Whipple's disease: endoscopic aspects before and after therapy.

This report describes the utility and the advantages of endoscopy in diagnosing and following the course of Whipple's disease. Sixteen patients, diagnosed over a period of 22 years, were identified via pathology records and retrospectively reviewed. Five patients were diagnosed before 1980 by means of peroral suction biopsy of the small intestine. The 11 patients diagnosed after 1980 all had upper gastrointestinal endoscopy and endoscopic small intestinal biopsies. Gross endoscopic lesions were observed in 9 of the 11 patients and disappeared in 5 of 6 treated patients at 6 months. These lesions include erosions, yellow plaques, and a pale yellow shaggy mucosa. The latter two lesions are macroscopically suggestive of Whipple's disease. After endoscopic "healing," periodic acid-Schiff-positive macrophages remained present in the endoscopic biopsies for years. The patients were followed for a median period of 4 years and 5 months. All patients were treated with antibiotics (eight tetracycline alone, four tetracycline + streptomycin + penicillin, and four trimethoprim). Five patients (four of the tetracycline alone group, none of the trimethoprim group) relapsed 2 to 11 years after the initial treatment.     

An?mie bei Patienten mit rheumatoider Arthritis

One of the most frequent extra-articular organ manifestations in rheumatoid arthritis (RA) is anemia. As anemia in RA patients may result in severe symptoms and aggravation of other disease manifestations (e.g. arteriosclerosis), the influence on the course of RA is profound. However, the importance of anemia in RA patients is frequently underestimated. The etiology of anemia in RA is complex. Anemia of inflammation (AI) and iron deficiency anemia, alone or in combination are the most frequent forms of anemia in RA. Changes in iron metabolism are the leading causes of anemia in RA patients and mainly induced by the altered synthesis and function of hepcidin and ferroportin. Hepcidin, a peptide produced in the liver and immunocompetent cells, impairs the expression of ferroportin on iron-secreting cells, thus reducing iron bioavailability. The typical changes of iron metabolism and hepcidin synthesis in RA are induced by proinflammatory cytokines, primarily interleukin-6. Hence, the treatment of RA with cytokine antagonists has significant therapeutic implications on anemia in the context of inflammation and impaired iron metabolism.     

Candida overgrowth in gastric juice of peptic ulcer subjects on short- and long-term treatment with H2-receptor antagonists

Candida overgrowth in gastric juice of peptic ulcer subjects under therapy with H2-receptor (H2-R) antagonists has been detected in 21.4 and 53.8% of cases after short- and long-term treatment respectively, and in 8% of controls. Both types of H2-R antagonists, ranitidine and cimetidine, were equally associated with production of yeasts. The location of ulcers, whether gastric or duodenal, seems to have no influence on fungal growth. Females were more susceptible than males to develop Candida in gastric juice. In the short-term course with H2-R blockers fungal colonization of gastric juice was associated with delay of the rate of ulcer healing. Fungal detection in gastric juice was not associated with mucosal invasion by Candida since in none of the patients who had a biopsy for gastric ulcer was Candida detected by histology.     

Overlooked Management and Risk Factors for Anemia in Patients with Intestinal Beh?et’s Disease in Actual Clinical Practice

Background/Aims

Anemia in patients with inflammatory bowel disease significantly affects the quality of life. The aim of this study was to investigate the frequency of and risk factors for anemia and to describe the management of anemia in patients with intestinal Behçet’s disease (BD) in actual clinical practice.

Methods

We included 64 patients with intestinal BD who visited the outpatient clinic of a tertiary referral center in June 2011 and had available laboratory data for the subsequent 6 months.

Results

Anemia was detected in 26 patients (40.6%). After 6 months, anemia was still present in 14 of these patients (53.8%). The cause of anemia was investigated in eight patients (30.8%), and oral iron supplementation was prescribed to four patients (15.4%). Of these four patients, two (50%) recovered completely within 6 months. Anemia was associated with a high Disease Activity Index for Intestinal Behçet’s Disease (DAIBD, p=0.024), erythrocyte sedimentation rate (p=0.003), and C-reactive protein (p=0.049) in univariate analysis. In multivariate analysis, the factor predictive for anemia in patients with intestinal BD was a higher DAIBD (≥40; odds ratio, 4.08; 95% confidence interval, 1.21 to 13.71; p=0.023).

Conclusions

Although anemia is common in intestinal BD patients, its clinical importance is overlooked in daily practice. Moderate to severe disease activity is predictive of anemia.     

Omeprazole in H2 receptor antagonist-resistant reflux esophagitis

We conducted a retrospective review of 25 patients with severe reflux esophagitis treated with omeprazole because of failure of H2 receptor antagonists to heal their esophagitis. Prior to beginning omeprazole (40 mg/day), all patients were on H2 antagonists for at least 9 months and still had endoscopic evidence of longitudinal (grade II) or circumferential (grade III) distal esophageal ulceration. Omeprazole therapy brought about complete endoscopic healing in 24 of 25 patients (96%). Twenty-three of 24 healed patients were then restarted on H2 antagonists as maintenance therapy. Repeat endoscopy was performed if symptoms recurred. Fourteen of 24 patients (58%) had recurrence of endoscopic esophagitis documented between 26 and 300 days from the time of starting maintenance therapy. Two of these 14 patients opted for antireflux surgery, whereas the remaining 12 were once again given omeprazole, which again resulted in symptom resolution in all patients. These data suggest that most patients with H2 receptor antagonist-resistant ulcerative esophagitis cannot be successfully maintained on H2 antagonists even after the ulcers have been healed with omeprazole. Further studies are required to determine the role of omeprazole compared to other treatments in the long-term maintenance therapy of these patients.     

Anemia management in cancer patients with chronic kidney disease

Anemia is a common complication of cancer and chronic kidney disease (CKD) associated with decreased physical performance as well as poor prognosis for life expectancy. Renal and cancer-induced anemia share common features regarding pathogenesis and therapeutic strategies. It is typically treated with iron substitution, erythropoiesis-stimulating agents (ESA) and in refractory cases with red blood cell transfusions. However, studies of the past few years unveiled numerous setbacks in the use of ESAs. These included a higher risk of cerebrovascular events and increased mortality without the improvement of cardiovascular outcomes in patients with CKD. Moreover, particularly negative results were observed in patients with previous cancer history under ESA therapy. These unfavorable findings have forced the clinicians to reevaluate the management of renal anemia. This led to decrease of ESA usage, while iron substitution and alternative therapeutic options gained more significance. Iron supplementation is also accompanied with certain risks ranging from gastrointestinal complications to severe allergic reactions and increased rate of infections. Furthermore, the evaluation of the long-term safety of excessive iron therapy is still lacking, especially in CKD patients with cancer. In the absence of these clinical studies, this review aims to summarize the currently available therapeutic strategies in anemia management of CKD patients with concomitant cancer.     

Microcytosis in Hodgkin disease associated with unbalanced globin chain synthesis

A review of 162 patients with Hodgkin disease disclosed 36 with microcytic anemia (mean corpuscular hemoglobin values [MCV] less than 80 fl). Three patients had iron deficiency, and one had beta-thalassemia. Of the remaining 32 patients, 24 had microcytic anemia at the time of diagnosis of Hodgkin disease, and ten, including two patients with this finding initially, developed microcytic anemia in association with recurrence of Hodgkin disease. Seven patients with Hodgkin disease and normal MCV had normal alpha-to-beta-globin chain ratios (1.0 +/- 0.14). Seven patients with Hodgkin disease and MCV less than 80 fl had significantly lower alpha-to-beta chain ratios (0.66 +/- 0.05). Twelve normal controls and four with iron-deficiency anemia and MCV less than 80 fl had normal ratios. Anemia was corrected, and MCV returned to normal in all patients who responded to therapy for Hodgkin disease. In the two patients studied sequentially, abnormal alpha-to-beta-chain ratio was corrected along with the anemia.     

Stimulating erythropoiesis in inflammatory bowel disease associated anemia

Anemia is a frequent complication in patients with inflammatory bowel disease (IBD), and is associated with decreased quality of life and increased rate of hospitalization. The primary therapeutic targets of IBD- associated anemia are iron deficiency and anemia of chronic disease. An important prognostic parameter of the success or failure of therapy is the outcome of the underlying disease. Iron deficiency should be appropriately managed with iron supplementation. However, the use of oral iron therapy is limited by several problems, the most important being gastrointestinal side effects leading occasionally to disease relapse and poor iron absorption. Intravenous iron preparations are more reliable, with iron sucrose demonstrating the best efficacy and tolerability. Treatment with erythropoietin or darbepoetin has been proven to be effective in patients with anemia, who fail to respond to intravenous iron. Patients with ongoing inflammation have anemia of chronic disease and may require combination therapy comprising of intravenous iron sucrose and erythropoietin. After initiating treatment, careful monitoring of hemoglobin levels and iron parameters is needed in order to avoid recurrence of anemia. In conclusion, anemia in the setting of IBD should be aggressively diagnosed, investigated, and treated. Future studies should define the optimal dose and schedule of intravenous iron supplementation and appropriate erythropoietin therapy in these patients.     

Zinc Deficiency Anemia and Effects of Zinc Therapy in Maintenance Hemodialysis Patients

Quantitative adjuvant zinc therapy using polaprezinc was performed to examine the correlation between zinc concentration and anemia in maintenance hemodialysis patients to propose appropriate treatment. Anemia and serum zinc concentration were measured in 117 patients with chronic renal failure receiving outpatient maintenance hemodialysis at Tsuyama Chuo Kinen Hospital. Two bags of polaprezinc (containing zinc 34 mg/day) were administered to 58 patients with lower than normal zinc levels (Zn < 80 mg/dl) as adjuvant zinc therapy to assess anemia improvement. Zinc concentration and all anemia parameters showed significant positive correlation, indicating that anemia improves in patients with high serum zinc levels. Regarding the effects of adjuvant zinc therapy for improving anemia, hemoglobin levels were found to increase significantly to the highest value at 3 weeks. During treatment, the dosage of erythropoietin was reduced significantly from baseline at all assessment points. No zinc poisoning from therapy was seen, but two patients had diarrhea (1.9%). Zinc‐treated patients required iron therapy due to the development of iron deficiency. Most maintenance hemodialysis patients suffer from zinc deficiency anemia, and zinc‐based polaprezinc has been confirmed to be an effective and safe adjuvant zinc treatment. Most patients diagnosed as refractory anemia with no response to erythropoietin also suffer from zinc deficiency anemia, many of whom are expected to benefit from zinc therapy to improve their anemia. Possible zinc deficiency anemia should be considered in the treatment of refractory anemia with no response to erythropoietin.     

Management of anemia in patients with congestive heart failure

Anemia is an independent risk factor for adverse patient outcomes. There are no guidelines for management of anemia in patients with congestive heart failure (CHF), despite its high incidence. Four objectives were defined by the International Anemia Management and Clinical Outcomes Expert Panel (AMCO), a multinational group of interdisciplinary experts identified by the Society for the Advancement of Blood Management (SABM) to: determine the prevalence of anemia in outpatients; to determine the prevalence of hospital‐acquired anemia; to assess the impact of anemia management on clinical outcomes such as quality of life and functional status; and to provide recommendations for primary care physicians and specialists for the diagnosis, evaluation, and management of anemia in patients with CHF. Anemia and iron deficiency were confirmed to be highly prevalent in patients with CHF. Intravenous iron therapy improves anemia, cardiac function and exercise tolerance, leading to improvement in quality of life. Anemia management has been demonstrated to be cost‐effective. Clinical care pathways to manage anemia in patients with CHF are recommended as best practices in order to improve patient outcomes. Am. J. Hematol. 92:88–93, 2017. © 2016 Wiley Periodicals, Inc.     

Anemia and chronic heart failure implications and treatment options

Anemia is a common comorbidity in patients with heart failure and is associated with worse long-term outcomes. Although the cause of anemia in heart failure is unclear, the weight of evidence suggests that renal dysfunction, along with neurohormonal and proinflammatory cytokine activation in heart failure, favors the development of anemia of chronic disease, with defective iron utilization, inappropriate erythropoietin production, and depressed bone marrow function. Similarly, the mechanisms by which anemia worsens heart failure outcomes are unknown but may be related to increased myocardial workload. If anemia is a mediator and not just a marker of poor outcomes, correcting anemia could become an important and novel therapeutic target to improve long-term outcomes in such patients. Indeed, several small-sized studies have shown the beneficial effects of empirically treating anemia in heart failure patients with recombinant erythropoietin and intravenous iron. However, the ideal threshold at which therapy should be initiated and the extent of correction considered safe and desirable in the individual patient with heart failure need to be known. These issues become more important because of increasing safety concerns that recombinant erythropoietin therapy for treating anemia may be associated with adverse cardiovascular outcomes in patients with chronic kidney disease and may worsen cancer in patients receiving chemotherapy to treat various types of cancer. Therefore, further prospectively designed studies are required to address some of these questions. Fortunately, 2 large mortality morbidity trials, TREAT (Trial to Reduce Cardiovascular Events with Aranesp Therapy) in patients with chronic kidney disease and RED-HF (Reduction of Events with Darbepoetin alfa in Heart Failure) in heart failure patients, are in progress and are likely to provide definitive answers.     

Management of Anemia and Iron Deficiency in Heart Failure

Anemia is independently associated with an increased risk of mortality and morbidity in patients with heart failure (HF). The diagnosis of anemia should prompt assessment of the underlying cause(s), first by using routine laboratory measurements (i.e., serum creatinine and estimated glomerular filtration rate [eGFR], serum iron, transferrin saturation, ferritin, vitamin B12, folic acid, and thyroid stimulating hormone). In clinical practice, it remains unclear whether using levels of the soluble transferrin receptor in HF patients to assess iron deficiency is warranted. Further investigation should follow these simple tests when judged appropriate (e.g., if occult gastrointestinal blood losses are suspected). Hemodilution may contribute significantly to anemia in patients with advanced HF and may be suspected when signs of hypervolemia are present. Euvolemia should be the first goal in such cases (as always), followed by optimization of the disease-modifying therapies used in HF (angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, β-blockers, or aldosterone antagonists and cardiac resynchronization therapy in selected cases). Erythropoiesis-stimulating agents (ESA) can be used to improve functional capacity in patients with significant chronic kidney disease (CKD), a frequent comorbidity in HF patients. ESA and iron therapy is recommended in patients with moderate-to-severe CKD (eGFR < 60 mL/min/1.73 m²), with a target hemoglobin level of 11.0 g/dL. In a recent randomized, placebo-controlled clinical trial, weekly administration of intravenous iron significantly improved symptoms, New York Heart Association class, quality of life, and exercise capacity in both anemic and non-anemic HF patients. A trend toward fewer hospitalizations was seen in the group treated with intravenous iron. The rates of adverse events were similar in the treatment and the placebo groups. Larger-scale and longer-term studies are needed to establish the safety and efficacy profile of intravenous iron in non-CKD HF patients and in HF patients without anemia. Studies designed to further unravel the pathophysiology of anemia in HF are essential in order to determine 1) novel treatment targets and 2) whether and how the treatment of anemia could improve outcomes.     

Current evaluation and management of anemia in patients with inflammatory bowel disease

Introduction: Anemia is a common extraintestinal manifestation in IBD patients and considerably impacts disease prognosis, hospitalization rates and time lost from work. While iron deficiency anemia is predominant, combinations of hematimetric and biochemical markers enable detection and targeted therapy of other etiologies including vitamin B12/folic acid deficiencies, hemolysis, myelosuppression and pharmacotherapies.

Areas covered: Current literature was searched for articles focusing on etiology, diagnostics and therapy of anemia in IBD. In the light of their own experience, the authors describe the physiology of anemia in IBD and present current evidence endorsing diagnostic and therapeutic options, focusing particularly on non-iron-related etiologies.

Expert commentary: Anemia in IBD is polyetiological, reaching far beyond iron deficiency anemia. While clinicians need to be aware of the increasing pallet of diagnostic tools and therapeutic options, detailed studies are needed to develop more convenient test procedures, long-term treatment and monitoring strategies, and unified guidelines for daily practice.     

Under-diagnosing and under-treating iron deficiency in hospitalized patients with gastrointestinal bleeding

AIM: To determine whether patients hospitalized with gastrointestinal(GI) blood loss anemia are being checked and treated for iron deficiency. METHODS: Retrospective chart review was conducted for all patients admitted to a single tertiary care hospital between 11/1/2011 and 1/31/2012 for any type of GI bleeding. The primary endpoint was the percentage of patients who had their iron studies checked during a hospitalization for GI blood loss anemia. Secondary outcomes included percentage of anemic GI bleeders who had adequate documentation of anemia and iron deficiency, and those who were treated for their iron deficiency. Then we tried to identify possible predictors of checking iron studies in an attempt to understand the thought process that physicians go through when managing these patients. Iron deficiency was defined as Iron saturation less than 15% or ferritin level less than 45 μg/L. Anemia was defined as hemoglobin level less than 13 g/dL for males and 12 g/dL for females.RESULTS: Three hundred and seven GI bleeders were hospitalized during the study period, and 282 of those(91.9%) had anemia during their hospital stay. Ninetyfive patients(30.9%) had iron studies performed during hospitalization, and 45 of those(47.4%) were actually found to be iron deficient. Only 29 of those 45 iron deficient patients were discharged home on iron supplements. Of the 282 patients that had anemia during hospitalization, 50(17.7%) had no documentation of the anemia in their hospital chart. Of the 45 patients that had lab proven iron deficiency anemia(IDA), only 22(48.5%) had documentation of IDA in at least one note in their chart. Predictors of checking iron studies in anemic GI bleeders were lower mean corpuscular volume, documentation of anemia, having fecal occult blood testing, not having hematemesis or past history of GI bleeding. There were no significant differences between the teaching and non-teaching services in any patient characteristics or outcomes. CONCLUSION: Iron deficiency is under-diagnosed, under-recognized even when iron studies were checked, and under-treated in hospitalized patients with GI bleeding.     

Effects of intravenous iron saccharate on improving severe anemia in rheumatoid arthritis patients

Anemia in rheumatoid arthritis (RA) is multifactorial. Iron deficiency, either definite or relative (defect in iron utilization), exists in RA patients with anemia. Intravenous iron therapy is indicated in severe and symptomatic cases or those with conditions precluding use of oral iron, but its safety and long-term efficacy have not been well-established. Forty severe anemic (hemoglobin < 9 g/dL) RA patients with or without demonstrable bone marrow iron stain were enrolled in this study. Fractionated administration of intravenous iron saccharate was undertaken and the median follow-up time was 1 year. All patients exhibited significant elevations of hemoglobin 3 months after treatment, which were more pronounced in the nonstainable iron marrow subjects {median (interquartile range): 3.8 (2.9–4.8) g/dL versus 2.9 (2.0–3.0) g/dL, p < 0.01}. Thereafter, hemoglobin remained at a plateau level that lasted during the observation period. Throughout the whole course, none of the cases exhibited side effects or flare up of disease activities. The use of intravenous iron saccharate, preferably administrated in a fractionated way, is effective in the correction of severe anemia in RA patients, especially those with nonstainable iron marrow.     

Anemia in non-celiac wheat sensitivity: Prevalence and associated clinical and laboratory features

BackgroundPatients suffering from non-celiac wheat sensitivity (NCWS) frequently report extra-intestinal symptoms, such as anemia.AimsWe investigated the prevalence and associated clinical features of anemia in NCWS patients.MethodsData from 244 NCWS patients, diagnosed by double-blind placebo-controlled wheat challenge, were retrospectively reviewed and compared with 2 control groups (celiac disease (CD) and irritable bowel syndrome (IBS)). Furthermore, 31 NCWS anemic patients were prospectively re-evaluated after at least 12 months on the “strict” wheat-free diet (WFD).ResultsAnemia prevalence in NCWS patients was 34.8% (mean hemoglobin 10.4 ± 1.4 g/dl), significantly higher than in IBS (17.4%, P = 0.03), but not in CD ones. The NCWS group, on the whole, had sideropenic-like features with low serum iron and altered iron deposits. Both anemia prevalence and sideropenic-like features were more evident in CD than in NCWS patients, whereas only a few IBS subjects showed such features. Significant differences were found in anemic vs non-anemic NCWS patients as regards to female sex, diagnostic delay, poly/hypermenorrhea, iron deficiency, and higher TSH values. A long-term WFD significantly reduced anemia and improved iron metabolism.ConclusionMicrocytic/hypochromic anemia and altered iron metabolism occur frequently in NCWS and can be treated with a long-term strict WFD. NCWS should be included in differential diagnosis of anemic patients with “functional gastrointestinal troubles”.     

Acid suppression in duodenal ulcer: a meta-analysis to define optimal dosing with antisecretory drugs

FVMany different dosage schedules of antisecretory drugs for the treatment of duodenal ulcer are recommended. The relationship between degree of acid suppression and therapeutic efficacy has not been precisely defined for these drugs. We have examined the association between suppression of intragastric acidity and duodenal ulcer healing rates for a number of therapeutic regimens. For the H2 receptor antagonists alone, the most significant correlation with healing rates was with suppression of intragastric acidity at night (r = 0.926; p = 0.0001). When other classes of drug: high dose antacid, omeprazole and a synthetic prostaglandin (enprostil) were included in the analysis, the closest correlation was with suppression of total 24 hour intragastric acidity (r = 0.911; p less than F0.0001). Stepwise linear regression analysis was used to investigate the relative contributions to healing of suppression of acidity during the day and night. Suppression of nocturnal acidity was found to be the single most important factor in explaining healing rates. No further benefit was obtained with daytime suppression for H2 receptor antagonists; suppression of acidity at night accounted for 86.1% of the observed variation in healing rates among different regimens of H2 receptor antagonists. When all classes of drugs were analysed, inclusion of daytime suppression produced a significant improvement in correlation over nocturnal suppression alone. Drug regimens providing potent suppression of nocturnal acidity produce the highest healing rates in controlled clinical trials. The healing rate for any dose regimen of an antisecretory drug can be predicted from a knowledge of its effect on intragastric acidity. For the H2 receptor antagonists, suppression of nocturnal acidity is the most relevant in this context. Moderate suppression of acidity achieves ulcer healing rates at four to eight weeks which are comparable with those seen with potent suppression at two to four weeks. Increasing degrees of suppression merely accelerate healing.     

Antacids: the past, the present, and the future

Antacids have served us well for over a century. The attitude in the late 1950s to 1970s that antacids should be taken only on demand was unjustified and was based on what can be seen nowadays as misinterpretation of scientific data. Twelve recent endoscopic controlled studies have confirmed the efficacy of antacids in the healing of duodenal ulcer, achieving about 75% healing in 4 weeks. Like H2-receptor antagonists, the efficacy of antacids in the healing of gastric ulcers is controversial, most probably related to the even greater pathogenetic heterogeneity of this condition. Antacids should be given at least four times a day and at least 1 hour after meals, since their therapeutic success most likely depends on neutralization of postprandial acid secretion. In vivo, the newer tablet forms are indistinguishable from the liquid forms in terms of neutralizing efficiency and healing efficacy. The ideal dose is one that neutralizes 400 mmol of acid. Combination with an anticholinergic drug is effective and a recent report suggests that this may lead to longer remission than with H2-receptor antagonists. As a long-term therapy, antacids appear to work but need to be taken in multiple daily doses, a regimen which is unlikely to meet with long-term patient compliance. The success of antacids in duodenal ulcer healing should alert us to the importance of controlling the meal-stimulated acid secretion in ulcer therapy, and to the hard fact that acid is a non-permissive factor in ulcer healing.     

Mechanisms and treatment of anemia in chronic heart failure

Anemia is highly prevalent in patients with chronic heart failure (HF) and is associated with poor clinical outcomes. Multiple mechanisms contribute to anemia in chronic HF, and subnormal compensatory rise in endogenous erythropoietin levels in response to anemia is one contributory factor. Randomized trials with recombinant human erythropoietin therapy in anemic patients with chronic kidney disease and concomitant heart disease have demonstrated a reduction in left ventricular hypertrophy but variable effects on clinical outcome. Preliminary clinical trials in anemic patients with chronic HF demonstrate that erythropoietin therapy is well tolerated and associated with short-term clinical improvement. The optimum target hemoglobin, erythropoietic agent, and dosing regimen, and the role of iron supplementation in patients with chronic HF, are not known. Additional studies are needed to determine the safety and efficacy of long-term erythropoietic therapy in chronic HF patients.     

Role of Helicobacter pylori in ulcer healing and recurrence of gastric and duodenal ulcers in longterm NSAID users. Response to omeprazole dual therapy.

BACKGROUND: The relation between Helicobacter pylori infection and non-steroidal anti-inflammatory drug (NSAID)-associated peptic ulcers remains unclear; in particular, it is not known whether H pylori plays a part in the healing and recurrence of these ulcers. AIMS: To evaluate prospectively in a consecutive series of arthritis patients receiving longterm NSAID treatment the prevalence of peptic ulcer as well as the effect of H pylori eradication on the healing and recurrence of gastric and duodenal ulcer found. PATIENTS: Some 278 consecutive patients underwent gastroscopy with multiple biopsies of the gastric antrum and corpus for histological examination and rapid urease test. One hundred peptic ulcers (59 gastric ulcers, 39 duodenal ulcers, and two gastric ulcers concomitant with a duodenal ulcer) were found. Seventy per cent of these ulcers were H pylori positive. METHODS: According to their H pylori status, ulcer patients were randomised to one of the following treatments: H pylori negative ulcers received omeprazole 20 mg twice daily for four to eight weeks, whereas H pylori positive lesions were treated with omeprazole 20 mg twice daily plus amoxycillin 1 g twice daily (the second of these for the first two weeks) or omeprazole alone for four to eight weeks while continuing NSAID therapy. Patients with healed ulcers were endoscopically followed up for six months after stopping antiulcer therapy while continuing NSAIDs. RESULTS: Endoscopic healing rates for gastric and duodenal ulcers in the three different groups were similar both at four and eight weeks. H pylori eradication did not influence healing, which occurred in 14 of 20 (70%) of patients in whom H pylori was eradicated, compared with 14 of 17 (82%) of patients with persistent infection. Cumulative recurrence rates at six months did not statistically differ among the three different groups (27% in H pylori negative, 46% in H pylori positive, and 31% in those where H pylori was eradicated during the healing phase), although a numerical trend in favour of a higher recurrence rate in infected patients was evident. CONCLUSIONS: H pylori eradication does not confer any significant advantage on the healing of gastric and duodenal ulcers associated with longterm NSAID use. It remains to be established with certainty whether eradication may be helpful in the reduction of recurrence in a specific subset of NSAID associated ulcer.