肝硬化患者胃粘膜病变与幽门螺杆菌感染的关系

近年来 ,肝硬化门脉高压性胃病 ( PHG)逐渐被人们所认识和重视 ,有关幽门螺杆菌 ( Hp)感染与慢性胃炎、消化性溃疡、胃癌等消化道疾病相关性的研究已见诸多报道 ,而有关 Hp感染与肝硬化胃粘膜病变相关性的研究鲜见报道。为探讨 Hp感染在肝硬化胃粘膜病变中的意义 ,我们对 5 8例肝硬化患者行胃镜检查及 Hp检测 ,并与 2 9例非肝硬化患者进行对照 ,现将结果报告如下。1　资料与方法1 .1　临床资料 :所选 5 8例均为我院住院患者 ,经临床确诊为肝硬化。其中男 45例 ,女 1 3例 ;年龄 2 8～71岁 ,平均 45 .2岁 ;肝硬化门脉高压组 38例 ,非门脉高…     

幽门螺杆菌感染和胃粘膜病变关系的研究

迄今许多研究证实幽门螺杆菌(Helicobacter pylori．HP)感染与慢性胃炎相关．称之为HP相关性胃炎。本文通过1000例胃粘膜活检标本的病理组织学观察．旨在进一步了解HP的致病性与胃粘膜主要病变的关系，从而探讨其发病学．     

肝硬化患者胃粘膜幽门螺杆菌检出的初步观察

本文对72例肝硬化患者进行了胃镜下胃粘膜活检检测幽门螺杆菌（HP）。组织学检查HP阳性42例，阳性率58．33％，HP感染和患者的肝功能Child分级无明显相关，亦和胃镜下食管静脉曲张的有无及曲张的严重程度无显著相关，而和胃粘膜活动性炎症及二十指肠溃疡的发生有明显相关。认为在肝硬化患者中，所存在的慢性活动性胃炎的主要病因仍是HP感染，HP可能在肝源性十二指肠溃疡的发病机制中起重要作用。     

幽门螺杆菌感染对猪胃粘膜上皮增生的影响

幽门螺杆菌(Hp)感染是慢性胃炎和消化性溃的主要病因,Hp亦可能是胃癌发生的危险因素,但是其直接关系尚难确定。在成功应用“中国1号小型猪”建立Hp相关性胃炎动物模型基础上,研究了Hp感染对猪胃粘膜上皮PCNA表达和NDA倍体的影响,以表明Hp与猪胃粘膜上皮增生的关系。     

幽门螺杆菌感染与肝硬化

探讨幽门螺杆菌(Hp)在肝硬化中的感染率并对其与肝功能、门脉高压、传播途径作相关分析。对30例胃十二指肠疾病患者和30例肝硬化患者进行胃镜检查、Hp快速尿素酶试验、14C呼吸试验同时记录年龄、饮食结构、习惯;肝功能指标(白蛋白、凝血酶原时间),门脉高压(腹水、脾大、食道静脉曲张),血常规(记录Hb)的相关资料。结果显示:Hp在肝硬化的感染率低于胃十二指肠疾病。Hp在肝硬化感染中的现象:分餐和低唾液可能是感染率低的一个主要因素,Hh减少、肝功能差、门脉高压增加与Hp感染率低有重要相关。肝硬化的低感染率与肝功能失代偿期、门脉高压和贫血不适宜Hp生存有关。口一口传播途径与Hp减少有重要相关性。     

慢性乙型肝炎和乙型肝炎肝硬化患者胃粘膜病变研究

目的 了解慢性乙型肝炎(CHB)和肝硬化患者胃粘膜病变发生率及其特征表现。方法 2017年1月～2019年1月海南医学院附属海南医院收治的70例慢性乙型肝炎、56例乙型肝炎肝硬化和同期在该院体检的50例健康人,接受胃镜检查,采用ELISA法检测血清胃蛋白酶原(PG)I和PGII水平,使用流式细胞仪检测外周血CD3⁺、CD4⁺和CD8⁺细胞百分比。结果 乙型肝炎肝硬化组血清PGI水平(93.8±28.3)μg/L,显著低于健康人【(135.7±21.6)μg/L,P<0.05】或CHB患者【(116.3±32.4)μg/L,P<0.05】,血清PGII水平为(13.3±5.7)μg/L,显著高于健康人【(9.2±2.4)μg/L,P<0.05】,血清PGI/PGII比例为(7.1±2.3),显著低于健康人【(14.8±3.4),P<0.05】或CHB患者【(9.6±2.9),P<0.05】;健康人、CHB和肝硬化组浅表性胃炎发生率分别为68.0%、32.9%和19.6%,差异显著(P<0.05),肝硬化组轻、中、重度萎缩性胃炎发生率分别为37.5%、25.0%和17.9%,与健康人(分别为8.0%、6.0%和2.0%,P<0.05)或CHB组(分别为37.1%、11.4%和5.7%,P<0.05)比,差异显著;肝硬化组外周血CD3⁺细胞百分比为(62.4±7.9)%,显著低于健康人【(68.3±5.8)%,P<0.05】或CHB组【(66.4±7.4)%,P<0.05】,CD4⁺细胞百分比为(35.7±7.4)%,显著低于健康人【(50.3±6.6)%,P<0.05】或CHB组【(45.4±6.4)%,P<0.05】,而CD8⁺细胞百分比为(34.4±4.7)%,显著高于健康人【(27.2±4.3),P<0.05】,CD4⁺/CD8⁺细胞比值为(1.8±0.3),显著低于健康人【(2.8±0.9),P<0.05】。结论 乙型肝炎肝硬化患者慢性萎缩性胃炎发生率高,血清PGI和PGII水平变化明显,其发生机制需要进一步探讨。     

幽门螺杆菌感染与胃黏膜病变的相关性研究

幽门螺杆菌(Hp)是慢性胃炎的主要病冈已得到多数学者认可,有关不同类型胃黏膜病变的Hp感染情况也有较多报道,然而由于检测方法的不同以及对胃黏膜病变的分类定义的差异,其结果差异甚大。我们采用病理组织切片H- E和Giemsa染色检测Hp,按照2000年全国慢性胃炎研讨     

幽门螺杆菌感染与胃粘膜上皮细胞增殖和凋亡

幽门螺杆菌（Ｈｐ）是定植于胃粘膜表面和粘液层之间的革兰阴性、生长缓慢的螺旋状微需氧菌．自１９８３年Ｗａｒｒｅｎ和Ｍａｒｓｈａｌｌ从胃内成功地分离出Ｈｐ以来，引起了医学界的广泛兴趣，从各方面对其在胃肠道疾病中的作用进行了深入的研究．大量研究表明，Ｈｐ是慢性胃炎和消化性溃疡的主要病因，流行病学［１］和组织病理学［２，３］研究指出，Ｈｐ感染和胃癌发生正相关．从慢性浅表性胃炎、萎缩性胃炎、肠上皮化生及异型增生到胃癌的演变过程已基本明确．Ｈｐ感染为慢性胃炎的主要病因，因此也有理由认为Ｈｐ感染是胃癌发生的危…     

胃粘膜刷检无创伤检测幽门螺杆菌感染

为探索一种检出率高、无创伤的检测幽门螺杆菌（Ｈｐ）感染的方法,我院在１９９８年３月～７月间,对６０例因出现消化道症状而就诊的门诊患者,进行胃粘膜刷检涂片检测Ｈｐ感染,从而探讨该方法的临床应用价值,现报告如下。１．资料与方法：本组６０例中男４６例,女１４例;年龄２２～６８岁,平均４８．５岁。除外近１个月内服用过抗生素、铋剂或奥美拉唑,排除胃部分切除术者,检查前停用Ｈ２受体阻滞剂至少１周。对６０例患者进行电子胃镜检查时采用ＰｅｎｔａｘＥＧ－２９３０Ｋ,用毛刷在胃窦部顺时针转向滚动涂刷２周,涂片１张立…     

幽门螺杆菌感染与胃黏膜损伤

自从1983年幽门螺杆菌（Hp）被发现，人们对胃黏膜损伤机制的认识发生了彻底的变革。Hp可通过定植、自身致病因子直接造成胃黏膜损伤，也可间接通过增加宿主细胞氧自由基和胃酸的产生，诱发免疫反应而损伤胃黏膜。此文就Hp与胃黏膜损伤关系的研究现状和进展作一综述。     

Helicobacter pylori infection accelerates human gastric mucosal cell proliferation

Helicobacter pylori causes chronic atrophic gastritis and intestinal type gastric cancer arises against a background of atrophic gastritis. Increased proliferation of epithelial cells is an important indicator of increased risk for gastric adenocarcinoma. We investigated gastric mucosal cell proliferation inH. pylori-associated gastritis and the effect of eradication therapy on this proliferation in 45 patients endoscopically diagnosed (31 with persistent eradication and 14 in whomH. pylori) recurred.H. pylori status was determined by culture and histology in biopsied specimens from the gastric antrum and corpus. Eradication of the infection was defined as reversal to negative on both tests. In vitro Ki-67 immunostaining of endoscopic biopsy specimens was used to measure mucosal cell proliferation inH. pylori-associated gastritis before and after therapy. The proliferative zone was defined as the distance of Ki-67-positive gastric epithelial cells between the highest and the lowest cells. In patients in whomH. pylori was eradicated, cell proliferation in both the antral and corpus mucosa had decreased 4 weeks after completion of the eradication therapy (P<0.01,P<0.001), and 6 months later, it had markedly decreased (P<0.05,P<0.05) and returned to normal. In patients in whomH. pylori recurred, only antral epithelial cell proliferation was reduced 4 weeks after eradication therapy, but whenH. pylori recurred, determined by culture and histology, cell proliferation level was the same as that before eradication. These results suggest thatH. pylori infection accelerates cell proliferation in gastric mucosa and may play a causal role in the chain of events leading to gastric carcinoma.     

幽门螺杆菌iceA基因型与胃黏膜病变的相关性

目的:研究幽门螺杆菌(H pylori)iccA基因型与胃黏膜病变的相关性.方法:用PCR方法检测552例慢性胃炎患者胃黏膜活检标本中H pylori的iceA基因在慢性炎症、活动性炎症、腺体萎缩和肠上皮化生中的存在情况.结果:在552例样本中,iceA1和iceA2亚型菌株单独检出率分别为67.2%,21.7%,iceA1和iceA2亚型均阳性的检出率7.6%,iceA1和iceA2亚型均阴性的比率3.4%.在H pylori感染的慢性炎症、活动性炎症、腺体萎缩、肠上皮化生的重度炎症iceA1的阳性率明显高于中度炎症.两者比较差异有统计学意义(83.1% vs 10.8%,85.5% vs 10.5%,75.6% vs13.0%,75.6% vs 13.0%,均,P<0.05).腺体萎缩和肠上皮化生iceA1的阳性率明显高于其他组(P<0.05).感染iceA1亚型菌株与未感染ieeA1亚型的胃黏膜病变程度差异有显著性(P<0.05).结论:iCeA1是河南地区的优势基因亚型,iceA1阳性率随炎症程度加重逐渐升高.iceA1亚型菌株与重度炎症特别是腺体萎缩和肠上皮化生关系密切.     

Helicobacter pylori infection and gastric emptying in cirrhotic patients with symptoms of dyspepsia

BACKGROUND/AIMS: Chronic gastric Helicobacter pylori infection is common in patients with dyspeptic symptoms. The effect of H. pylori infection on gastric emptying, in cirrhotic patients with dyspeptic symptoms, has never been studied. Therefore, we investigated the incidence of H. pylori infection and its relationship with gastric emptying in cirrhotic patients with dyspepsia. METHODOLOGY: A solid-phase gastric emptying study and 14C urea breath test were performed in 80 cirrhotic patients with dyspepsia. The severity of cirrhosis was assessed according to Child-Pugh's classification. RESULTS: The overall incidence of delayed gastric emptying was 75%. Delayed gastric emptying incidences according to severity of cirrhosis were 71.4% for Child-A, 73.1% for Child-B, and 80.8% for Child-C. The differences were not significant. The incidence of H. pylori infection was 52.5% overall. H. pylori infection rates were 46.4% for Child-A, 42.3% for Child-B, and 69.2% for Child-C. Although there was a tendency for the infection rate to increase with the severity of liver cirrhosis, the difference was not significant. In addition, there were no significant differences in the incidences of H. pylori infection among patients with normal and delayed gastric emptying. CONCLUSIONS: Delayed gastric emptying is common in cirrhotic patients with dyspepsia. However, the status of H. pylori infection does not seem to play a role in delayed gastric emptying in these patients.     

Treatment of Helicobacter pylori infection favourably affects gastric mucosal superoxide dismutases.

BACKGROUND AND AIMS: Excessive production of reactive oxygen metabolites (ROMs) by phagocytic cells is thought to contribute to the mucosal pathology of Helicobacter pylori infection. Previously, H pylori infection was shown to have a differential effect on some gastric mucosal scavenger enzymes of ROMs-namely, mitochondrial and cytoplasmic superoxide dismutases-reflected by a large increase in the cytokine inducible manganese superoxide dismutase and a marginal decrease in the constitutive copper/zinc superoxide dismutase. The present study was performed to evaluate whether these altered mucosal superoxide dismutase concentrations and activities in H pylori associated gastritis are reversed to normal by successful treatment of the infection. PATIENTS AND METHODS: In two different treatment groups-namely, omeprazole or ranitidine, in combination with clarithromycin and metronidazole (OME/AB (n = 33) and RAN/AB (n = 30))-manganese superoxide dismutase and copper/zinc superoxide dismutase concentrations were evaluated by enzyme linked immunosorbent assays in homogenates of gastric antrum and corpus biopsy specimens obtained before and eight weeks after successful treatment of H pylori infection. Superoxide dismutase activities in these homogenates were determined spectrophotometrically in eight patients of both groups before and after successful treatment. The concentrations of gastric mucosal superoxide dismutases were also determined in 12 patients with a persistent H pylori infection, with (n = 4) or without (n = 8) eradication therapy. Infection and eradication of H pylori were confirmed by a combination of culture and histology. RESULTS: Concentrations of manganese superoxide dismutase were significantly lower after than before therapy in antral (p < 0.001 in both treatment groups) and corpus (p < 0.001 in both treatment groups) mucosa. By contrast, copper/zinc superoxide dismutase concentrations were significantly higher (p < 0.001) only in antral mucosa of the OME/AB treated group. Manganese superoxide dismutase activity was significantly lower after than before treatment in antral (OME/AB p < 0.01, RAN/AB p < 0.001), but not in corpus mucosa. Copper/zinc superoxide dismutase activity was not significantly altered by therapy. In the 12 patients with a persistent H pylori infection no major changes in the gastric mucosal superoxide dismutase concentrations were found. CONCLUSIONS: The raised manganese superoxide dismutase and reduced copper/ zinc superoxide dismutase concentrations and activities in H pylori associated gastritis were reversed towards normal by successful treatment of the infection.     

Helicobacter pylori infection in dyspeptic cirrhotic patients

BACKGROUND/AIMS: To date, few studies have focused on the role of Helicobacter pylori (H. pylori) in cirrhotic patients with gastroduodenal disease and reported results are conflicting. The aim of this study was to assess the H. pylori infection rate in dyspeptic cirrhotic patients with or without gastroduodenal lesions at endoscopy. METHODOLOGY: In a prospective study, 226 consecutive dyspeptic cirrhotic patients were enrolled in the study upon assessment of H. pylori infection. Two-hundred dyspeptic non-cirrhotic patients were also included as controls. The presence of H. pylori was detected by rapid urease test and histology (Giemsa staining) in 3 biopsy specimens from the antrum and 3 from the gastric body. RESULTS: H. pylori infection was found in 135 (59.7%) cirrhotics and in 121 (60.5%) controls (p = NS). The prevalence of gastric ulcer was higher in cirrhotics than in controls (16% vs. 2.5%, p = 0.0001), while the prevalence of duodenal ulcer was similar (11% vs. 12%, respectively). The H. pylori infection rate was similar between cirrhotics and controls, both with gastric (83% vs. 80%) and with duodenal (88% vs. 96%) ulcers. Moreover, in our study, a H. pylori-related peptic lesion was the cause of previous gastroduodenal bleeding in 6 of 50 (12%) cirrhotic patients. CONCLUSIONS: Our results indicated that H. pylori infection is implicated in the pathogenesis of peptic ulcer in cirrhotic patients, similar to findings in non-cirrhotic patients.     

Human gastric mucosal hydrophobicity does not decrease with Helicobacter pylori infection or chronological age.

BACKGROUND AND AIMS: Infection with cytotoxin-associated gene A (cagA) Helicobacter pylori is associated with severe gastric diseases. Previous studies in humans have reported a decreased gastric hydrophobicity with H pylori infection. The aim of the present study was to differentiate between the effect of cagA+ and cagA- strains on gastric mucus hydrophobicity. METHODS: One hundred patients without peptic ulcers and not on medication were randomly recruited from endoscopy clinics; each patient had six biopsies. Contact angle measurements were performed using a goniometer assisted by computer software. H pylori status was assessed by histology, Campylobacter-like organism test and culture, and cagA+ status was determined by polymerase chain reaction. RESULTS: In age- and sex-matched patients, there was no significant difference (P=0.27) in contact angle between H pylori-positive (61+/-2.8 degrees ) and H pylori-negative patients (65.5+/-3.0 degrees ). There was also no significant difference (P=0.36) in contact angle among H pylori-negative, cagA- and cagA+ patients (65.5+/-3.0 degrees , 58.6+/-3.6 degrees and 63.4+/-4.9 degrees , respectively). However, a trend of increased mean contact angles in cagA+ compared with cagA- and H pylori-negative patients was observed in patients 50 years and younger (68.3+/-8.3 degrees , 61.1+/-6.1 degrees and 63.6+/-2.2 degrees , respectively; P=0.70) and in patients without atrophy (71.1+/-8 degrees , 59.6+/-4 degrees and 66+/-2 degrees , respectively; P=0.30). In addition, there was no significant correlation between contact angles and patient age (r=0.104, P=0.306). CONCLUSIONS: The present study shows that H pylori infection and the chronological age have no effect on the gastric mucus hydrophobicity, but it highlights a trend of increased mucus hydrophobicity with cagA+ infection that needs to be supported by future studies.     

Gastric mucosal superoxide dismutases in Helicobacter pylori infection.

BACKGROUND--The mucosal pathology of Helicobacter pylori infection may in part be due to excessive production of reactive oxygen metabolites (ROMs) by phagocytes. The influence of H pylori infection on mucosal superoxide dismutases, some major scavenger enzymes of ROM was investigated. In humans superoxidase dismutase is present in at least two forms-that is, mitochondrial manganese (Mn)-superoxide dismutase and cytoplasmic copper-zinc (CuZn)-superoxide dismutase. METHODS--The amount and activity of both superoxide dismutases were measured, respectively by enzyme linked immunosorbent assay (ELISA) and spectrophotometrical enzyme activity assay, in gastric biopsy homogenates of patients with normal mucosa (n = 39) and in patients with H pylori related gastritis (n = 71). Infection and gastritis were confirmed by a combination of culture, serology, and histology. RESULTS--The amount (p < 0.001) and activity (p < or = 0.05) of Mn-superoxide dismutase were increased by about twofold to three-fold, whereas the amount and activity of CuZn-superoxide dismutase showed a slight decrease in gastric mucosa of patients with H pylori gastritis, in both antrum and corpus, compared with normal mucosa of patients without H pylori infection. Mn-superoxide dismutase concentrations in biopsy specimens of histologically normal corpus from patients with an inflamed antrum were significantly higher (p < 0.01) than that of patients with a histologically normal antrum. CONCLUSION-- H pylori infection has a differential effect on mitochondrial and cytoplasmic superoxide dismutase in the gastric mucosa, reflected by a pronounced increase in the cytokine inducible Mn-superoxide dismutase and a marginal decrease in the constitutive CuZn-superoxide dismutase.     

Gastroduodenal mucosal vitamin-C levels in Helicobacter pylori infection.

BACKGROUND: Vitamin C is an important endogenous antioxidant, and epidemiologic evidence suggests that it may protect against the development of gastric cancer. We therefore determined mucosal vitamin-C levels in the stomach and duodenum of subjects with and without Helicobacter pylori infection. METHODS: The patients were 30 subjects undergoing routine gastroscopy for investigation of dyspepsia. High-performance liquid chromatography with electrochemical detection was used to determine mucosal ascorbic acid and total vitamin-C levels. RESULTS: In H. pylori-negative subjects with normal gastroduodenal histology the antrum contained significantly higher levels of ascorbic acid and total vitamin C than the corpus or duodenum (P < 0.05). No significant changes were seen in gastric mucosal ascorbic acid or total vitamin-C levels in the presence of H. pylori infection and related inflammation. The presence of gastric atrophy did not affect mucosal ascorbic acid or total vitamin C levels. Duodenal ascorbic acid and total vitamin-C levels did not change significantly in the presence of gastric H. pylori or duodenal inflammation. CONCLUSIONS: Although high levels of vitamin C are present in the gastroduodenal mucosa, these are not altered in the presence of H. pylori infection and inflammation. These observations suggest that the mucosal antioxidant potential of vitamin C is not impaired by H. pylori infection.