Relapsed duodenal ulcer after cure of Helicobacter pylori infection

We report a patient—a 42-year-old man—who had suffered from recurrent duodenal ulcer for about 20 years. Successful curative therapy for Helicobacter pylori infection was performed for 2 weeks with new triple omeprazole, anoxicillin, clarithromycin (OAC) treatment in October 1995, and cure of the infection was repeatedly confirmed by histology, culture, and the ¹³C urea breath test. One month after the curative therapy, recurrence of a small duodenal ulcer was observed and in February another duodenal ulcer and reflux esophagitis occurred, with severe symptoms, despite the continuous administration of ranitidine. None of the examinations to reconfirm cure of the infection revealed the presence of H. pylori. As the patient experienced continual psychological stress and smoked more frequently during the recurrent episode and had not used nonsteroidal anti-inflammatory drugs, stress and smoking appeared to play important roles in the relapse of duodenal ulcer in this patient after cure of H. pylori infection. (Received Aug. 18, 1997; accepted Jan. 23, 1998)     

Should we eradicate Helicobacter pylori infection in patients receiving nonsteroidal anti‐inflammatory drugs or low‐dose aspirin?

Whether Helicobacter pylori infection alters the risk of ulcer disease in patients receiving nonsteroidal anti‐inflammatory drugs (NSAIDs) or low‐dose aspirin is one of the most controversial topics in peptic ulcer research. This is an important management issue, particularly in countries where peptic ulcer disease is common and the prevalence of H. pylori infection is high. Current evidence shows that H. pylori infection increases the ulcer risk associated with NSAIDs or low‐dose aspirin. Eradication of H. pylori reduces the subsequent risk of endoscopic and complicated ulcers in patients who are about to start long‐term NSAIDs. Among patients with H. pylori infection and a history of ulcer bleeding who continue to use low‐dose aspirin, 1 week of eradication therapy prevents recurrent ulcer bleeding. Failure of eradication and concomitant use of NSAIDs, however, account for most cases of recurrent bleeding with low‐dose aspirin. The apparent protective effect of H. pylori in long‐term NSAIDs users reported in some studies was actually the weeding out of susceptible patients who were intolerant to NSAIDs. There is no convincing evidence that eradication of H. pylori has any clinically important adverse effect on the healing and prevention of ulcers in NSAIDs users.     

Inhibitory effects of aspirin and indometacin on the growth of Helicobacter pylori in vitro

OBJECTIVE: The interactions between non‐steroidal anti‐inflammatory drugs and Helicobacter pylori have not been sufficiently documented to date. The aim of this study was to investigate the possible effects of aspirin and indometacin on the growth of H. pylori and to determine the effects of aspirin on the susceptibility of H. pylori to some antimicrobials. METHODS: Kinetic studies were performed by inoculating strains of H. pylori in brucella broth with different concentrations of aspirin and indometacin. Growth of bacteria in the broth was assessed spectrophotometrically and by viable colony counts after incubation for 24 and 48 h. Bacterial morphology was determined by Gram stain under light microscopy. The minimal inhibitory concentration (MIC) of aspirin and indometacin was determined by the standard agar dilution method. The MIC of amoxicillin, clarithromycin and metronidazole was measured in the presence and absence of aspirin by the E‐test method. RESULTS: Kinetic studies revealed that aspirin and indometacin inhibited the growth of H. pylori in a dose‐dependent manner. The bactericidal activity of these agents was expressed by cell lysis. Aspirin at 400 µg/mL produced an almost 2‐log decrease in the number of CFU/mL at 48 h. Similar inhibitory effects were obtained when 100 µg/mL indometacin was tested. The MIC at which 90% of H. pylori was inhibited was 512 µg/mL and 128 µg/mL for aspirin and indometacin, respectively. Increased susceptibility of H. pylori to amoxicillin, clarithromycin and metro­nidazole was found in the presence of aspirin. CONCLUSIONS: Aspirin and indometacin could significantly inhibit the growth of H. pylori when incubated in brucella broth in vitro. A subinhibitory concentration of aspirin enhanced the susceptibility of H. pylori to some antimicrobial agents.     

Medical treatment of duodenal ulcer: Acid inhibition or Helicobacter pylori eradication?

To ascertain whether acid inhibition or Helicobacter pylori (HP) colonization is the decisive factor in the healing of duodenal ulcer, we treated 54 patients with famotidine and carried out long-term follow-up. Helicobacter pylori colonization was found in 70.4% of patients before treatment. There were no differences in the pre-treatment characteristics between patients with HP positive or HP negative ulcers. The 4-week and 8-week healing rates after famotidine treatment were 72.5% and 82.4% respectively. No difference in HP colonization was found between patients with ulcer healed and those with ulcer not healed (78.4% vs 64.3% at 4th week and 77.3% vs 71.4% at 8th week, P greater than 0.05). In patients with ulcer healed at 4th week, the intragastric pH was raised significantly and the antral acute inflammation was less severe than those with ulcer not healed. Ulcer recurrence was found in 76.9% of patients within 1 year, but there was no difference in ulcer recurrence between the patients with positive or negative HP colonization at the time of ulcer healing. Our results suggest that duodenal ulcer healing and recurrence are closely related to acid inhibition rather than to HP colonization.     

内镜对十二指肠溃疡幽门螺杆菌感染的预测

目的 分析内镜下十二指肠溃疡对H.pylori感染的预测价值。并评价对十二指肠溃疡病人予经验性根除H.pylori治疗的合理性。方法 以盲法比较311例病人胃粘膜病变与H.pylori感染的关系,H.pylori感染以胃粘膜Giemsa染色和^14C-尿素呼吸试验确定,选择十二指肠溃疡作为H.pylori感染的预测指标并计算敏感性、特异性、预测值和似然比。结果 311例病人H.pyloi感染162例,H.pylori感染者十二批肠溃疡发生率显著高于H.pylori阴性之者（21.6%vs4.7%)。以十二指肠溃疡预测H.pylori感染其行异性、阳性预测值和阳性似然比分别为95.3%(C191.9-98.7%)、83.3%(C172.0-94.6%)和4.59。结论 内镜下十二指肠小疡对H.pylori感染具有较高的阳性预测价值;建议临床对十二指肠溃疡病人应于内镜诊断后即直接予经验性根除H.pylori治疗。     

Effect of Helicobacter pylori eradicated therapy on water gastric emptying in patients with active duodenal ulcer

BACKGROUND AND AIMS: It remains debatable if duodenal ulcer (DU) or Helicobacter pylori infection has a definite impact on human gastric emptying (GE). We explored the nature of water GE in active DU patients before and after ulcer healing and the influence of H. pylori eradication on GE. METHODS: A home made applied potential tomography (APT) was used to measure liquid GE. Twelve electrodes were placed in a circular array around the upper abdomen of studied subjects. After drinking 500 mL of ion-free water, paired electrodes injected electrical current and the remaining 10 electrodes recorded signals, one-by-one in a rotating order. Based on tomographical calculation, the serial changes of averaged signals from altered resistivities were constructed to display GE. Initially, 64 H. pylori infected active DU patients were enrolled. After APT measurement, one-week triple therapy (omeprazole, amoxicillin and clarithromycin) was dispensed. Patients were asked back to determine ulcer/H. pylori status and GE on a scheduled date 3 months later. Finally, 58 patients finished the trial with valid and readable GE data obtained. RESULTS: The ulcer healing and H. pylori eradicated rates were 91.4% and 82.8%, respectively. In general, liquid GE was prolonged in all DU patients at follow up. Of 48 eradicated patients, 35.4% manifested either enhanced or delayed GE before treatment, whereas only five (10.4%) had abnormal GE after treatment (P < 0.0001). In contrast, this characteristically normalized GE was not found in non-eradicated patients. CONCLUSIONS: Water GE of active DU patients ranges from enhanced to delayed, while an effective H. pylori triple therapy is useful not only for healing ulcers, but also for restoring abnormal GE.     

Duodenal gastric metaplasia and Helicobacter pylori infection in high and low duodenal ulcer-prevalent areas in India

Background: Previous reports, based on surgery, showed duodenal ulcer (DU) to be more common in the rice‐eating areas of southern India than in the northern wheat‐eating areas. Aims: Does this difference persist? Can it be explained by risk factors other than diet? Methods: A total of 20 053 records from patients undergoing endoscopy for dyspepsia, and 590 endoscopy patients from two northern and two southern centers in India were studied prospectively. Records were scrutinized to determine the relative incidence of DU and non‐ulcer dyspepsia in wheat‐ and rice‐eating areas. Age, sex, length of history, smoking and medication were recorded. Three antral biopsies and one from each duodenal quadrant were taken. A rapid urease test was carried out on one of the antral biopsies; the others were examined for Helicobacter pylori, gastritis, duodenitis and duodenal gastric metaplasia. Results: The difference in diet‐associated prevalence persisted. No differences in smoking, Helicobacter pylori infection or duodenal gastric metaplasia were found between the two regions, but all three were more common in DU than in non‐ulcer dyspeptic patients from both dietary areas. Conclusions: The dietary differences between the regions remain the only factor to account for the differences in DU prevalence. A strong interrelationship between duodenal gastric metaplasia and cigarette smoking is demonstrated.     

Association of the CagA status of Helicobacter pylori and serum levels of interleukin (IL)‐17 and IL‐23 in duodenal ulcer patients

OBJECTIVE: It has been reported that the cytotoxin‐associated gene A (cagA+) H. pylori strains induce severe gastric mucosal inflammation. The aim of this study was to investigate the association of the virulence factor CagA with IL‐17 and IL‐23 serum levels in duodenal ulcer (DU) patients and H. pylori‐infected asymptomatic (AS) carriers. METHODS: In total, 45 H. pylori‐infected DU patients were enrolled to study: 23 tested positive for the anti‐CagA antibody (anti‐CagA+) and 22 tested negative for the anti‐CagA antibody (anti‐CagA‐), 30 were AS carriers (15 were anti‐CagA+ and 15 were anti‐CagA‐) and 15 were healthy uninfected participants (as a control group). The IL‐17 and IL‐23 serum levels of participants were measured by enzyme‐linked immunosorbent assay method. RESULTS: The mean IL‐17 levels in DU patients were significantly higher than those in AS and control groups (P < 0.001 and P < 0.0001 respectively). In the DU group, the mean IL‐17 levels in participants testing positive for anti‐CagA (10.84 ± 5.79 pg/mL) were significantly higher than those observed in participants testing negative for anti‐CagA (7.65 ± 4.74 pg/mL; P < 0.05). The mean IL‐23 levels in the DU and AS groups were significantly higher than in the control group (P < 0.02 and P < 0.03 respectively) but were not significantly different in participants testing positive and negative for anti‐CagA. CONCLUSION: These results showed higher IL‐17 and IL‐23 serum levels in H. pylori‐infected participants than in the control group. In the DU group the expression of IL‐17 was influenced by the CagA factor.     

胃十二指肠疾病幽门螺杆菌检出的意义

目的:研究幽门螺杆菌(Hp)与消化性溃疡及慢性胃炎致病的关系。方法:因胃十二指肠疾病而做胃镜的患者,采取胃粘膜进行组织快速检菌,一分钟尿素酶(1min UT)试验和血清间接免疫荧光法进行检菌分析。结果:对5000例胃及十二指肠疾病Hp的组织检出率为88.1％。1min UT阳性率为62.9％,两种检菌法有显著差异(P<0.01)。十二指肠溃疡Hp检出为96.0％,胃癌和萎缩性胃炎Hp感染率为50.0％和59.2％,而1min UT只有41.5％阳性率。结论:胃癌和萎缩性胃炎均有粘膜层萎缩,腺体减少、粘液分泌功能降低,Hp茵不能适应强酸环境下生存。十二指肠溃疡和慢性胃炎多伴引起幽门口水肿和幽门变型,胃排空减缓。是导致Hp茵高检出率的重要因素。     

消化性溃疡与幽门螺杆菌L型感染相关性研究

目的　探讨消化性溃疡 (PU)与幽门螺杆菌 L型 (HP- L )感染的关系。方法　取 386例 PU患者胃窦、胃体及十二指肠粘膜组织 ,常规切片后以革兰氏染色和免疫组化染色镜检 HP- L 型细菌 ,并计算检出率。结果　 HP- L 型检出率为 5 3.37% ,其中革兰氏染色和免疫组化染色检出率分别为 5 6 .73%、5 4 .2 9% ,差异无显著性(P>0 .0 5 ) ;胃溃疡、十二指肠溃疡 HP- L 型检出率分别为 5 8.33%、5 5 .5 0 % ,差异无显著性 (P>0 .0 5 ) ;男女患者HP- L 检出率前者 (6 1.18% )明显高于后者 (38.17% ) (P<0 .0 1) ;30岁以下、30岁～、4 0岁～、5 0岁～患者 HP- L检出率依次为 32 .0 5 %、4 1.94 %、5 9.18%、71.79% ,差异显著 (P<0 .0 1)。结论　 PU患者 Hp- L型感染率较高 ,且男性高于女性 ,HP- L型检出率随年龄增长而增高。 PU患者 HP- L型变异可能是导致溃疡迁延不愈、反复发作的重要原因之一     

幽门螺杆菌感染、服用非甾体抗炎药与消化性溃疡的关系

目的 研究消化性溃疡患者由于幽门螺杆菌（H.pylori）感染或服用非甾体抗炎药（NSAIDs）的发生率.方法 选取湖北省武汉市武昌医院2010年3月-2012年7月诊治的152例消化性溃疡患者,将其作为治疗组,同时选取同一时间段到消化科就诊的234例非消化性溃疡患者,将其作为对照组.结果 胃溃疡组感染H.pylori的几率是对照组的2.308倍,十二指肠溃疡组是对照组的8.186倍;胃溃疡组服用NSAIDs的几率是对照组的6.072倍,十二指肠溃疡组是对照组的2.823倍;胃溃疡组同时感染H.pylori和服用NSAIDs的几率是对照组的14.972倍,十二指肠溃疡组是对照组的28.873倍.结论 H.pylori感染同时服用了NSAIDs患者增加消化性溃疡的发生危险性,两种因素同时存在可以起协同作用,增加消化性溃疡的发生几率.     

Role of Helicobacter pylori virulence factor and genotypes in non‐ulcer dyspepsia¶

Background and Aim: The role of Helicobacter pylori (HP) in non‐ulcer dyspepsia is debatable. Eradicating HP will help a small group of non‐ulcer dyspeptic patients. However, it is unclear which subgroup of patients will benefit from eradication therapy. The aim of the present study was to compare the cagA and cagE status, as well as vacA genotypes, of HP in non‐ulcer dyspeptic patients who responded successfully to eradication therapy compared with those patients who did not. Methods: Consecutive patients with moderate to severe (Likert 2 or 3) non‐ulcer dyspepsia with HP were recruited prospectively. Gastric biopsies were taken, DNA extracted and polymerase chain reaction performed to determine the cagA and cagE status and vacA alleles. Eradication therapy was offered until HP was eradicated successfully. The HP status was checked 1 month after eradication therapy using the [¹³C]‐urea breath test. All patients were assessed by one interviewer using Gastrointestinal Symptom Rating Scale (GSRS), a four‐point Likert scale, and SF‐36 for quality of life over 12 months. Treatment success was defined as minimal or no symptoms (Likert 1 or 0). The cagA, cagE and vacA status was blinded to the investigators until completion of the study. Results: Seventy‐three patients (36 males, 37 females) were recruited to the study. The mean ± SD patient age was 53.38 ± 12.09 years. When the 36 patients who improved (group A) were compared with the 37 (group B) who did not, no significant difference was found in the cagE positive rate (55.6 vs 43.2%, respectively; P = 0.638), cagA positive rate (83.1 vs 73.0%, respectively; P = 0.247), vacA m1 versus m2 subtype (84.0 vs 55.6%, respectively; P = 0.472) or vacA s1a versus s1c (39.4 vs 57.1%, respectively; P = 0.166). There was also no significant difference noted in the SF‐36 scores between the two groups after the conclusion of eradication therapy. Conclusions: Stratification of HP genotypes and virulence factor has no significant impact on the treatment success of non‐ulcer dyspepsia.     

Helicobacter pylori infection in bleeding peptic ulcer patients after non-steroidal antiinflammatory drug consumption

AIM:To establish the prevalence of Helicobacter pylori (H. pylori ) infection in patients with a bleeding peptic ulcer after consumption of non-steroidal antiinflamma- tory drugs (NSAIDs). METHODS:A very early upper endoscopy was performed to find the source of upper gastrointestinal bleeding and to take biopsy specimens for analysis of H. pylori infection by the rapid urease (CLO) test, histological examination, and bacterial culture. IgG anti-CagA were also sought. The gold standard for identifying H. pyl...     

Helicobacter pylori eradication improves gastric histology and decreases serum gastrin, pepsinogen I and pepsinogen II levels in patients with duodenal ulcer

Background and Aim: The aim of this study was to assess the gastric histopathology and serum gastrin‐17 and pepsinogens profiles in patients with duodenal ulcer before and after Helicobacter pylori eradication in a population with a very high prevalence of H. pylori. At the same time we assessed the role of H. pylori density on these variables. Methods: Eighty Caucasian patients with H. pylori–associated duodenal ulcer before treatment and 1 year after randomized eradication were studied. Among patients with unsuccessful eradication two groups were distinguished according to the data obtained after treatment: the group with negative rapid urease test and decreased bacterial density according to morphological score (partial elimination group); the group with positive rapid urease test and high bacterial density (failed eradication group). Results: One year after successful eradication, serum levels of gastrin‐17, pepsinogen I and pepsinogen II decreased. Similar changes of serum pepsinogen I and pepsinogen II levels were observed in patients with partial elimination of H. pylori infection. In the group with successful eradication, inflammation, activity, atrophy and number of lymphoid follicles in the antral mucosa fell. In the group with partial elimination, antral mucosa activity and H. pylori score reduced. Other morphological changes were statistically non‐significant. Conclusion: Patients with duodenal ulcer after successful eradication have improvement of morphological and functional characteristics of gastric mucosa.     

抗菌和抑酸治疗十二指肠溃疡的差别

目的 研究抗菌疗法、奥美拉唑及雷尼替丁对十二指肠溃疡治疗作用的差别。 方法 尿素酶试验、幽门螺杆菌的组织学检测、胃窦及溃疡周围组织的炎症变化的光镜和电镜观察。 结果 抗菌疗法组对幽门螺杆菌的清除和溃疡组织的恢复最优,奥美拉唑组次之,雷尼替丁组上述变化不明显。(治疗前后尿素酶试验阳性率分别为:100％→9％,88％→54％,89％→89％;溃疡周边炎症积分分别为:2.9±0.1→1.8±0.2,2.6±0.2→2.6±0.3,2.7±0.3→2.6±0.2)。 结论 抗菌治疗由于可清除幽门螺杆菌,促进溃疡愈合的质量最好,可能是其复发率低的因素。奥美拉唑虽不能清除幽门螺杆菌,却能抑制该菌的活性。     

幽门螺杆菌与消化性溃疡并出血的研究现状

幽门螺杆菌是消化性溃疡的确定性致病因素,其在溃疡并出血的作用尚不十分明确.目前,幽门螺杆菌在消化性溃疡并出血的感染率受检测方法、药物等影响不尽相同.幽门螺杆菌感染在一定程度上增加了消化性溃疡并出血的危险性,从长远上根除幽门螺杆菌可以降低溃疡出血风险,促进溃疡愈合.     

幽门螺杆菌阳性十二指肠溃疡患者表皮生长因子分泌减少的意义(英文)

目的检测胃液和唾液表皮生长因子、胃泌素和生长抑素浓度的变化并评价表皮生长因子分泌减少在幽门螺杆菌（Ｈｐ）阳性十二指肠溃疡发病中的意义．方法１４例健康人、２７例慢性胃炎和１２例十二指肠溃疡．用尿素酶试验、组织学检查和细菌培养判断Ｈｐ感染状态．胃液和唾液表皮生长因子、胃泌素和生长抑素的检测用放免法．结果Ｈｐ阳性的慢性胃炎和十二指肠溃疡患者胃液中胃泌素的浓度高于健康人（Ｐ＞００５），但生长抑素的浓度却显著低于对照组．另外，Ｈｐ感染的十二指肠溃疡患者胃液和唾液中ＥＧＦ的浓度（ｎ＝１０，２７２０ｎｇ／Ｌ±９６３ｎｇ／Ｌ和８３ｎｇ／Ｌ±２４ｎｇ／Ｌ）显著低于健康人（ｎ＝１２，４０５６ｎｇ／Ｌ±３５６ｎｇ／Ｌ和２２０ｎｇ／Ｌ±１７０ｎｇ／Ｌ）和Ｈｐ阳性的慢性胃炎患者（ｎ＝２５，４２３０ｎｇ／Ｌ±１０４０ｎｇ／Ｌ和２２０ｎｇ／Ｌ±１１１ｎｇ／Ｌ）（Ｐ＜００５）．结论ＥＧＦ的分泌减少可能在Ｈｐ阳性十二指肠溃疡发病中起着重要作用．     

广州胃病患者幽门螺杆菌多株感染的研究

目的了解我国Ｈｐ感染人群中的多株感染状况．方法取因上腹不适行内镜检查的２０例Ｈｐ阳性患者（胃溃疡６例,十二指肠溃疡８例,慢性胃炎６例）的胃窦和胃体粘膜组织,进行Ｈｐ培养．初代培养后,分别取胃窦和胃体各１０个菌落进行传代,抽提各菌落ＤＮＡ,应用聚合酶链反应随机引物扩增的ＤＮＡ多态指模技术［ＲＡＰＤＰＣＲ］进行菌株鉴定．结果ＰＣＲ扩增产物电泳分析显示有１８例患者胃窦和胃体的ＨｐＤＮＡ指模一致,提示这１８例患者均是单株感染;另有２例胃体菌株表现为两种指模形态,提示为２株Ｈｐ感染．结论广州地区存在Ｈｐ多株感染,但不普遍．