慢性乙肝、丙肝患者胃蛋白酶原水平的变化及其与肝功能异常的关系

目的：探讨慢性乙肝、丙肝患者血清胃蛋白酶原（PG）水平是否受肝功能异常的影响。方法：选择130例肝功能异常的慢性乙肝、丙肝患者（肝病组）和200例健康体检者（正常对照组）,采用ELISA法检测血清PGⅠ、PGⅡ浓度,计算PGⅠ/PGⅡ比值,比较两组血清PGⅠ、PGⅡ浓度及其比值。将肝病患者按照谷丙转氨酶、谷草转氨酶、白蛋白、总胆红素单项指标是否正常分组,比较PGⅠ、PGⅡ以及其比值的差异。结果：肝病组PGⅠ（155.21±93.55 ng/mL）、PGⅡ（16.27±11.95 ng/mL）水平明显高于正常对照组（P<0.001）,PGⅠ/PGⅡ比值（12.82±8.1）低于正常人群（P<0.05）。谷丙转氨酶、谷草转氨酶、白蛋白、总胆红素水平与PGⅠ、PGⅡ及其比值无关（P>0.05）。结论：病毒感染导致的慢性肝病可影响血清PGⅠ、PGⅡ水平,而这种影响作用并不依赖肝细胞损伤或肝脏合成功能损伤,可能与病毒导致的胃粘膜损伤有关。     

时间分辨荧光微球免疫层析技术定量检测人血清胃蛋白酶原Ⅰ的实验研究

目的 研制快速定量检测人血清胃蛋白酶原Ⅰ (pepsinogens Ⅰ,PGⅠ)试纸,并评价试纸性能.方法 以包裹有时间分辨荧光的纳米微球作为标记示踪物,运用免疫层析试纸技术,研制PG Ⅰ检测试纸;考察试纸的检测线性、灵敏度、精密度、与对比试剂的符合率.结果 试纸定量检测的线性良好,方程为Y=0.027 9+0.004 8X,r=0.997 8;灵敏度为0.27 μg/L;批内CV小于10％,批间CV11.03％;与市售PG Ⅰ试剂平行检测489份血清样本,有良好的相关性(YTRFIA =0.856 6Xstrip+7.545 6,R2 =0.989 1,P＜0.01).结论 PG Ⅰ时间分辨荧光纳米微球免疫层析试纸操作简单、快速、经济、可定量,满足临床检测血清PG Ⅰ的需求.     

肝硬化合并门脉高压性胃病患者血清胃蛋白酶原变化及临床意义

目的 探讨肝硬化合并门脉高压性胃病(Portal Hypertension Gastropathy,PHG)患者血清胃蛋白酶原变化及临床意义.方法 选择2015年1月至2016年1月本院住院治疗的122例肝硬化患者作为研究对象,根据胃镜下检查有无PHG,分为肝硬化合并PHG组62例和肝硬化无PHG组60例;同期选择在本院进行健康体检人群60例作为对照组.肝功能进行根据Child-Pugh评分分级为A级、B级、C级,检测血清胃蛋白酶原(Pepsinogen,PG)水平,并计算PG Ⅰ/PGⅡ比值(PGR),分析血清PG水平与胃黏膜病变的关系.结果 肝硬化PHG组肝功能明显低于无PHG组(x 2=6.588,P=0.037);PHG组较无PHG组血清PG Ⅰ水平显著降低(t=7.378,P=0.000);重度胃黏膜病变患者血清PG Ⅰ、PGR水平较轻度患者明显降低(t=2.392、4.292,P=0.009、0.000);肝硬化病变不同部位各组血清PG水平比较,差异无统计学意义(t=1.803、2.632、0.658,P=0.174、0.080,0.522).结论 肝硬化合并门脉高压性胃病患者血清PG Ⅰ水平显著降低,可反映肝硬化胃黏膜受损程度,对评价胃黏膜功能状态具有一定价值.     

血清胃蛋白酶原及胃泌素-17水平与胃癌的相关性研究

目的 探讨血清胃蛋白酶原(PG)I、PGⅡ、PG I/PGⅡ(PGR)及胃泌素-17(GAS-17)水平在胃癌患者中的诊断价值及相关性.方法 选取该院454例胃部疾病患者,104例健康者(对照组),分别检测各组血清PG I、PGⅡ、PGR及GAS-17水平.绘制受试者工作特征(ROC)曲线评价血清PGⅠ、PGⅡ、PGR及GAS-17水平在胃癌和非胃癌组中的诊断价值,并应用Lo-gistic回归模型分析胃癌的独立危险因素.结果 胃癌组、萎缩性胃炎组和非萎缩性胃炎组血清PGI及PGR明显低于对照组(P＜0.05),且胃癌组血清PG I及PGR明显低于萎缩性胃炎组、非萎缩性胃炎组和胃溃疡组(P＜0.05).胃癌组血清GAS-17水平明显高于对照组、非萎缩性胃炎组和胃溃疡组(P＜0.05).胃癌组与对照组血清PGⅡ水平比较差异无统计学意义(P＞0.05).进展期胃癌组血清PGI及PGR明显低于早期胃癌组(P＜0.05),而血清GAS-17水平明显高于早期胃癌组(P＜0.05).胃癌TNM分期越高,血清PG I水平降低越明显(P＜0.05),血清GAS-17水平升高越明显(P＜0.05).ROC曲线显示,血清PGI、PGⅡ、PGR、GAS-17及联合检测对胃癌组的诊断效能优于非胃癌组,且4项联合检测的曲线下面积(AUC)高于单项检测,其灵敏度和特异度分别为83.7％和76.8％.多元Logistic回归分析发现胃癌家族史、不正确的饮食习惯、PG I及GAS-17进入回归模型,其OR值及95％CI分别为6.481(3.562～11.316)、2.843(1.103～6.918)、2.624(1.094～4.521)、1.735 (1.046～3.912).结论 血清PGI、GAS-17及PGR水平变化与胃癌的病程进展及分化程度相关,联合检测有助于提高胃癌的阳性诊断率.     

Gastric cancer screening in 16 villages of Zhuanghe region: a mass screeningreport from a high risk area of stomach cancer in China

AIM To study the comprehensive prevention and treatment of gastric cancer among high-risk population inthe high risk areas.METHODS A gastrocarcinoma mass screening was performed in 16 villages of Zhuanghe region. About50 000 population were involved and 3033 cases aged above 35 suffering from gastric diseases, and/or hadfamily history of gastric cancer were screened. Clinical epidemiological investigation, double-contrast X-ray,serum pepsinogen monitor, gastroscopic biopsies and histopathologic examinations were adopted in thescreening.RESULTS The ratio of the examined patients with gastric disorder reached up to 82% and 32 patients withgastric cancer were detected (1.06%) and 18 cases were early gastric cancer (56.25%). Patients with gastriccancer were treated successively. Aside from gastric cancer, several gastric lesions were also detected, whichlaid a good foundation for further interventional treatment. It was also found in the examination that93.97% of the local residents were addicted to salted pork and more than 60% of the residents had Hpinfection.CONCLUSION Gastric diseases, Hp infection of gastric mucosa and eating salted pork are very common inZhuanghe region. These are very dangerous factors causing gastric cancer. It is feasible to quit eating saltedpork and eradicate Hp infection and cure precancerous diseases.     

抑萎灵治疗慢性萎缩性胃炎癌前病变临床观察

目的观察抑萎灵治疗慢性萎缩性胃炎胃癌前病变的临床疗效。方法将60例患者随机分为治疗组和对照组（各30例）,分别给予抑萎灵方和胃复春片治疗,疗程6个月。观察两组临床疗效及治疗前后胃蛋白酶原（PG）含量变化。结果治疗组的总体疗效优于对照组（P〈0．05）;治疗后两组中医证候积分较治疗前降低（P〈0．05,P〈0．01）,且治疗组降低幅度大于对照组（P〈0．01）;治疗后两组PGI、PGⅡ、PGI／PGll都增加（P〈0．01）,且两组问诸指标有显著差异（P〈0．05）。结论抑萎灵治疗慢性萎缩性胃炎胃癌前病变疗效确切,其机制可能与其修复胃黏膜功能有关。     

Gastric atrophy and oesophageal squamous cell carcinoma: possible interaction with dental health and oral hygiene habit

Background:

Gastric fundal atrophy has been hypothesised to increase the risk of oesophageal squamous cell carcinoma (OSCC), but studies have shown inconsistent results.

Methods:

We measured serum pepsinogen I (PGI) and pepsinogen II (PGII) among 293 incident cases and 524 matched neighbourhood controls in a high-risk area of Northern Iran. Conditional logistic regression model was used to estimate odds ratios (ORs) and their 95% confidence intervals (CIs).

Results:

After controlling for age, sex, residence area and other potential confounders, gastric atrophy (defined by a validated criterion, PGI <55 μg dl⁻¹) was associated with a two-fold increased risk (OR=2.01, 95% CI: 1.18, 3.45) of OSCC in the absence of nonatrophic pangastritis (defined as PGII <11.8 μg dl⁻¹). Stratification by PGII decreased the misclassification errors due to cancer-induced gastritis. Presence of both poor dental health, indicated by higher than median sum of decayed, missing, and filled teeth (DMFT score), and gastric atrophy further increased the risk of OSCC (OR=4.15, 95% CI: 2.04, 8.42) with relative excess risk due to interaction (RERI) of 1.47 (95% CI: −1.15, 4.1). Coexistence of poor oral hygiene habit with gastric atrophy elevated OSCC risk eight times (OR=8.65, 95% CI: 3.65, 20.46) and the additive interaction index was marginally statistically significant (RERI=4.34, 95% CI: −1.07, 9.76).

Conclusion:

Gastric atrophy is a risk factor for OSCC, and poor dental health and oral hygiene habit may act synergistically in increasing the risk.     

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。     

Preventive effects of etodolac,a selective cyclooxygenase‐2 inhibitor,on cancer development in extensive metaplastic gastritis,a Helicobacter pylori‐negative precancerous lesion

The present study investigated the preventive effects of etodolac, a selective cyclo‐oxygenase (COX)‐2 inhibitor, on metachronous cancer development after endoscopic resection of early gastric cancer. Among 267 early gastric cancer patients who underwent endoscopic resection, 47 patients with extensive metaplastic gastritis were selected based on endoscopic findings and our previously described criteria of serum pepsinogen (PG) test‐positive and Helicobacter pylori antibody‐negative conditions. Nonrandomized etodolac treatment (300 mg/day) was administered to 26 patients (Group A), while the remaining 21 patients were untreated (Group B). No significant differences in age, sex distribution, lifestyle factors or extent of metaplastic gastritis at baseline were identified between groups. Patients were followed for metachronous cancer development with endoscopy every 6–12 months for up to 5 years. Mean (standard deviation) follow‐up period was 4.2 (0.9) years. In Group B, 5 cancers developed (incidence rate = 6,266/100,000 person‐years), significantly more than the 1 cancer in Group A (incidence rate = 898/100,000 person‐years; p < 0.05). Long‐term etodolac treatment did not influence the extent of metaplastic gastritis as revealed by endoscopic findings or by serum PG levels, but effectively reduced metachronous cancer development in patients with extensive metaplastic gastritis. These results strongly suggest that chemoprevention of cancer in the metaplastic stomach is possible by controlling COX‐2 expression.