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This study examines the effects of environmental hazards, including tobacco, alcohol/alcohol flush response, areca nut, and Helicobacter pylori (H pylori) infection on upper digestive diseases. This is a multi‐hospital‐based endoscopy‐survey cross‐sectional study. Subjects were received upper endoscopies in outpatient clinics at four hospitals in Taiwan between 2008 and 2013. Biopsy‐based methods or urea breath test were used confirm the status of H pylori infection. In total, 8135 subjects were analyzed. Higher cumulative amounts of alcohol consumption were at higher risk of Barrett's esophagus and esophageal squamous cell carcinoma (ESCC), higher cumulative amounts of tobacco consumption were at higher risk of peptic ulcer, and higher cumulative amounts of areca nut consumption were at higher risk of duodenitis. Alcohol flush response was significant risk for reflux esophagitis and Barrett's esophagus (adjusted odds ratio [aOR] = 1.18 and 1.32, 95% confidence interval [CI] = 1.07‐1.31 and 1.06‐1.65, respectively). H pylori infection was inversely associated with ESCC risk (aOR = 0.20, 95% CI = 0.10‐0.40). In addition, H pylori infection was consistently and significantly risk factors for gastrointestinal diseases, including peptic ulcer, gastric adenocarcinoma, and duodenitis (aOR = 5.51, 1.84, and 2.10, 95% CI = 4.85‐6.26, 1.03‐3.26, and 1.71‐2.56, respectively). Besides the cumulative risk of alcohol, tobacco, and areca nut for Barrett's esophagus, ESCC, and peptic ulcer, respectively, presence of facial flushing was the significant risk for reflux esophagitis and Barrett's esophagus. H pylori infection was positively associated with peptic ulcer, gastric adenocarcinoma, and duodenitis, but inversely associated with ESCC.

An 82‐year‐old man was presented to our hospital due to epigastric and right hypochondrial pain 17 weeks after the initiation of intravenous treatment with nivolumab for recurrent lung adenocarcinoma as multiple lung and sternal metastases. Urgent gastroscopy revealed macroscopic duodenitis such as severe erythema, oedema, black‐coloured erosions, and ulcers located throughout the second portion of the duodenum, which was confirmed by abdominal computed tomography as circumferential thickening of the duodenal wall. Those lesions were pathologically considered as non‐specific inflammation and spontaneously disappeared within a month, suggesting nivolumab‐induced immune‐related adverse events., Immune‐related adverse events usually occur in the colon; however, the duodenum could be affected by the immune checkpoint inhibitors. This is an extremely rare phenomenon that is characterized by pathologically non‐specific inflammation.

Objectives The risk of cytomegalovirus (CMV) reactivation in multiple myeloma (MM) patients treated with bortezomib-based induction regimens is increased following autologous stem cell transplantation (ASCT). There is paucity of data regarding the risk of CMV infections in MM patients who did not receive bortezomib and ASCT. Methods We herein report three cases of heavily pretreated MM patients, receiving daratumumab-containing combination regimens, in whom ASCT had been performed long ago and who recently developed severe CMV-related gastrointestinal disease. Results All the three patients had a prolonged CMV disease course requiring a long-term antiviral treatment. All the patients suffered from CMV colitis. One patient had concurrent CMV duodenitis and another patient had a concurrent CMV retinitis. Conclusion Novel myeloma treatments prolong patient survival and more patients with profound immunosuppression following multiple lines of therapies are seen in clinical practice. These patients may present with opportunistic infections that were rare in the past. Our findings suggest a possible association between daratumumab therapy (in combination with other immunosuppressive therapies) and severe CMV gastrointestinal disease. A longer follow-up is needed to explore long-term side effects of novel agents like daratumumab in newly diagnosed as well as heavily pretreated MM patients.

Lanthanum (La) deposition has been observed in gastrointestinal mucosa of dialysis patients treated with La carbonate to treat hyperphosphatemia in the 6 years since its authorization in Japan. We investigated gastrointestinal biopsies from 112 dialysis patients, and found 15 cases of histiocytic aggregation with crystalloids and one case of duodenitis with histiocyte aggregation without crystalloids in the 30 patients treated with La carbonate. No histiocytic lesions were observed in the 82 patients without La carbonate administration. So far in total 70 cases of La deposition in the alimentary tract have been reported, including our 16 cases. Neither clinical nor histological findings other than histiocytic aggregation were specific in the patients with La deposition. We also compared the groups with and without La deposition, revealing that the daily and total doses of La carbonate showed statistically significant correlations with La deposition. However the causality with their histologic features, e.g. intestinal metaplasia and degree of inflammation, were inconclusive between the two groups. Although no critical symptoms have been reported, it is necessary to accumulate more cases to clarify the mechanism of La deposition, because dialysis patients must take phosphate buffers for a long period.

Purpose Whereas some studies suggest that statins exert a gastroprotective effect against gastrointestinal hemorrhage, others report that statin use is associated with increased risk of gastrointestinal hemorrhage. Aim of report: To investigate the risk of gastrointestinal hemorrhage among statin-users compared with non-users. Methods This was a retrospective cohort study using clinical, administrative, and pharmacy data encompassing October 2003 to March 2012 from patients enrolled in the San Antonio military health care system. Two treatment groups were defined: statin-users (use for at least 90 days) and non-users (never received statin). A propensity score-matched cohort was generated to match statin-users and non-users based on 82 variables. Main outcome measures were defined by the International Classification of Diseases, ninth revision-clinical modification diagnoses codes or procedural codes for gastrointestinal hemorrhage, gastritis/doudenitis, gastroduodenal ulcers, endoscopy procedures, and endoscopy procedures related to gastrointestinal hemorrhage. Results A total of 43 438 patients were identified; 13 626 (31.4%) were statin-users and 29 812 were non-users. We propensity score-matched 6342 non-users with 6342 statin-users. The risk of outcomes was similar between the two groups for gastrointestinal hemorrhage (Odds Ratio [OR]: 1.0; 95% confidence interval [95%CI]: 0.91, 1.11); gastrointestinal ulcers (OR: 0.99; 95%CI [0.80, 1.24]); gastritis/duodenitis (OR: 0.92; 95%CI [0.83, 1.02]); and endoscopic procedures (OR: 1.07; 95%CI [0.98, 1.17]). Conclusion Statin use was not significantly associated with either an increased or decreased risk of gastrointestinal hemorrhage. Choice of statin therapy should not be limited in those patients at risk of gastrointestinal hemorrhage. Copyright © 2015 John Wiley & Sons, Ltd.

SummaryBackground Lymphocytic gastritis (LG) is an uncommon entity with varying symptoms and endoscopic appearances. This condition, as well as two forms of H. pylori-negative gastritis [chronic active gastritis (CAG) and chronic inactive gastritis (CIG)], appears to be more common in patients with coeliac disease (CD) based on single-centred studies. Aim To compare the prevalence of LG, CAG and CIG among those with normal duodenal histology (or nonspecific duodenitis) and those with CD, as defined by villous atrophy (Marsh 3). Methods We analysed all concurrent gastric and duodenal biopsy specimens submitted to a national pathology laboratory during a 6-year period. We performed multiple logistic regression to identify independent predictors of each gastritis subtype. Results Among patients who underwent concurrent gastric and duodenal biopsy (n = 287 503), the mean age was 52 and the majority (67%) were female. Compared to patients with normal duodenal histology, LG was more common in partial villous atrophy (OR: 37.66; 95% CI: 30.16–47.03), and subtotal/total villous atrophy (OR: 78.57; 95% CI: 65.37–94.44). CD was also more common in CAG (OR for partial villous atrophy 1.93; 95% CI: 1.49–2.51, OR for subtotal/total villous atrophy 2.42; 95% CI: 1.90–3.09) and was similarly associated with CIG (OR for partial villous atrophy 2.04; 95% CI: 1.76–2.35, OR for subtotal/total villous atrophy 2.96; 95% CI: 2.60–3.38). Conclusions Lymphocytic gastritis is strongly associated with coeliac disease, with increasing prevalence correlating with more advanced villous atrophy. Chronic active gastritis and chronic inactive gastritis are also significantly associated with coeliac disease. Future research should measure the natural history of these conditions after treatment with a gluten-free diet.

There is increasing evidence to suggest the presence of chronic inflammation in the gastrointestinal (GI) tract of cystic fibrosis (CF) patients. Some CF patients continue to have very severe gastrointestinal symptoms despite conventional CF treatment. In our center, these patients are managed in a CF gastroenterology clinic, jointly with a pediatric gastroenterologist. A number have required GI endoscopy and biopsy. The aim of our study was to characterize these patients and determine whether endoscopy and biopsy changed their management. We reviewed all the patients seen in the CF gastroenterology clinic from 2004 to 2009, who had GI endoscopies performed. The GI symptoms these patients were experiencing included abdominal pain, nausea and vomiting, rectal bleeding, failure to thrive, loose stools, and constipation. Twelve patients had GI endoscopies with mucosal biopsies performed. The median [interquartile range (IQR)] age at referral to the CF gastroenterology clinic was 4 years [0.9-8]. Their body mass index (BMI) was 15.2 [13.7-15.5]. Twenty-five percent were homozygous delta F508. Two patients had previously had meconium ileus as neonates requiring surgical intervention. One other patient had needed abdominal surgery for intussusception. Ninty-two percent were pancreatic insufficient, 25% were chronically infected with Pseudomonas aeruginosa and 17% were on regularly 3 monthly intravenous antibiotics. Of the 10 patients who were able to perform spirometry, FEV1 was 101% [67-125] predicted. Nine of the 12 patients had evidence of mucosal inflammation in their biopsies, including duodenitis with eosinophilic infiltrate, chronic non-specific inactive gastritis, enteropathy with partial villous atrophy, and non-specific colitis. Immunosuppressive and anti-inflammatory therapies were commenced in these nine patients, including prednisolone, azathioprine, methotrexate, ketotifen, mesalazine, and sulfasalazine as well as the use of parenteral nutrition and elemental feeds. All the patients clinically responded to therapy. Five of the patients commenced on anti-inflammatory therapy had repeat biopsies 1-5 years following commencement of treatment and all showed histological improvement of the mucosal inflammation. GI endoscopy with mucosal biopsy has a significant role to play in the management of CF children with severe GI disease. In our study, it influenced the management in the majority of patients with severe GI symptoms. Furthermore, if GI mucosal inflammation is identified on biopsy, management with immunomodulatory agents may be clinically beneficial.

Summary Background Helicobacter-negative gastritis and duodenitis occur more often in patients with inflammatory bowel disease (IBD) than in non-IBD controls. Preliminary evidence suggests that they are particularly common among children. Aim To study the age-specific occurrence of gastritis and duodenitis among paediatric IBD patients. Methods From a computerised database of surgical pathology reports, we selected 344 IBD patients and 4241 non-IBD controls between the age 0 and 21 years, who underwent colonoscopy and oesophago-gastro-duodenoscopy with biopsy results from both procedures. Results Helicobacter-negative chronic active gastritis was found in 2% of controls and 20% of IBD patients (Crohn's disease (CD) 26%, ulcerative colitis (UC) 13%). Duodenitis was found in 2% of controls and 17% of IBD patients (Crohn's disease 28%, UC 8%). Similar prevalence rates were observed in male and female patients. The most striking age-specific patterns were seen in Crohn's disease, with chronic active gastritis being highest in the 5–9 years age-group and declining in all subsequent age-groups. The age-specific rise and fall of duodenitis appeared more protracted, reaching a peak at age 10–14 years and then gradually declining. Conclusions Helicobacter-negative gastritis and duodenitis occur significantly more often in paediatric IBD patients than in non-IBD controls, as well as in adult IBD patients. Such upper gastrointestinal inflammation appears to be particularly common in patients with Crohn's disease.

Background/Aims The upper gastrointestinal (GI) toxicity associated with non-steroidal anti-inflammatory drugs (NSAID) use among cirrhotic patients remains unclear. The objective of this study was to evaluate the risk of upper GI adverse events associated with celecoxib and oral and parenteral non-selective NSAIDs in cirrhotic patients. Methods All the patients aged ≥ 20 years with a diagnosis of cirrhosis hospitalized for variceal bleeding and non-variceal upper GI adverse events (oesophageal, gastric, duodenal ulcer, bleeding; gastritis and duodenitis) in 2006 were identified using ICD-9-CM diagnosis codes from inpatient claims from the Taiwan National Health Insurance Database. In the case-crossover study design, the case period was defined as 1–30 days and the control period as 31–60 days before the date of hospitalization. The information for individual NSAID use was obtained from the outpatient pharmacy prescription database. Adjusted self-matched odds ratios (OR) and their 95% confidence intervals (CI) were estimated with a conditional logistic regression model. Results A total of 4876 cirrhotic patients were included. The adjusted OR (95% CI) was 1.44 (0.89–2.31) for celecoxib, 1.87 (1.66–2.11) for oral non-selective NSAIDs and 1.90 (1.55–2.32) for parenteral NSAIDs overall. Risks were similar for variceal and non-variceal events. Concomitant use of proton pump inhibitors and histamine-2 receptor antagonists tended to decrease the upper GI toxicity associated with non-selective NSAIDs and celecoxib. Conclusion The use of nsNSAIDs but not celecoxib was associated with a two-fold increased risk of variceal and non-variceal upper GI events among cirrhotic patients.

Background: Long-term Helicobacter pylori infection leads to chronic gastritis, peptic ulcer, and gastric malignancies. Indigenous microflora in alimentary tract maintains a colonization barrier against pathogenic microorganisms. This study is aimed to observe the gastric and duodenum microflora alteration after H. pylori infection in Mongolian Gerbils model. Materials and Methods: A total of 18 Mongolian gerbils were randomly divided into two groups: control group and H. pylori group that were given H. pylori NCTC J99 strain intragastrically. After 12 weeks, H. pylori colonization was identified by rapid urease tests and bacterial culture. Indigenous microorganisms in stomach and duodenum were analyzed by culture method. Histopathologic examination of gastric and duodenum mucosa was also performed. Results: Three of eight gerbils had positive H. pylori colonization. After H. pylori infection, Enterococcus spp. and Staphylococcus aureus showed occurrences in stomach and duodenum. Lactobacillus spp. showed a down trend in stomach. The levels and localizations of Bifidobacterium spp., Bacteroides spp., and total aerobes were also modified. Bacteroides spp. significantly increased in H. pylori positive gerbils. No Enterobacteriaceae were detected. Positive colonization gerbils showed a higher histopathologic score of gastritis and a similar score of duodenitis. Conclusions: Long-term H. pylori colonization affected the distribution and numbers of indigenous microflora in stomach and duodenum. Successful colonization caused a more severe gastritis. Gastric microenvironment may be unfit for lactobacilli fertility after long-term H. pylori infection, while enterococci, S. aureus, bifidobacteria, and bacteroides showed their adaptations.

SUMMARY Endoscopy alone, without histology, has poor sensitivity and specificity for diagnosing diffuse mucosal diseases of the oesophagus, stomach and duodenum. Erosive lesions with exudate at the distal end of the oesophagus are a reliable sign of oesophagitis, but are present in only approximately 50% of patients with gastro-oesophageal reflux. Erythema and friability are unreliable are subject to considerable inter-observer variation. Numerous macroscopic abnormalities of the gastric and duodenal mucosa have been identified, but these show no consistent histological pattern.

Background and Aim: To validate an early discharge policy in patients admitted with upper gastrointestinal bleeding (UGIB) due to ulcers. Methods: Patients with gastroduodenal ulcer or erosive gastritis/duodenitis were included in a previous study aiming to develop a practice guideline for early discharge of patients with UGIB. Variables associated with unfavorable evolution were analyzed in order to identify patients with low-risk of re-bleeding. After that, a one-year prospective analysis of all UGIB episodes was carried out. Results: A total of 341 patients were identified in the retrospective study. Variables associated with unfavorable evolution were: systolic blood pressure ≤ 100 mmHg, heart rate ≥ 100 bpm, and a Forrest endoscopic classification of severe. 10% of patients were immediately discharged; however, if predictive variables obtained in the multivariate analysis had been used, hospitalization could have been prevented in 34% of patients. A total of 77 patients were included in the prospective analysis. Although only 19.5% of patients were immediately discharged without complications, 29 patients (37.7%) were theoretically suitable for early discharge. Conclusions: Patients with UGIB who have clean-based ulcers and are stable on admission can be safely discharged immediately after endoscopy. Implementation of the clinical practice guideline safely reduced hospital admission for those patients.

OBJECTIVE: To discover whether scattered white spots (SWS) in the duodenum are related to a specific kind of disease. We also scrutinized other upper endoscopic findings which might be associated with SWS. METHODS: Among the patients who were admitted for upper gastrointestinal system endoscopy, those having the endoscopic appearance of SWS in duodenum were enrolled in this study. In total 107 patients [70 women, 37 men, mean age: 51.6 ± 16.88 years (range: 17-82 years)] were included. At least three duodenal biopsies were taken from each patient and histopathological examinations were done by experienced pathologists. RESULTS: The histopathological examination revealed that 39 (36.4%) patients had intestinal lymphangiectasia (IL), 15 (14%) patients had giardiasis (G) and 30 (28.1%) patients had chronic non-specific duodenitis (CD). Two patients with IL were also found to have G. Twenty patients had both IL and CD. One had both G and CD. G was the least common etiology for SWS in the duodenum. The most common reasons for SWS in the duodenum in this study group were IL and CD, in order of decreasing frequency. There was no significant relationship with the other upper endoscopic findings in all these patients. CONCLUSION: Histopathological examinations should be provided for each patient with SWS in the duodenum to assess the etiology. © 2009 The Authors. Journal compilation © 2009 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology and Blackwell Publishing Asia Pty Ltd.

Reasons for performing study: Based on clinical observation, it is hypothesised that horses with duodenitis-proximal jejunitis (DPJ) that are treated surgically have a shorter duration, smaller volume, and slower rate of nasogastric reflux (NGR) compared to horses treated medically, are more likely to develop diarrhoea than medically managed cases, and have a higher incisional infection rate than a sample population of horses undergoing abdominal exploration for gastrointestinal disease other than DPJ.Objectives: To compare: 1) duration, volume and rate of NGR and the percentage of horses with diarrhoea between medically and surgically treated DPJ cases; and 2) incisional infection rate in horses with DPJ undergoing abdominal exploration to a sample population of horses undergoing abdominal exploration for gastrointestinal disease other than DPJ.Methods: Medical records of cases with DPJ diagnosed 1995-2006 were reviewed. Information obtained included subject details, presenting clinical findings, treatment category (medical/surgical), complications (diarrhoea, incisional infection), and outcome (survival/nonsurvival). Data were analysed using a Chi-squared test and a mixed model analysis of variance. Level of significance was P

Background: Peptic ulcers and erosions (PU&E) are thought to be uncommon in children. Patients with early exposure to Helicobacter pylori may be at a higher risk for early onset PU&E. Children in Israel have a high prevalence and early acquisition of Helicobacter pylori (H. pylori) and have easy access to pediatric gastroenterologists and endoscopy. Our aim was to describe the prevalence and characteristics of PU&E in this population referred by Pediatric Gastroenterologists for an upper endoscopy. Methods: We conducted a retrospective study over the years January 2003–May 2006. Over these years we had information on 751 diagnostic upper endoscopies. PU&E was regarded as erosive gastritis/duodenitis or ulcer in either the stomach or duodenum. H. pylori status was assessed using rapid urease test and gastric biopsies. Results: PU&E was detected in 169 (22.5%) patients (ulcers 51 (6.8%), erosions 118 (15.7%)). One hundred twenty-four had gastric PU&E and 58 had duodenal PU&E. H. pylori was positive in 112 (66.3%). H. pylori-associated PU&E becomes common after age 10 years, with gastric PU&E presenting much earlier than duodenal disease. Most of the H. pylori-negative PU&E were idiopathic and improved symptomatically on PPI treatment. Interestingly, 43% of patients with PU&E in our cohort were either immigrants from the former Soviet Union or of Israeli Arab origin. Conclusions: PU&E appears to be common in this selected population with a relatively high incidence of gastric PU&E. H. pylori associated PU&E becomes common after age 10 years with gastric PU&E presenting much earlier than duodenal disease. Non H. pylori PU&E in children comprises approximately a third of all PU&E, are mostly idiopathic and appear earlier than H. pylori associated PU&E.

Background: Helicobacter pylori is implicated in the etiology of gastric and duodenal ulcer, non-ulcer dispepsia, atrophic gastritis, gastric adenocarcinoma and lymphoma. Methods: Between November 1995 and December 2004, the presence of H. pylori was investigated using the CLO test in 9239 patients who underwent upper gastrointestinal endoscopy at a single institution in Istanbul, Turkey. The results were evaluated as early–late positive, and negative. Results: There were 4667 women (50.51%) with a mean age of 44.5 years (range, 13–90 years), and 4572 men (49.49%) with a mean age of 45.7 years (range, 11–85 years). The CLO test was positive in 41.44% of cases. The most frequent symptoms on admission were epigastric pain (46.2%) and burning (19.6%). The most frequent endoscopic diagnosis was pangastritis (64%) and non-erosive duodenitis (30.5%). The H. pylori positivity was 61.53% during the first 5-year period and 38.47% during the second 5-year period. The H. pylori positivity was significant in patients using non-steroidal anti-inflamatory drugs and tobacco (P

Overnight gastric secretion was studied in 32 patients with acute duodenal ulcers before treatment and whilst taking cimetidine 400 mg b.d. After 6 weeks of treatment with cimetidine 400 mg b.d. 13 patients had healed ulcers, seven patients had healed ulcers but a persistent erosive duodenitis, and 12 patients had persisting ulceration. Inhibition of nocturnal gastric secretion by cimetidine 400 mg b.d. was most profound in patients who healed their ulcers completely; a less profound inhibition of nocturnal gastric secretion was seen in the non-healing and duodenitis groups. In patients with persisting ulcers and poor inhibition of nocturnal gastric secretion by cimetidine, gastric secretion could be suppressed by either cimetidine 400 mg b.d. in combination with pirenzepine 50 mg b.d., or by cimetidine 1600 mg nocte, but suppression of nocturnal gastric secretion was more effective with cimetidine 1600 mg than cimetidine with pirenzepine.

SUMMARY Forty-five patients taking long-term indomethacin and with endoscopic erosions or superficial ulcers in the oesophagus, stomach or duodenal bulb were randomized in a double-blind study to continue with standard indomethacin or receive a ‘delayed-release’ formulation. This consisted of microgranules of indomethacin coated with an acrylic resin, Eudragit L, which releases drug in the small intestine. Endoscopy was repeated after 8 weeks and biopsies taken on both occasions. Changes in endoscopic lesions and histological appearances were similar in both groups, although mucosal erythema was less in those given Eudragit L indomethacin. Systemic, rather than topical, effects of indomethacin may therefore be responsible for persistence of gastro-duodenal mucosal lesions in these patients. There is reason to question the clinical practice of using expensive, delayed-release preparations.

Summary Reasons for perfoming study: Feeding concentrate has been putatively associated with risk of development of duodenitis-proximal jejunitis (DPJ); however, this association has not been evaluated systematically in a controlled study. Objectives: To determine whether there was evidence that feeding practices were associated with increased odds of developing DPJ employing a case control study. Hypothesis: The amount of concentrate fed daily to horses is significantly greater among horses that develop DPJ than control horses with either lameness or other types of colic. Methods: Feeding practices of cases of DPJ diagnosed between 1997 and 2003 were compared with those of 2 populations of control horses (colic controls and lameness controls) admitted to the clinic from the same time period. Following multiple imputation of missing data, comparisons were made using polytomous logistic regression. Results: Horses with DPJ were fed significantly more concentrate and were significantly more likely to have grazed pasture than either control populations; DPJ horses were significantly more likely to be female than were lameness horses. Results were unchanged after adjusting for bodyweight of the horse. Conclusions: Feeding and grazing practices differ among horses with DPJ relative to horses with other forms of colic and lame horses. Potential relevance: The observed magnitudes of association were not sufficiently strong to merit diagnostic/predictive application; however, these observations, if substantiated by other studies, might provide important aetiological clues.

We report three pediatric liver transplant recipients receiving tacrolimus immunosuppression presented with vomiting, heme-positive stools and failure to thrive, who had subtotal villous atrophy in their histology because of food protein sensitivity. Case findings and current literature of the casual relationship between tacrolimus and food allergies briefly reviewed.

Intestinal intraepithelial lymphocytes (IELs) belong to a unique T-cell population interspersed between epithelial cells of both the small and large intestine. It is becoming increasingly recognised that an increased number of IELs with a normal villous architecture is within the wide spectrum of histological abnormalities observed in coeliac disease. An increased number of IELs is the earliest pathological change following gluten challenge and a high IEL count may be the only sign of gluten sensitivity. Therefore, the finding of a raised IEL count with normal villous architecture is of sufficient clinical importance to be reported in routine small bowel biopsies. However, it is evident that not all small intestinal biopsy specimens showing increased IELs are explained by gluten sensitivity. Increased IELs in small bowel mucosa have also been associated with autoimmune disorders, tropical sprue, food protein intolerance, Helicobacter pylori-associated gastritis, peptic duodenitis, parasitic and viral infections, as well as the development of intestinal lymphoma. Histological examination of a biopsy specimen of the small bowel remains the diagnostic gold standard for coeliac disease. There will be an ever increasing demand for histological confirmation of gluten sensitivity in patients in whom the classic microscopic appearance of flattened villi may not have fully developed. The more widespread recognition by histopathologists of the pattern of injury manifested by increased numbers of IELs in intestinal biopsy specimens will certainly help in early diagnosis of coeliac disease, lessen diagnostic confusion and influence the modern practice of gastrointestinal tract medicine. This review discusses some of the recent developments in clinical pathology pertaining to increased IELs in small bowel mucosal biopsies.

Peptic ulcer disease (PUD) can present with many complications including inflammation, ulceration and perforation. Improvements in CT have enabled better imaging of the gastroduodenal area. Three cases of complicated PUD detected on CT are presented with a brief review of the current literature.

Background: Cytomegalovirus (CMV) is considered to be the major cause of upper gastrointestinal (GI) symptoms in organ transplant recipients. In the diagnosis of GI CMV infection the detection of the virus in the mucosa is essential. The aim of the study was to evaluate the significance of CMV, detected in biopsy specimens from stomach and duodenum of solid organ transplant recipients. Methods: Data of 227 elective upper endoscopies on symptomatic organ transplant recipients were evaluated for clinical symptoms, endoscopic changes and conventional histologic alterations of mucosal biopsy samples. Qualitative PCR was performed for detection of the presence of CMV-DNA in each biopsy materials. Results: CMV-DNA was detected in biopsy samples of 91 patients (40.1%) while only in 20 cases (8.8%) the signs of CMV infections were found by conventional histology (p

Objective: Eradication of Helicobacter pylori is effective in preventing ulcer relapse after simple repair of perforated duodenal ulcers. However, when and how the H. pylori status should be determined remains unclear. The study investigated the role of early endoscopic follow up in managing patients with simple omentopexy for duodenal ulcer perforation. Patients and Method: Patients below the age of 75 years who had simple repair of perforated duodenal ulcer were recruited. They were given a 4-week course of H2 receptor antagonist upon discharge and advised to return for a follow-up endoscopy at 8 weeks after operation. During endoscopic examination, ulcer healing and other gastroduodenal pathology were noted. Random biopsies were taken from the antrum and body of the stomach for determination of H. pylori infection. Results: In a 30-month period, 112 patients were admitted with perforated duodenal ulcers. The perforation was repaired by either laparoscopic (n = 41) or open method (n = 71). Eleven patients died during hospitalization. Of the 101 patients who recovered, 16 were lost to follow up. Nine patients were considered unfit for endoscopy as a result of medical comorbidities. Among the 76 patients who attended the follow-up endoscopy, 47 were shown to have H. pylori infection (61.8%). Active duodenal ulcers were found in 15 patients, significant erosions in five patients and severe duodenitis in seven patients. Patients infected by H. pylori had a significantly higher proportion of persistent duodenal pathology compared with the uninfected patients (23/47 vs 4/29; P = 0.003). Multivariate analysis revealed that smoking and H. pylori infection were the two independent factors predicting persistent duodenal lesions. Conclusion: Patients treated with simple closure for duodenal ulcer perforation are recommended to have their H. pylori status determined by early follow-up endoscopy, and an eradication regimen should be prescribed to those who are positive for the infection. Chinese Abstract Figure Chinese Abstract. Figure Chinese Abstract. Figure Chinese Abstract. Figure Chinese Abstract. Figure Chinese Abstract.

Background: Treatment for Helicobacter pylori reduces ulcer recurrence. Eradication rates of the organism vary with different drug regimens from 30% to 90%. There is a need to identify patients who have failed treatment. [14C]-Urea breath test (UBT) is non-invasive, sensitive, safe and highly reliable test for diagnosis of H. pylori infection. As there is a paucity of reports on the utility of [14C]-UBT in confirming H. pylori eradication, this study was undertaken. Methods: Thirty-eight patients (age 34 ± 17 years, range 16–84 years, 27 men) with upper gastrointestinal symptoms underwent upper gastrointestinal endoscopy. Baseline H. pylori infection was diagnosed by identification of the organism on antral biopsies and positive rapid urease test (RUT). After 1 month of completion of treatment, repeat RUT and histological examination of antral endoscopic biopsies were performed. Eradication of H. pylori was defined as absence of the organism on histology, and negative RUT. The [14C]-UBT was performed using 185 kBq [14C]-urea dissolved in 300 mL water. Breath samples were collected once before ingestion of [14C]-urea, and subsequently at 5 and 15 min. Results were expressed as 14CO2/mmol CO2 exhaled as per cent of administered urea. Results: Endoscopy revealed antral gastritis (n = 14), duodenal ulcer (n = 8), duodenitis (n = 2), oesophagitis (n = 1), antral gastritis and duodenal ulcer (n = 3), antral gastritis and duodenitis (n = 7) and normal upper gastrointestinal endoscopy (n = 3). All the 20 patients who were negative for H. pylori on RUT and histology, tested negative for H. pylori on [14C]-UBT. However, of 18 patients shown to have H. pylori infection on RUT and histology, 16 were positive for H. pylori on [14C]-UBT. The sensitivity, specificity, positive predictive value, negative predictive value and accuracy of [14C]-UBT were 100, 89, 91, 100 and 95% respectively. Conclusions: The [14C]-UBT is a reliable indicator of H. pylori eradication after treatment. It can obviate the need for antral biopsies to confirm eradication of H. pylori after completion of treatment.

Aims Helicobacter pylori (H. pylori) eradication rate varies according to the treatment regimen used and other factors, e.g. antimicrobial resistance and patient compliance. The aim of the present study was to evaluate the influence of patient counselling and follow-up on H. pylori eradication rates and to document the effectiveness of a 1 week eradication regimen consisting of lansoprazole (30 mg once daily), amoxicillin (1 g twice daily) and clarithromycin (500 mg twice daily). Methods Seventy-six dyspeptic patients, who at endoscopy were found to have gastritis, duodenitis or ulceration, and a positive H. pylori urease test, were recruited. Patients were randomly assigned to an intervention group (n = 38) or a control group (n = 38). Intervention patients received their medicines via the hospital pharmacy and were counselled (and followed up) by a hospital pharmacist. Control patients were given a standard advice sheet and referred to their GP who prescribed the same therapy. Results Intervention patients exhibited a statistically significant improvement in the H. pylori eradication rate (94.7% vs 73.7%; P = 0.02) and compliance (92.1% vs 23.7; P

Background and Aims: The purpose of this study was to investigate the relationship between gastric metaplasia and Helicobacter pylori in patients with endoscopic duodenitis. Methods: The subjects were 57 patients with endoscopic duodentitis with or without H. pylori-associated gastritis. Biopsy specimens were obtained from the stomach and duodenal bulb to assess the histological findings and H. pylori infection. Gastric metaplasia was divided into three types: complete, intermediate and incomplete, according to the amount of mucus in the metaplastic cells. In 10 H. pylori-positive patients, endoscopic and histological findings of duodenitis were compared before and after eradication of the bacteria. Results: There was no significant difference in the extent of gastric metaplasia or the appearance and severity of endoscopic duodenitis between H. pylori-positive and -negative groups. The complete type of gastric metaplasia was frequently detected in the H. pylori-negative group, whereas the incomplete type was frequently observed in the H. pylori-positive group. After eradication of H. pylori, the incomplete type changed to the complete type with a decrease of histological inflammation. Conclusions: The complete type of gastric metaplasia occurred frequently without H. pylori infection, whereas the incomplete type was frequently associated with H. pylori infection.

BACKGROUND AND AIMS: To verify whether a triple therapy bismuth citrate plus amoxicillin and tinidazole eradicates H. pylori infection in pediatric patients. METHODS: Fifty children (30 females; mean age 12.4 +/- 1.1 years, range 10-15 years) suffering from upper abdominal complaints and Helicobacter pylori (H. pylori)-associated gastroduodenal disease were treated with a 4 week course of ranitidine bismuth citrate (400 mg, twice daily) plus oral tinidazole (20 mg/kg) and amoxicillin (50 mg/kg) for the first 2 weeks. RESULTS: The endoscopic diagnoses were: esophagitis (seven cases), gastritis (six cases), gastroduodenitis (43 cases), duodenitis (one case), gastric ulcer (two cases) and duodenal ulcer (13 cases). Helicobacter pylori was eradicated in 40 (80%) patients and clinical improvement was noticed in 39 (78%) of symptomatic subjects. Duodenal ulcers were healed in all the children, but lymphoid nodular hyperplasia was persistent in all patients, independent of the H. pylori status. The potentially drug-related adverse events (blackening of the tongue, six patients; diarrhea, one patient; disturbance of taste, two patients) were registered in seven (14%) patients and dark stools were observed in 48 (96%) patients. No children withdrew from the study because of either side-effects or clinical laboratory changes. No patient had toxic levels of blood bismuth (values ranged between 2.1 and 5.4 microg/L, mean value 3.4 +/- 1.04 microg/L). CONCLUSIONS: Findings suggest that the present treatment regimen is effective enough in the resolution of H. pylori-associated peptic ulcer disease of childhood.

BACKGROUND To the authors' knowledge, multiple carcinoid tumors of the duodenum have not been reported previously. However, multiple carcinoids in the stomach, ileum, and rectum, which were accompanied by the proliferation of endocrine cells, have been reported in the published literature. METHODS A patient with multiple carcinoids including argyrophilic cell hyperplasia of the duodenum and hypergastrinemia underwent surgery. The resected stomach and duodenum were analyzed histopathologically. RESULTS There were 11 carcinoid lesions, each of which was accompanied by peripheral endocrine cell micronests (ECMs). Increasing gastrin positive cells in the antral region and chronic duodenitis in the duodenal bulb also were observed. The peripheral ECMs usually were adjacent to proliferating argyrophilic cells in the Brunner gland ducts or the crypts of Lieberkuhn, which showed focal pyloric gland metaplasia. CONCLUSIONS In the case presented in the current study, the development of the multiple carcinoid lesions may be strongly related to the presence of multifocal pyloric gland metaplasia, as well as to the trophic action of gastrin, which is present at high levels in the setting of chronic duodenitis. Cancer 2000;89:963–9. © 2000 American Cancer Society.

Background: Few data are available on the efficacy of second-line H. pylori eradication regimens. Aim: To compare the efficacy of either omeprazole or ranitidine in a second-line quadruple regimen in patients with duodenal ulcer or erosive duodenitis. Patients and methods: A total of 37 patients with erosive duodenitis and 119 with duodenal ulcer who have failed eradication of H. pylori with double or triple regimens, without metronidazole, were randomly assigned to receive tripotassium dicitrato bismuthate 600 mg t.d.s. + metronidazole 500 mg t.d.s. + tetracycline hydrochloride 500 mg t.d.s. combined with either omeprazole 20 mg b.d. (group O, 78 patients) or ranitidine 300 mg b.d. (group R, 78 patients) for 14 days. H. pylori eradication was verified by histology, rapid urease test and 13C-urea breath test. Statistics: t-test, χ2-test. Results: A total of 143 patients had a post-treatment endoscopy. Eradication rates were: intention-to-treat: group O 77% (67–87), group R 76% (66–85), P=0.85; per protocol analysis: group O 86% (77–95), group R 82 (71–93), P=0.58. Side-effects were frequent but mild. Conclusions: Omeprazole 20 mg b.d. and ranitidine 300 mg b.d. were equally effective as antisecretory agents combined in a second-line quadruple eradication regimen.

Background: The role of Helicobacter pylori infection in the development of Barrett’s oesophagus and its complications is uncertain. The aim of the present study was to determine the importance of H. pylori infection in this disease by comparing the frequency of oesophageal and gastric H. pylori infection in a group of patients with Barrett’s oesophagus or adenocarcinoma, with the frequency of infection in a control group without Barrett’s disease. Methods: The study group included 160 patients (123 male, 37 female; mean age: 61.2 years) who were classified (according to the highest grade pathological lesion in the oesophagus) as having Barrett’s intestinal metaplasia (IM; 88 patients), Barrett’s oesophagus with low-grade dysplasia (LGD; 28 patients), high-grade dysplasia (HGD; five patients), Barrett’s indefinite for dysplasia (n = 4), and Barrett’s adenocarcinoma (33 patients). A total of 91 of these patients had gastric antral specimens available for study. The control group consisted of 214 consecutive, prospectively enrolled symptomatic patients (122 male, 92 female; mean age: 57.2 years) who underwent upper gastrointestinal endoscopy and in whom Barrett’s oesophagus or Barrett’s adenocarcinoma was not found. A modified Warthin–Starry method was used to detect H. pylori infection. Results: Oesophageal H. pylori infection was found in eight of 160 (5%) patients with Barrett’s oesophagus or Barrett’s adenocarcinoma. Helicobacter pylori organisms in the oesophagus were found only on non-intestinalized cardiac or oxyntocardiac mucosa. All patients with oesophageal H. pylori infection and an antral biopsy available for study had antral H. pylori infection. Gastric antral H. pylori infection was significantly less prevalent in patients in the Barrett’s study group (15/91, 16.5%) than in the non-Barrett’s control group (67/214, 31.3%; Fisher’s exact test, P = 0.01). Patients from the control group with an endoscopic diagnosis of duodenal ulcer, gastric ulcer, gastritis, or duodenitis had a significantly higher prevalence of infection compared with the Barrett’s group, but there was no difference in the infection prevalence in patients in the Barrett’s group and patients with reflux oesophagitis, hiatal hernia, no endoscopic abnormality, or any other diagnosis. Conclusions: Oesophageal H. pylori infection is uncommon in patients with Barrett’s IM, dysplasia, or adenocarcinoma, and may be restricted to non-intestinalized columnar epithelium. Gastric H. pylori infection may have a protective effect for the development of Barrett’s oesophagus.

Purpose— To estimate the incidence of adverse gastrointestinal events in alendronate users. Methods— The computerized pharmacy claims of 12 geographically dispersed United Health Group-affiliated health plans were used to identify 1421 persons who received alendronate prescriptions. The medical claims data of these individuals were searched for subsequent diagnoses of oesophagitis, ulcer of the oesophagus, oesophageal perforation, gastric ulcer, and gastritis/duodenitis. The incidence level was estimated as cumulative incidence and incidence density and their 95% confidence intervals. Results— Thirty-nine persons had a diagnostic code indicating an incident oesophageal or gastric diagnosis of interest, including 22 with oesophagitis, two with oesophageal ulcer, one with gastric ulcer, and 15 with gastritis/duodenitis. Thirteen cases (33.3%) underwent upper endoscopic examination. Five (12.8%) patients were hospitalized. Reflecting alendronate use, 95% of patients were female. The cumulative incidence of oesophageal and gastric events for alendronate users was 3.1% in females, 2.0% in males, and 3.0% overall. The incidence density of a diagnosis of oesophageal or gastric events was 9.0 per 100 woman-years of exposure. There was no significant variation in the cumulative incidence among different age groups. Conclusions— These results suggest the incidence of oesophageal and gastric diagnostic codes is high among alendronate users. Further research is needed to assess the possible association between alendronate and adverse upper gastrointestinal events. Copyright © 2000 John Wiley & Sons, Ltd.

Objective To examine the spectrum of urological complications associated with bladder drainage of pancreatic allografts. Patients and method Between July 1991 and October 1996, 140 consecutive bladder–drained pancreatic allografts were performed and were reviewed retrospectively to determine the spectrum of post-operative urological complications. Ninety-five patients (68%) underwent simultaneous pancreas-kidney transplantation, 35 (25%) had the pancreas transplanted after the kidney, while 10 (7%) had a pancreas transplant alone. The mean follow–up was 35 months. Results Seventy patients (50%) had urological complications necessitating intervention: 17 (12%) had retained foreign bodies, bladder tumours occurred in three, 14 had bladder calculi and 15 (11%) had cystoscopic evidence of duodenitis. One patient developed an arteriovenous fistula and one had a necrotic duodenal allograft. Reflux pancreatitis occurred in six patients. Other complications included urethral stricture (three), urethral erosion (three), epididymitis (three), acute prostatitis (one) and prostatic abscess (one). One patient developed a urethrocutaneous fistula and another developed a vesicocutaneous fistula. In the series, 30 of the 140 patients (21%) required eventual conversion to enteric drainage of their allograft as definitive therapy. Conclusions Pancreatic transplantation with bladder drainage is associated with a wide range of significant urological problems. Although appropriate treatment can resolve most of the complications, this often entails additional operative intervention, which may increase the long-term morbidity or jeopardize graft function. As a result of the severity of these urological complications, some centres use primary enteric drainage as the method of choice for pancreatic transplantation.

Background. The purpose of this study was to determine whether oral immunization of ferret kits with a whole-cell sonicate of Helicobacter mustelae lysate (Hml) and the adjuvant muramyl dipeptide (MDP) would reduce the incidence of natural colonization with H. mustelae and the extent of Helicobacter-associated gastritis by enhancing the host mucosal immune response. Materials and Methods. Between the ages of 4 and 11 weeks, 44 ferret kits were gavaged with Hml and various doses of MDP. The extent of gastritis and duodenitis and the immune response to H. mustelae were evaluated. Results. All kits became colonized naturally with H. mustelae and the majority developed mild to severe gastritis and duodenitis. Kits that received Hml with MDP developed significantly greater inflammation of the gastric antrum and duodenum, as compared to kits vaccinated with Hml alone. Vaccination with Hml and 50 μg of MDP was associated with severe lesions in the proximal duodenum characterized by accumulation of mononuclear inflammatory cells, mucosal erosion, and ulceration. Although serum antibody specific for H. mustelae in 4-week-old kits was approximately 50% of adult levels, a finding attributable to passively acquired maternal antibody, both systemic and mucosal antibody levels became depressed over time despite oral vaccination. The humoral immune response was sufficiently low to prevent detection of any significant dose effect of MDP on antibody levels among experimental groups. Conclusions. Oral vaccination of young ferrets with Hml and 50 μg MDP increased the risk of Helicobacter-associated mucosal ulceration in the proximal duodenum, which was associated with low humoral (but significant cell-mediated) immune responses to H. mustelae. In retrospect, the frequency of vaccination may have suppressed the systemic humoral immune response, thereby promoting mucosal damage by H. mustelae. The 50-μg dose of MDP enhanced the cell-mediated immune response, which indirectly contributed to development of severe lesions. The increased frequency of mucosal damage associated with this vaccination regimen enhances the value of the ferret model for studying duodenal ulceration secondary to Helicobacter infection.

To investigate the prevalence and the significance of Helicobacter pylori duodenal colonization, endoscopic duodenal biopsies were performed in 168 children with chronic abdominal pain, gastroesophageal reflux, gastrointestinal bleeding, and malabsorption syndrome. Helicobacter pylori infection was detected in 68 children (40.4%): in 31 of them H. pylori was present in the gastric antrum, and in 37 in the duodenum also. Duodenitis was observed in 25 children with duodenal H. pylori; gastric metaplasia in 3. Scanning electron microscopy revealed the presence of the micro-organism in 3/13 cases; the bacteria were located in the intercellular spaces and alterations of the epithelial surface were found. In conclusion, H. pylori gastritis in children is often associated with duodenal colonization which can cause duodenitis, and also without gastric metaplasia, which indicates a possible role of the micro-organism in the pathogenesis of the lesions.

The prevalence of peptic ulcer in cirrhotic patients is similar to that reported for the general population. Although gastric acid outputs ar normal or lower in cirrhotic subjects compared with non-cirrhotics, the frequency of non-response to histamine H2-receptor antagonists is higher. Peptic ulcer disease in the cirrhotic seems to pursue a more virulent course compared with that in the non-cirrhotic subject. Peptic ulcer prevalences in patients dying of uraemia or in uraemic patients on maintenance dialysis treatment are comparable with those in the general population. However, the frequency of peptic ulcer, especially complicated ulcer, is increased following renal transplantation. Ulcer complications in this context are associated with a high mortality rate. Pre-transplant risk factors for subsequent development of peptic ulcer remain to be identified and the value of histamine H2-receptor antagonists in prophylaxis is as yet unproven.

The systemic humoral immune response to Helicobacter pylori antigens was investigated in 36 children with recurrent abdominal pain (RAP). H. pylori was cultured and Helicobacter-like organisms (HLO) were seen in six children, three of whom had active and two inactive chronic gastritis. None of these children had endoscopic abnormalities. All sex children had increased IgG antibodies to heat-stable H. pylori antigens which were of the IgG1 and IgG3 subclasses. Using six other IgG tests, four of which were commercially available, two to five H. pylori-positive children were found seropositive. Five of six H. pylori-negative children with inactive chronic gastritis and no endoscopic abnormalities had increased IgM antibody levels in addition to increased or borderline increased IgG antibody levels to H. pylori, indicating activity in a chronic H. pylori infection. Five children without H. pylori and with no morphological changes, but with gastritis or duodenitis by endoscopy, had significantly lower IgG and IgA antibody levels compared to other groups. Six of nineteen children without H. pylori, and with no morphological or endoscopic changes had increased IgG and IgM antibody levels to H. pylori. All H. pylori-negative children were seronegative by the four commercial kits. Overall, 12 (33%) of 36 children with RAP were either H. pylori positive by culture and microscopy or had increased IgG antibody levels to H. pylori, which is significantly different from the 10-14% seropositive rate of asymptomatic children. H. pylori may therefore be a cause of RAP in one quarter to one third of the children with RAP in whom other etiologies of RAP are excluded. Further studies on a large number of children are needed for an extended evaluation of the humoral immune response to H. pylori and for further examination of commercial kits which seem to give a high number of false-negative results.

The medical records of 75 horses with duodenitis-proximal jejunitis (DPJ) were reviewed. Ages, physical parameters, laboratory values, and treatment data were compared between horses surviving DPJ and horses not surviving DPJ (Table 1). Fifty of 75 horses (66.6%)survived. Sixty-six horses (88.0%)were managed with medical treatment alone and nine horses (12.0%) were managed with medical treatment plus surgical intervention. Using a logistic regression model, the association of each of the 19 physical and laboratory parameters with death was evaluated retrospectively in the 75 horses. Three parameters (anion gap, abdominal fluid total protein concentration, and volume of gastric fluid for the first 24 hours of hospitalization) were significantly associated with death by univariate analysis. Using a stepwise multiple logistic regression, two parameters remained significantly associated with death (P> 0.05), anion gap and abdominal fluid total protein concentration. (Journal of Veterinary Internal Medicine 1992; 6:307–311)

Disseminated intravascular coagulation (DIC) secondary to colic was diagnosed in 23 horses. Each horse was categorized retrospectively as to the cause of the colic based on surgical and/or necropsy findings: group 1 consisted of 14 horses with compromised intestine that required resection and anastomosis; group 2 consisted of 3 horses with nonstrangulating intestinal displacement and/or impactions; and group 3 consisted of 6 horses with colic associated with enteritis and/or colitis. Horses were considered to be affected with DIC if at least three of five hemostatic parameters were significantly abnormal: decreased antithrombin III (AT III) values, increased level of fibrin degradation products (FDP), thrombocytopenia, prolonged activated partial thromboplastin time, and prolonged prothrombin time. The most consistent hemostatic abnormalities were decreased AT III activity, increased FDP titers, and thrombocytopenia. Clotting times were more variable and did not always correlate with the presence of excessive hemorrhage. Excessive hemorrhage was present during surgery in seven horses and occurred within 1 to 12 hours after surgery in nine other horses. In addition to treatment of the primary disease, 19 horses received treatment for DIC consisting of heparin and/or plasma or fresh whole blood transfusions. Heparin alone was used in 12 horses. Heparin, in addition to fresh whole blood transfusions or fresh plasma, was administered to four horses. Three horses were treated with plasma alone. Four other horses were not treated specifically for the DIC. Eight horses (34%) survived the acute coagulopathy. Although a greater proportion of the surviving horses received heparin therapy (87.5%; 7/8) than did those that died (60%; 9/15), the difference was not statistically significant (P = 0.345).(ABSTRACT TRUNCATED AT 250 WORDS)

Biopsy specimens were taken from the duodenal bulb and the distal duodenum in 45 duodenal ulcer patients before and after treatment with histamine-2 antagonists, prostaglandin analogues or antacids. After four weeks of treatment, the ulcer had healed in 31 patients. The treatment did not lead to a reduced frequency of helicobacter-associated duodenitis or gastric metaplasia of the duodenal epithelium. We found gastric metaplasia in 52.3% of all biopsy specimens from the duodenal bulb, chronic active duodenitis in 71.9% and helicobacter-like structures in 15.9%. The helicobacter organisms were found only in areas of gastric metaplasia, and an accompanying chronic active duodenitis was found in 94.1%. In the distal duodenum, we observed chronic active duodenitis in 15.0% of the specimens. Here the inflammation was not associated with gastric metaplasia or helicobacter-like structures. These observations support the hypothesis that Helicobacter pylori colonizes the duodenal mucosa only in areas of gastric metaplasia, and that such colonization may lead to an active duodenitis.

A total of 370 children who underwent upper gastrointestinal endoscopy (534 procedures) were retrospectively studied. All procedures were performed successfully. Side effects were demonstrated in only one case (0.2%), which was complicated by perioral cyanosis during the procedure. As to pre-endoscopic medication, it was thought that topical pharyngeal anesthesia alone may well be used for school-age children over 7 years of age, general anesthesia with endotracheal intubation for neonates, and intravenous sedation for infants and younger children. Of 370 patients studied, 70.8% had endoscopic diagnoses. The most common diagnosis was gastritis (136 cases), followed by peptic ulcer (75), duodenitis (29), and esophagitis (20). Several conclusions for indications were drawn from the present study. Pediatric upper gastrointestinal endoscopy is a safe and useful method for diagnostic and therapeutic approach, if adequate pre-endoscopic medication is chosen.

Biopsy specimens from duodenal mucosa in 34 patients with upper gastrointestinal symptoms and endoscopically abnormal mucosa (including duodenitis, active duodenal ulcer, and healed duodenal ulcer) and in 9 patients with histologically normal mucosa were examined histologically for gastric metaplasia and endogenous alkaline phosphatase (AP) activity. Using haematoxylin and eosin (H&E) and periodic acid-Schiff (PAS), we found gastric metaplasia in 91-2 per cent (31 out of 34) of patients with altered duodenal mucosa and in 33·3 per cent (3 out of 9) of patients with histologically normal, non-inflamed duodenal mucosa (P < 0·001). To characterize gastric metaplasia further, histochemical methods for AP activity were applied to duodenal mucosa specimens. No AP activity was detected in complete metaplastic cells, but focal or diffuse loss of AP activity was frequently shown in otherwise normal appearing enterocytes next to metaplastic cell groups. Focal loss of AP activity was also detected in seven out of nine healthy controls ( = 77·8 per cent) which appeared normal when stained with H&E. Our results suggest that the loss of AP activity in enterocytes may be an early marker of developing gastric metaplasia or at least a morphological manifestation of cell damage.

We present here our findings on patients with an elevated lesion of the duodenal bulb. All these patients were treated in our clinics between the years 1984 and 1988. These lesions were present in 36 of 8,802 patients who underwent upper gastrointestinal pan-endoscopy. Two patients had a duodenal carcinoma, 2 an adenoma, and 1 a Brunner's gland adenoma. There were 15 with a hyperplastic polyp, 3 with a heterogenic gastric mucosa, 3 with Brunner's gland hyperplasia, 6 with duodenitis, and 4 with regenerative mucosa. Among these 36 lesions, only 69% (25 lesions) were evident on the upper gastrointestinal X-ray series. Adenoma and Brunner's gland adenoma were of a pedunculated form of the gross type and had an irregular surface mucosa. Both duodenal carcinomas were detected by endoscopic biopsy and were resected. Histologically, these lesions were limited to the submucosal layer and were of the non-pedunculated polypoid form, but there were no other characteristic endoscopic features, in comparison with other elevated lesions. Thus, upper gastrointestinal endoscopy with routine observations of the duodenal bulb plus endoscopic biopsy will lead to a definite diagnosis of these elevated lesions and to the early detection and treatment of this rare malignant lesion.

Sixty-five patients with a clinical suspicion of peptic ulcer disease were evaluated with fluid-aided sonography (US). The results were compared with endoscopic and upper gastrointestinal (UGI) series findings. Fifteen normal volunteers were examined by US only. The stomach and duodenum were both adequately visualized in 12 of the normal volunteers and in 51 of the study patients. US detected wall abnormalities in 21 of 23 patients (91%) with abnormal UGI series and endoscopy in the antropyloric and duodenal regions, although none of the 17 documented ulcers were visible by US. Abnormalities detected with US included increased wall thickness (mean, 12.85 mm), asymmetric thickening of the mucosa and muscularis, spasm, and deformity. US was considered normal in 25 of 28 patients (89%) with normal UGI series and endoscopy. The results suggest that US may be a useful nonstressful procedure in the evaluation of peptic ulcer disease previously diagnosed by UGI series or endoscopy.