Helicobacter pylori infection, gastrin and cyclooxygenase-2 in gastric carcinogenesis

Gastric cancer is one of the most frequent neoplasms and a main cause of death worldwide, especially in China and Japan. Numerous epidemiological, animal and experimental studies support a positive association between chronic Helicobacter pylori(H. pylori) infection and the development of gastric cancer. However, the exact mechanism whereby H. pylori causes gastric carcinogenesis remains unclear. It has been demonstrated that expression of cyclooxygenase-2(COX-2) is elevated in gastric carcinomas and in their precursor lesions. In this review, we present the latest clinical and experimental evidence showing the role of gastrin and COX-2 in H. pylori-infected patients and their possible association with gastric cancer risk.

Reduced secretion of epidermal growth factor in duodenal ulcer patients with Helicobacter pylori infection

AIM To investigate the concentration changes of epidermal growth factor (EGF) in duodenal ulcer patients with H. pylori infection.

Helicobacter pylori upregulates prion protein expression in gastric mucosa: A possible link to prion disease

AIM： Pathological prion protein （PrP^sc） is responsible for the development of transmissible spongiform encephalopathies （TSE）. While PrPc enters the organism via the oral route, less data is available to know about its uptake and the role of gastrointestinal inflammation on the expression of priori precursor PrPc, which is constitutively expressed in the gastric mucosa.METHODS： We studied PrPc expression in the gastric mucosa of 10 Helicobacter pylori-positive patients before and after successful H pylori eradication compared to non-infected controls using RT-PCR and Western blotting. The effect of central mediators of gastric inflammation, i.e., gastrin, prostaglandin E2 （PGE2）, tumor necrosis factor alpha （TNF-α） and interleukin 1 beta （IL-1β） on PrPc expression was analyzed in gastric cell lines.RESULTS： PrPc expression was increased in H pyloriinfection compared with non-infected controls and decreased to normal after successful eradication. Gastrin, PGE2, and IL-1β dose-dependently upregulated PrPc in gastric cells, while TNF-α had no effect.CONCLUSION： H pylori infection leads to the upregulation of gastric PrPc expression. This can be linked to H pylori induced hypergastrinemia and increased mucosal PGE2 and IL-1β synthesis. H pylori creates a milieu for enhanced propagation of prions in the gastrointestinal tract.

Changes with aging in gastric biomarkers levels and in biochemical factors associated with Helicobacter pylori infection in asymptomatic Chinese population

AIM To observe changes in gastric biomarker levels with age and effects of Helicobacter pylori(H. pylori) infection in a healthy population, and explore factors associated with gastric biomarkers.METHODS Three hundred and ninety-five subjects were selected and underwent physical examinations, biochemical tests, and measurement of serum pepsinogen(PG)Ⅰ and Ⅱ, gastrin-17(G-17) and H. pylori antibody levels. Analyses were made by Student's t-test, ANOVA, Pearson's correlation and multiple linear regressions.RESULTS PGII levels were higher in the ≥ 65-years-old age group(P < 0.05) and PGI/PGII were lower in the ≥ 75-years-old age group(P = 0.035) compared to the 35-44-years-old age group. Levels of low-density lipoprotein cholesterol(LDL-C) were higher(P = 0.009) in H. pylori-infected subjects that were male. LDL-C levels were higher in 55-74-years-old age group(P < 0.05) for H. pylori-infected subjects and 45-64-yearsold age group(P < 0.05) for non-infected subjects compared to 35-44-years-old age group. Hp-Ig G level positively correlated with PGⅠ, PGⅡ and G-17(P < 0.001, P < 0.001, P = 0.006), and negatively correlated with PGI/PGII(P < 0.001). Creatinine positively correlated with PGⅠ, PGⅡ and G-17(P < 0.001, P < 0.001, P < 0.001). Fasting blood glucose(FBG) positively correlated with PGⅠ/PGⅡ and G-17(P < 0.001, P = 0.037). Age positively correlated with PGII and G-17(P = 0.005, P = 0.026).CONCLUSION PGII levels increased while PGI/PGII declined with age in a healthy population. H. pylori infection had an effect on raising LDL-C levels to increase the risk of atherosclerosis in males, especially those of elderly age. Age, H. pylori infection, levels of renal function and FBG were associated with levels of pepsinogens and gastrin.

Family-based Helicobacter pylori infection status and transmission pattern in central China,and its clinical implications for related disease prevention

BACKGROUND Helicobacter pylori(H.pylori)has characteristics of family cluster infection;however,its family-based infection status,related factors,and transmission pattern in central China,a high-risk area for H.pylori infection and gastric cancer,have not been evaluated.We investigated family-based H.pylori infection in healthy households to understand its infection status,related factors,and patterns of transmission for related disease prevention.AIM To investigate family-based H.pylori infection status,related factors,and patterns of transmission in healthy households for related disease prevention.METHODS Blood samples and survey questionnaires were collected from 282 families including 772 individuals.The recruited families were from 10 selected communities in the greater Zhengzhou area with different living standards,and the family members’general data,H.pylori infection status,related factors,and transmission pattern were analyzed.H.pylori infection was confirmed primarily by serum H.pylori antibody arrays;if patients previously underwent H.pylori eradication therapy,an additional 13C-urea breath test was performed to obtain their current infection status.Serum gastrin and pepsinogens(PGs)were also analyzed.RESULTS Among the 772 individuals examined,H.pylori infection rate was 54.27%.These infected individuals were from 246 families,accounting for 87.23%of all 282 families examined,and 34.55%of these families were infected by the same strains.In 27.24%of infected families,all members were infected,and 68.66%of them were infected with type I strains.Among the 244 families that included both husband and wife,spouse co-infection rate was 34.84%,and in only 17.21%of these spouses,none were infected.The infection rate increased with duration of marriage,but annual household income,history of smoking,history of alcohol consumption,dining location,presence of gastrointestinal symptoms,and family history of gastric disease or GC did not affect infection rates;however,individuals who had a higher education level showed lower infection rates.The levels of gastrin-17,PGI,and PGII were significantly higher,and PGI/II ratio was significantly lower in H.pylori-infected groups than in H.pylori-negative groups.CONCLUSION In our study sample from the general public of central China,H.pylori infection rate was 54.27%,but in 87.23%of healthy households,there was at least 1 H.pylori-infected person;in 27.24%of these infected families,all members were infected.Type I H.pylori was the dominant strain in this area.Individuals with a higher education level showed significantly lower infection rates;no other variables affected infection rates.

Impact of Helicobacter pylori infection on ghrelin and various neuroendocrine hormones in plasma

AIM: Ghrelin, an endogenous ligand for growth hormone secretagogue receptor, influences appetite, energy balance, gastric motility and acid secretion. The stomach is the main source of circulating ghrelin. There are inconsistent reports on the influence of Helicobacter pylori (H pylori) infection on circulating ghrelin levels. We sought to elucidate the relationship between ghrelin and various peptides in plasma, with special reference to H pylori.METHODS: Plasma ghrelin levels were measured by radioimmunoassay in 89 subjects who were referred for upper gastrointestinal endoscopy, consisting of 42 H pylori infected and 47 uninfected ones. Plasma gastrin,somatostatin, leptin, insulin-like growth hormone 1 (IGF-1)and chromogranin A concentrations were also measured.Twelve patients were treated with anti- H pylori regimen.RESULTS: Ghrelin circulating levels were greatly decreased in H pylori-positive than negative individuals (194.2±90.2fmol/mL and 250.4±84.1 respectively, P＜0.05), but did not significantly alter following the cure of infection (176.5±79.5 vs 191.3±120.4). There was a significant negative correlation between circulating ghrelin and leptin levels, as well as body mass index, for the whole and uninfected population, but not in H pylori-infected patients. Plasma ghrelin concentrations correlated positively with IGF-1 in H pylori-negative group and negatively with chromogranin A in the infected group.There were no significant correlations among circulating levels of ghrelin, gastrin and somatostatin irrespective of H pylori status.CONCLUSION: H pylori infection influences plasma ghrelin dynamics and its interaction with diverse bioactive peptides involved in energy balance, growth and neuroendocrine function.

Helicobacter pylori and colorectal neoplasia:Is there acausal link?

Ever since Helicobacter pylori(H. pylori) was recognized as an infectious cause of gastric cancer, there has been increasing interest in examining its potential role in colorectal carcinogenesis. Data from casecontrol and cross-sectional studies, mostly relying on hospital-based samples, and several meta-analyses have shown a positive statistical relationship between H. pylori infection and colorectal neoplasia. However, the possibility exists that the results have been influenced by bias, including the improper selection of patients and disparities with respect to potential confounders. While the evidence falls short of a definitive causal link, it appears that infection with H. pylori /H. pylori-related gastritis is associated with an increased, although modest, risk of colorectal adenoma and cancer. The pathogenic mechanisms responsible for this association remain uncertain. H. pylori has been detected in colorectal malignant tissues; however, the possibility that H. pylori is a direct activator of colonic carcinogenesis remains purely hypothetical. On the other hand, experimental data have indicated a series of potential oncogenic interactions between these bacteria and colorectal mucosa, including induction and perpetuation of inflammatory responses, alteration of gut microflora and release of toxins and/or hormonal mediators, such as gastrin, which may contribute to tumor formation.

Helicobacter pylori infection and gastrointestina hormones:a review

INTRODUCTIONHelicobacter pylori(Hp)infection is closely relatedto gastrointestinal hormones and involves theformation of gastritis,gastric carcinoma and pepticulcer.Its pathogenesis relevant

Assessing GastroPanel serum markers as a non-invasive method for the diagnosis of atrophic gastritis and <i>Helicobacter pylori</i>infection

Gastric colonization by Helicobacter pylori increases the risk of gastric disorders, including atrophic gastritis which can be diagnosed based on levels of serum biomarkers like Gastrin and Pepsinogen. We therefore examined the efficacy of a serological-based method namely GastroPanel Blood kit, in diagnosing and scoring gastritis associated to Helicobacter pylori infection. Patients with dyspeptic symptoms were prospectively recruited on voluntary basis at the Yaounde Central Hospital and University Teaching Hospital, from March to July 2011. The degree of atrophy was classified according to levels in patient serum of pepsinogens I and II (PGI and PGII) and Gastrin 17 (G17) and compared with histological profiles as reference method. A specific ELISA test was used for the detection of H. pylori IgG antibodies. In total, 86 volunteers from 21 to 83 years old (mean = 46.4 ± 3.3) were enrolled, including 74.4% of women and 25.6% of men. The prevalence of gastritis was statistically similar between Gastro Blood Panel test and histology used as reference method (89.5% versus 83.7%: p > 0.20). Diagnosis based on serum makers showed high sensitivity (93.1%) in comparison with the reference method. However, the serological based method has diagnosed more atrophic gastritis than the reference (17.4% versus 7.0%: p 0.05). Furthermore, the prevalence of H. pylori infection did not differ significantly between serological method (84.9%) and reference method (81.4%). These results suggest that diagnosis of atrophic gastritis and H. pylori infection obtained with an optional serological method (GastroPanel) is in a strong agreement with the biopsy findings, and thus can be a useful non endoscopic assessment of stomach mucosal atrophy in patients with dyspepsia.

Ascorbic acid secretion in the human stomach and the effect of gastrin

AIM To investigate the changes of gastricmucosal ascorbic acid secretion in patients withnonulcer dyspepsia and the effect of gastrin onit,and to relate any observed changes to H.pylori infection and mucosal histology.METHODS Ascorbic acid secretions in patientswere examined by collecting continuouslygastric juice for one hour after having aspiratedand discarded fasting gastric juice.Using theclearance rate(mL/min)of ascorbic acid fromblood to gastric juice represented ascorbic acidsecretion in the gastric mucosa.Ascorbic acidconcentrations in plasma and juice weremeasured by ferric reduced method.RESULTS Gastric ascorbic acid secretions inH.pylori-positive patients(1.46 mL/min,range0.27-3.78)did not significantly differ fromthose in H.pylori-negative patients(1.25 mL/min,0.47-3.14)(P】0.05).There were nosignificant differences in ascorbic acidsecretions between patients with mild(1.56 mL/min,0.50-3.30),moderate(1.34 mL/min,0.27-2.93)and severe(1.36 mL/min,0.47-3.78)inflammation(P】0.05).There were nosignificant differences in ascorbic acidsecretions between patients without activity(l.45mL/min,0.27-3.14)and with mild(1.32mL/min,0.61-2.93),moderate(1.49mL/min,0.50-3.78)and severe(1.43 mL/min,0.51-3.26)activity of chronic gastritis either(P】0.05).Ascorbic acid secretions in patientswith severe atrophy(0.56 mL/min,0.27-1.20)were markedly lower than those in patientswithout atrophy(1.51 mL/min,0.59-3.30)and with mild(1.43 mL/ min,0.53-3.78)andmoderate(1.31 mL/min,0.47-3.16)atrophy(P【0.005).There was a significant negativecorrelation between ascorbic acid secretion andseverity of atrophy(correlation coefficient=-0.43,P【0.005).After administration ofpentagastrin,ascorbic acid secretions weremarkedly elevated(from 1.39 mL/min,0.36-2.96 to 3.53mL/min,0.84-5.91)(P【0.001).CONCLUSION Ascorbic acid secretion ingastric mucosa is not affected by H.pyloriinfection.Gastric ascorbic acid secretion ismarkedly related to the severity of atrophy,whereas not related to the severity ofinflammation and activity.Gastrin may stimulategastric ascorbic acid secretion.A decreasedascorbic acid secretion may be an importantfactor in the link between atrophic gastritis andgastric carcinogenesis.

益生菌疗法根除不同分型H.pylori对胃泌素-17、胃蛋白酶原的影响

目的探讨联合益生菌根除不同分型H.pylori对胃泌素-17(gastrin-17,G-17)、胃蛋白酶原(pepsinogen,PG)的影响。方法将116例H.pylori阳性慢性胃炎患者随机分为四联疗法组和联合益生菌疗法组,疗程均为2周。选取H.pylori阳性健康体检者100名作为健康对照组。对H.pylori抗体CagA、VacA、UreA和UreB进行血清学检测,并检测治疗前后血清中PGⅠ、PGⅡ、PGⅠ/Ⅱ比值(PGⅠ/PGⅡratio,PGR)及G-17水平。结果四联疗法组、联合益生菌疗法组及健康对照组的H.pyloriⅠ型阳性率均高于H.pyloriⅡ型,且两治疗组H.pyloriⅠ型的阳性率明显高于健康对照组(P<0.05);三组CagA+VacA抗体阳性率均高于各组CagA、VacA抗体阳性率(P<0.05)。三组VacA、UreA、UreB抗体阳性率均高于各组CagA抗体阳性率(P<0.05)。不同炎症程度慢性胃炎CagA、UreB抗体的阳性率差异均无统计学意义(P>0.05);重度慢性胃炎与轻度慢性胃炎比较,VacA抗体阳性率显著升高,而UreA抗体阳性率显著下降(P<0.05)。治疗前,与H.pyloriⅡ型感染者相比,三组H.pyloriⅠ型感染者PGⅡ及G-17水平显著升高,PGR水平显著下降(P<0.05),而PGⅠ水平差异无统计学意义(P>0.05);治疗后,联合益生菌疗法组H.pyloriⅠ型患者的PGⅠ、PGⅡ及G-17水平显著下降,PGR水平升高(P<0.05)。结论H.pyloriⅠ型菌株是慢性胃炎的主要致病菌株,并且影响患者血清PGⅠ、PGⅡ、PGR及G-17的水平。联合益生菌疗法治疗H.pyloriⅠ型慢性胃炎,能降低血清PGⅠ、PGⅡ、G-17水平,提高PGR水平。

米曲菌胰酶片配合四联疗法治疗功能性消化不良伴H.pylori感染的效果观察

目的观察米曲菌胰酶片配合四联疗法治疗功能性消化不良伴幽门螺杆菌(H.pylori)感染的效果。方法前瞻选取2018年4月至2019年12月医院就诊的功能性消化不良伴幽门螺杆菌(H.pylori)感染患者82例作为研究对象,随机分为对照组和观察组,每组41例。对照组实施莫沙必利+四联疗法,观察组在对照组基础上配合米曲菌胰酶片治疗,均于治疗2周时评估效果。治疗前、治疗2周时,评估并比较2组临床症状改善情况;各时点,评估并比较2组血清胃泌素-17(G-17)水平;治疗期间,记录2组不良反应现象。结果治疗2周,2组临床各症状积分及总分均较治疗前降低,且观察组低于对照组,差异有统计学意义(P<0.05);治疗2周时,2组G-17水平较治疗前降低,且观察组低于对照组,差异有统计学意义(P<0.05);2组不良反应发生率比较相近,差异无统计学意义(P>0.05)。结论米曲菌胰酶片配合四联疗法更利于减轻功能性消化不良伴H.pylori感染患者主要症状,患者G-17水平明显降低,且不会增加不良反应风险,安全可靠。

血清胃泌素17、胃蛋白酶原Ⅱ及血脂水平检测对结直肠腺瘤性息肉患者幽门螺杆菌Ⅱ型感染的诊断价值

目的:探讨血清胃泌素17(G-17)、胃蛋白酶原Ⅱ(PGⅡ)和血脂水平对结直肠腺瘤性息肉患者幽门螺杆菌(HP)Ⅱ型感染的诊断价值。方法:选取结直肠腺瘤性息肉患者160例,进行HP检测,并根据有无HP感染分为HP阳性组(100例)和HP阴性组(60例)。检测两组血清G-17、PGⅡ及血脂水平,并分析其对患者感染HPⅡ型的诊断价值。结果:与HP阴性组比较,HP阳性组G-17、PGⅡ、胃蛋白酶原Ⅰ(PGⅠ)水平升高(均P<0.05)。与HP阴性组比较,HP阳性组总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)水平升高(均P<0.05)。与HPⅠ型组比较,HPⅡ型组G-17、PGⅡ、PGⅠ水平升高(均P<0.05)。与HPⅠ型组比较,HPⅡ型组TG、HDL-C水平升高,TC、LDL-C水平降低(均P<0.05)。以HP阳性结直肠腺瘤性息肉患者是否感染HPⅡ型为变量,做关于血清G-17、PGⅡ、PGⅠ、TG、TC、LDL-C、HDL-C水平的ROC曲线分析,其曲线下面积(AUC)分别为0.891、0.812、0.742、0.559、0.820、0.66、0.619,进行筛选后将AUC高于0.7的因子纳入联合诊断中建立模型,进行逻辑回归分析,并根据模型输出结果对患者是否发生HPⅡ型感染进行诊断,结果显示G-17、PGⅡ、PGⅠ及TC联合诊断的AUC为0.934。结论:在结直肠腺瘤性息肉患者中,HP阳性患者血清G-17、PGⅡ、PGⅠ、TC、TG、LDL-C水平明显升高,感染HPⅡ型患者G-17、PGⅡ、PGⅠ、TG、HDL-C水平高于感染HPⅠ型患者,TC和LDL-C水平低于感染HPⅠ型患者,且G-17、PGⅡ、PGⅠ及TC联合应用对患者感染HPⅡ型具有较高的诊断价值。

不同毒力型的幽门螺旋杆菌对胃内微环境的影响

目的 通过观察不同毒力型的幽门螺旋杆菌(helicobacter pylori,Hp)感染对胃液、胃蛋白酶及炎症因子的影响。方法 收集2021年12月至2023年3月收治的110例患者,根据碳13呼气试验结果,分为Hp阳性组(n=79),Hp阴性组(n=31)。其中Hp阳性组根据其Hp抗体分型,分为Ⅰ型组(n=52)、Ⅱ型组(n=11)、未定型组(n=16);Hp阴性组挑选抗体全阴者分为空白对照组(n=12)。所有患者均进行胃液pH值、钠离子(Na+)、钾离子(K+)、氯离子(Cl-)、白介素6 (Interleukin-6,IL-6)、白介素8 (Interleukin-8,IL-8)、胃泌素17 (Gastrin-17,G-17)、胃蛋白酶原Ⅰ(Pepsinogen I,PGⅠ)、胃蛋白酶原Ⅱ(Pepsinogen I,PGⅡ)检测。结果 Hp阳性组与Hp阴性组相比pH值、Na+、Cl-、K+,差异无统计学意义(P> 0.05);Hp阳性组相比Hp阴性组Cl-含量降低(P <0.05)。Hp阳性组较Hp阴性组相比IL-6、IL-8、G-17、PGⅠ、PGⅡ均有上升(P <0.05)。Ⅰ型组与Ⅱ型组、未定型组、空白对照组相比pH值、Na+、K+,差异均无统计学意义(P> 0.05)。Ⅰ型组、未定型组与空白对照组比较,Cl-含量均降低(P <0.05)。Ⅰ型组分别与Ⅱ型组、未定型组、空白对照组比较,IL-6、IL-8、PGⅠ均有上升(P <0.05)。空白对照组分别与其他各组之间PGⅡ存在明显差异(P <0.05)。Ⅰ型组与未定型组的G-17含量差异无统计学意义(P> 0.05)。Ⅰ型组与Ⅱ型组、空白对照组比较G-17均有上升(P <0.05)。结论 Ⅰ型Hp菌感染可能通过增加IL-6、IL-8、G-17的表达造成胃黏膜损伤,进而导致消化功能异常。

慢性萎缩性胃炎病人幽门螺杆菌感染特征及胃功能状态评估研究

目的:探讨血清胃蛋白酶原Ⅰ(PGⅠ)、胃蛋白酶原Ⅱ(PGⅡ)、PGⅠ/PGⅡ比值(PGR)、胃泌素-17(G-17)与幽门螺旋杆菌(Hp)抗体分型检测在慢性萎缩性胃炎(CAG)诊断中的应用价值。方法:选取170例慢性胃炎病人,其中CAG组79例,慢性非萎缩性胃炎(CNAG)91例,比较2组指标的变化。结果:170例病人中Hp阳性92例,阳性率54.12%。与CNAG组比较,CAG组Hp抗体阳性率、Ⅰ型Hp感染阳性率、PGⅡ和G17水平均明显升高(P<0.05~P<0.01),PGR水平降低(P<0.01)。Ⅰ型Hp阳性组与Ⅱ型Hp阳性组相比,PGⅡ和G17的表达水平升高(P<0.05),PGR水平降低(P<0.05)。PGⅠ、PGⅡ、PGR、G17和Hp抗体分型的AUC分别为0.548、0.606、0.361、0.660、0.589;联合检测的AUC为0.690。结论:PGⅡ、PGR、G17水平变化及Hp抗体分型可作为萎缩性胃炎筛查指标,联合检测可为临床诊疗提供更可靠的实验室依据。

胃蛋白酶原、胃泌素-17和幽门螺旋杆菌抗体与萎缩性胃炎的相关性

萎缩性胃炎也称慢性萎缩性胃炎,是由多种因素诱导胃黏膜上皮和腺体细胞萎缩导致黏膜上皮变薄的一种慢性胃部疾病。萎缩性胃炎与胃黏膜的肠上皮化生甚至癌变具有密切的关系,因此在临床上如何准确地对其进行判断是萎缩性胃炎监测的重点。目前临床确诊萎缩性胃炎主要依靠胃镜和胃黏膜活检,但其检查步骤繁杂,对医生的技能有着较高的要求,且手术费用高昂,故而并不适用于人群的普遍筛查。因此,寻找方便快捷、敏感性又高的检查方法具有十分重要的现实意义。近年来许多研究表明,胃黏膜上皮细胞分泌的胃蛋白酶原(PG)、胃泌素-17(G-17)和血清中的幽门螺旋杆菌(Hp)抗体可以有效地辅助诊断萎缩性胃炎,本文就其在萎缩性胃炎中的研究进展作一综述,旨在评估这三者对筛查和确定萎缩性胃炎的临床适用性。

幽门螺杆菌抗体谱、胃泌素及胃蛋白酶原表达与消化性溃疡的关系分析

目的分析幽门螺杆菌(Hp)抗体谱、胃泌素-17(G-17)及胃蛋白酶原(PG)表达与消化性溃疡的关系。方法回顾性分析2021年4月—2022年4月我院消化内科收治的经消化内镜及病理组织检查确诊为消化性溃疡或胃癌的125例患者的病例资料,其中诊断为消化性溃疡的90例患者纳入消化性溃疡组,诊断为胃癌的35例患者纳入胃癌组,另选取同时期健康体检者50例纳入对照组。比较3组入院时G-17、PGⅠ、PGⅡ水平、Hp抗体谱及Hp阳性率,分析消化性溃疡患者中Hp阳性与Hp阴性患者G-17、PGⅠ、PGⅡ水平差异,绘制受试者工作特征(ROC)曲线评估G-17、PGⅠ、PGⅡ水平对Hp阳性消化性溃疡的诊断效能。结果入院时,消化性溃疡组G-17、PGⅡ水平均明显低于胃癌组,PGⅠ水平明显高于胃癌组(P<0.05);对照组G-17、PGⅡ水平均低于其他两组(P<0.05),PGⅠ水平高于其他两组(P<0.05);消化性溃疡组与胃癌组Hp抗体谱比较差异无统计学意义(P>0.05);消化性溃疡组和胃癌组各抗体阳性率均高于对照组(P<0.05)。90例消化性溃疡患者中Hp阳性67例,35例胃癌患者中Hp阳性31例,消化性溃疡组和胃癌组Hp阳性率比较差异无统计学意义(P>0.05)。消化性溃疡Hp阴性患者G-17、PGⅡ水平均明显低于Hp阳性患者,PGⅠ水平明显高于Hp阳性患者(P<0.05);G-17、PGⅠ、PGⅡ及其联合检测诊断Hp阳性消化性溃疡的曲线下面积(AUC)分别为0.633、0.768、0.761、0.854。结论消化性溃疡患者较胃癌患者G-17、PGⅡ水平下降,PGⅠ水平升高,并且消化性溃疡患者中Hp阳性患者以上指标变化更为显著,可辅助临床诊断胃肠疾病。

体检人群幽门螺杆菌感染的危险因素及其与血清PGⅠ、PGⅡ、G-17的相关性

目的 探讨体检人群幽门螺杆菌(Hp)感染的危险因素及其与血清胃蛋白酶原Ⅰ(PGⅠ)、胃蛋白酶原Ⅱ(PGⅡ)、胃泌素-17(G-17)的相关性。方法 选择2020年1月至2022年1月在山西省大同市第五人民医院体检中心行Hp筛查的816例体检者为研究对象。根据Hp感染情况分观察组(Hp感染,310例)和对照组(Hp未感染,506例)。统计Hp感染情况及影响因素,比较两组血清PGⅠ、PGⅡ、G-17水平,并分析Hp感染者与血清PGⅠ、PGⅡ、G-17的相关性。结果 816例受检者中男426例,女390例。男性阳性感染率高于女性,差异有统计学意义(P<0.05)。不同年龄、文化程度体检者Hp感染率比较,差异无统计学意义(P>0.05)。不同饮酒、经常喝生水、经常在外就餐、经常吃辛辣食物、胃病诊疗史、Hp家族传染史体检人群Hp感染阳性率比较,差异有统计学意义(P<0.05)。多因素logistic回归分析显示,饮酒、经常喝生水、经常在外就餐、经常吃辛辣食物、胃病诊疗史、有Hp家族传染史是体检者发生Hp感染的危险因素(P<0.05)。观察组血清PGⅠ、PGⅡ、G17水平高于对照组,差异有统计学意义(P<0.05)。体检人群Hp感染与血清PGI、PGⅡ、G-17水平呈正相关(r>0,P<0.05)。结论 体检人群Hp感染与多种因素有关,尤其血清PGⅠ、PGⅡ、G-17水平异常与Hp感染有关,具有较高的临床价值。

胃泌素与胃息肉相关性的研究进展

胃泌素是一种主要由G细胞分泌的肽类激素,具有促进胃酸分泌和促进细胞增殖的生理作用。多种因素均可引起胃泌素升高,而胃泌素升高也与一系列消化系统疾病相关,因此,调节胃泌素的分泌对人体健康十分重要。胃息肉是一种凸出于胃壁的局限性隆起性病变,主要通过胃镜检查诊断,虽然胃息肉是一种良性病变,但仍具有恶变潜能,可进展为胃癌。本文将胃泌素与胃息肉的研究现状及相关性研究进行以下综述。

PGⅠ、PGⅡ、G-17联合幽门螺杆菌IgG抗体检验在胃癌中的诊断价值

目的 分析胃蛋白酶原Ⅰ(PGⅠ)、胃蛋白酶原Ⅱ(PGⅡ)、胃泌素-17(G-17)、幽门螺杆菌免疫球蛋白G(IgG)抗体联合检验在胃癌中的诊断价值。方法 选取76例胃癌患者作为胃癌组,选取同一时间段健康志愿者114例作为对照组。对纳入本研究的所有研究对象进行PGⅠ、PGⅡ、G-17、幽门螺杆菌IgG抗体检验。分析比较两组PGⅠ、PGⅡ、G-17水平及幽门螺杆菌IgG抗体阳性率(幽门螺杆菌Ⅰ型、Ⅱ型)。结果 胃癌组患者PGⅠ(61.73±2.47)μg/L明显低于对照组的(76.75±3.46)μg/L,PGⅡ(16.57±0.46)μg/L、G-17(23.66±1.47)pmol/L均高于对照组的(12.89±1.74)μg/L、(11.13±1.74)pmol/L,差异有统计学意义(P<0.05)。胃癌组幽门螺杆菌抗体Ⅰ型阳性率50.0%高于对照组的29.8%,差异有统计学意义(P<0.05);但两组幽门螺杆菌抗体Ⅱ型阳性率比较无明显差异(P>0.05)。结论 对胃癌患者用PGⅠ、PGⅡ、G-17联合幽门螺杆菌IgG抗体检验有助于提高疾病诊断准确率,可为胃癌疾病临床诊断提供科学依据,对胃癌早期防治意义重大,值得推广应用。