Severe Gastritis Research Articles

The role of endoscopy and biopsy in the management of severe gastrointestinal disease in cystic fibrosis (CF) patients

AimThere 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 GI...

Value of the Likert Dyspepsia Scale in Differentiation of Functional and Organic Dyspepsia in Children

Dyspeptic symptoms may not allow clinicians to differentiate organic and functional gastrointestinal disorders. According to our dyspeptic patients' answers to dyspepsia questionnaire, we aimed to define the symptom scores directing organic dyspepsia (OD) before upper gastrointestinal endoscopy. One hundred sixty-one patients (ages 10-17 years, mean 13.5 ± 2.3 years, male/female: 2/3) with chronic upper gastrointestinal system symptoms lasting for at least 3 months were enrolled. Patients with predominated reflux symptoms were excluded by 24-hour pH monitoring. Before upper gastrointestinal endoscopy, severity and incidence of 8 gastrointestinal symptoms (epigastric pain, upper abdominal discomfort, retrosternal pyrosis, bitter or sour taste in mouth, halitosis, belching, nausea, and early satiety) were measured by 5-point Likert scale. Total score indicated severity score multiplied by incidence score. Antral biopsy samples were obtained. OD is defined as peptic ulcer, erosive esophagitis, erosive or nodular gastritis, and erosive duodenitis in endoscopy and/or moderate to severe antral gastritis in histology. Functional dyspepsia (FD) is defined as normal findings/mucosal hyperemia in endoscopy and/or mild antral gastritis in antral histology. We evaluated the relation among severity and incidence scores of each dyspeptic symptom in patients with OD or FD. Age, sex, body mass index, drug history, nutritional habits, the quality of life related to dyspepsia were also investigated in patients with OD and FD. According to patients' histological and endoscopic findings, 100 (62%) patients were in the OD group and 61 (38%) patients were in the FD group. Of the dyspeptic complaints, the severity, incidence, and total scores of epigastric pain were significantly correlated with dyspepsia type (respectively, P = 0.042, P = 0.028, and P = 0.005). Of 93 patients who had an epigastric pain severity of 4 and 5 (namely, moderate to severe pain), 65 (70%) patients were in the OD group and 28 (30%) patients were in the FD group. Of 68 patients who had an epigastric pain severity of 0 to 3 (no epigastric pain or mild pain), 33 (48.5%) were in the OD group and 35 (51.5%) were in the FD group, and the difference was statistically significant (P = 0.042). After analyzing the total scores of 8 dyspeptic symptoms, one by one or in different combinations, we could not find a threshold (cutoff) score value that was able to indicate OD definitely. Age, sex, body mass index, and nutritional habits were not significantly different between patients with OD or FD. Nocturnal abdominal pain, pain before meals, and resolution of symptoms after meals or ingestion of antacid drugs were not significantly related to OD. Nocturnal abdominal pain was observed to be higher in the group with moderate to severe gastric inflammation. In the present study, the severity, incidence, and total scores of epigastric pain were significantly related to OD; however, a cutoff value of dyspepsia symptom score for differentiation of OD and FD could not determined. In our study, Likert dyspepsia scale was not beneficial in differentiation of the OD/FD groups. We suggest that the Likert dyspepsia scale should be redesigned for children or the same scale should be applied in a larger cohort of dyspeptic children.

Elevated risk of colorectal adenoma with Helicobacter pylori‐related chronic gastritis: A population‐based case‐control study

This study investigated correlations between Helicobacter pylori infection or chronic atrophic gastritis (CAG) and risk of colorectal adenoma in a population-based case-control study. Subjects comprised asymptomatic, middle-aged, male Japanese factory workers who participated in an annual health check-up program, including cancer screening with colonoscopy. We selected 239 colorectal adenoma cases based on histological evaluation and 239 age-matched adenoma-free controls, and evaluated colorectal adenoma risk according to stage of H. pylori-related chronic gastritis as determined by serum tests for H. pylori antibody titer and pepsinogen. Subjects with colorectal adenoma were more likely to be smokers and have hypercholesterolemia. H. pylori infection was a risk factor for adenoma as a whole (crude odds ratio [OR]: 2.26, 95% confidence interval [CI]: 1.44-3.55). Analysis of distal adenoma cases showed that adenoma risk was significantly increased in the presence of H. pylori infection, but there was no further increase in risk with CAG. In contrast, proximal adenoma risk increased stepwise with the presence and progression of H. pylori-related chronic gastritis and showed a maximal and significant increase with CAG (crude OR: 4.51, 95% CI: 1.43-14.2). Subjects with more extensive and severe gastritis showed still higher risk not only for proximal but also for distal adenoma. H. pylori-related chronic gastritis is likely to be involved in the development of colorectal neoplasms, and its progression appears to increase the risk, particularly for proximal adenomas. Knowing the H. pylori-related chronic gastritis stage will probably be useful for evaluation of risk for colorectal neoplasia.

H. pylori cagL amino acid sequence polymorphism Y58E59 induces a corpus shift of gastric integrin α5β1 related with gastric carcinogenesis

We tested whether cagL amino acid sequence polymorphisms of Helicobacter pylori correlated to clinico-histological outcomes and gastric α5β1 integrin expressions. One hundred forty five patients with H. pylori infection and 47 noninfected controls were enrolled to check gastric integrin α5β1 intensities topographically. The collected isolates were screened for cagL-genotype by polymerase chain reaction (PCR), and assessed for amino acid sequence polymorphisms using sequence translation. Our H. pylori isolates were predominantly (98.6%) cagL-genopositive, 95.8% of which had the RGD motif in their amino acid sequences. The isolates from the gastric cancer (GCA) patients indicated a higher rate of amino acid sequence polymorphisms-Y58 and E59-than those of the non-GCA patients (P < 0.05). The polymorphisms as Y58E59 noted with increased risk of GCA up to 4.6-fold (95%CI: 1.8-11.9). H. pylori-infected patients had higher integrin α5β1 than noninfected patients (P < 0.05). Furthermore, cagL-Y58E59 H. pylori infection predisposed an upward shift in integrin α5β1 (P = 0.007) in the corpus, leading to more severe corpus chronic inflammation (P < 0.05). H. pylori CagL amino acid polymorphisms like Y58E59 correlate with a higher risk of GCA, and may regulate a corpus shift of gastric integrin α5β1 to lead to severe corpus gastritis during gastric carcinogenesis.

A randomized controlled trial of rebamipide plus rabeprazole for the healing of artificial ulcers after endoscopic submucosal dissection

Endoscopic submucosal dissection (ESD) is an increasingly common technique for the resection of early gastric cancers. Although 8 weeks of treatment with a proton pump inhibitor (PPI) reportedly heals most patients with ESD-derived artificial ulcers, it does not heal those with severe atrophic gastritis, for whom there is little data. This study examined whether healing rates of the latter especially were improved by the addition of the non-PPI mucosal healing agent rebamipide after ESD. Patients were randomly assigned to two treatment groups for 8 weeks following ESD: patients in the PPI group received daily rabeprazole alone (20 mg), whereas those in the combination group received daily rabeprazole (20 mg) and rebamipide (300 mg). At the primary endpoint (56 days after ESD) we determined the proportion of patients in whom ulcers had healed to scar-stage (S-stage, complete healing). A pre-specified subgroup analysis examined ulcer healing in patients with severe atrophic gastritis. Overall, progression to S-stage occurred in 54.8% in the PPI group, and 86.7% in the combination group (odds ratio 5.3, 95% confidence interval 1.50-19.02, p = 0.006). Among those patients with severe atrophic gastritis, healing to S-stage occurred in 30.0% in the PPI group, and in 92.9% in the combination group (odds ratio 30.3, 95% confidence interval 2.63-348.91, p = 0.0023). Treatment with a PPI plus rebamipide improved healing rates at 8 weeks for patients with ESD-derived artificial ulcer, and appeared to be particularly effective for patients with severe atrophic gastritis.

IL‐9 is a Th17‐derived cytokine that limits pathogenic activity in organ‐specific autoimmune disease

IL-9 is a pleiotropic cytokine with key functions in tolerance and inflammation, and its expression is considered a hallmark of Th2-lineage cells. Here, we report that human and mouse Th17 cells are a significant source of IL-9. The expression of IL-9 by Th17 cells was strictly dependent on the presence of TGF-β and IL-1β, and inhibited by IL-4. IL-9-deficient Th17 cells induced more severe autoimmune gastritis following transfer to nu/nu recipient mice. Th17 cells did not appear to be the target of IL-9 bioactivity as Th17 expansion and differentiation was comparable using IL-9-deficient CD4(+) cells or when IL-9 was neutralized with antibodies in vitro. However, reduced mast cell activity was associated with the increased pathogenicity of IL-9-deficient Th17 cells. Together, these results demonstrate a previously unappreciated role for IL-9 in dampening the pathogenic activities of Th17 cells.

Molecular Aspects ofH. pylori-Related MALT Lymphoma

Helicobacter pylori-related extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue is a paradigm for malignancy arising in an inflammatory background. While the diagnosis of H. pylori gastritis is often straightforward, distinction between severe gastritis and early lymphoma can be difficult and requires careful assessment of clinical findings in addition to histological features and immunohistochemical results. A number of cytogenetic abnormalities have been discovered in H. pylori-related lymphomas and several have clinical importance, related to the responsiveness of lymphoma to H. pylori eradication therapy, but routine molecular studies are not widely utilized. While molecular methods may be used in equivocal cases, a trial of conservative therapy is warranted given the propensity for these lymphomas to regress with eradication of the organism. Once therapy is initiated, care must be taken to avoid a premature assignment of disease refractoriness because complete response can take several months to more than a year. Cases truly refractory to H. pylori eradication therapy may be treated with adjuvant chemoradiation with a high response rate.

Lesions associated with plerocerci (Platyhelminthes: Cestoda: Trypanorhyncha) in the gastric wall of a cownose ray, Rhinoptera bonasus (Mitchill), (Myliobatiformes: Rhinopteridae) from the northern Gulf of Mexico

We describe lesions associated with a seemingly intense infection of trypanorhynch plerocerci (Platyhelminthes: Cestoda: Trypanorhyncha) in the gastric wall of a female cownose ray, Rhinoptera bonasus (Myliobatiformes: Rhinopteridae) captured in the northern Gulf of Mexico. Grossly, the multitude of encapsulated, encysted plerocerci imparted a bumpy and cobbled appearance to the serosa of the stomach, and none was observed in any other tissue during routine parasitological necropsy. Histologically, the plerocerci were associated with severe intramural granulomatous gastritis, vascular ectasia and mesothelial polyposis with the exclusion of the mucosa. To our knowledge, this is the first published case study documenting platyhelminth-associated histopathological changes in the gastrointestinal tract of R. bonasus as well as that of the efficacy of immunocytochemical markers for smooth muscle actin, Factor VIII, S-100, and proliferating cell nuclear antigen in Myliobatiformes. It also may serve as a potential primer for much needed ecological investigations regarding the potential role of elasmobranchs as intermediate or 'paratenic' hosts in the life cycles of trypanorhynch cestodes.

How to assess the severity of atrophic gastritis.

Atrophic gastritis, is the main consequence of long-standing Helicobacter pylori infection, and is linked to the development of gastric cancer. The severity of atrophic gastritis is related to the lifetime risk of gastric cancer development, especially in terms of its degree and extent of mucosal damage. Therefore, it is important for clinicians to assess the severity of atrophic gastritis, interfere with the disease progress, and reverse gastric mucosal atrophy. In the article, we demonstrated some methods (conventional endoscopy, modern endoscopic technology and noninvasive methods) that may help assess the severity of atrophic gastritis and select the reasonable treatment protocols.

Unexpected Death in a Heart Transplant Recipient

Patient: 55-year-old Hispanic male Chief Complaint: Three weeks pre-mortem: pleuritic chest pain, shortness of breath, and fatigue. History of Present Illness: The patient presented for routine monitoring of his heart transplant and complained of body weakness and positional chest discomfort. An echocardiogram showed a large pericardial effusion. A pericardiocentesis was performed and 550 mL of serosanguinous fluid was removed. Following pericardiocentesis, his symptoms improved temporarily. His condition worsened over the next 3 weeks, and he died. Past Medical History: Ischemic cardiomyopathy treated with a heart transplant 1 month prior to hospitalization, type II diabetes mellitus, hypertension, hyperlipidemia, severe gastritis, and status-post cholecystectomy. He was currently taking tacrolimus, mycophenolate mofetil, and prednisone to prevent rejection of his heart allograft. At presentation, a level of tacrolimus measured at its trough was supratherapeutic. Family History: The patient’s father and brother have a history of coronary artery disease. Social History: The patient is an ex-smoker, who quit 20 years ago (10 pack years). He denies alcohol and illicit drug use. He was a landscaper until the month before his heart transplant. Autopsy Findings: 1. Solid white embolus filling the left anterior descending coronary artery. There were multifocal white areas consistent with acute ischemia, most notable in the distribution of this artery (Image 3A and Image 3B). Multiple sections of myocardium at autopsy showed no change in his grade of cellular rejection, and confirmed the absence of humoral rejection. 2. The pleural surfaces of the lungs show multi-focal fibrous patches consistent with adhesions (Image 3C). The lungs were diffusely congested, and the tracheobronchial tree was free of obstructions. There were bilateral serosanguinous effusions, totaling more than 2 liters. 3. Bile-stained liver (1300 g) with centrilobular necrosis and perisinusoidal fibrosis. Laboratory and Pathology Findings: A number of abnormal laboratory values were identified 1 day premortem (Table 1). A cardiac …

Autofluorescence imaging for predicting development of metachronous gastric cancer after Helicobacter pylori eradication

Although Helicobacter pylori eradication decreases the incidence of metachronous gastric cancer after endoscopic treatment for early gastric cancer (EGC), metachronous cancer still develops after successful eradication, particularly in patients with severe corpus gastritis. We investigated whether the extent of atrophic fundic gastritis diagnosed by autofluorescence imaging (AFI) videoendoscopy is predictive of development of metachronous gastric cancer after H. pylori eradication in patients treated with endoscopic submucosal dissection (ESD) for EGC. A total of 82 patients who underwent ESD for EGC from 2003 to 2006, who received eradication therapy participated in this study. The extent of chronic atrophic fundic gastritis was evaluated by AFI and categorized into closed and open type. The main outcome was the incidence of metachronous gastric cancer detected by annual surveillance endoscopy. During a median observation period of 55 months, metachronous gastric cancer developed in 12 of 82 patients (14.6%). Multivariate Cox's proportional hazard analysis revealed that open-type, atrophic fundic gastritis diagnosed by AFI was significantly associated with development of metachronous gastric cancer (hazard ratio: 4.88, 95% confidence interval [CI]: 1.32-18.2, P = 0.018) after adjustment for age, sex, histological intestinal metaplasia, serum pepsinogen level, and H. pylori status. Metachronous EGC developed after successful H. pylori eradication, and extensive atrophic fundic gastritis diagnosed by AFI was a significant predictor, thus it could identify patients undergoing ESD for EGC who still required intensive surveillance after eradication.

Long‐Term Statin Therapy Affects the Severity of Chronic Gastritis

Helicobacter pylori (H. pylori) is a major cause of chronic gastritis. Statins have several pleotropic effects and their mechanisms of action could be related to anti-inflammatory, antioxidants, and immunomodulatory effects. To determine whether statin therapy affects the severity of chronic gastritis. In a retrospective study, we evaluated 516 patients who underwent upper endoscopy. One-hundred and ninety-eight patients had chronic gastritis, The 198 patients with chronic gastritis were divided into two groups: group 1 comprised patients with a history of statin therapy and group 2 comprised patients with no history of statin therapy. Both groups were compared for age, gender, body mass index (BMI), underlying diseases, drug therapy, alcohol consumption, smoking and the serum levels of C-reactive protein (CRP). The presence of H. pylori was determined by gastric biopsy and rapid urease test. The grade and severity of gastritis were assessed using the updated Sydney classification system in two gastric biopsy specimens that were taken from each participant in each group. Of the 198 patients with chronic gastritis, 49% of the patients had mild gastritis and 51% had moderate to severe gastritis. From the results of a multiple logistic regression analysis after adjusting for confounding variables that included age, gender, and BMI, we found that elevated serum CRP levels (odds ratio (OR) 2.33; 95% confidence interval (CI) = 0.8-2.6, p = .02), H. pylori (OR 1.99; CI 0.14-2.4, p = .04), and the use of statin (OR 1.64; CI = 0.71-1.77, p = .05) independently predict the severity of chronic gastritis. Long-standing statin therapy may reduce the severity of chronic gastritis. Mild increased CRP levels in absence of obvious source can predict the severity of chronic gastritis. Further researches are needed to assess the effect of statin in chronic gastritis.

Topography of gastritis and its severity in 864 first degree relatives of gastric cancer patients.

Studies on gastric mucosal histological findings among first degree relatives (FDR) of gastric cancer (GC) patients are scarce. The aim is to evaluate the topography and the severity of gastritis among FDR of GC patients. A total of 989 subjects who were FDR of GC patients, ages 40-65 years underwent gastroscopies. When no gross lesion was found, five specimens were evaluated according to the Sydney Classification and one for urease testing in order to determine the type of gastritis and its severity. Of the 989 subjects, 107 had significant lesions, including two with GC and one with esophageal cancer. The 864 subjects who had complete morphological data taken from five gastric areas (two from the antrum and three from the corpus) comprised 419 males (mean age 48.5±7 years) and 445 females (mean age 47±6.4 years). The H. pylori rate was 76.6%. Normal mucosa was seen in 6.9%, antrum-restricted gastritis in 7.4%, antrum-predominant gastritis in 63.5% and corpus-predominant gastritis in 20% (both had >80% H. pylori infection) and corpus-restricted gastritis in 2%. More atrophy was seen in the antrum and corpus of FDR females than males. The severity did not differ between those with one or more GC patients' relatives. Forty-nine percent of FDR had atrophy and 9.4% intestinal metaplasia (IM) in the corpus. After the age of 40, there was progression of intestinal metaplasia from 12.2 to 27.3% in the antrum and from 6.7% to 26.2% in the corpus during two decades. No high grade dysplasia was found in this mid-age population. Only one-fifth of FDR have H. pylori-induced corpus-predominant gastritis who are at risk for cancer and suitable for eradication. Corpus-restricted gastritis is a rare disease in this area.

Helicobacter pylori infection and the severity of gastritis are not associated with iron deficiency in a group of Brazilian patients

Helicobacter pylori (H. pylori) infection has been associated with iron deficiency anemia. However, results reported in the literature are contradictory. The goal of the present study was to study the possible association between H. pylori infection and iron deficiency in a sample of adults. One hundred and fifty individuals were studied (H. pylori-positive n=75; H. pylori-negative n=50). The presence of anemia was determined using red cell indices and reticulocyte hemoglobin content (CHr). Iron status was assessed based on serum iron and ferritin levels. Possible involvement of inflammatory activity in erythropoiesis was investigated by measuring the correlation between C-reactive protein (CRP) and red cell indices and iron status. There were no significant differences in the hematological or biochemical parameters for the two groups. Iron deficiency was diagnosed in six individuals, but no difference in prevalence was found between the H. pylori-positive and H. pylori-negative groups. A weak but significant inverse correlation was observed between CRP and CHr concentrations and between serum gastrin and CHr in the H. pylori-positive group. These results suggest a reduction in iron availability for reticulocyte hemoglobinization, but insufficient to cause anemia. H. pylori infection was not a determining factor for development of iron deficiency in our study population.

A Woman with Black Spheres in Her Stomach

Purpose: Selective internal radiation therapy (SIRT) delivers targeted, high dose intra-arterial radiation to liver tumors via beta radiation-emitting Yttrium-90 microspheres, sparing contiguous hepatic parenchyma and adjacent viscera. However, inadvertent radiation injury to abdominal organs may occur. We report a case of radiation-induced gastric ulceration to alert clinicians to the diagnostic difficulties and diverse clinical spectrum associated with this underappreciated and potentially catastrophic complication of SIRT. A 57 year-old woman with stage IV breast cancer including liver and lung metastases presented in Jan. 2010 complaining of 2 months of worsening nausea and vomiting. She had received chemotherapy in Nov. 2009, consisting of 5-FU, gemcitabine, cyclophosphamide and trastuzumab; that month she also received SIRT with Yttrium-90 microspheres, a targeted radioembolization treatment aimed at her liver metastases. She was hospitalized elsewhere in early Dec. 2009 for nausea and vomiting, treated symptomatically with ondansetron, and discharged. On exam, vital signs were normal, physical exam was unremarkable. CBC and basic chemistries were normal. Abdominal CT scan: diffuse gastric antral thickening. A GI consultant performed UGI endoscopy: diffuse, severe gastritis and extensive, circumferential antral ulceration. Overlying blood clots and duodenal bulb ulcerations were also present; biopsies were taken. On histologic examination, black, spherical foreign bodies, consistent with Yttrium-90 microspheres, were visualized, documenting radiation gastritis and extrahepatic dissemination of radioactive particles. She received IV omeprazole and steroids, which improved symptoms. The patient was discharged home on a steroid taper, liquid hydromorphone, lorazepam, and ondansetron. GI complications of SIRT involving Yttrium-90 microspheres have been reported to be as high as 8%. Diverse sequelae of radiation damage may occur, including esophagitis, gastroduodenal ulceration, acute cholecystitis, pancreatitis, and small bowel obstruction or perforation. Mechanisms of unintended microsphere spread may include unrecognized vascular variants, collateral circulation, or changes in flow dynamics during infusion. Misdiagnosis and diagnostic delay of these potentially fatal complications of SIRT are common, as this case illustrates. Reasons for delay include non-specific, diverse symptoms which may be immediate, early or delayed as long as a year. These complaints may be attributed to widespread malignancy or chemotherapy. Clinicians must consider radiation-associated toxicity in SIRT-treated patients developing abdominal symptoms.

Comparison of Endoscopically Evaluated Etiologies of Upper GI Bleeding of Adult Sri Lankans with International Studies Admitted to a Medical Unit of a Tertiary Care Center

Purpose: To compare etiology of upper GI bleeding affecting adult Sri Lankans, with results of international studies, admitted to a medical unit of a tertiary care center. Methods: Case notes of 1500 patients who had undergone upper GI endoscopy for varices from 13.3.2002 to 13.2.2004 were retrospectively analyzed and those who had clinical evidence of upper GI bleeding were selected.Table: [1394]Results: A total of 345 patients had upper GI bleeding with a male:female ratio of 229:114 (2:1). The majority was in the 51-70 age range. Endoscopy showed presence of severe antral gastritis with duodenitis, esophagitis, peptic ulcer disease, esophageal varices, pangastritis, erosions and malignancies in 48%, 28%, 28%, 32%, 15%, 17% and 5% of the instances, respectively. Vast majority showed overlapping pathologies. Only about 50% of the varices showed evidence of bleeding. 12% showed negative endoscopies. 10% were on NSAIDS and 9% were alcohol abusers. The table below depicts a comparison of above etiologies with several international studies. Table 01 is a comparison of causes of UGIB of other published studies with the current data. Conclusion: Upper GI bleeds are a major cause of acute medical admissions in Sri Lanka constituting about 25% of the endoscopy work. Amongst aetiological lesions of upper GI bleeding, AGML, osophagitis, and varices had been the major pathologies in this part of the world, in contrast to the West. NSAIDs and alcohol had been important associated contributory factors and there was a clear male preponderance in the bleeders. National and regional guidelines should be formulated based on these observations to educate general public of the contributory factors, mainly alcohol and NSAIDs.

PA35 HISTOLOGICAL EVALUATION OF GASTRIC MUCOSA IN COELIAC DISEASE CHILDREN AND ADOLESCENTS. THE ROLE OF APCA DETECTION

Objectives: Lymphocytic gastritis (LG) has been described in coeliac disease (CD) patients and in patients with Helicobacter pylori (Hp) infection but the pathogenetic mechanism remains unknown. Aims: The aim of our study was to evaluate the characteristics of the gastric mucosa and the prevalence of lymphocytic gastritis in a large series of CD children and adolescents. Methods: 167 CD children at the diagnosis (F 108; range 11 months–18 years), consecutive performing the upper-intestinal endoscopy at our Department over the period Jan 2008-Dec 2009, were enrolled. Duodenal (2 bulb and 4 distal duodenum samples) together with gastric antral biopsies, were performed. CD diagnosis was performed according to the NASPGHAN criteria. Hp infection was diagnosed by histology and the rapid urease test. Gastric lesions and duodenal biopsies were classified according to the modified Updated Sydney System and to the modified Marsh classification, respectively. Anthropometric and clinical data of each patient were registered at the diagnosis. Moreover, gastric parietal cells antibodies (APCA) were determined with an ELISA. Results: Gastric alterations was found in 38/167 CD children (23%). Particularly, lymphocytic gastritis was found in 13 CD patients (7.8%); superficial chronic gastritis (SCG) was detected in 24 celiacs (14.4%); and one child (0.6%) showed severe interstitial chronic gastritis (ICG). 3/38 children (one with LG, one with SCG and one with ICG) presented Hp infection. Ten patients with LG were symptomatic (7 typical and 3 atypical) while four were silent. Among patients with SCG, 16 children were typical, 5 atypical and 3 silent, and the prevalent symptoms were diarrhoea, abdominal pain and low weight growth. In the table are shown histological grading of the gastric mucosa in LG and SCG patients. The most frequent duodenal lesion, total villous atrophy (Marsh 3C), was detected in 100% and 92% of LG and SCG CD patients. Among CD children, no APCA were found in patients without gastritis, while 3/22 with gastric lesions were positive for APCA (one with mild LG and the other two with mild SCG).

PA37 RETROSPECTIVE ANALYSIS OF COAGULATION DISORDERS IN CHILDREN AND ADOLESCENTS WITH COELIAC DISEASE AT DIAGNOSIS

Objectives: Lymphocytic gastritis (LG) has been described in coeliac disease (CD) patients and in patients with Helicobacter pylori (Hp) infection but the pathogenetic mechanism remains unknown. Aims: The aim of our study was to evaluate the characteristics of the gastric mucosa and the prevalence of lymphocytic gastritis in a large series of CD children and adolescents. Methods: 167 CD children at the diagnosis (F 108; range 11 months–18 years), consecutive performing the upper-intestinal endoscopy at our Department over the period Jan 2008-Dec 2009, were enrolled. Duodenal (2 bulb and 4 distal duodenum samples) together with gastric antral biopsies, were performed. CD diagnosis was performed according to the NASPGHAN criteria. Hp infection was diagnosed by histology and the rapid urease test. Gastric lesions and duodenal biopsies were classified according to the modified Updated Sydney System and to the modified Marsh classification, respectively. Anthropometric and clinical data of each patient were registered at the diagnosis. Moreover, gastric parietal cells antibodies (APCA) were determined with an ELISA. Results: Gastric alterations was found in 38/167 CD children (23%). Particularly, lymphocytic gastritis was found in 13 CD patients (7.8%); superficial chronic gastritis (SCG) was detected in 24 celiacs (14.4%); and one child (0.6%) showed severe interstitial chronic gastritis (ICG). 3/38 children (one with LG, one with SCG and one with ICG) presented Hp infection. Ten patients with LG were symptomatic (7 typical and 3 atypical) while four were silent. Among patients with SCG, 16 children were typical, 5 atypical and 3 silent, and the prevalent symptoms were diarrhoea, abdominal pain and low weight growth. In the table are shown histological grading of the gastric mucosa in LG and SCG patients. The most frequent duodenal lesion, total villous atrophy (Marsh 3C), was detected in 100% and 92% of LG and SCG CD patients. Among CD children, no APCA were found in patients without gastritis, while 3/22 with gastric lesions were positive for APCA (one with mild LG and the other two with mild SCG).

PA36 PSYCHOLOGICAL IMPACT OF COELIAC DIAGNOSIS AND GLUTEN-FREE DIET IN SILENT SALIVARY SCREENING-DETECTED SCHOOL CHILDREN

Objectives: Lymphocytic gastritis (LG) has been described in coeliac disease (CD) patients and in patients with Helicobacter pylori (Hp) infection but the pathogenetic mechanism remains unknown. Aims: The aim of our study was to evaluate the characteristics of the gastric mucosa and the prevalence of lymphocytic gastritis in a large series of CD children and adolescents. Methods: 167 CD children at the diagnosis (F 108; range 11 months–18 years), consecutive performing the upper-intestinal endoscopy at our Department over the period Jan 2008-Dec 2009, were enrolled. Duodenal (2 bulb and 4 distal duodenum samples) together with gastric antral biopsies, were performed. CD diagnosis was performed according to the NASPGHAN criteria. Hp infection was diagnosed by histology and the rapid urease test. Gastric lesions and duodenal biopsies were classified according to the modified Updated Sydney System and to the modified Marsh classification, respectively. Anthropometric and clinical data of each patient were registered at the diagnosis. Moreover, gastric parietal cells antibodies (APCA) were determined with an ELISA. Results: Gastric alterations was found in 38/167 CD children (23%). Particularly, lymphocytic gastritis was found in 13 CD patients (7.8%); superficial chronic gastritis (SCG) was detected in 24 celiacs (14.4%); and one child (0.6%) showed severe interstitial chronic gastritis (ICG). 3/38 children (one with LG, one with SCG and one with ICG) presented Hp infection. Ten patients with LG were symptomatic (7 typical and 3 atypical) while four were silent. Among patients with SCG, 16 children were typical, 5 atypical and 3 silent, and the prevalent symptoms were diarrhoea, abdominal pain and low weight growth. In the table are shown histological grading of the gastric mucosa in LG and SCG patients. The most frequent duodenal lesion, total villous atrophy (Marsh 3C), was detected in 100% and 92% of LG and SCG CD patients. Among CD children, no APCA were found in patients without gastritis, while 3/22 with gastric lesions were positive for APCA (one with mild LG and the other two with mild SCG).

Unusual Presentation of Fever of Unknown Origin in a 78-Year-Old White Male

Purpose: The manifestations of Crohn's disease can afflict any part of the gastrointestinal tract from the mouth to the anus. Because it is often a disease of unknown etiology, and can result in many clinical dilemmas, Crohn's disease is a formidable diagnostic challenge. This clinical vignette features observations made during the diagnosis of new onset Crohn's disease in a 78-year-old white male and presents pertinent training points for practicing physicians.[961] Figure 1: CT showing thickening of terminal ileum.[961] Figure 2: EGD showing severe gastritis in the stomach.[961] Figure 3: Colonoscopy showing a mildly erythematous terminal ileum.[961] Figure 4: Video capsule endoscopy showing ulcerations in the distal ileum.