿瘤病理分型与性别、生长部位等的关系。方法对经支气管镜检查取材确诊的469例40岁以下肺癌进行回顾性分析。结果469例40岁以下患者肺癌患者中,男性332例,女性137例,男女性别比为2.42:1,病理分型,鳞状细胞癌155例(33.0%),其次是腺癌122例(26.0%),小细胞癌96例(20.5%),男性鳞癌的比例40.7%,明显高于女性14.6%,腺癌比例19.0%明显低于女性43.1%,男性和女性的肿瘤病理类型分布构成有显著差异(P<0.05)。病变部位以双上叶居多,右侧多于左侧。镜下改变新生物及黏膜浸润等直接征象占81.4%。结论40岁以下肺癌患者中,男性以鳞癌为主,女性以腺癌居多。青年人肺癌易漏诊和误诊,支气管镜检查是其诊断的重要手段,应该提高对青年肺癌的警惕和认识,及早进行支气管镜检查。     

慢性胃炎导致胃癌的多因素分析

目的探讨慢性胃炎导致胃癌的相关因素。方法回顾性分析111例胃癌患者的临床资料,用胃癌风险指数(GCRI)表示相关因素的危险程度。结果 111例慢性胃炎性胃癌患者,幽门螺杆菌感染(AHPI)阳性患者77例(69.40%),其中45%AHPI阳性患者出现各类胃炎。AHPI患者GCRI得分偏高(高风险指数)。幽门螺杆菌阴性的其他胃炎性胃癌患者GCRI得分<3分(P=0.001)。结论幽门螺杆菌导致的慢性胃炎更容易诱发胃癌。     

Helicobacter pylori infection-negative gastric cancer in Japanese hospital patients: incidence and pathological characteristics

We used Helicobacter pylori sero-positivity and mucosal atrophy as detected by the serum pepsinogen method to identify H. pylori infection-negative gastric cancer patients with or without atrophy. One hundred and six of 748 (14.2%) primary gastric cancer patients were infection-negative by a serum antibody detection system. Further, 121 (16.2%) of the 748 were negative for gastric mucosal atrophy by the pepsinogen method, of whom 15/748 (2.0%) were H. pylori-negative by pepsinogen I level (>70 ng/mL) and pepsinogen I/II ratio (>3.0). Twenty-seven of 782 (3.6%) gastric cancer patients were H. pylori-negative by antibodies and severe atrophy as determined by pepsinogen I level (<30 ng/mL) and pepsinogen I/II ratio (<2.0). H. pylori-negative gastric cancer patients with severe atrophy likely had a previous infection. These results indicate that the actual number of H. pylori-negative patients is 2.0% at minimum and 10.6% (14.2% minus 3.6%) at maximum in the general Japanese population. Five of 15 (33%) cases displaying neither anti-H. pylori antibodies nor atrophy were intestinal-type and 10 (67%) were diffuse-type adenocarcinomas. Thirteen surgical patients with primary gastric cancer displaying neither antibodies nor mucosal atrophy were further analyzed for pathological and phenotypic characteristics. The mucin phenotype was divided into four gastric, five gastric and intestinal, two intestinal and two null types, independent of histological classification. Intestinal phenotype elements were detected by Cdx2 immunohistochemical methods in nine of 13 (70%) cases examined. We conclude that a small fraction of gastric cancer patients displayed multifactorial carcinogenesis without H. pylori infection, indicating that gastric cancer risk still exists in the absence of H. pylori infection, at an incidence of 2.0% at minimum and 10.6% at maximum in the general Japanese population.     

Serum pepsinogen levels in gastric cancer patients and their relationship with Helicobacter pylori infection: a prospective study.

BACKGROUND: Our aim was to study the serum pepsinogen levels in gastric cancer patients in our population in relation to histology and the presence of Helicobacter pylori. METHODS: Forty-six patients with gastric cancer and 70 controls were studied prospectively in a 1-year period. Serum levels of pepsinogen I (PG I), pepsinogen II (PG II), and gastrin were measured by radioimmunoassay. RESULTS: The mean PG I levels for cancer patients and controls were 83.5 microg/l and 60.9 microg/l, respectively (P = 0.03), the mean PG II levels were 27.2 microg/l and 12.1 microg/l respectively (P < 0.0001). The PG I/II ratio was significantly lower in cancer patients (P = 0.04) and in those with Helicobacter infection. Serum pepsinogen levels were not affected by any pathological characteristics. Histology showed that the prevalence of chronic gastritis, intestinal metaplasia, and gastric atrophy was 97%, 56%, and 15%, respectively. CONCLUSION: The prevalence of gastric atrophy is low in our population, and serum pepsinogen measurement is not useful as a screening tool for gastric cancer in this population.     

幽门螺杆菌联合血清胃蛋白酶对胃癌的诊断价值

目的探讨幽门螺杆菌(helicobacter pylori,Hp)联合血清胃蛋白酶原(pepsinogen,PG)对胃癌的诊断价值。方法选择诊治的胃部疾病患者189例,其中胃癌患者39例(观察组),胃炎患者150例(对照组),检测2组的Hp阳性率,同时检测血清PGⅠ、PGⅡ含量并判断诊断价值。结果观察组与对照组的Hp阳性率分别为82.1%和40.0%,观察组显著高于对照组(P<0.05)。观察组的血清PGⅠ和PGⅡ阳性率为92.3%、100.0%,显著高于对照组的44.0%和28.7%(P<0.05)。在观察组中,PGⅡ的诊断敏感性最高(96.0%),PGⅠ的诊断特异性最高(32.0%)。结论Hp联合血清PG对胃癌的早期诊断具有很好的临床应用价值,能反映胃部疾病患者癌变的可能。     

胃癌高危因素评分模型构建及对筛查时机、方案选择的价值研究

背景与目的：伺机性筛查也称为个体筛查,是一种基于临床表征的筛查方法,花费少,患者依从性高,是目前提高我国早期胃癌检出率的可行途径。基于患者基线资料及血液学检查等常用指标,构建一套关于胃癌高危因素评分模型,探讨其对胃癌高危患者筛查时机、方案选择的价值,以期为临床高效筛查提供更多依据。方法：收集2014年6月—2017年12月甘肃省人民医院普外科收治的387例胃黏膜相关疾病患者为研究对象。收集幽门螺杆菌（Helicobacter pylori,HP）感染情况、血清胃蛋白酶原（pepsinogen,PG）Ⅰ及PGⅠ/Ⅱ等指标,采用病例-对照的研究方法,构建胃癌高危评分模型。结果：受试者工作特征（receiver operating characteristic,ROC）曲线显示,当PGⅠ为43.7 μg/L时,曲线下面积最大为0.736,其灵敏度为0.529,特异度为0.779。当PGⅠ/Ⅱ为2.2 μg/L时,曲线下面积最大为0.780,其灵敏度为0.578,特异度为0.849。将二者并联时,对胃癌诊断的灵敏度为71.8%、特异度为75.5%,可确定PGⅠ≤43.7 μg/L且PGⅠ/Ⅱ≤2.1 μg/L是最佳筛查临界值。单因素分析结果显示,两组患者的性别构成、年龄、饮用水类型、家族史、食用腌制品、HP感染、PGⅠ及PGⅠ/Ⅱ等差异有统计学意义（P＜0.05）。进一步行多因素Logistic分析发现,患者性别、饮用水类型、HP感染、家族史、PGⅠ、PGⅠ/Ⅱ及年龄是影响患者胃癌发生的独立危险因素（P＜0.05）。在Logistic分析基础上,对各危险因素进行赋值,建立评分模型：Y=A×年龄+30×性别+30×饮用水+30×HP（+）+50×家族史+B×PG水平（35~45岁：A=20;46~55岁：A=40;56~65岁：A=70;≥66岁：A=80。当PGⅠ≤43.7 μg/L且PGⅠ/Ⅱ＞2.1 μg/L：B=10;PGⅠ＞43.7 μg/L且PGⅠ/Ⅱ≤2.1 μg/L：B=30;PGⅠ≤43.7 μg/L且PGⅠ/Ⅱ≤2.1 μg/L：B=80）。根据构建模型对两组患者评分进行验证,结果发现,病例组评分［（209.78±46.98）分］显著高于对照组［（122.37±56.37）分］,差异有统计学意义（χ ² =13.962,P＜0.001）。ROC曲线显示,当临界值为156分时,曲线下面积最大为0.876,灵敏度为0.880,特异度为0.716,Youden指数=0.595。拟合优度经Hosmer-Lemeshow检验后发现,模型HL指标为13.492,P=0.095,表明模型拟合度较好。结论：根据建立的胃癌评分模型,对评分≥156且因消化道相关不适而就诊的患者,应视为高危人群,建议至少每年进行1次胃镜随访。     

Helicobacter pylori infection on the risk of stomach cancer and chronic atrophic gastritis.

Helicobacter pylori infection is associated with gastric adenocarcinoma. However, the mechanisms of this interaction are still unclear. This study was conducted to explore the effects of H. pylori infection on early and late stage gastric carcinogenesis. This study included 134 patients with adenocarcinoma of the stomach (ACS), 67 patients with chronic atrophic gastritis (CAG), and 65 normal controls recruited at Memorial Sloan-Kettering Cancer Center (MSKCC) from November 1, 1992 to November 1, 1994. Epidemiologic data were collected by a modified National Cancer Institute Health Habits History Questionnaire. H. pylori infection was diagnosed by pathological evaluation. Risk factors were analyzed using logistic regression. The odds ratio (OR) associated with H. pylori infection was 10.4 [95% confidence interval (CI): 2.6-41.6] for CAG and 11.2 (95% CI: 2.5-50.3) for gastric cancer in comparison with normal controls, with adjustment for pack-years of smoking, alcohol drinking, body mass index, total caloric intake, dietary fat and fiber intake, and Barrett's esophagus. But H. pylori infection was not associated with risk of stomach cancer when patients with stomach cancer were compared with patients with CAG (OR = 0.6, 95% CI: 0.3-1.3) after controlling for potential confounding variables. This association was persistent when only patients with both gastric cancer and chronic gastritis were considered as cases and patients with CAG were considered as controls (OR = 0.7, 95% CI: 0.3-2.0) in the multivariate analysis. Our results suggest that H. pylori infection may be involved in the early stage of development of CAG, but not in the development of stomach cancer from CAG, and indicate that strategies for prevention of stomach cancer should target the early stage to eliminate H. pylori infection in high-risk populations.     

Effect of Helicobacter pylori infection combined with CagA and pepsinogen status on gastric cancer development among Japanese men and women: a nested case-control study.

BACKGROUND: Although accumulating evidence suggests that Helicobacter pylori plays a role in gastric carcinogenesis, the magnitude of the risk remains uncertain. Aim: We aimed to estimate the magnitude of the risk of gastric cancer associated with H. pylori infection by a large case-control study nested within a prospective cohort. Possible effect modification by CagA status, and serum pepsinogen status, as a marker of atrophic gastritis, was also considered to see its effect on developing gastric cancer. Subjects and METHODS: Subjects (n = 123,576) were followed up from 1990 to 2004; 511 gastric cancer cases matched to 511 controls were used in the analysis. Plasma immunoglobulin G antibody to H. pylori, CagA, and pepsinogen I and II were measured. RESULTS: The adjusted odds ratio (95% confidence interval) of gastric cancer associated with H. pylori infection was 5.1 (3.2-8.0). Assuming all CagA-positive subjects are true H. pylori positives doubled this risk. Atrophic gastritis was also associated with an elevated risk of gastric cancer and the risk increased further with pepsinogen levels. CONCLUSIONS: Subjects with pepsinogen levels indicative of severe atrophic gastritis may need careful examination regularly regardless of H. pylori infection. Those who have other pepsinogen levels but who are H. pylori seropositive are likely to benefit from H. pylori eradication therapy. Considering both the cost and the potential for misclassification that may occur using multiple serologic tests, caution is needed in interpreting or extrapolating these findings into a screening strategy.     

胃癌患者围术期胃蛋白酶原和胃泌素-17变化对术后医院感染的影响

目的探讨胃癌患者围术期胃蛋白酶原(PG)和胃泌素-17变化对术后医院感染的影响,为胃癌患者术后医院感染的防治提供参考。方法选取拟行胃癌手术治疗的患者150例(胃癌组),选取门诊同期行健康体检无异常者150例为对照(对照组),胃癌组在术前和术后7 d时、对照组在纳入研究时检测血清PG-Ⅰ和PG-Ⅱ、胃泌素-17水平,观察术后医院感染。结果胃癌组血清PG-Ⅰ和PG-Ⅱ、胃泌素-17分别为(73.94±11.65)ng/ml、(22.47±4.95)ng/ml、(15.58±7.77)pmol/l,明显高于对照组(P<0.05);胃癌组患者术后7 d时血清PG-Ⅰ和PG-Ⅱ、胃泌素-17分别为(65.23±10.21)ng/ml、(14.67±3.85)ng/ml、(8.76±4.47)pmol/l,明显低于术前(P<0.05)。术后共有23例发生医院感染,感染率为15.33%,分别为呼吸道感染11例、泌尿系感染5例、切口感染5例、胃肠道感染2例。术后感染患者术前血清PG-Ⅰ和PG-Ⅱ、胃泌素-17分别为(81.90±11.87)ng/ml、(26.40±4.23)ng/ml、(18.52±6.45)pmol/l,明显高于无感染患者(P<0.05);术后感染患者术后7 d时血清PG-Ⅰ和PG-Ⅱ、胃泌素-17分别为(69.15±10.12)ng/ml、(16.54±3.90)ng/ml、(11.73±4.58)pmol/l,明显高于无感染患者(P<0.05)。结论胃癌患者术后PG和胃泌素-17水平明显低于术前。术前PG和胃泌素-17水平较高患者术后更容易发生医院感染,同时术后感染患者PG和胃泌素-17水平下降幅度相对较小。     

血清PG和G-17及幽门螺杆菌抗体表达与胃癌发病率相关性分析

目的:探讨福建省胃癌高、中、低发地区居民血清胃蛋白酶原(PG)Ⅰ、PGⅡ、胃泌素(G-17)水平及幽门螺杆菌(Hp)感染的分布趋势。方法:选择长乐市江田镇、同安区大同镇和福安市赛歧镇分别代表福建省胃癌的高、中、低发地区,以ELISA检测3地区居民(共725人)的血清PGⅠ、PGⅡ、G-17含量及Hp IgG抗体,统计学检验比较各指标在3地区间的差异。结果:长乐江田镇、同安大同镇和福安赛歧镇PGⅠ中位数分别为110.75、131.00和107.32μg/L,PGⅡ为13.90、14.70和7.79μg/L,PGⅠ/PGⅡ比值为7.91、8.66和13.09,G-17为2.90、1.10和1.00ρmol/L,Hp感染率分别为49.6%、33.5%和29.3%。各指标在3个地区间的差异均有统计学意义,z值为47.15～121.76,χ2=22.47,P值均<0.001。3地区居民血清指标异常者(PGI<25μg/L、PGⅠ/PGⅡ比值<2.5或G-17≥2ρmol/L)所占的比例差异有统计学意义,χ2值为13.45～94.46,P值均≤0.001。Hp感染阳性者的血清PGⅠ、PGⅡ和G-17均高于阴性者,而PGⅠ/PGⅡ比值则低于阴性者。无论Hp阳性或阴性,3个地区居民的血清学指标差异都有统计学意义,z值为-3.32～70.36,P值均<0.05。结论:福建省胃癌高、中、低发地区居民血清PGⅠ、PGⅡ、G-17水平及Hp感染率分布有明显的地区差异,提示这些血清学指标的变化可能与胃癌的发生密切相关。     

血清胃蛋白酶原联合Ca724在胃癌患者中的诊断及预后价值

目的 探讨联合血清胃蛋白酶原及糖类抗原724(Ca724)检查在胃癌诊断及预后评价中的应用价值。方法 以120例疑似胃癌患者作为观察对象,所有患者均接受血清胃蛋白酶原Ⅰ(PGⅠ)、血清胃蛋白酶原Ⅱ(PGⅡ)、Ca724及胃镜检查,以胃镜下活检病理检查结果作为确诊标准,分析PGⅠ/PGⅡ(PGR)、Ca724及PGR联合Ca724检查对胃癌的诊断价值。结果 所有观察者中,共有92例确诊为胃癌。PGR联合Ca724检查的诊断灵敏性及准确性均高于PGR检查及Ca724检查,而诊断特异性低于PGR检查及Ca724检查。同时,PGR检查、Ca724检查及PGR联合Ca724检查对于胃癌均有一定的诊断价值,而PGR联合Ca724检查的诊断价值高于PGR检查及Ca724检查(P＜0.05)。此外,不同病理分期间PGR及Ca724存在统计学差异,以Ⅳ期组PGR最低,Ca724最高(P＜0.05)。结论 联合血清胃蛋白酶原及Ca724检查在胃癌的诊断及预后评价中具有明确的应用价值。     

Epidemiologic findings on serologically defined chronic atrophic gastritis strongly depend on the choice of the cutoff-value

Chronic atrophic gastritis (CAG), a precursor of intestinal gastric cancer, is mostly ascertained noninvasively by serum pepsinogens in epidemiologic studies. However, serological definitions vary widely. We aimed to investigate the impact of this variation on estimated prevalence of CAG and its association with its main risk factors, age and Helicobacter pylori infection. Serum pepsinogen I and II and antibodies against H. pylori were measured by ELISA among 9,444 women and men aged 50-74 years in a population-based cohort study in Saarland/Germany. Application of the various definitions resulted in a wide range of prevalence estimates of CAG prevalence (2.1%-8.2%, with an outlier of 18.8% for one particular definition) and its associations with age and H. pylori infection (age adjusted odds ratios, OR, for CagA positive H. pylori infection: 0.98-4.48). Definitions of CAG based on both pepsinogen I and the pepsinogen I/II ratio or on the pepsinogen I/II ratio only revealed much clearer associations with both age and H. pylori infection than definitions of CAG based on pepsinogen I only (ORs for H. pylori infection: 1.45-4.48 and 0.86-1.30, respectively). Epidemiologic findings on CAG lack comparability due to the heterogeneity in serologic definitions of CAG. The association of age and H. pylori infection with CAG may be strongly underestimated in studies in which CAG is defined by pepsinogen I only.