老年幽门螺杆菌相关性胃炎患者抗幽门螺杆菌根除治疗前后的病理学研究

目的分析老年幽门螺杆菌（Hp）相关性胃炎患者抗Hp根除治疗前后胃黏膜病理炎症变化程度,探讨老年Hp相关性胃炎患者行抗Hp根除治疗的重要性。方法收集1989年4月至2011年6月经内镜活检病理、13C-尿素呼气试验、粪便Hp抗原检测,有长期随访资料的老年Hp相关性胃炎患者共239例,观察抗Hp根除治疗前后胃黏膜病理炎症改变程度。结果Hp彻底根除的199次治疗中,179次镜下组织学慢性炎症程度明显好转,治疗前64次有活动性炎症,治疗后27次有活动性炎症;Hp未彻底根除的66次治疗中,42次镜下组织学慢性炎症程度明显好转,治疗前39次有活动性炎症,治疗后22次有活动性炎症。Hp达根除标准的老年患者较Hp未能根除者镜下组织学慢性炎症及活动性炎症程度均明显好转（P〈0．05）。结论对老年Hp相关性胃炎患者进行抗Hp根除治疗,可明显改善患者的胃黏膜组织学慢性炎症及活动性炎症程度,有效地减少慢性胃炎的发病及减轻病变程度。     

幽门螺杆菌相关性胃部疾病的病理变迁

目的：探讨幽门螺杆菌（Hp)清除与否与胃黏膜病理转归的关系。方法：191Hp感染的胃炎或溃疡病患者分别随机给予抗Hp或非抗Hp治疗,1年后复查胃镜,病理分型根据悉系统。结果191例患者中,慢性炎症1年后的炎症程度较1年前减轻（P＜0．05）。其中萎缩和肠化生的程度也较前减轻（P＜0．05）,但活性动性炎症和蔼前后比较差异无显著性（P＜0．05）。根据1年后胃镜复查有无Hp清除分为两个队列,Hp清除列有107例,Hp未肖除列有84例,Hp清除列较未清除列1年后慢性炎症程度轻（P＜0．05）活动性炎症者少（P＜0．05）。对不疾病和不同的治疗分层后发现,Hp清除者的胃黏膜炎症程度总是较Hp未清除者轻（P＜0．05）。结论本研究提示,Hp感染与胃黏膜活动性炎症关系较为密切。Hp清除有利于胃黏膜炎症程度的减轻。     

中西医结合根除幽门螺杆菌对萎缩性胃炎核因子-κB表达的影响

[目的]观察以胃舒散为主的三联疗法（胃舒散、呋喃唑酮和克拉霉素）治疗幽门螺杆菌（Hp）阳性慢性萎缩性胃炎（CAG）的临床效果及其对核因子-κB（NF-κB）表达的影响。[方法]41例Hp阳性CAG患者服用胃舒散2．0g，呋喃唑酮0．1g，各3次／d，克拉霉素0．25g，2次／d，1周后再继服胃舒散4周。治疗前及治疗结束1年后行内镜及病理组织学检查，取活检观察病理组织学改变及NF-κB表达变化，采用银染色法、^14C-尿素呼气试验或快速尿素酶试验检测Hp。[结果]三联疗法结束1年后，Hp根除率为85．4％；根除Hp能显著减轻患者胃窦部慢性炎症（P〈0．05）和活动程度（P〈0．01），下调NF-κB表达（P〈0．01），但胃炎的萎缩和肠化生等病理无明显改变。[结论]以胃舒散为主的三联疗法对Hp有较高根除率。根除Hp可抑制NF-κB的表达，减轻活动性炎症，但近期观察对萎缩、肠化生等病理改变无明显作用。     

幽门螺杆菌感染与白细胞介素-8、粒细胞集落刺激因子含量的关系

目的：探讨幽门螺杆菌（Hp)与胃黏膜白细胞介素（IL）－8和粒细胞集落刺激因子（G－CSF）相关胃炎间的关系。方法：应用酶联免疫吸附试验法测定60例接受胃镜检查患者胃窦黏膜组织培养上清中IL－8、G－CSF的含量，比较Hp感染与非感染患者其含量的差异。其中慢性浅表性胃炎14例，胃溃疡13例，十二指肠溃疡13例，胃黏膜正常者20例。结果：60例受检者中Hp感染40例，其胃黏膜IL－8及G－CSF含量明显高于14非Hp感染者（P＜0．01）。慢性浅表胃炎、胃溃疡Hp阳性者IL－8）及G－CSF明显高于正常组织Hp阳性者（P＜0．01）。慢性浅表性胃炎中，Hp阳性组的IL－8及G－CSF含量高于Hp阴性组（P＜0．05）。结论：Hp感染可以诱导胃黏膜炎症细胞合成和释放IL－8及G－CSF，IL－8及G－CSF可能在Hp相关性胃十二指肠疾病的发病过程中发挥关键作用，是引起炎症反应以及进一步病理损害的重要途径。     

根除Hp感染患者胃黏膜组织学变化及胃癌患病率的随访研究

目的研究幽门螺杆菌（Hp）阳性患者根除Hp后对胃黏膜炎症、萎缩和肠上皮化生（IM）及胃癌患病率的影响。方法采用随机、对照研究方法,对在我院行胃镜检查同时行Hp及胃黏膜组织学检查者236例进行随访观察,3a后复查胃镜和组织病理学,评定组织学变化。分析Hp阳性组和阴性组在胃黏膜炎症、萎缩及IM的变化。结果Hp阳性组中胃黏膜的炎症、腺体的萎缩和肠化的总人数明显高于Hp阴性组（P〈0．05）。结论根除Hp感染可减轻胃黏膜活动性炎症、萎缩和肠上皮化生以及胃癌的发病率。     

根除幽门螺杆菌对胃黏膜癌前病变的影响的Meta分析

目的探讨根除幽门螺杆菌（Hp）对萎缩性胃炎、肠化生等癌前病变的逆转效用。方法全面检索1984年至2008年底国内外生物医学期刊发表的根除Hp对胃黏膜癌前病变影响的临床研究文献及学术会议的交流论文,共6个随机对照试验524例患者进入本系统评价。采用胃黏膜组织学评分、组织学变化作为观察指标。结果（1）Hp根除组胃黏膜萎缩程度改善率显著高于对照组（OR=0．27,95％CI0．17～0．46,P=0．000）;但胃黏膜肠化生改善率在Hp根除组和对照组之间无显著差异（OR=0．55,95％CI0．28～1．08,P=0．082）;（2）Hp根除组Hp根除后胃窦部、胃体、胃底部黏膜的活动性炎症、慢性炎症以及萎缩评分均显著低于对照组（P〈0．01）,但各部位黏膜的肠化生评分改善在Hp根除组和对照组之间无显著差异（P〉0．05）。结论本Meta分析表明,根除Hp可改善慢性萎缩性胃炎的萎缩程度,活动性炎症和慢性炎症程度,但是对胃黏膜肠化生的改善不明显。     

幽门螺杆菌感染慢性胃炎患者红细胞膜补体受体1型分子的表达及其临床价值

[目的]观察幽门螺杆菌（Hp）感染慢性胃炎患者红细胞膜补体受体1型（CR1）分子表达特点以及治疗对其表达的影响，并探讨其临床价值。[方法]Hp阳性（＋）慢性胃炎58例，给予抗Hp三联和胃动力药（得乐冲剂、普瑞博思、阿莫西林和甲硝唑）治疗2周。治疗前及治疗结束后分别进行胃镜及Hp检测，并采用免疫酶联（ELISA）法定量测定CR1分子的数量。[结果]Hp（＋）组治疗后有2例胃黏膜无炎症，较治疗前轻度例数显著增高，中、重度例数显著降低（P〈0．01）。Hp（＋）组治疗前外周血红细胞CR1分子数量显著低于正常对照组（P〈0．01），治疗后显著升高（P〈0．01）。[结论]Hp感染慢性胃炎患者抗Hp三联和胃动力药联用，不仅能显著改善黏膜炎症表现，还能增加红细胞CR1分子活性，提高红细胞免疫功能。     

慢性胃炎伴良性结节状改变与幽门螺杆菌及淋巴滤泡的关系

目的研究慢性胃炎伴良性结节状改变与幽门螺杆菌（Hp）及胃黏膜淋巴滤泡的关系。方法从2004年7月1日-2005年6月30日行内镜检查患者中，筛选出胃窦黏膜有良性结节样改变者为研究对象，在患者胃窦黏膜处喷洒靛胭脂作色素内镜观察，确定有结节状形态改变，并在有明显结节处取活检组织3块，其中1块立刻作Hp快速试验，判定有无Hp感染；另外2块送病理检查，观察胃黏膜淋巴滤泡形成和淋巴细胞浸润情况，并采用亚甲蓝-硼酸染色法进一步明确诊断Hp感染情况。结果将胃黏膜良性结节状改变的慢性胃炎患者分为三组：结节性胃炎组、萎缩性胃炎组和疣状胃炎组，患者平均年龄分别为（31．OO±11．62）岁、（58．61±12．14）岁和（51．29±12．99）岁，其中结节性胃炎组患者发病年龄最小（P〈0．01）；Hp感染率分别为92．86％、82．56％和69．89％，其中结节性胃炎组的感染率明显高于其他两组（P〈0．01）；有淋巴组织增生所见依次为94．90％、27．9％、18．28％，其中结节性胃炎患者淋巴组织增生明显高于其他胃炎患者（P〈0．01）。伴有结节样改变的萎缩性胃炎患者中萎缩和肠化生百分率分别为100％和59．3％，远高于疣状胃炎组的7．53％、8．60％和结节状胃炎组的4．03％、0．00％。结论在三种常见的胃黏膜良性结节状改变的胃炎中，结节性胃炎与Hp感染及胃黏膜淋巴滤泡形成之间存在密切相关性。可以把Hp感染及淋巴组织滤泡形成和淋巴细胞浸润作为诊断结节性胃炎的病理诊断依据。     

幽门螺杆菌感染与C-myc基因和P53基因表达与胃癌的相关性研究

目的探讨幽门螺杆菌（Hp）感染情况与C-myc基因及P53基因的表达与胃癌的相关性。方法用w—s染色法观察不同胃病黏膜组织中Hp感染情况，采用免疫组化检测技术检测不同胃病组织的C-myc基因和P53基因表达产物。结果胃癌及癌前病变组Hp感染率明显高于慢性浅表性胃炎组（P〈0．01），C-myc基因和P53基因的表达也显著高于慢性浅表性胃炎组（P〈0．01）。Hp感染阳性组的C-myc基因和P53基因表达明显高于Hp感染阴性组（P〈0．01）。结论Hp感染可能通过激活C-myc基因，同时使P53基因失活从而诱发胃黏膜的癌变。     

纾萎方治疗慢性萎缩性胃炎的临床研究

[目的]观察纾萎方治疗慢性萎缩性胃炎（CAG）的临床疗效和安全性。[方法]采用随机与阳性对照药平行对照的方法，将81例CAG患者分为治疗组（纾萎方）41例，对照组（胃复春）40例。观察2组临床症状改善情况及病理检查胃黏膜腺体萎缩、肠上皮化生（IM）、异型增生（ATP）和幽门螺杆菌（Hp）感染的变化。[结果]病理疗效：治疗组总有效率75．61％，对照组50．00％（P〈0．05）；症候疗效：治疗组总有效率95．12％，对照组47．50％（P〈0．01）。[结论]纾萎方治疗CAG不仅能明显改善临床症状，而且对CAG、IM及ATP有逆转作用，并有效提高CAG胃黏膜腺体形态的恢复质量。     

Delta (13)C-urea breath test value is a useful indicator for Helicobacter pylori eradication in patients with functional dyspepsia

BACKGROUND: Eradication of Helicobacter pylori is not routinely recommended for the symptomatic relief and the prevention of gastric cancer in patients with functional dyspepsia. The present study investigated a useful indicator of H. pylori eradication in such patients by determining the optimal cutoff value of a 13C-urea breath test (UBT). METHODS: One hundred dyspeptic patients participated in the study. Dyspepsia was scored, and a 13C-UBT administered. A level of delta 13C-UBT of>4 per thousand was diagnosed as H. pylori-positive. After the stomach was endoscopically sprayed with phenol red, biopsy specimens were taken from the antrum, body and cardia of the stomach for the assessment of H. pylori density, and activity (neutrophil infiltration) and degree (lymphocyte infiltration) of gastritis. RESULTS: Correlation between delta 13C-UBT and dyspepsia score was not found. Delta 13C-UBT significantly correlated with H. pylori density score in the total stomach (r = 0.53, P < 0.0001), neutrophil (r = 0.34, P = 0.0005) and lymphocyte score (r = 0.69, P < 0.0001). Twenty-six of the 100 subjects had a neutrophil score of >or=4, lymphocyte score of >or=4, and H. pylori score of >or=4. Their 95% confidence interval of mean was 58.2 per thousand, which reflects moderate to marked acute and chronic gastritis, and dense H. pylori colonization. CONCLUSIONS: The 13C-UBT is a reliable semiquantitative test to assess H. pylori density and the activity and degree of gastritis. It is proposed that H. pylori eradication therapy might be beneficial for patients with functional dyspepsia with a delta 13C-UBT of >58.2 per thousand.     

Significance of cagA status and vacA subtypes of Helicobacter pylori in determining gastric histopathology: virulence markers of H. pylori and histopathology

BACKGROUND: It has been suggested that Helicobacter pylori strains containing the cytotoxin-associated gene A (cagA), and s1m1 genotype of vacuolating cytotoxin gene A (vacA) may have been associated with peptic ulcer disease. The aim of the present study was to analyze such an association of cagA presence and vacA subtypes of H. pylori with histopathological findings in patients with gastritis. METHODS: Sixty-five independent H. pylori strains isolated from Turkish patients with gastritis were analyzed. The antral biopsy specimens were processed for culture and histopathology. Histopathological features were recorded and graded according to updated Sydney system. The vacA subtypes and cagA gene were tested by polymerase chain reaction. RESULTS: Mild degree of antral density was associated with mild degree of gastric neutrophil infiltration (P = 0.010). Positive cagA status correlated significantly with the presence of atrophy (P = 0.035) and neutrophil infiltration (P < 0.001), but not with H. pylori density (P = 0.754) nor the degree of mononuclear cell infiltration (P = 0.945). The vacA subtypes were independent of gastric histopathology. The odds ratios for atrophy and neutrophil infiltration of cagA+ versus cagA- strains were 3.62 (95% confidence interval [CI]: 1.04-12.66) and 53.18 (95%CI: 11.08-255.23), respectively. CONCLUSION: The presence of the cagA gene is strongly associated with atrophic and active gastritis. Distinct vacA subtypes of H. pylori appear to have no association with histopathological findings of gastritis.     

Gastric epithelial cell CXC chemokine secretion following Helicobacter pylori infection in vitro

BACKGROUND AND AIMS: Helicobacter pylori infection of the stomach is commonly associated with infiltration of neutrophils. Gastric epithelial cells are recognized as central mediators of tissue responses to this organism. The aim of the present study was to ascertain patterns of production of three neutrophil chemoattractant chemokines following infection of gastric epithelial cells with H. pylori in vitro. METHODS: Two gastric cancer-derived epithelial cell lines were infected with H. pylori organisms of previously defined cagE and cagA status for periods of up to 24 h. The production of three chemokines (interleukin [IL]-8, epithelial neutrophil activating protein [ENA]-78 and growth-related oncogene [GRO]-alpha) over this time was measured in culture supernatants using immunoassays. RESULTS: Both IL-8 and GRO-alpha were produced by both AGS and KATO-III cells in response to H. pylori infection, and in a cag PAI-dependent manner. ENA-78, however, was not increased following H. pylori infection. CONCLUSIONS: GRO-alpha is expressed by epithelial cells following H. pylori infection along with IL-8. Both may contribute to neutrophilic infiltration present in gastric mucosa associated with H. pylori infection. In contrast, H. pylori infection does not lead to an increased synthesis of ENA-78, suggesting that this may not be as important in vivo.     

Effect of H. pylori on COX-2 expression in gastric remnant after distal gastrectomy

BACKGROUND/AIMS: Helicobacter pylori infection is known to induce gastritis, oxidative stress, and cyclooxygenase (COX)-2 expression in the gastric mucosa. However, the effect of H. pylori infection on remnant gastritis has not been studied. We investigated whether the severity of remnant gastritis and COX-2 expression were affected by H. pylori infection after distal gastrectomy. METHODOLOGY: The study included 97 patients with gastric cancer who underwent curative distal gastrectomy with lymphadenectomy in our department between May 1999 and April 2001. All patients underwent endoscopic examination 2 weeks before and 12 weeks after surgery. The presence of H. pylori infection was determined by urease activity, hematoxylin-eosin staining, and immunochemical staining. Histologic remnant gastritis was graded based on the degree of neutrophil infiltration using the updated Sydney System. COX-2 expression was estimated immunohistochemically. RESULTS: Both the degree of neutrophil infiltration and the level of COX-2 expression were significantly higher in patients with than without H. pylori (p<0.05). There was a significant correlation between the degree of neutrophil infiltration and the degree of COX-2 expression (p<0.001). CONCLUSIONS: H. pylori eradication may become a treatment for preventing both remnant gastritis as well as remnant gastric carcinoma after distal gastrectomy.     

Effect of Helicobacter pylori Infection on Gastric Emptying and Gastrointestinal Hormones in Dyspeptic and Healthy Subjects

There is no general agreement as regards the effect of Helicobacter pylori infection on gastric emptying in patients with functional dyspepsia. Food releases several gastrointestinal hormones, and some of these are known to contribute to the regulation of gastric emptying. The aim of this study was to investigate the influence of H. pylori on gastric emptying in dyspeptic and healthy subjects and to verify whether different hormone secretion patterns are affected by the presence of the bacterium. Twenty-seven patients affected by functional dyspepsia and 30 asymptomatic healthy subjects entered the study. H. pylori presence was assessed in controls by IgG antibodies to H. pylori and [¹³C] urea breath test, and that in patients by Warthin-Starry stain on gastric biopsies. After ingesting a standard solid-liquid meal, an ultrasound examination of gastric emptying was performed. Plasma concentrations of gastrin, cholecystokinin, and pancreatic polypeptide were measured in the fasting and postprandial period for 4 hours. The incidence of H. pylori infection was not higher in functional dyspepsia patients than in controls. As regards gastric emptying, no difference was detected between patients and controls with and without H. pylori infection. On the contrary, the presence of H. pylori infection determined alterations in gastrin levels, which were higher in controls than in patients. Basal CCK levels were higher in the H. pylori-negative patients than H. pylori-positive patients and controls. In conclusion, H. pylori infection seems not to cause alterations in gastric emptying, but rather alterations in gastrin levels. In contrast, the altered levels of CCK account for its involvement in the pathophysiology of H. pylori-negative dyspepsia.     

Differential roles of interleukin-1beta and interleukin-8 in neutrophil transendothelial migration in patients with Helicobacter pylori infection

BACKGROUND: Little information is currently available on the contribution of locally generated inflammatory and chemotactic cytokines to endothelial cell activation and subsequent neutrophil transendothelial migration in patients with Helicobacter pylori (H. pylori)-associated gastritis. METHODS: The contents of interleukin (IL)-1beta and IL-8 in the organ culture supernatants of antral mucosal tissues were measured with an enzyme-linked immunosorbent assay. The effects of the endogenous IL-1beta and IL-8 in mucosal tissues on neutrophil adherence and transendothelial migration were investigated using an experimental model of human umbilical vein endothelial cells (HUVEC). RESULTS: The contents of IL-1beta and IL-8 in organ cultures of antral mucosal tissues were significantly higher in patients with H. pylori infection than in those without infection. The organ culture supernatants from H. pylori-positive patients induced the expression of intercellular adhesion molecule-1 mRNA in HUVEC with increased binding of neutrophils, and these stimulatory effects were inhibited when HUVEC were pretreated with a nuclear factor-kappaB inhibitor, MG-132. Moreover, neutrophil adherence to HUVEC induced by the supernatants decreased after preincubation with neutralizing anti-IL-1beta antibody. As compared with the supernatants from H. pylori-negative patients, the samples from H. pylori-positive patients exhibited a significantly higher chemotactic activity for neutrophils, which was inhibited almost completely by preincubation of the supernatants with anti-IL-8 antibody. CONCLUSIONS: Locally generated IL-1beta and IL-8 could coordinate with each other during the process of neutrophil infiltration into the gastric mucosa in patients with H. pylori infection.     

Relationship between antral lymphocyte density and basal gastrin levels in patients with Helicobacter pylori infection

BACKGROUND: The mechanism by which Helicobacter pylori causes hypergastrinaemia is not completely understood. AIM: To evaluate whether antral lymphocyte density could play a role in this alteration. METHODS: A total of 12 patients with active duodenal ulcer and 10 with non-ulcer dyspepsia were enrolled upon detection of Helicobacter pylori infection at endoscopy Enrolled as controls were 7 matched dyspeptic patients without Helicobacter pylori infection. Biopsy specimens were collected for Helicobacter pylori and histological assessments, and for antral lymphocyte density assessment by a histomorphometric method. A blood sample was obtained from each patient to determine basal gastrin levels. All patients were controlled by a further endoscopy 4 weeks after the end of Helicobacter pylori treatment. RESULTS: Antral lymphocyte density (5,464 +/- 1,328 and 5,635 +/- 1,186 vs 2,267 +/- 557 lymphocytes/mm2; p<0.001 and p<0.001, respectively) and gastrin levels (66.7 +/- 14.1 and 60.4 +/- 21.7 vs 40.7 +/- 7.8 pg/dl; p=0.004 and p=0.02, respectively) were higher in duodenal ulcer and non-ulcer dyspepsia patients than in controls, while no significant differences emerged between duodenal ulcer and non-ulcer dyspepsia patients. There was a significant direct correlation between antral lymphocyte density and gastrin levels both in duodenal ulcer (r=0.77; p=0.003) and in non-ulcer dyspepsia (r=0.75; p=0.03) patients, while no correlation was found in controls [r=0.12; p=0.8). After treatment, this correlation persisted in 10 eradication failure patients (r=0.68; p=0.027), but disappeared in those successfully cured. CONCLUSIONS: These data suggest that lymphocyte density in the antral mucosa could play a role in the impaired gastrin production occurring in patients with Helicobacter pylori infection.     

Correlation between duodenogastric reflux and remnant gastritis after distal gastrectomy

BACKGROUND/AIMS: Many patients who undergo distal gastrectomy develop remnant gastritis. This report describes the correlation between remnant gastritis and the amount of duodenogastric reflux and looks at the relationship between Helicobacter pylori infection and duodenogastric reflux in remnant gastritis. METHODOLOGY: Sixty-two patients who underwent curative distal gastrectomy for gastric cancer with radical lymphadenectomy were studied. The period of bile reflux (percent time) into the gastric remnant was measured with the Bilitec 2000 under standardized conditions. Remnant gastritis was semi-quantified using the neutrophil infiltration score based on the updated Sydney System, and the presence of H. pylori infection was determined 12 weeks after the surgery. RESULTS: Overall, the correlation was not significant between the neutrophil infiltration score and the percent time (p=0.08). Similarly, the correlation was not significant in patients with H. pylori infection (p=0.30), but it was significant in patients without H. pylori infection (p=0.03). CONCLUSIONS: Duodenogastric reflux after distal gastrectomy can cause remnant gastritis in patients without H. pylori infection. Reconstruction with biliary diversion is protective against the development of remnant gastritis.     

Enhanced somatostatin secretion into the gastric juice with recovery of basal acid output after Helicobacter pylori eradication in gastric ulcers

BACKGROUND AND AIM: Antral somatostatin interacts with gastric acid secretion. We aimed to investigate the effect of eradication on gastric acid, somatostatin secretion and mucosal histology in gastric ulcer patients with Helicobacter pylori (H. pylori) infection. METHODS: Twenty-eight patients (21 male, 7 female) with H. pylori-positive gastric ulcer were treated with dual therapy. Before and 4-8 weeks after the therapy, the histology of biopsy specimens, basal acid output (BAO) and maximal acid output (MAO) after stimulation with tetragastrin were assessed. Somatostatin concentration in the gastric juice was measured by radioimmunoassay, and somatostatin output during either the basal or gastrin-stimulated period was also examined. RESULTS: Eradication was successful in 22 patients. Before treatment, the acid and somatostatin output were inversely related to the severity of neutrophil infiltration in the corpus and antrum, respectively. After successful eradication, improvement of histological inflammation and an increase in BAO, basal and gastrin-stimulated somatostatin output were observed. Eradication had no effect on atrophy and MAO. There was a positive correlation between gastric acid and somatostatin output in the basal or stimulated condition, irrespective of H. pylori infection. CONCLUSIONS: The present results suggest that recovery of gastric BAO may be caused by an improvement in corpus neutrophil infiltration, but not by an increase in parietal cell volume or a change in atrophy. Also, there was an increase in basal and gastrin-stimulated somatostatin-containing cell activity accompanied by improved antral neutrophil infiltration in the early phase after H. pylori eradication in gastric ulcers.