Effects of Helicobacter pylori and nonsteroidal anti-inflammatory drugs on peptic ulcer disease: a systematic review.

BACKGROUND & AIMS: The aim was to systematically review the interactions between Helicobacter pylori (HP) infection and NSAID use on the risk of uncomplicated or bleeding peptic ulcer. METHODS: All relevant full articles published in MEDLINE from January 1989-June 2004 were included. Sensitivity analyses for type of controls or use of aspirin or non-aspirin NSAIDs were performed. RESULTS: In 21 studies involving 10,146 patients, uncomplicated peptic ulcer was more common in HP-positive than HP-negative patients (pooled odds ratio [OR], 2.17) or in HP-positive than HP-negative NSAID users (OR, 1.81). In 6 age-matched controlled studies, ulcer was more common in HP-positive than HP-negative patients (OR, 4.03), irrespective of NSAID use, and in NSAID users than non-users (OR, 3.10), irrespective of HP status; the risk of ulcer was 17.54-fold higher in HP-positive NSAID users than HP-negative non-users. The use of aspirin or non-aspirin NSAIDs did not affect the results. Ulcer bleeding was evaluated in 17 studies involving 4084 patients. NSAID use was more frequent in bleeding patients than control subjects (OR, 5.13), irrespective of HP status and type of controls. In contrast, HP infection in bleeding patients compared with control subjects was less frequent in the 8 studies with ulcer cases as control subjects (OR, 0.40) and more frequent in the 9 studies with uninvestigated subjects as controls (OR, 2.56). In the latter studies, presence compared with the absence of both HP and NSAIDs increased the risk of bleeding 20.83-fold. CONCLUSION: HP infection and NSAID use represent independent and synergistic risk factors for uncomplicated and bleeding peptic ulcer.     

Risk of ulcer bleeding in patients infected with Helicobacter pylori taking non-steroidal anti-inflammatory drugs

OBJECTIVE: To determine whether Helicobacter pylori is an independent risk factor for bleeding peptic ulcer in users of non-steroidal anti-inflammatory drugs (NSAIDs), including aspirin. DESIGN: A prospective matched case-control study. SETTING: Odense University Hospital, Denmark. SUBJECTS: 132 patients with a bleeding peptic ulcer (n=124) or haemorrhagic gastritis (n=8) at endoscopy who had taken an NSAID in the previous week and 136 controls who had taken NSAIDs without gastrointestinal complications. The controls were recruited from rheumatology and geriatric outpatient clinics. MEASUREMENTS: H pylori status assessed by serology and 13C-urea breath test and regarded as positive if either test was positive. Data on potential confounding factors including smoking and alcohol were collected by interview. MAIN RESULT: H pylori was present in 57% of cases and 43% of controls. The adjusted odds ratio of bleeding from a peptic ulcer owing to H pylori infection in NSAID users was 1.81 (95% CI 1.02 to 3.21) and was similar in aspirin and non-aspirin NSAID users. Peptic ulcer bleeding was also statistically significantly associated with a history of previous ulcer bleeding, dyspepsia within the previous 3 months, drinking alcohol but not with smoking. About 16% of bleeding peptic ulcers in NSAID users could be attributed to H pylori infection. CONCLUSION: NSAID users infected with H pylori have an almost doubled risk of bleeding peptic ulcer compared with uninfected NSAID users.     

Helicobacter pylori and risk of ulcer bleeding among users of nonsteroidal anti-inflammatory drugs: a case-control study.

BACKGROUND & AIMS: Peptic ulcer complications related to use of nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most common serious adverse drug reactions. Whether Helicobacter pylori infection potentiates this gastrointestinal toxicity of NSAIDs is still unresolved. In this study, we investigated the role of H. pylori as a cause of bleeding peptic ulcer among NSAID users. METHODS: A case-control study of current users (n = 132) of NSAIDs (including acetylsalicylic acid), admitted because of bleeding peptic ulcer, was performed. Controls were 136 NSAID users without gastrointestinal complications. H. pylori was diagnosed by either increased levels of serum immunoglobulin G or by 13C-urea breath test. RESULTS: Fifty-eight (44%) case subjects had a bleeding gastric ulcer, 54 (41%) had a bleeding duodenal ulcer, 12 (9%) had both gastric and duodenal ulcers, and 8 (6%) had hemorrhagic gastritis. H. pylori was present in 75 (57%) cases compared with 59 (43%) controls. The adjusted odds ratio of bleeding peptic ulcer among NSAID users associated with H. pylori infection was 1.81 (95% confidence interval, 1.02-3.21). H. pylori accounted for approximately 24% of bleeding peptic ulcers among elderly NSAID users. CONCLUSIONS: NSAID users infected with H. pylori have an almost twofold increased risk of bleeding peptic ulcer compared with NSAID users without H. pylori.     

Peptic ulcer bleeding: interaction between non-steroidal anti-inflammatory drugs, Helicobacter pylori infection, and the ABO blood group system

BACKGROUND: Helicobacter pylori infection is found in almost all patients with an uncomplicated ulcer. Non-steroidal anti-inflammatory drug (NSAID) use is the main risk factor for bleeding peptic ulcer. In the older literature ABO blood groups were mentioned as a risk factor. There is continuing uncertainty about the interaction between these risk factors and the development of peptic ulcer bleeding. We therefore determined the separate and combined effect of NSAIDs, H. pylori infection, and the ABO blood group system in patients with a bleeding peptic ulcer. METHODS: The prevalence of NSAID use, H. pylori infection, and blood group O was determined in 227 patients who were admitted with a bleeding gastric or duodenal ulcer between 1990 and 1997. These results were compared with the expected frequency of these risk factors in the Dutch population. RESULTS: NSAID use was reported in 48.2% of the patients with a bleeding peptic ulcer. The H. pylori prevalence was 62.0%, whereas blood group O was present in 49.3% of the patients. NSAID use was the strongest risk factor for hemorrhage caused by a peptic ulcer (relative risk, 8.4), whereas the relative risk associated with H. pylori infection and blood group O was 1.5 and 1.2, respectively. With univariate analysis NSAID use and H. pylori infection seemed to be separate risk factors and did not really potentiate each other's effect. Moreover, blood group O did not potentiate the strong effect of NSAIDs. CONCLUSION: H. pylori infection may add only a little to the important risk of NSAID use in the development of bleeding peptic ulcers.     

Management of NSAID-associated peptic ulcer disease

Non-steroidal anti-inflammatory drug (NSAID) use increases the risk of gastrointestinal complications such as ulcers or bleeding. The presence of factors like advanced age, history of peptic ulcer, Helicobacter pylori infection and the use of anticoagulants or antiplatelet agents increase this risk further. COX-2 inhibitors and antisecretory drugs, particularly proton pump inhibitors, help to minimize the risk of gastrointestinal complications in high-risk patients. This review presents a practical approach to the prevention and treatment of NSAID-associated peptic ulcer disease and examines the new advances in the rational use of NSAIDs.     

Peptic ulcer disease today

Over the past few decades, since the introduction of histamine H(2)-receptor antagonists, proton-pump inhibitors, cyclo-oxygenase-2-selective anti-inflammatory drugs (coxibs), and eradication of Helicobacter pylori infection, the incidence of peptic ulcer disease and ulcer complications has decreased. There has, however, been an increase in ulcer bleeding, especially in elderly patients. At present, there are several management issues that need to be solved: how to manage H. pylori infection when eradication failure rates are high; how best to prevent ulcers developing and recurring in nonsteroidal anti-inflammatory drug (NSAID) and aspirin users; and how to treat non-NSAID, non-H. pylori-associated peptic ulcers. Looking for H. pylori infection, the overt or surreptitious use of NSAIDs and/or aspirin, and the possibility of an acid hypersecretory state are important diagnostic considerations that determine the therapeutic approach. Combined treatment with antisecretory therapy and antibiotics for 1-2 weeks is the first-line choice for H. pylori eradication therapy. For patients at risk of developing an ulcer or ulcer complications, it is important to choose carefully which anti-inflammatory drugs, nonselective NSAIDs or coxibs to use, based on a risk assessment of the patient, especially if the high-risk patient also requires aspirin. Testing for and eradicating H. pylori infection in patients is recommended before starting NSAID therapy, and for those currently taking NSAIDs, when there is a history of ulcers or ulcer complications. Understanding the pathophysiology and best treatment strategies for non-NSAID, non-H. pylori-associated peptic ulcers presents a challenge.     

Effect of helicobacter pylori infection on the risk of upper gastrointestinal bleeding in users of nonsteroidal anti-inflammatory drugs

PURPOSE: We evaluated whether infection with Helicobacter pylori, including specific cytotoxic-associated antigen (CagA)-positive strains, increase the risk of upper gastrointestinal bleeding in users of nonsteroidal anti-inflammatory drugs (NSAIDs). METHODS: Cases with upper gastrointestinal bleeding and recent NSAID use, including aspirin, who were admitted during 2001, were compared with age- and sex-matched outpatient controls who had recent NSAID use. H. pylori infection was diagnosed by serum antibodies or the (13)C-urea breath test; and CagA seropositivity was diagnosed by enzyme-linked immunoassay. RESULTS: H. pylori was detected significantly more frequently in cases of bleeding than controls (79% [63/80] vs. 56% [45/80], P = 0.004). Cases of bleeding were more likely than controls to have a history of peptic ulcer (34% [n = 27] vs. 13% [n = 10], P = 0.003), previous upper gastrointestinal bleeding (19% [n = 15] vs. 6% [n = 5], P = 0.03), recent dyspepsia (29% [n = 23] vs. 15% [n = 12], P = 0.06), and <3 months of NSAID use (58% [n = 46] vs. 40% [n = 32], P = 0.04). CagA positivity was not associated with gastrointestinal bleeding. In a multivariate analysis, H. pylori infection was the only significant risk factor for upper gastrointestinal bleeding (odds ratio = 1.7; 95% confidence interval: 1.2 to 2.5; P = 0.004). CONCLUSION: H. pylori infection almost doubles the risk of upper gastrointestinal bleeding among users of NSAIDs.     

Impact of non-steroidal anti-inflammatory drug and aspirin use on the prevalence of dyspepsia and uncomplicated peptic ulcer disease

BACKGROUND: Non-steroidal anti-inflammatory drug and aspirin (here collectively called NSAIDs) use is the second most common aetiologic factor for peptic ulcer disease and a major factor for peptic ulcer complications. The role of NSAIDs in the pathogenesis of uncomplicated peptic ulcer is less well understood and the interaction between NSAIDs and Helicobacter pylori infection on ulcer development is controversial. The aim of the present study was to examine the role of NSAIDs in the occurrence and clinical features of uncomplicated peptic ulcer disease. METHODS: A total of 1091 consecutive patients referred for open-access upper gastrointestinal endoscopy by general practitioners (GPs) were enrolled. The use of NSAIDs was gathered from a structured questionnaire completed by the patients and from patient files by GPs. The exclusion criteria were previous H. pylori eradication and gastric surgery, as well as symptoms and/or signs suggestive of acute gastrointestinal bleeding. RESULTS: Of the whole study group (n = 1091), 76 (7%) patients had a peptic ulcer. Thirty patients had an NSAID-use-associated peptic ulcer and 46 patients a non-NSAID-use peptic ulcer. Of patients with chronic gastritis (n = 599), 71% were H. pylori-positive and 108 used NSAIDs. Of those with chronic gastritis, 23 had an NSAID-use-associated peptic ulcer and 38 a non-NSAID ulcer. Of patients with normal gastric histology (n = 492), 75 patients used NSAIDs, 7 had an NSAID ulcer and 8 a non-NSAID ulcer. The only independent risk factor for peptic ulcer in patients using NSAIDs was H. pylori infection (odds ratio (OR) 3.1, 95% confidence interval (CI) 1.3-7.3), whereas dyspepsia (OR 1.0, 95% CI 0.4-2.4), male sex (OR 1.4, 95% CI 0.6-3.4), age (OR 1.0 per decade, 95% CI 0.8-1.3) and anaemia (OR 2.9, 95% CI 0.9-8.7) were not risk factors. In patients not using NSAIDs, independent risk factors for peptic ulcer were dyspepsia (OR 4.3, 95% CI 2.1-8.8), male sex (OR 2.0, 95% CI 1.1-2.8), age (OR 1.2 per decade, 95% CI 1.0-1.5), anaemia (OR 6.2, 95% CI 2.6-14.9) and H. pylori infection (OR 7.5, 95% CI 3.4-16.6). When comparing patients using NSAIDs or not, the OR of patients on NSAIDs for peptic ulcer was 2.7 (95% CI 1.5-5.0) among patients with chronic H. pylori gastritis (n = 424) and 5.3 (95% CI 1.8-15.0) among patients with normal gastric mucosa (n = 492). CONCLUSIONS: The use of NSAIDs increases the risk of peptic ulcer 3- and 5-fold in H. pylori-positive and H. pylori-negative patients, respectively. Dyspepsia is a poor predictor of peptic ulcer among patients using NSAIDs, and serologic H. pylori testing and treatment for chronic NSAID users is recommended.     

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.     

幽门螺杆菌感染和长期服用阿司匹林与上消化道出血关系研究

目的:探讨幽门螺杆菌(Hp)感染患者长期服用阿司匹林与上消化道出血的关系。方法:选取门诊每日服用100mg阿司匹林的患者,进行胃镜检查并检测Hp。根据Hp检测结果将3809例入选对象分为Hp阳性组和Hp阴性组,随访2年,观察上消化道出血情况;Hp阳性伴上消化道出血患者抗Hp治疗根除Hp后分组,分别给予法莫替丁40mg睡前顿服(干预组),或不加干预者作为对照组,2组均继续服用阿司匹林,随访2年,观察其再出血情况。结果:60岁以上老年患者服用小剂量阿司匹林上消化道出血率明显高于60岁以下患者(P<0.05);Hp阳性组2802例患者中上消化道出血146例(5.21%),Hp阴性组共1007例患者,上消化道出血为30例(2.98%),2组相比差异有统计学意义(P<0.05);144例患者根除Hp法莫替丁干预组72例,上消化道再出血2例(2.78%),对照组72例,上消化道再出血8例(11.1%),2组相比差异有统计学意义(P<0.05)。结论:60岁以上老年患者服用小剂量阿司匹林增加上消化道出血风险;Hp感染并长期服用小剂量阿司匹林可增加患者上消化道出血风险;法莫替丁干预能有效降低长期服用小剂量阿司匹林患者上消化道再出血风险。     

Role of Helicobacter pylori eradication in aspirin or non-steroidal anti-inflammatory drug users

Helicobacter pylori(H pylori) infection and the use of non steroidal anti-inflammatory drugs (NSAIDs) including aspirin at any dosage and formulation represent well-established risk factors for the development of uncomplicated and complicated peptic ulcer disease accounting for the majority of such cases. Although the interaction between H pylori and NSAID/aspirin use in the same individuals was questioned in some epidemiological studies, it has now become widely accepted that they are at least independent risk factors for peptic ulcer disease. According to data from randomized intervention trials, naive NSAID users certainly benefit from testing for H pylori infection and, if positive, H pylori eradication therapy prior to the initiation of NSAID. A similar strategy is also suggested for naive aspirin users, although the efficacy of such an approach has not been evaluated yet. Strong data also support that chronic aspirin users with a recent ulcer complication should be tested for H pylori infection and, if positive, receive H pylori eradication therapy after ulcer healing, while they appear to benefit from additional long-term therapy with a proton pump inhibitor (PPI). A similar approach is often recommended to chronic aspirin users at a high risk of ulcer complication. H pylori eradication alone does not efficiently protect chronic NSAID users with a recent ulcer complication or those at a high-risk, who certainly should be treated with long-term PPI therapy, but H pylori eradication may be additionally offered even in this setting. In contrast, testing for H pylori or PPI therapy is not recommended for chronic NSAID/aspirin users with no ulcer complications or those at a low risk of complications.     

Epidemiology of acute upper gastrointestinal bleeding

Acute upper gastrointestinal bleeding is an important emergency situation. Population-based epidemiology data are important to get insight in the actual healthcare problem. There are only few recent epidemiological surveys regarding acute upper gastrointestinal bleeding. Several surveys focusing on peptic ulcer disease showed a significant decrease in admission and mortality of peptic ulcer disease. Several more recent epidemiological surveys show a decrease in incidence of all cause upper gastrointestinal bleeding. The incidence of peptic ulcer bleeding remained stable. Peptic ulcer bleeding is the most common cause of upper gastrointestinal bleeding, responsible for about 50% of all cases, followed by oesophagitis and erosive disease. Variceal bleeding is the cause of bleeding in cirrhotic patients in 50-60%. Rebleeding in upper gastrointestinal bleeding occurs in 7-16%, despite endoscopic therapy. Rebleeding is especially high in variceal bleeding and peptic ulcer bleeding. Mortality ranges between 3 and 14% and did not change in the past 10 years. Mortality is increasing with increasing age and is significantly higher in patients who are already admitted in hospital for co-morbidity. Risk factors for peptic ulcer bleeding are NSAIDs use and H. pylori infection. In patients at risk for gastrointestinal bleeding and using NSAIDs, a protective drug was only used in 10%. COX-2 selective inhibitors do cause less gastroduodenal ulcers compared to non-selective NSAIDs, however, more cardiovascular adverse events are reported. H. pylori infection is found in about 50% of peptic ulcer bleeding patients. H. pylori should be tested for in all ulcer patients and eradication should be given.     

Role of Helicobacter pylori Infection on Upper Gastrointestinal Bleeding in the Elderly (A Case-Control Study)

Nonsteroidal antiinflammatory drug (NSAID) useis known to be associated with a high incidence of uppergastrointestinal tract bleeding in the elderly. Theincreased prevalence of Helicobacter pylori (HP) infection, which also occurs with age, suggeststhat an interaction between NSAID use and HP infectionmay explain the higher incidence of ulcer complicationsin the elderly. The aim of the present study was to determine if a relationship existsbetween HP infection and NSAID use in elderly patientswith upper gastrointestinal bleeding. This was a case-control study on 146 elderly patients (73/group). The bleeding group consisted of 37 males and 36females (mean age 80.4 years, range 70-96) with symptoms(hematemesis, melena, anemia with loss of more than 3 ghemoglobin), and endoscopic stigmata of bleeding. The control group consisted of 73 age- andsex-matched patients with the same endoscopic diagnosisbut with no endoscopic stigmata of bleeding. NSAID usewas evaluated by interview at the time of endoscopy, and HP infection was confirmed in all cases byhistology and the rapid urease test. Statisticalanalyses were performed using the chisquare test andlogistic regression. In both groups, 46.57% of patients were affected with gastric ulcer, 36.98% withduodenal ulcer, and 16.43% with erosive gastritis. Thebleeding group had a significantly higher percentage ofNSAID users (53.42% vs 19.17%, P < 0.0001) and a lower percentage of HP-positive patients(47.94% vs 72.60%, P = 0.004). The NSAID use pattern wasas follows: occasional users (sporadic, as needed duringthe previous week): 53.8% of bleeding cases and 50% of controls; acute users (continuoustherapy for less than one month): 17.9% of bleedingcases and 28.5% of controls; and chronic users(continuous therapy for more than one month): 28.2% ofbleeding cases and 21.4% of controls. The logisticregression demonstrated that NSAID use was significantlyrelated to an increase risk of bleeding both in gastric(odds ratio: 4.98, 95% CI: 1.83-13.6) and duodenal ulcer patients (odds ratio: 10.2, 95% CI: 2.25-46.7) while HP-positivity presented a significantinverse relationship with bleeding only in subjects withgastric lesions (odds ratio: 0.20, 95% CI: 0.07- 0.55). NSAID use and HP infection were alsoshown to be independent, unrelated factors, with theoverall risk of bleeding in HP-positive NSAID usersidentified to be significantly less than in HP-negative NSAID users. In conclusion, in elderlypatients: (1) NSAID use increases the risk of uppergastrointestinal bleeding while HP infection wasassociated with a low risk for gastric bleeding; and (2)the two factors are independent variables, thereforethe HP-positive NSAID user has a lower risk than theHP-negative NSAID user.     

The association of Helicobacter pylori infection and nonsteroidal anti-inflammatory drugs in peptic ulcer disease.

BACKGROUND AND AIM: Peptic ulcer disease (PUD) affects 10% of the world population. Helicobacter pylori infection and the use of a nonsteroidal anti-inflammatory drug (NSAID) are the principal factors associated with PUD. The aim of the present study was to evaluate a cohort of patients with PUD and determine the association between H pylori infection and NSAID use. PATIENTS AND METHODS: The medical charts of patients with endoscopic diagnosis of PUD were retrospectively reviewed from September 2002 to August 2003. Patients were divided into three groups according to ulcer etiology: H pylori infection (group 1); NSAID use (group 2); and combined H pylori infection and NSAID use (group 3). RESULTS: One hundred two patients were evaluated: 36 men (35.3%) and 66 women (64.7%). Forty patients had H pylori infection, 43 had used NSAIDs and 15 had combined H pylori infection and NSAID use; four patients with ulcers secondary to malignancy were excluded. The frequency of women was significantly higher in group 2 (P=0.01). The mean age of patients in group 1 was significantly lower than in the other two groups (P=0.003). PUD developed earlier in group 3 than in group 2 (5.0+/-4.7 months versus 1.4+/-2.1 months, respectively, P=0.018). Thirty-two patients (32.7%) had bleeding peptic ulcer. Group 2 had a higher risk of bleeding peptic ulcer than the other two groups (P=0.001). CONCLUSIONS: The development of PUD was observed earlier in the combined H pylori and NSAID group than in patients with only NSAID use. This suggests a synergic effect between the two risks factors in the development of PUD.     

Should coronary patients chronically taking a low-dose of aspirin receive gastroprotective agents?]

The use of low-dose aspirin (75-300 mg/day) is associated with an increased risk of gastrointestinal bleeding, which is lower than that observed with common NSAIDs. Risk factors for the development of GI bleeding in patients taking low-dose aspirin are not well defined, although patients with a previous history of peptic ulcer, concomitant NSAID use and serious diseases should receive gastroprotection. Among the available drugs, proton pump inhibitors associated, when present, to Helicobacter pylori erradication, have shown the highest efficacy. The best cost-effectiveness treatment is still undefined.     

Risk and preventive factors of low-dose aspirin-induced gastroduodenal injuries: a comprehensive review

The risk of peptic ulcer complications, particularly bleeding, is increased in association with the use of low-dose aspirin (LDA). Risk factors for upper gastrointestinal (GI) ulcer or bleeding among LDA users include a history of prior GI events, older age, chronic renal failure, combined antithrombotic therapy and nonsteroidal anti-inflammatory drugs (NSAIDs). Helicobacter pylori and aspirin seem to be independent risk factors for peptic ulcer and bleeding. The studies report conflicting findings about the effect of H. pylori infection on NSAID-related ulcers, and proton-pump inhibitors (PPIs) seem to be superior to eradication only to prevent recurrent ulcer bleeding with LDA. Previous studies indicate that hypoacidity related to corpus atrophy, as well as taking PPIs and co-treatment with angiotensin type 1 receptor blockers (ARBs) and statins seem to reduce peptic ulcer among LDA users. In addition, the interleukin-1β (IL-1β)-511 T allele and angiotensinogen (AGT)-20 CC, which work as the high-producer allele of IL-1β and AGT, are significantly associated with ulcer or ulcer bleeding. The SLCO1B1*1b haplotype, which has the highest transport activity, may diminish the preventive effect of statins or ARBs. The data are still lacking and further prospective studies are needed to identify the specific risk or protective factors for upper GI ulcer and its complications associated with LDA.     

Upper non-variceal gastrointestinal bleeding-review the effectiveness of endoscopic hemostasis methods

Upper non-variceal gastrointestinal bleeding is a conditionthat requires immediate medical intervention and has a high associated mortality rate(exceeding 10%). The vast majority of upper gastrointestinal bleeding cases are due to peptic ulcers. Helicobacter pylori infection, non-steroidal anti-inflammatory drugs and aspirin are the main risk factors for peptic ulcer disease. Endoscopic therapy has generally been recommended as the firstline treatment for upper gastrointestinal bleeding as it has been shown to reduce recurrent bleeding, the need for surgery and mortality. Early endoscopy(within 24 h of hospital admission) has a greater impact than delayed endoscopy on the length of hospital stay and requirement for blood transfusion. This paper aims to review and compare the efficacy of the types of endoscopic hemostasis most commonly used to control non-variceal gastrointestinal bleeding by pooling data from the literature.     

Peptic ulcer bleeding: is Helicobacter pylori a risk factor in an endemic area?

BACKGROUND/OBJECTIVE: A high prevalence of Helicobacter pylori infection has been reported in Iran. Although the importance of H. pylori in the induction of peptic ulcer disease is clearly defined, only few studies have addressed its role in bleeding from peptic ulcers. We evaluated the role of H. pylori in peptic ulcer bleeding. METHODS: Patients with acute peptic ulcer bleeding (PUB) and those with peptic ulcer disease without bleeding ('controls') were enrolled. Upper GI endoscopy and rapid urease test were performed in both groups. Histological study for detection of H. pylori was performed in patients with active bleeding, if RUT was negative. Other variables evaluated included sex, age, smoking, previous history of bleeding, non-steroidal anti-inflammatory drugs use, ulcer size, ulcer location, and duration of acid-peptic disease. Multivariate logistic regression analysis was performed to identify independent risk factors. RESULTS: 161 patients with PUB and 287 control patients were enrolled. H. pylori infection was seen more frequently in patients with duodenal ulcer than gastric ulcer (88.9% vs. 60.5%, p< 0.001). Univariate analysis showed that patients with PUB were more often male, older in age, used NSAID, had history of PUB in the past, had ulcer located in the stomach and not in the duodenum, and more often had large ulcer (>1 cm). Logistic regression analysis showed that H. pylori infection was protective in PUB after controlling for confounders (OR 0.41, 95% CI 0.21-0.79), when ulcer location was not entered in the model. A second model including ulcer location (to test for a residual effect) showed that H. pylori infection was not a significant risk factor in PUB (OR 0.61, 95% CI 0.30-1.24). CONCLUSIONS: H. pylori may not be an independent factor in bleeding from peptic ulcers. The lower frequency of this infection in these patients can be described by the higher frequency of bleeding from gastric ulcers, which are less H. pylori related compared with duodenal ulcer.