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Background: Methotrexate-associated lymphoproliferative disorder (MTX-LPD) can present as a benign lymphoid proliferation or a malignant lymphoma in patients taking MTX. Almost 50% of MTX-LPD cases show spontaneous remission after withdrawal of MTX treatment. Studies have suggested that the hyper-immune state of rheumatoid arthritis, the immunosuppressive state associated with MTX, and the carcinogenicity of the Epstein-Barr virus might contribute to MTX-LPD development. Although most cases of MTX-LPD occur at extranodal sites, few cases of MTX-LPD affecting the stomach and duodenum have been reported. To our knowledge, no other study has reported on the endoscopic observations of dramatic withdrawal and appearance of multiple digestive tract lesions in a short period of time. Herein, we report the clinical course and imaging findings of our case, which may be useful for understanding the pathological condition of MTX-LPD., Case Presentation: We describe the case of a 70-year-old woman with MTX-LPD of the stomach and duodenum. Disease regression was temporarily achieved after cessation of MTX treatment; however, it subsequently recurred, and complete response was only achieved after six cycles of rituximab, cyclophosphamide, hydroxydaunorubicin, oncovin, and prednisolone (R-CHOP) chemotherapy., Conclusions: The first-choice therapy for patients taking MTX who develop suspected MTX-LPD should be the withdrawal of MTX treatment. Even after remission is achieved, patients should be kept under careful observation, and if the disease recurs, chemotherapy should be commenced promptly.

Competing Interests: Competing interests: None declared.

Introduction: The association between olmesartan and an enteropathy histologically indistinguishable from untreated celiac disease has recently been described. However, pathogenetic mechanisms leading to villous atrophy, prevalence, natural history and genetic background of this condition have not yet been defined., Patients: We describe here two cases of olmesartan-associated enteropathy and discuss some aspects of the natural history of this condition., Results: In both patients, an infectious episode seems to have triggered the severe malabsorption syndrome which led them to hospitalization. High titer positive antinuclear antibodies with homogeneous pattern were found., Conclusions: Our reports add to a growing body of evidence suggesting that olmesartan-associated enteropathy should be considered in the presence of villous atrophy and negative celiac serology and in the diagnostic algorithm of non-responsive celiac disease.

An 88-year-old woman on long-term intravitreal bevacizumab presented with acute gastrointestinal hemorrhage. She was stabilized and underwent nonrevealing upper endoscopy. She continued to require intermittent blood transfusions, and resulting computed tomography of the abdomen revealed an aortoduodenal fistula. The patient was undergoing treatment for her macular degeneration with intravitreal bevacizumab, an angiogenesis inhibitor frequently used to treat solid organ malignancies. Systemic administration has been associated with serious adverse events, including gastrointestinal hemorrhage, perforation, and fistula formation. Intravitreal bevacizumab has been used off-label to treat macular degeneration, but data on the safety of this therapy are limited. Given her lack of other risk factors, the authors postulate a potential association between intravitreal bevacizumab and aortoduodenal fistula formation in this patient.

Background: Regional chemotherapy is used successfully in the treatment of both primary and secondary malignancies, in particular of the peritoneal surface and the liver, and is currently explored as an attractive approach for patients with locally advanced pancreatic ductal adenocarcinoma. To establish the feasibility and toxicity of regional intra-arterial gemcitabine delivered as a 24-h continuous infusion to the pancreas as a novel treatment option for patients with locally advanced PDAC a phase I clinical trial was conducted., Methods: Between April 2011 and September 2013 six patients with biopsy confirmed, borderline or unresectable pancreatic adenocarcinoma, and having received at least one line of systemic chemotherapy, underwent vascular redistribution of the inflow to the head of the pancreas by arterial coil embolization followed by perfusion catheter placement within the splenic artery. Patients were treated with increasing doses of gemcitabine administered by continuous splenic arterial infusion over 24 h with inter-patient and intra-patient dose escalation scheme. The primary endpoint was toxicity of the intra-arterial gemcitabine regimen and to establish the maximum tolerated dose., Results: Catheter placement and gemcitabine infusion was successful in all patients enrolled to date (n = 6). Four out of six patients experienced catheter tip migration requiring replacement or revision. Patients received a median of four doses of 24-h gemcitabine infusion. Two patients developed grade 3 and 4 duodenal ischemia and upper gastrointestinal bleeding. Median overall survival was 15.3 months and median time to progression was 3 months. Three patients (50 %, n = 3/6) progressed systemically. Two patients had stable disease >4 months following treatment and underwent pancreaticoduodenectomy., Conclusions: While technically feasible to treat locally advanced pancreatic ductal adenocarcinoma, prolonged regional pancreatic perfusion with gemcitabine following pancreatic arterial redistribution carries a high risk for gastrointestinal toxicity. Shorter infusion schedules with frequent on treatment evaluations should be considered for future clinical trials.

Vascular endothelial growth factor (VEGF) receptor tyrosine kinase (RTK) inhibitors are reported to cause reversible mucosal hyperplasia (adenosis) in the duodenum of rats; however, the pathogenesis is not fully elucidated. Using lenvatinib, a VEGF RTK inhibitor, we characterized the histologic time course of this duodenal change in rats. At 4 weeks, there was degeneration and necrosis of Brunner's gland epithelium accompanied by neutrophil infiltration around the affected glands. At 13 weeks, the inflammation was more extensive, and Brunner's gland epithelium was attenuated and flattened and was accompanied by reactive hyperplasia of duodenal epithelium. At 26 weeks, the changes became more severe and chronic and characterized by marked cystic dilation, which extended to the external muscular layer. These dilated glands exhibited morphological characteristics of duodenal crypt epithelium, suggestive of replacement of disappeared Brunner's glands by regenerative duodenal crypt epithelial cells. Similar changes were not present in similar time course studies in dog and monkey studies, suggesting that this is a rodent- or species-specific change. Based on the temporal progression of Brunner's gland lesion, we identify degeneration and necrosis of the Brunner's glands as the primary change leading to inflammation, cystic dilatation, and regeneration with cells that are morphologically suggestive of duodenal crypt epithelium., (© 2014 by The Author(s).)

Therapy with non-steroidal anti-inflammatory drugs (NSAIDs) is a diffcult task. Good anti-inflammatory effect increases the risk of gastrointestinal complications with a frequency of 10-50%. The risk further increases with age (above 60-70 yr), the history of ulcer disease concomitant intake of acetylsalicylic acid, anticoagulants, and glucocorticosteroids. Long-term antisecretory therapy with proton pump inhibitors, e.g., esomeprazole, was shown to be an effective prophylactic tool. This drug maintains the intragastric pH value above 4 for 15 hr on the average. The risk of erosive and ulceraive lesions in the stomach and duodenum significantly decreases by selective cyclooxygenase-2 inhibitors, e.g., coxibs, that however increase the risk of thrombotic cardiovascular complications. The author proposes recommendations on the use of NSAIDs in the patients at risk of serious gastrointestinal and cardiovascular pathology. Naproxen in combination with proton pitmp inhibitors is the drug of choice among NSAIDs. Vimovo is a fixed combination of naproxen and esomeprazole. Results of comparative studies on the efficacy of vimovo and celecoxib are presented along with the data on the safety of this. combination compared with that of naproxen monotherapy

Warfarin is an anticoagulant agent known to have a common complication, bleeding. Intramural intestinal haematoma is an uncommon incidence of warfarin-induced haemorrhage. Abdominal pain is its most frequent symptom and presentation with upper-gastrointestinal haemorrhage is rarely seen. Here, we present a 67-year-old male who was admitted to the hospital with active upper-gastrointestinal haemorrhage. In this case, the cause of bleeding has been attributed to duodenal intramural haematoma due to warfarin overuse., (Copyright © 2013 Arab Journal of Gastroenterology. Published by Elsevier Ltd. All rights reserved.)

In a process of medical care and supervision on staff and military personnel, eliminating the chemical weapons, it was revealed that they are more susceptible to esophagogastroduodenal pathology in comparison with the control group. Moreover, the given pathology has an asymptomatic disease course but associated with high contamination of Helicobacter pylori. Marked inflammation changes, atrophic and fibrosis manifestation and microcirculation dysfunction have been confirmed by histological analysis of gastric mucosa. We supposed that the complex of occupational health risk factors, including possible subliminal toxic influence of eliminated CW components determines this pathological dysfunction. Negative influence of shift work and irregular nutrition rhythm are not excluded. The findings of this research are dictating the necessary of revision of military medical expertise principles and the development of the more effective treatment and prophylactic methods.

ACE inhibitors are the leading cause of drug-induced angio-oedema in the USA. ACE inhibitor-induced intestinal angio-oedema, a much rarer complication of this medication, has been reported. The author reports a patient presenting with a 1-day history of severe abdominal pain. The patient was started on lisinopril 2 days prior to this presentation. Computer axial tomography (CAT) scan of the abdomen demonstrated extensive and marked thickening, and oedema involving the duodenum and proximal jejunum associated with significant mesenteric oedema. Concerns for visceral angio-oedema and a possible association with lisinopril according to the Naranjo algorithm were raised. Lisinopril was discontinued and the patient was treated with antihistamines. The patient improved clinically in the next 24 h and discharged home with education and documentation of this serious allergy. ACE inhibitor-induced visceral angio-oedema is under-reported and most often missed resulting in waste of hospital resources towards working up this clinical diagnosis.

Background: Low-dose acetylsalicylic acid (LDA, 75 mg/day to 325 mg/day) is recommended for primary and secondary prevention of cardiovascular events, but has been linked to an increased risk of upper gastrointestinal bleeding (UGIB)., Objective: To analyze the magnitude of effect of LDA use on UGIB risk., Methods: The PubMed and Embase databases were searched for randomized controlled trials (RCTs) reporting UGIB rates in individuals receiving LDA, and observational studies of LDA use in patients with UGIB. Studies were pooled for analysis of UGIB rates., Results: Eighteen studies were included. Seven RCTs reported UGIB rates in individuals randomly assigned to receive LDA (n=22,901) or placebo (n=22,923). Ten case-control studies analyzed LDA use in patients with UGIB (n=10,816) and controls without UGIB (n=30,519); one cohort study reported 207 UGIB cases treated with LDA only. All studies found LDA use to be associated with an increased risk of UGIB. The mean number of extra UGIB cases associated with LDA use in the RCTs was 1.2 per 1000 patients per year (95% CI 0.7 to 1.8). The number needed to harm was 816 (95% CI 560 to 1500) for RCTs and 819 (95% CI 617 to 1119) for observational studies. Meta-analysis of RCT data showed that LDA use was associated with a 50% increase in UGIB risk (OR 1.5 [95% CI 1.2 to 1.8]). UGIB risk was most pronounced in observational studies (OR 3.1 [95% CI 2.5 to 3.7])., Conclusions: LDA use was associated with an increased risk of UGIB.

Spontaneous small-bowel hematomas most commonly involve the jejunum, followed by the ileum and duodenum, and occur in patients who receive excessive anticoagulation with phenprocoumon/warfarin or who have additional risk factors for bleeding. We report three cases of intramural small-bowel hematoma, all complications of treatment with phenprocoumon, which nowadays is used extensively for therapeutic and prophylactic purposes. Diagnosis can be readily attained by sonography and confirmed using computed tomography. Early diagnosis is crucial because most patients can be treated successfully without surgery. Based on this experience and data from the literature, conservative treatment is recommended for intramural intestinal hematomas, when other complications needing laparotomy have been excluded.

Objective: Perchloroethylene (PCE) is a known animal carcinogen and probable human carcinogen. Dry cleaning exposures, particularly PCE, are also associated with renal toxicity. The objective was to follow-up a cohort of dry cleaners to evaluate mortality and assess end-stage renal disease (ESRD) morbidity., Methods: This study adds 8 years of mortality follow-up for 1704 dry cleaning workers in four cities. Employees eligible for inclusion worked for ≥1 year before 1960 in a shop using PCE as the primary solvent. Life table analyses for mortality and ESRD morbidity were conducted. Only employees alive on 1 January 1977 were included in ESRD analyses., Results: Overall cancer deaths were in significant excess in this cohort (standardised mortality ratio (SMR) 1.22, 95% CI 1.09 to 1.36). Oesophageal, lung and tongue cancers had significant excesses of deaths. Oesophageal cancer risk was highest among those employed in a PCE-using shop for ≥5 years with ≥20 years' latency since first such employment. Deaths from non-malignant underlying diseases of the stomach and duodenum were in significant excess. Hypertensive ESRD morbidity was significantly elevated in the entire cohort (standardised incidence ratio (SIR) 1.98, 95% CI 1.11 to 3.27), and among workers employed only in PCE-using dry cleaning shops for ≥5 years., Conclusion: Employment in the dry cleaning industry and occupational exposure to PCE are associated with an increased risk for ESRD and for cancer at several sites. The employment duration findings for oesophageal cancer and hypertensive ESRD further support an association with PCE exposure instead of lifestyle or socioeconomic factors.

Intramural duodenal haematoma (IDH) is uncommon and usually presents with upper gastrointestinal bleeding. Trauma, anticoagulant therapy, blood coagulation disorders and endoscopic interventions have been reported to cause IDH. IDH secondary to antiplatelet therapy has not been previously reported in the literature. We report IDH secondary to aspirin therapy that was associated with transient obstructive jaundice and acute cholecystitis in a 47-year-old woman. The patient was successfully managed with conservative management.

The purpose of this study was to describe the clinical and gross pathological findings, treatment, and outcome in three dogs receiving deracoxib that developed proximal duodenal perforation and subsequent septic peritonitis. Clinical findings were acute vomiting and anorexia following initiation of deracoxib therapy. Deracoxib dosages ranged from 2 to 3 mg/kg per os q 24 hours. In each dog, exploratory laparotomy revealed duodenal perforations approximately 1 cm orad to the major duodenal papilla. Two out of three dogs survived following exploratory laparotomy. Two of three dogs in the present case series received the approved deracoxib dosage. Dogs receiving deracoxib, even at labeled dosages, should be monitored judiciously for signs of gastrointestinal disease.

We describe a case of 78 year-old woman under anticoagulant therapy who presented abdominal pain, nausea, vomiting and an elevated prothrombin time levels (INR = 9.03). The ultrasound and abdominal CT showed a thickened small bowel wall mainly involving duodenum and jejunum. The endoscopy showed an ecchymotic aspect of duodenum and jejunum. The patient received conservative medical treatment and her symptoms spontaneously subsided.

Objective: To evaluate the type, frequency, and severity of macroscopic small bowel mucosal injury after chronic NSAID intake as assessed by capsule endoscopy (CE), as well as to correlate the severity of gastroduodenal and intestinal damage in these patients., Material and Methods: A prospective, endoscopist-blind, controlled trial. Sixteen patients (14F/2M; age: 57.06 +/- 10.16 yrs) with osteoarthritis (OA) on chronic therapy with NSAIDs underwent CE and upper gastrointestinal endoscopy (UGE). Seventeen patients with OA (9F/2M; age: 57.47 +/- 9.82 yrs) who did not take NSAIDs were included as a control group. A scale ranging from 0 to 2 (0 = no lesions, 1-minor = red spots or petechiae, denuded areas and/or 1-5 mucosal breaks; 2-major = > 5 mucosal breaks and/or strictures, or hemorrhage) was designed to assess the severity of small bowel mucosal injuries., Results: CE found intestinal lesions in 75% (12/16) of patients in the study group and in 11.76% (2/17) of controls (p < 0.01). Seven out of 16 NSAID consumers (43.75%) and none in the control group (0%) had a major small bowel mucosal injury (p < 0.01). The percentages of patients with grade 1 and 2 gastroduodenopathy in the study group, as assessed by UGE, were 37.14 and 23.81%, respectively. There was no significant difference in the rate of major enteropathy between patients with none or minor gastroduodenal injury, and those with major gastroduodenopathy (43.75 vs. 40%; p = N.S.)., Conclusions: Chronic NSAID intake is associated with a high rate of small bowel mucosal injuries. Our data have failed to demonstrate a relationship between the severity of gastroduodenal and intestinal injury.

Lugol's solution is an iodinated agent used for treating thyroid crisis. It is primarily used in diagnostic tests for esophageal diseases. However, Lugol's solution can cause local mucosal injury and hemorrhage. We report, for the first time, a case of 34-year-old man who exhibited severe duodenal hemorrhage induced by Lugol's solution that was used to treat thyroid crisis. The quantity of Lugol's solution used for treating thyroid crisis is much higher than that used for mucosal disease investigation. Clinical practitioners should be aware of gastrointestinal hemorrhage when using Lugol's solution for the treatment of thyroid crisis.

Purpose of Review: This article reviews selected publications related to nonsteroid anti-inflammatory drug (NSAID)-induced gastroduodenal toxicity in recent years., Recent Findings: This article provides a comprehensive review of the latest evidence on the epidemiology of NSAID-induced gastroduodenal injury, recommendations on optimal gastroprotective regimens among patients in need of NSAID, risk stratification approach by considering gastrointestinal and cardiovascular risks, and negative interaction between proton pump inhibitors (PPIs) and clopidogrel., Summary: Current evidence indicates that a PPI and a cyclooxygenase (COX)-2-selective NSAID provides the best gastric protection. In light of potential cardiovascular hazard of NSAIDs, physicians should select an NSAID according to individual patients' cardiovascular risk (i.e., naproxen vs. a nonnaproxen NSAID). The choice of gastroprotective therapy depends on the number and nature of gastrointestinal risk factors. PPI co-therapy is recommended in patients with high gastrointestinal risk on aspirin. Whether there is any clinically important interaction between PPIs and clopidogrel remains uncertain.

Background: Low-dose acetylsalicylic acid (ASA; aspirin; 75-325 mg/day) is effective for the prevention of cardiovascular events, and its use in this indication is rapidly increasing. However, the use of ASA and, indeed, other non-steroidal anti-inflammatory drugs (NSAIDs) is limited by the incidence of adverse gastroduodenal events. OBJECTIVES AND SCOPE: To review the clinical evidence for, and the pharmacodynamic basis of, ASA-induced gastroduodenal toxicity in comparison with NSAIDs, and address the question of whether low-dose ASA is 'safe' from a gastroduodenal perspective. This was a narrative, descriptive review, rather than a formal systematic review., Findings: Adverse gastroduodenal effects, which are well known to occur with NSAIDs, are also prevalent in patients receiving low-dose ASA for cardiovascular protection even at doses as low as 75 mg/day. The risk of gastroduodenal toxicity is particularly high among 'at-risk' low-dose ASA patients (aged >70 years, previous ulcer or upper gastrointestinal bleeding and users of antiplatelets or NSAIDs). There are important differences in the mechanism of ASA-induced gastroduodenal toxicity, relative to NSAIDs. These differences include the effects on the cyclooxygenase (COX)-1 isoenzyme, local effects on the gastroduodenal mucosa specific to ASA and a reduction in platelet aggregation., Conclusion: Data suggest that ASA causes significant gastroduodenal damage even at the low doses used for cardiovascular protection. These effects (both systemic and possibly local) may be pharmacodynamically distinct from the gastroduodenal toxicity seen with NSAIDs. Studies are required to establish strategies for improving the tolerability of low-dose ASA, allowing patients to continue to benefit from the cardiovascular protection associated with such therapy.

Non-steroidal anti-inflammatory drugs (NSAIDs) are the most commonly prescribed drugs worldwide, which attests to their efficacy as analgesic, antipyretic and anti-inflammatory agents as well as anticancer drugs. However, NSAID use also carries a risk of major gastroduodenal events, including symptomatic ulcers and their serious complications that can lead to fatal outcomes. The development of "coxibs" (selective cyclooxygenase-2 [COX-2] inhibitors) offered similar efficacy with reduced toxicity, but this promise of gastroduodenal safety has only partially been fulfilled, and is now dented with associated risks of cardiovascular or intestinal complications. Recent advances in basic science and biotechnology have given insights into molecular mechanisms of NSAID-induced gastroduodenal damage beyond COX-2 inhibition. The emergence of newer kinds of NSAIDs should alleviate gastroduodenal toxicity without compromising innate drug efficacy. In this review, novel strategies for avoiding NSAID-associated gastroduodenal damage will be described.

The herbicide, pendimethalin, is used worldwide, but its acute toxicity is not yet widely known. There have been some reported acute pendimethalin poisoning cases in humans and most of them intentionally ingested the concentrated formulation. We describe a 73-year-old man who developed corrosive gastroduodenal injury after accidental ingestion of the diluted (300 times with water) pendimethalin formulation. He had a history of reflux oesophagitis and had been taking omeprazol (10 mg/day) for a year. He consumed alcohol two hours after the accidental ingestion and then had nausea and epigastric pain. Endoscopy performed three days post-exposure revealed gastroduodenal injury. As he had consumed alcohol every day for years and had no history of gastroduodenal ulcer, the accidental ingestion may be associated with this injury. He was successfully treated by increasing his dosage of omeprazol (20 mg/day) for two weeks. This case indicates that ingestion of a small quantity of pendimethalin can provoke gastroduodenal injury.

An intramural hematoma of the duodenum was first reported in an article in the Lancet in 1838. At least, 90% of cases are caused by blunt abdominal trauma, typically accidents involving bicycles or motor vehicles. Intramural duodenal hematoma is a rare complication of anticoagulant therapy. It occurs in patients who receive excessive anticoagulation with warfarin or who have some other risk factor for bleeding. CT characteristics include circumferential wall thickening, intramural hyperdensity, luminal narrowing, and intestinal obstruction. Early diagnosis is crucial because most patients are treated nonoperatively with a good outcome.