慢性萎缩性胃炎患者幽门螺杆菌根除后胃黏膜G细胞数量和血清胃泌素含量的变化

背景:幽门螺杆菌(H.pylori)感染是慢性萎缩性胃炎(CAG)最重要的致病因素,根除H.pylori能否阻止或逆转胃黏膜萎缩目前尚不清楚.目的:通过观察CAG患者H.pylori根除前后胃黏膜G细胞数量和血清胃泌素含量的变化,探讨H.pylori感染对胃黏膜G细胞数量及其分泌功能的影响.方法:60例H.pylori阳性的CAG患者进行了根除治疗,在治疗前和治疗结束3个月后分别行胃镜检查.采用免疫组织化学法和放射免疫分析法测定H.pylori根除前后胃窦黏膜G细胞数量和血清胃泌素含量.结果:31例H.pylori感染的CAG患者在根除治疗3个月后进行了复查,根除率为77.4%.G细胞数量和血清胃泌素含量随胃黏膜萎缩程度的加重而逐渐显著减少(P<0.01).轻度萎缩组H.pylori根除后G细胞数量与治疗前相比无显著差异(P<0.05),而升高的血清胃泌素含量显著降低(P<0.01);中、重度萎缩组H.pylori根除后减少的G细胞数量显著增加(P<0.05),血清胃泌素含量呈上升趋势(P<0.05).结论:CAG患者根除H.pylori后胃黏膜G细胞数量及其合成、分泌胃泌素的功能可出现恢复性变化,可能有助于阻断CAG的进一步发展.     

根除幽门螺杆菌对胃黏膜病变的影响

幽门螺杆菌（H.pylori）被认为是导致胃黏膜病变的重要因子，根除H.pylori能使胃黏膜病变改善。目的：观察根除H.pylori对胃黏膜病变的影响。方法：予100例经胃镜和组织病理学检查确诊为萎缩性胃炎伴H．pylori感染患者抗H.pylori治疗，1年后复查胃镜和组织病理学，评定组织学变化。结果：所有患者均有不同程度的活动性炎症和慢性炎症。抗H.pylori治疗后，86例被根除。与根除前相比，根除后慢性炎症、活动性炎症、腺体萎缩程度评分均明显下降（P〈0．01），肠化生评分无显著改善。结论：根除H.pylori对胃黏膜病变具有临床治疗意义。     

不同数量~(13)C-UBT检测值与幽门螺杆菌根除率的关系及影响因素

目的探讨不同数量13C-UBT检测值与幽门螺杆菌(Helicobacter pylori,H.pylori)根除率的关系及影响因素。方法收集2016年1月至2016年8月新疆维吾尔自治区人民医院消化科门诊患者中13C-UBT检测结果阳性并行胃黏膜组织病理切片检查者634例,分析不同数量13C-UBT检测值与H.pylori根除率的关系及影响因素。结果不同数量13C-UBT检测值的H.pylori根除率随13C-UBT检测值的增加而降低(90.0%、89.7%、85.0%、77.2%),onetile组根除率较quartile组根除率高,且差异有统计学意义(90.0%vs 77.2%,P=0.029)。H.pylori根除率与不同数量13C-UBT检测值相关。H.pylori密度与十二指肠溃疡、胃黏膜糜烂、13C-UBT检测值、胃黏膜萎缩、肠化相关。结论不同数量13C-UBT检测值与H.pylori根除率相关,十二指肠溃疡、胃黏膜糜烂、胃黏膜萎缩、肠化及13C-UBT检测值可能影响H.pylori密度的程度。     

Kawamura分类法在评价幽门螺杆菌感染和胃炎中的价值

目的 探讨Kawamura分类法在诊断幽门螺杆菌(H.pylori)感染和评价胃黏膜炎症及萎缩程度中的价值。方法 在放大内镜下观察71例H.pylori感染患者的胃体上段大弯侧和小弯侧胃黏膜的腺管开口(COs)。根据腺管开口特点分为“白边黑点(white-edged dark spot)”型、“白色(white)”型、“纯白色(dense white pit，DWP)”型，分别取病理活检。对患者行H.pylori根除治疗，6个月后对根除成功的65例患者复查胃镜，比较根除治疗前后3种分型的分布及不同分型胃黏膜炎症活动度和萎缩程度的差异。结果 H.pylori根除后3种分型的分布与根除前比较差异有统计学意义(P<0.001)。根除治疗前以“white”型为主，根除治疗后以“white-edged dark spot”型为主。“white-edged dark spot”型、“white”型、“DWP”型胃黏膜的炎症程度依次升高，每两组间炎症活动度分布比较差异均有统计学意义(P<0.001)。不同Kawamura分型胃黏膜萎缩程度分布比较差异无统计学意义(P>0.05)。结论 Kawamura分类法有助于评价H.pylori感染及胃黏膜炎症活动度，但在评价胃黏膜萎缩程度方面无显著优势。     

紧密连接蛋白Occludin及ZO-1在根除幽门螺杆菌慢性胃炎组织中的表达

目的观察闭锁蛋白(Occludin)及闭锁小带蛋白(zonula occludens-1,ZO-1)在根除幽门螺杆菌(Helicobacter pylori,H.pylori)慢性胃炎组织中的表达变化,探讨其与患者临床病理及预后的关系。方法采用免疫组织化学法检测H.pylori阴性正常人(25例)、根除H.pylori前后慢性浅表性胃炎(30例)及慢性萎缩性胃炎(30例)患者胃窦黏膜标本中Occludin、ZO-1的蛋白表达。结果 H.pylori阴性的正常人胃黏膜Occludin、ZO-1蛋白表达较H.pylori阳性慢性胃炎患者高,差异有统计学意义(P0.05),H.pylori阳性的慢性浅表性胃炎组织Occludin及ZO-1蛋白表达较慢性萎缩性胃炎增强,差异有统计学意义(P0.05);H.pylori根除治疗后,慢性浅表性胃炎组织中Occludin及ZO-1表达量较治疗前增强(P0.05),慢性萎缩性胃炎组织Occludin、ZO-1表达无明显变化(P0.05);H.pylori未根除患者,Occludin及ZO-1蛋白变化差异无显著性(P0.05)。结论 H.pylori阳性的慢性胃炎患者胃黏膜屏障受损,萎缩发生前根除H.pylori治疗可提高Occludin及ZO-1蛋白表达,进而修复H.pylori引起的胃黏膜损伤。     

幽门螺杆菌根除疗法结合叶酸对慢性萎缩性胃炎患者的远期效果

目的探讨幽门螺杆菌(Helicobacter pylori,H.pylori)根除疗法结合叶酸对慢性萎缩性胃炎(chronic atrophic gastritis,CAG)患者的远期效果.方法选取2013-07/2014-06于永嘉县中医医院门诊的123例行H.pylori根除治疗的CAG患者为研究对象,根据治疗方案分为联合组(n=71)和单纯根除组(n=52),单纯根除组患者给予标准三联H.pylori根除治疗,联合组患者在根除H.pylori成功后口服叶酸片3 mo.在治疗后2年进行胃镜随访,比较2组患者治疗前后可操作的与胃癌风险联系的肠化生评估(operative link for gastric intestinal metaplasia assessment,OLGIM)和萎缩评估(operative link for gastritis assessment,OLGA)分期,根据治疗后2年的13C尿素呼气试验结果将联合组患者分为H.pylori根除成功组(n=49)和H.pylori再感染组(n=22),比较3组治疗前后的CAG病变评分.结果治疗后2年,联合组的OLGIM和OLGA分期明显优于单纯根除组,差异均有统计学意义(P0.05).治疗后2年,H.pylori根除成功组和单纯根除组患者的CAG病变评分显著低于同组治疗前,差异均有统计学意义(P0.05),而H.pylori再感染组治疗前后的CAG病变评分比较,差异无统计学意义(P0.05).组间比较,H.pylori根除成功组的CAG病变评分显著低于H.pylori再感染组和单纯根除组,差异均有统计学意义(P0.05),H.pylori再感染组与单纯根除组治疗后的CAG病变评分比较,差异无统计学意义(P0.05).结论 H.pylori根除治疗联合叶酸能显著改善CAG患者的胃黏膜萎缩和肠化生程度,促进其病情恢复,远期应用效果令人满意,且H.pylori成功根除者的效果更好.     

萎缩性胃炎患者幽门螺杆菌根除后表皮生长因子及其受体的变化

目的　研究幽门螺杆菌 (Helicobacterpylori,H .pylori)感染对胃黏膜表皮生长因子受体 (epidermalgrowthfactorreceptor ,EGFR)、血清表皮生长因子 (epidermalgrowthfactor,EGF)水平的影响。方法　对 60例H pylori检测阳性的慢性萎缩性胃炎患者进行根除治疗 ,在治疗前及疗程结束 3个月后分别进行胃镜检查 ,并采用免疫组化及放射免疫法测定H pylori根除前后胃黏膜EGFR和血清EGF含量。 3 0例H pylori检测阴性且胃镜检查无明显异常者作为正常对照组。结果　 60例H pylori检测阳性的CAG患者的胃黏膜EGFR阳性率及血清EGF水平均高于正常对照 ,其差异有显著性 (P <0 0 5 ,P <0 0 1)。有 3 1例在根除治疗 3个月后进行了复查 ,其中 2 4例H pylori得到成功根除。 2 4例H pylori得到根除的CAG患者 ,根除后血清EGF水平明显下降 (P <0 0 1) ,而EGFR阳性率无改变 (P >0 0 5 )。结论　H pylori感染引起胃黏膜EGFR阳性率及血清EGF水平增加 ,根除H pylori后血清EGF可恢复至正常水平 ,而胃黏膜EGFR阳性率在短期内没有明显改变     

马来酸伊索拉定联合三联疗法对幽门螺杆菌感染小鼠治疗作用的实验研究

目的观察马来酸伊索拉定(Irsogladine Maleate,IM)联合三联疗法对幽门螺杆菌(H.pylori)感染小鼠的根除作用其及对H.pylori所致胃黏膜炎症的修复作用。方法 60只KM小鼠随机分为6组,空白对照组、H.pylori感染模型组和4个药物治疗组。治疗组分别给予标准三联、铋剂四联、小剂量IM+标准三联及大剂量IM+标准三联药物灌胃治疗。快速尿素酶试验(RUT)联合组织病理学Giemsa染色判断H.pylori根除情况,HE染色判断胃黏膜炎症情况。结果标准三联组7例H.pylori根除成功,铋剂四联组、小剂量IM+标准三联组及大剂量IM+标准三联组均有8例根除成功,四组根除率两两比较,差异无统计学意义(P0.05)。大剂量IM+标准三联组对胃黏膜慢性炎性反应的修复作用与铋剂四联组相当,优于标准三联组,差异有统计学意义(P0.05)。结论大剂量或小剂量IM联合标准三联对H.pylori感染小鼠的H.pylori根除率与铋剂四联相当,略高于标准三联,IM联合标准三联可明显改善H.pylori感染根除后的胃黏膜慢性炎性反应,且具有剂量依赖性。     

幽门螺旋杆菌对克拉霉素、甲硝唑、左氧氟沙星耐药的研究进展

幽门螺旋杆菌(Helicobacter pylori,H.pylori)感染可导致慢性胃炎、消化性溃疡、胃癌和胃黏膜相关淋巴组织(mucosa-associated lymphoid tissue,MALT)淋巴瘤。而H.pylori根除治疗失败与克拉霉素、甲硝唑及左氧氟沙星高的耐药率有关。现已证实这些抗生素的耐药机制与H.pylori基因突变有关。提高对这些抗生素耐药机制的了解对发展和证实以活检组织为基础的耐药性检测方法很有必要。快速检测H.pylori耐药的基因突变有助于H.pylori根除治疗方案的选择。     

功能性消化不良是否需要根除幽门螺杆菌——支持的观点

幽门螺杆菌（H.pylori）阳性的功能性消化不良（FD）或非溃疡性消化不良（NUD）相当于有消化不良症状的慢性活动性胃炎，前者强调消化不良症状,后者则强调胃黏膜组织学改变。根除H.pylori可使部分患者的症状得到长期改善,胃黏膜活动性炎症消退，逆转或防止萎缩／肠化生的发展,预防胃癌和消化性溃疡，与其他治疗措施相比具有费用,疗效比优势。     

Future candidates for indications of Helicobacter pylori eradication: Do the indications need to be revised?

Since the discovery of Helicobacter pylori in 1982, the development of several treatment guidelines has allowed a consensus on the indications for H. pylori eradication. Beyond these currently accepted indications, including various upper gastrointestinal disorders and extragastric diseases, a significant amount of new information regarding H. pylori eradication is emerging. Certain types of acute gastritis, such as nodular gastritis, hypertrophic gastritis, Ménétrier's disease, hemorrhagic gastritis, and granulomatous gastritis are reversible after H. pylori eradication. Further, for chronic gastritis, closed-type atrophic gastritis and complete-type intestinal metaplasia appear to be more reversible after H. pylori eradication than open-type atrophic gastritis and incomplete-type intestinal metaplasia. Eradication can also be considered in subjects younger than 40 years who have a family history of gastric cancer and in subjects with long-term medications that might lead to bleeding (antiplatelet agents) or atrophy (proton pump inhibitors). Emerging evidence indicates that H. pylori eradication could be an effective treatment for some extragastric diseases that are unresponsive to conventional therapy. In such conditions, routine screening for eradication of H. pylori has not previously been recommended; a "test-and-treat" approach is suggested in the aforementioned situations. Given that H. pylori eradication is effective when the gastritis is reversible, future indications should be expanded to include acute gastric lesions that show marked improvement upon H. pylori eradication rather than just focusing on chronic gastric lesions. Future indications for H. pylori eradication should focus more on reversible lesions before preneoplastic conditions develop.     

根除幽门螺杆菌对胃窦黏膜萎缩和肠上皮化生逆转影响的前瞻性研究

目的 探讨根除幽门螺杆菌(Hp)对逆转胃窦黏膜萎缩和肠上皮化生(肠化生)病理改变的作用.方法 对行胃镜检查的门诊患者,于胃窦处取黏膜活检行病理学检查,并确定Hp感染状态.将Hp感染的慢性胃炎伴胃窦黏膜萎缩或(和)肠化生患者作为入选对象并分为两组,一组行Hp根除治疗,为Hp根除组(48例);另一组未行抗Hp治疗,为对照组(38例).分别在1年和5年后对两组患者进行胃镜随访,并在同一部位取材,根据2次病理结果的不同分为逆转和未逆转两种情况.结果 胃窦黏膜萎缩逆转率在Hp根除组显著高于对照组(37.1%比12.0%).5年后Hp根除组的胃窦黏膜萎缩逆转率显著高于1年后,45岁以下者显著高于45岁以上者.而在对照组中,胃窦黏膜萎缩逆转和随访的时间及年龄无明显关系.在2次随访中,肠化生逆转率在Hp根除组和对照组间差异均无统计学意义(P>0.05).结论 根除Hp尚不能逆转胃窦黏膜肠化生,但对逆转胃窦黏膜萎缩有作用,这种作用与随访观察时间及患者的年龄有关.因此,对有Hp感染的胃窦黏膜萎缩者应及早行根除Hp治疗.     

Improvement of gastric atrophy after Helicobacter pylori eradication therapy

BACKGROUND: It remains controversial whether gastric atrophy is reversible after Helicobacter pylori eradication therapy. AIM: To clarify whether gastric atrophy improves after H. pylori eradication therapy using a histologic approach. METHODS: Subjects were 87 H. pylori infection-cured patients (treatment group) and 29 continuously H. pylori-infected patients (control group). The subjects in the treatment and control groups were followed for 10-49 months (mean, 22 months) and 11-50 months (mean, 22 months), respectively. Biopsy specimens were obtained from the greater curvature of the antrum and corpus at the beginning and end of the observation period; histologic analyses of these specimens were performed for detection of activity, inflammation, atrophy, and intestinal metaplasia. Results were scored without any clinical information according to the Sydney system. RESULTS: In the treatment group, the histologic score for atrophy was improved in the corpus but not in the antrum. Intestinal metaplasia was not improved in either the antrum or the corpus. There were no significant differences during the follow-up in gastric atrophy and intestinal metaplasia in the control group. CONCLUSION: Gastric atrophy was improved in the corpus approximately 2 years after H. pylori eradication therapy.     

Nutrition status and Helicobacter pylori infection in patients receiving hemodialysis

Chronic kidney disease(CKD) patients receiving hemodialysis(HD) often develop gastrointestinal abnormalities over their long treatment period. In general, prognosis in such patients is poor due to the development of protein-energy wasting(PEW). Therefore, it is important to clarify the etiology of PEW and to establish better strategies to deal with this condition. Chronic Helicobacter pylori(H. pylori) infection in the gastric mucosa has a close association with not only the development of peptic ulcer disease and gastric cancer, but is also associated with abnormal plasma and gastric mucosal ghrelin levels that are seen in malnutrition. It is unclear whether H. pylori infection of the gastric mucosa is directly associated with prognosis in HD patients by affecting ghrelin levels. Recent studies show that the prevalence of H. pylori infection in HD patients is significantly lower than in subjects with normal renal function. In the natural history of H. pylori infection in HD patients, the prevalence of infection decreases as the length of time on HD increases. The severity of gastric mucosal atrophy has been suggested as the major determinant of ghrelin levels in these patients, and eradication therapy of H. pylori improves nutritional status by increasing serum cholinesterase and cholesterol levels, especially in patients with mildto-moderate gastric mucosal atrophy. Prompt H. pylori eradication to inhibit the progress of gastric atrophy may be required to prevent this decrease in ghrelin levels and subsequent PEW and improve the prognosis of HD patients by improving their nutritional status.     

Characteristics and predictors of gastric cancer after Helicobacter pylori eradication

Helicobacter pylori(H. pylori) eradication can reduce gastric cancer. However, gastric cancer still develops after eradication, and cases who received eradication therapy are increasing. In this study, we have reviewed the characteristics and predictors of primary gastric cancer developing after H. pylori eradication. In terms of the characteristics, endoscopic, histologic, and molecular characteristics are reported. Endoscopically, gastric cancer after eradication is often depressedtype and shows a gastritis-like appearance, which sometimes makes the diagnosis difficult. Histologically, most gastric cancer after eradication is intestinal type, and non-neoplastic epithelium, also called epithelium with low-grade atypia, is frequently seen over the tumor, which is presumably the cause of the endoscopic gastritis-like appearance. As for molecular characteristics, some markers, such as Ki67, MUC2, and Wnt5a expression, are lower in cancer from patients in whom H. pylori has been eradicated. In terms of predictors, several Japanese studies have reported that severe endoscopic atrophy at eradication is a risk factor for gastric cancer development. Histologic intestinal metaplasia, especially in the corpus, and long-term use of proton pump inhibitors, are also reported as risk factors for gastric cancer after H. pylori eradication. These studies on the characteristics and predictors of gastric cancer development will become the cornerstone for establishing a novel surveillance program based on the gastric cancer risk stratification specific to H. pylori-eradicated patients.     

Reversal of fundic atrophy after eradication of helicobacter pylori

Objectives: We sought to evaluate the effect of Helicobacter pylori eradication in patients with fundic atrophic gastritis.
Methods: Acid secretion, gastric emptying, and histology were evaluated in 20 patients with fundic atrophic gastritis and H. pylori infection. After investigation, 10 patients (Group 1) received an eradicating treatment and 10 (Group 2) did not receive any treatment. One year later, the baseline investigations were repeated. Subsequently, patients in Group 2 received the same treatment given to patients in Group 1 and were reevaluated 12 months later. A further follow-up was performed in both groups 36 months after the treatment.
Results: At 1-yr follow-up, all the patients in Group 1 were H. pylori negative whereas all the patients in Group 2 were still infected. In Group 1, there was a significant improvement of both fundic atrophy and acid secretion, compared with baseline ( p < 0.01 ). In Group 2, no substantial modification of either histological or functional parameters was observed at the first follow-up; conversely, a significant ( p < 0.01 ) improvement of fundic atrophy and acid secretion was detected in these patients 12 months after eradication of the bacterium. Histological pattern remained unchanged at 36 months of follow-up in both groups. Gastric emptying remained, on the average, unaffected by the treatment; however, three patients with delayed gastric emptying at entry had normal gastric emptying after eradication of H. pylori.
Conclusions: Our data suggest that mucosal atrophy can be reduced or even reversed by the eradication of H. pylori , and this is associated with a recovery of gastric function.     

Implications of corpus gastritis, atrophy and cyclooxygenase in the development of gastric erosions after curing Helicobacter pylori infection

BACKGROUND: Helicobacter pylori eradication decreases recurrence of peptic ulcers with marked improvement in histological inflammation, but gastric mucosal injuries may be developed even after eradication. PURPOSE: To investigate the mechanisms responsible for the development of gastric erosions after eradication, we analysed the relationship between clinicopathological risk factors and the occurrence of gastric erosion after curing H. pylori infection. PATIENTS: Sixty patients underwent endoscopy before, and 3, 6 and 12 months after the completion of H. pylori eradication. METHODS: Risk factors associated with the development of gastric erosions after eradication were assessed by multivariate analysis, and cyclooxygenase-1 and -2 immunoreactivity was histologically examined in the gastric mucosa before and after eradication. RESULTS: The cumulative prevalence of gastric erosions after H. pylori eradication was 38.3% within 1 year. Using multivariate analysis, corpus gastritis scores (inflammation score+activity score), corpus atrophy scores and an age of more than 50 years were found to be independent factors associated with the development of gastric erosion after eradication with odds ratios of 7.39, 0.13 and 5.00, respectively. Cyclooxygenase-2 immunoreactivity of the corpus was decreased for the non-erosion group after eradication, but not for the erosion group. CONCLUSIONS: Severe gastritis or less severe atrophy in oxyntic glands but not in pyloric glands before eradication may be involved in the development of gastric erosions after curing H. pylori infection.     

Helicobacter pylori eradication in the healing of atrophic gastritis: a one-year prospective study

OBJECTIVE: Whether gastric atrophy or intestinal metaplasia heals after successful treatment of Helicobacter pylori (H. pylori) infection is still a matter of controversy. The aim of this article was to clarify whether, after one year, H. pylori eradication is associated with healing in glandular atrophy and intestinal metaplasia in the corpus and antrum. MATERIAL AND METHODS: Ninety-two H. pylori-positive peptic ulcer patients with atrophic gastritis (panatrophy, antral or corpus predominant) participated in the baseline study, 1-year prospective follow-up data being available from 76 patients. Mean age was 58+/-12.6 years (mean+/-SD) and the male/female ratio 2/1. The patients participated in an H. pylori eradication study in which they randomly received active eradication therapy. Endoscopy was performed before H. pylori eradication therapy and after 8 and 52 weeks, with specimens examined according to the Sydney system. RESULTS: Of the 92 patients, 8 (9%) had panatrophy, 58 (63%) had antral- and 26 (28%) had corpus-predominant atrophic gastritis. After H. pylori eradication, the mean atrophy score declined in patients with antral-predominant atrophy from 1.5 (mean) to 0.7 (p<0.05), in corpus-predominant atrophy from 1.7 to 0.2 (p=NS) and in patients with panatrophy from 1.2 to 0.8 (p=NS). Atrophy healing was seen in 55% of antral-predominant atrophy patients who had successful H. pylori eradication.The mean antral atrophic score in one year declined in patients with duodenal ulcer (from 1.0 mean to 0.4) whereas it remained the same (1.3) in those with gastric ulcer (p<0.05). CONCLUSIONS: Atrophy can diminish or even disappear, especially in the antrum, during a 1-year follow-up after eradication of infection. Atrophy progression seems milder in patients with duodenal ulcer than in patients with gastric ulcer.     

Histological changes of gastric atrophy and intestinal metaplasia after Helicobacter pylori eradication]

BACKGROUND/AIMS: Long-term Helicobater pylori infection results in atrophic gastritis and intestinal metaplasia, and increases the risk of gastric cancer. However, it is still controversial that eradication of H. pylori improves atrophy or metaplasia. Therefore, we investigated histological changes after the H. pylori eradication in patients with atrophy or metaplasia. METHODS: One hundred seven patients who received successful eradication of H. pylori infection in Hanyang University, Guri Hospital from March 2001 to April 2006, were enrolled. Antral biopsy was taken before the eradication to confirm the H. pylori infection and grade of atrophy or metaplasia by updated Sydney System. After a certain period of time, antral biopsy was repeatedly taken to confirm the eradication and investigate histological changes of atrophy or metaplasia. RESULTS: Mean age of the patients was 55.3+/-11.3, and average follow-up period was 28.7+/-13.9 months. Endoscopic diagnosis included gastric ulcer, duodenal ulcer, non-ulcer antral gastritis. Atrophy was observed in 41 of 91 and their average score was 0.73+/-0.92. After the eradication of H. pylori, atrophy was improved (0.38+/-0.70, p=0.025). However, metaplasia which was observed in 49 of 107, did not significantly improve during the follow-up period. Newly developed atrophy (7 of 38) or metaplasia (18 of 49) was observed in patients who without atrophy or metaplasia initially. Their average scores were slightly lower than those of cases with pre-existing atrophy or metaplasia without statistical significance. CONCLUSIONS: After the eradication of H. pylori infection, atrophic gastritis may be improved, but change of intestinal metaplasia is milder and may take longer duration for improvement.     

Improvement of long-standing iron-deficiency anemia in adults after eradication of Helicobacter pylori infection

We report two cases of long-standing iron-deficiency anemia in premenopausal women that improved after eradication of H. pylori infection. There were no ulcerations or hemorrhagic lesions in the gastrointestinal tract and no bleeding focus in gynecological organs. Both cases showed H. pylori infection in the stomach and gastric atrophy. After successful eradication of H. pylori infection, the iron-deficiency anemia in both patients dramatically improved, and neither patient suffered from anemia for about 2 years. The cure of H. pylori infection is an optional treatment for iron-deficiency anemia in one fraction of the patients.