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A number of complications are associated with COVID-19 due to reduced immunity. Of these, opportunistic infections are of great significance because of their atypical presentation and low detection rates. Co-infection of various parts of the gastrointestinal system with cytomegalovirus (CMV) is a common occurrence in COVID- 19 patients. Dysphagia and odynophagia are the main complaints of oesophagitis caused by CMV. Colitis due to CMV presents with melena, diarrhoea, or constipation. However, gastritis due to the same agent can be asymptomatic or associated with atypical symptoms like fever and epigastric pain. Cytomegalovirus gastritis can be fatal if not detected early. Hence, continued monitoring of routine baseline investigations is imperative until the complete resolution of COVID-19, as prompt diagnosis improves the outcomes.

Background: Cytomegalovirus (CMV) gastritis is occasionally reported in case reports and limited case series. Up to now, it is the largest and most comprehensive retrospective study of CMV gastritis., Methods: All patients who were histologically diagnosed with CMV gastritis at Linkou Chang Gung Memorial Hospital between January 2000 and April 2020 were included. Patients were divided into two groups according to immunity. Between-group differences in characteristics, manifestations, endoscopic features, prognostic factors, and outcomes were analyzed. The main endpoint was 3-month mortality., Results: A total of 54 patients (34 immunocompromised, 20 immunocompetent) were enrolled. Common presentations included gastrointestinal bleeding (35.2%), abdominal pain (33.3%) and fever (31.5%). The endoscopic features included ulcer (88.9%) and inflammation (11.1%). The 3-month mortality rate was 20.4% and overall mortality rate was 40.7%. Acute kidney injury was the only independent risk factor for 3-month mortality (OR 53.89, 95%CI 1.56-1861.73, p = 0.027). Anti-viral therapy and host immune status did not affect 3-month mortality., Conclusion: Both immunocompromised and immunocompetent patients with CMV gastritis have high mortality rates, without significant between-group differences. Acute kidney injury is the only independent predictive factor for 3-month mortality. Prevention of acute kidney injury may possibly improve the 3-month mortality rate., (Copyright © 2020 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.)

Background/aims: The association of Epstein-Barr virus (EBV) with gastric malignancies has been proven by many studies in the literature. However, information about EBV-associated inflammation/gastritis remains limited. The aim of this study is to establish the prevalence of latent EBV infection in patients with chronic gastritis without H. pylori infection., Materials and Methods: In this study, 119 patients with gastritis without H. pylori infection were included. Furthermore, 28 patients with H. pylori gastritis were included in the study as a control group. Chromogenic in situ hybridization (EBV-encoded RNA) and immunohistochemistry (LMP-1 antibody) were performed in all 147 cases. The prevalence of EBV and its relationship with age, sex, the affected part of the stomach, the density of inflammation, inflammatory activity, intestinal metaplasia, and atrophy were analyzed., Results: In this study, 14 cases showed positive immunostaining for EBV. EBV positivity was seen mostly in the lymphoid tissue (13 cases), but it was also detected at the gastric epithelium (7 cases). The mean age of the patients was 44 years, which was slightly younger than that of the EBV-negative cases (48 years). The inflammation density was higher in EBV-positive cases than the EBV-negative gastritis cases (p=0.002). Intestinal metaplasia was detected in 7% of the cases. EBV-positive cases had a higher incidence of atrophy without intestinal metaplasia (21% vs 3.8% without EBV)., Conclusion: EBV was detected in 12% of the cases with gastritis without H. pylori infection. Endoscopic follow-up may be appropriate for patients with gastritis, who have atrophy without intestinal metaplasia and are H. pylori negative but EBV positive.

Primary cytomegalovirus (CMV) infection is rare in immunocompetent hosts and generally asymptomatic. CMV infective gastritis in patients without immunosuppression is very unusual. A 44-year-old man presented with complaints of intermittent epigastric pain. He had no history of organ transplantation, human immunodeficiency virus infection, or immunosuppression of any type. Upper gastrointestinal endoscopy revealed ulcers in the gastric antrum and uplift of the gastric body. Computed tomography scan showed obvious thickening of the gastric wall and enlargement of retroperitoneal lymph nodes, suggesting malignancy. However, the first biopsy only showed ulcerative inflammation, necrosis, and mucosal erosions around the ulcer. Repeat biopsy and histopathological examination showed CMV inclusions in glandular endothelial cells. Immunohistochemistry findings supported the diagnosis of CMV infective gastritis. Symptoms subsided after treatment with intravenous ganciclovir, and the gastric ulceration and surrounding mucosal inflammation decreased. This case report and review of literature is presented to increase awareness regarding this rare disease., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Background: Human papillomavirus (HPV), the causative agent of cervical cancer, is also suggested as a risk factor for gastric adenocarcinoma. Many infectious agents besides Helicobacter pylori have been associated with gastritis. The aim of this study was to investigate HPV DNA and genotyping HPV type 16 DNA in gastric adenocarcinoma and Helicobacter pylori gastritis cases., Methods: A hundred and six gastric adenocarcinoma and Helicobacter pylori gastritis samples and 26 controls were included. After deparaffinization by xylene, DNA extraction was performed by the phenol-chloroform-isoamyl alcohol method and 106 samples were studied with a G6PDH control kit (Eurogentec, Seraing, Belgium). Fifty-three adenocarcinoma and 43 Helicobacter pylori samples were thought to have enough tissue and were studied for HPV DNA. HPV types other than 16 and HPV type 16 DNA were detected by Real Time PCR using the L1 region. Amplifications of MY09/11 products were done by GP5+/GP6+ primers and Cyanine-5 labeled HPV DNA and HPV 16 DNA specific probe in Light Cycler 2.0 (Roche Diagnostics, Germany) device., Results: Among gastric adenocarcinoma and Helicobacter pylori gastritis samples, 20/53 (38%) and 18/43 (41.8%) were HPV DNA positive, respectively. Five (19.2%) of 26 controls were HPV DNA positive., Conclusions: Our 38% positive result in the gastric carcinoma group is in concordance with previous reports. This is the first study revealing the HPV-H. pylori relationship in gastritis cases and we concluded that with regard to the nearly three-fold higher HPV DNA (41.8%) in gastritis cases compared to controls, Helicobacter pylori positive cases should also be evaluated in favor of HPV in the gastritis group.

Herein, we describe an extremely rare case of gastritis due to concurrent infection with Epstein-Barr virus (EBV) and cytomegalovirus (CMV) occurring in an immunocompetent adult. The patient was a 35-year-old man who presented with slight fever, nausea, anorexia, weight loss for 3 weeks, mild transaminitis, and leukocytosis with atypical lymphocytes in peripheral blood. The clinical presentation and elevated IgM titers to both EBV-VCA and CMV strongly suggested infectious mononucleosis syndrome caused by co-infection with EBV and CMV. A computed tomographic scan of the abdomen showed diffuse thickening of the gastric wall mimicking linitis plastica, and upper endoscopy revealed thickened and eroded mucosa throughout the stomach. Histologic examination of gastric biopsies showed a dense lymphoid and neutrophilic infiltrate in the lamina propria with erosion. In situ hybridization assay revealed many lymphocytes positive for EBV-encoded RNA. Moreover, immunohistochemistry using an anti-CMV monoclonal antibody identified some CMV-positive cells (i.e. foveolar epithelium and endothelium). We finally diagnosed this case as gastric involvement in infectious mononucleosis, and the patient recovered without the administration of antiviral drugs. To our knowledge, this is the first reported case of gastritis co-infected with EBV and CMV, as a manifestation of infectious mononucleosis in an immunocompetent adult.

Background: Cytomegalovirus (CMV) is a common viral pathogen in transplant patients which often targets the stomach. However, the endoscopic characteristics of gastric CMV infection are not well established. We aimed to develop a predictive model using endoscopic findings for gastric CMV infection in renal transplant patients., Methods: A retrospective study of 287 kidney transplant recipients who underwent endoscopy with biopsy for suspected CMV infection from January 2006 to November 2015 at a tertiary referral hospital was performed. CMV infection was defined based on inclusion bodies in hematoxylin and eosin and immunohistochemical staining. Endoscopic and clinical parameters related to gastric CMV infection were selected by univariate analyses. Multivariate logistic regression was used to create a predictive model from β-coefficients., Results: CMV was present in 107 (37.7%) of the 287 patients. Multivariate analysis found age (odds ratio [OR], 0.964; 95% confidence interval [CI], 0.938-0.99; P = 0.008), erosions with surface exudate (OR, 5.34; 95% CI, 2.687-10.612; P < 0.001), raised shape of erosions (OR, 3.957; 95% CI, 1.937-8.083; P < 0.001), and antral location of ulcers (OR, 15.018; 95% CI, 5.728-39.371; P < 0.001) as independent predictive factors for gastric CMV infection. Using the predictive model created from this analysis, the sensitivity, specificity, positive predictive value, negative predictive value, and accuracy were 71.03%, 85.56%, 74.51%, 83.24%, and 80.14%, respectively. The area under the receiver operating characteristic curve of this model for detecting CMV infection was 0.850 (95% CI, 0.803-0.889; P < 0.001)., Conclusions: The predictive model with typical endoscopic findings may be useful for detecting gastric CMV infection in renal transplant patients.

The Epstein-Barr virus (EBV) is one of the infectious agents found in stomach tissue. Recently, EBV-associated gastric carcinoma (EBVaGC) was classified as a new subtype of gastric carcinoma. To date, there is a lack of knowledge about the distribution and prevalence of EBV infection in both the normal stomach and various gastric lesions, including EBVaGC, in the Thai population. In this study, we detected EBV in the normal stomach (NS; n = 19), chronic gastritis (CG; n = 36), intestinal metaplasia (IM; n = 40), gastric dysplasia (GD; n = 15), and gastric adenocarcinoma (GC; n = 33) by polymerase chain reaction (PCR) amplification of the latent membrane protein (LMP1) gene of EBV. EBV-PCR amplification was positive in 42.1%, 36.1%, 22.5%, 13.3%, and 33.3% of NS, CG, IM, GD, and GC, respectively. For further clarification in EBVaGC, we performed EBV-encoded small RNA in situ hybridization (EBER-ISH) in PCR-positive cases of GD and GC. Four GC cases were EBER-ISH positive (12.1%), while both GD cases were EBER-ISH negative. In addition, we determined the distribution of the EBV strain (type A or B) based on EBNA3C sequence and EBV variants based on LMP1 variation (wild-type and 30-bp deletion variants; wt-LMP1 or del-LMP1). The results showed that type A and wt-LMP1 were the most prevalent in all lesions. In conclusion, EBV is common in both the NS and gastric lesions, and the frequency of EBVaGC was 12.1% in Thai patients., (© 2018 Wiley Periodicals, Inc.)

Cytomegalovirus (CMV) infection is a common infectious complication in immunocompromised patients. The colon is the most common site of CMV infection in the gastrointestinal tract. Rarely, however, invasion of the upper gastrointestinal tract, such as the esophagus or stomach, has been reported. Herein, we describe the first reported case of CMV gastritis in a patient with end-stage renal disease and uremic symptoms (including nausea, vomiting, and poor appetite) who had begun hemodialysis therapy. This patient was not a transplant recipient and was not receiving immunosuppressant treatment. As CMV gastritis is easily over looked in patients with end-stage renal disease, physicians should maintain a high index of suspicion and establish the diagnosis as early as possible using an upper GI endoscopic biopsy and adequate staining., (Copyright © 2018 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.)

Epstein-Barr virus-associated gastric cancer (EBVaGC) is a representative EBV-infected epithelial neoplasm, which is now included as one of the four subtypes of The Cancer Genome Atlas molecular classification of gastric cancer. In this review, we portray a gastritis-infection-cancer sequence of EBVaGC. This virus-associated type of gastric cancer demonstrates clonal growth of EBV-infected epithelial cells within the mucosa of atrophic gastritis. Its core molecular abnormality is the EBV-specific hyper-epigenotype of CpG island promoter methylation, which induces silencing of tumor suppressor genes. This is due to the infection-induced disruption of the balance between DNA methylation and DNA demethylation activities. Abnormalities in the host cell genome, including phosphatidylinositol-4,5-biphosphate 3-kinase catalytic subunit α (PIK3CA), AT-rich interaction domain 1A (ARID1A), and programmed death-ligand 1 (PD-L1), are associated with the development and progression of EBVaGC. Furthermore, posttranscriptional modulation affects the transformation processes of EBV-infected cells, such as epithelial mesenchymal transition and anti-apoptosis, via cellular and viral microRNAs (miRNAs). Once established, cancer cells of EBVaGC remodel their microenvironment, at least partly, via the delivery of exosomes containing cellular and viral miRNAs. After exosomes are incorporated, these molecules change the functions of stromal cells, tuning the microenvironment for EBVaGC. During this series of events, EBV hijacks and uses cellular machineries, such as DNA methylation and the miRNA delivery system. This portrait of gastritis-infection-cancer sequences highlights the survival strategies of EBV in the stomach epithelial cells and may be useful for the integration of therapeutic modalities against EBV-driven gastric cancer.

A 35-year-old woman who had previously undergone a lung transplantation presented with severe abdominal pain and vomiting. The gastroscopy showed diffuse ulcerative gastric lesions. Tests for varicella zoster virus and Epstein-Barr virus via polymerase chain reactions (PCR) on endoscopically obtained gastric biopsies were found to be positive and confirmed varicella gastritis. Intravenous antiviral therapy with acyclovir was administered resulting in a normalization of all clinical symptoms, especially of abdominal pain and inflammation parameters.

We report varicella-zoster virus (VZV) gastritis in a 70-year-old woman postchemotherapy for lymphoma, presenting with abdominal pain, vomiting, and delirium without rash. A gastric biopsy demonstrated viral inclusions but posed a diagnostic challenge as immunohistochemistry for cytomegalovirus and herpes simplex virus were negative, and VZV immunohistochemistry was not available. The patient developed a vesicular rash 7 days after her symptoms began. Molecular testing of the gastric biopsy and a skin swab both confirmed VZV infection. She also had probable involvement of her liver and pancreas based on imaging and serum chemistry, and possible central nervous system involvement. She recovered with appropriate antiviral therapy but later developed a postherpetic neuralgia, and chronic intrahepatic biliary strictures; liver biopsy demonstrated a cholangiopathy of uncertain etiology. A literature review of the pathogenesis, epidemiology and sequelae of VZV infection is included.

Spasmolytic polypeptide-expressing metaplasia (SPEM) and intestinal metaplasia (IM) have been recognized as neoplastic precursors in gastric carcinogenesis. We explored the relationship between SPEM and IM in Epstein-Barr virus-associated (EBVaGC) and Epstein-Barr virus-negative (EBVnGC) gastric cancer. Sixty-four EBVaGC and one hundred and fifty-four EBVnGC patients were included. EBV positivity was identified using Epstein-Barr virus-encoded RNA-1 in situ hybridization. SPEM was subclassified into absent, early, and advanced SPEM. Acute and chronic inflammation was graded as absent, mild, moderate, and marked. Univariate and multivariate logistic regression analyses were conducted to analyze the correlation between SPEM, IM, and inflammation. Our study revealed that SPEM was detected in 87.5% EBVaGC and 85.1% EBVnGC patients. Distribution of patients according to the SPEM classification was significantly different between EBVaGC and EBVnGC groups (P=.038). IM was observed less frequently in EBVaGC when compared with EBVnGC patients (P<.001). No difference was observed between EBVaGC and EBVnGC in the levels of acute and chronic inflammation. A positive correlation between IM and SPEM status was observed in both EBVaGC and EBVnGC patients. Furthermore, advanced SPEM was an independent influential factor to IM in EBVnGC (P=.013). In conclusion, SPEM was associated with both EBVaGC and EBVnGC more frequently than IM. Moreover, advanced SPEM had a stronger association with IM than early SPEM in EBVnGC. These results suggest that identification of SPEM should be used as a high-risk indicator for detecting early gastric carcinoma, and should be brought to the attention of pathologists and clinicians., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Purpose: Helicobacter pylori secretory peptidyl prolyl isomerase, HP0175, is progressively identified as a pro-inflammatory and pro-carcinogenic protein, which serves to link H. pylori infection to its more severe clinical outcomes. Here, we have analyzed host HP0175-specific antibody responses in relation to the severity of gastritis., Methods: The HP0175 gene fragment was PCR-amplified, cloned, expressed and purified by Ni-NTA affinity chromatography. Serum antigen-specific antibody responses of non-ulcer dyspeptic patients (N = 176) against recombinant HP0175 were detected by western blotting. The infection status of these subjects was determined by rapid urease test, culture, histology, and serology. The grade of inflammation and stage of atrophy were scored blindly according to the OLGA staging system., Results: The recombinant HP0175 (rHP0175) was expressed as a ~35 kDa protein and its identity was confirmed by western blotting using anti-6X His tag antibody and pooled H. pylori-positive sera. Serum IgG antibodies against rHP0175 segregated our patients into two similar-sized groups of sero-positives (90/176, 51.1 %) and sero-negatives (86/176, 48.9 %). The former presented with higher grades of gastric inflammation (OR = 4.4, 95 % CI = 1.9-9.9, P = 0.001) and stages of gastric atrophy (OR = 18.3, 95 %CI = 1.4-246.6, P = 0.028)., Conclusion: Our findings lend further support to the pro-inflammatory nature of H. pylori peptidyl prolyl isomerase (HP0175) and recommends this antigen as a non-invasive serum biomarker of the severity of H. pylori-associated gastritis.

Purpose: Gastritis caused by infection with Helicobacter pylori is characterized by chronic inflammation and damage in gastric tissue, which is a main risk factor for gastric cancer. Associated with H. pylori, the TP53 gene tumor suppressor and the cell adhesion glycoprotein epithelial cadherin develop a relevant role in the integrity and carcinogenesis of the epithelium. We aimed to detection of H. pylori and its main virulence markers and measured the messenger RNA (mRNA) expression levels of E-cadherin and TP53 genes., Methods: The detection of H. pylori and its virulence markers, as well as the mRNA expression levels of E-cadherin and TP53 genes, were obtained for 161 samples of gastric biopsies including 37 with normal gastric tissue, 70 with gastritis, 24 from neoplastic tissue, and 27 from adjacent non-neoplastic by means of a quantitative real-time polymerase chain reaction., Results: The mRNA expression levels of E-cadherin and TP53 were found to be decreased in patients with gastritis, independently of H. pylori infection. In samples from gastric patients, the neoplastic tissue showed an accentuated decrease of expression; on the other hand, the expression of E-cadherin was normal in adjacent non-neoplastic., Conclusions: No evidence was found of the involvement of the cagA and vacA genes in the decreased expression of E-cadherin and TP53. The process of carcinogenesis is complex, and the decrease of the E-cadherin gene expression and TP53 gene expression appears to contribute significantly.

We report a case of fatal respiratory and gastric herpesvirus infection in a vaccinated, adult cat with no known immunosuppression or debilitation. The disease was characterized by severe necrotizing bronchopneumonia, fibrinonecrotic laryngotracheitis, and multifocal necrotizing gastritis associated with eosinophilic intranuclear inclusion bodies and a large amount of feline herpesvirus-1 antigen detected with immunohistochemistry.

Background: The tumor suppressor p53 is as a regulator of cell proliferation, apoptosis and many other biological processes as well as external and internal stress responses. Mdm2 SNIP309 is a negative regulator of 53. Therefore, this study aimed to determine the role of the Mdm2 SNIP 309 polymorphism in the gastric mucosal morphological patterns in patients with Helicobacter pylori associated gastritis., Materials and Methods: A prospective cross-sectional study was carried out from November 2014 through November 2015. Biopsy specimens were obtained from patients and infection was proven by positive histology. Gastric mucosa specimens were sent to the Molecular Genetics Unit, Institute of Medicine, Suranaree University of Technology where they were tested by molecular methods to detect the patterns of Mdm2 SNIP 309 polymorphism using the real-time PCR hybridization probe method. The results were analyzed and correlated with gastric mucosal morphological patterns by using C-NBI endoscopy., Results: A total of 300 infected patients were enrolled and gastric mucosa specimens were collected. In this study the percentage of Mdm2 SNIP 309 T/T homozygous and Mdm2 SNIP309 G/T heterozygous was 78% and 19 % respectively whereas Mdm2 SNIP309 G/G homozygous was 3%. Mdm2 SNIP 309 T/T homozygous and Mdm2 SNIP309 G/T heterozygosity correlated with type 1 to type 3 gastric mucosal morphological patterns (P<0.01) whereas Mdm2 SNIP309 G/G homozygous correlated with type 4 and type 5 (P<0.01)., Conclusions: Our study finds the frequency of Mdm2 SNIP309 G/G in a Thai population is very low, and suggests that this can explain ae Thailand enigma. Types 1 to type 3 are the most common gastric mucosal morphological patterns according to the unique genetic polymorphism of MDM2 SNIP 309 in the Thai population.

Background: Helicobacter pylori is now recognized as a causative factor of chronic gastritis, gastroduodenal ulcers, gastric cancer and mucosaassociated lymphatic tissue lymphoma. Tolllike receptors are important bacterial receptors in gastric epithelial cell signaling transduction and play critical roles in gastric carcinogenesis., Materials and Methods: A total of 400 patients undergoing esophagogastroduodenoscopy for investigation of chronic abdominal pain were genotyped for singlenucleotide polymorphisms (SNPs) in TLR1 (rs4833095) using TagMan SNPs genotyping assay by realtime PCR hybridization. Relationships with susceptibility to H. pylori infection and premalignant gastric mucosa morphological patterns, classified by magnifying NBI endoscopy, were investigated., Results: The percentages of TLR1 rs4833095, CC homozygous, CT heterozygous and TT homozygous cases were 34, 46.5 and 19%, respectively. CC showed statistical differences between H. pylori positive and negative cases (P<0.001). CT and TT correlated with type 1 and type 2 gastric mucosal morphological patterns (P<0.01) whereas CC correlated with types 3 and 4 (P<0.01)., Conclusions: This study demonstrated good correlation of TLR1 rs4833095 genotype with severity of inflammation in H. pylori infected gastric mucosa according to gastric mucosal morphologic patterns with magnifying NBI endoscopy.

Phosphorylation of PTEN at residues Ser380/Thr382/383 leads to loss of phosphatase activity and tumor suppressor function. Here, we found that phosphorylation of PTEN at residues Ser380/Thr382/383 was increased with gastric carcinogenesis, and more importantly, Helicobacter pylori was a trigger of this modification in chronic non-atrophic gastritis. H. pylori could phosphorylate and inactivate PTEN in vivo and in vitro, resulting in survival of gastric epithelial cells. Furthermore, stable expression of dominant-negative mutant PTEN or inhibition of Akt prevented the enhanced survival induced by H. pylori. These results indicate that PTEN phosphorylation at residues Ser380/Thr382/383 is a novel mechanism of PTEN inactivation in gastric carcinogenesis, and H. pylori triggers this modification, resulting in activation of the PI3K/Akt pathway and promotion of cell survival.

The cytomegalovirus (CMV) disease spectrum is very wide, with symptomatic infections being rare in immunocompetent hosts. We present the case of a 31-year-old immunocompetent man diagnosed with CMV gastritis in the context of primary infection. The most important laboratory abnormalities leading to diagnosis were: elevation of liver enzymes (3-4× the upper limit of normal), thrombocytopenia (133 G/L), lymphocytosis (55%-4.2 G/L) with activated lymphocytes, CMV IgM positive (negative IgG), CMV viral load of 5700 copies/mL (real-time PCR); autoimmunity study showed antiparietal cell antibodies; abdominal ultrasonography detected homogenous splenomegaly (14.6×13.4 cm) and endoscopy unveiled superficial erosions of the gastric antrum that were biopsied. Anatomopathology and immunohistochemistry of the samples identified cytomegalic inclusions in endothelial cells. Cellular and humoral immunity deficits were excluded. As the patient developed severe asthaenia, adynamia and epigastric pain, he was administered gancyclovir 5 mg/kg intravenously twice daily for 7 days, with resolution of symptoms and gastric lesions confirmed by re-evaluation through endoscopy., (2015 BMJ Publishing Group Ltd.)

Objectives: Skin grafting has been evolving as an important application in reconstructive surgery. Mixed reports about the survival of allogeneic and xenogeneic keratinocytes require further substantiation to determine the role of these cells in wound healing., Materials and Methods: Rabbit and rat skins were recovered and cultured in vitro. Full-thickness wounds were created on the dorsum of rabbits (2 cm × 2 cm; n = 4). Cultured epithelial autograft, allograft, and xenograft cells were sprayed onto 3 freshly created wounds, with 1 wound acting as a control. The wounds were monitored every 2 days for 4 weeks. After 4 weeks, the rabbits were killed; skin biopsies were taken from each healed wound and stained with hematoxylin and eosin, and epidermal thickness was measured., Results: All examined grafts showed favorable healing outcomes because the wounds appeared similar to normal skin upon healing. The only observed significant difference was the thickness of the epidermis layer, which was thinner in the xenograft (P = .002) than the autograft or allograft. Morphologic evaluation of the skin surface showed that the rat skin was thinner than the rabbit skin. The graft that achieved the best result was the autograft because the thickness was similar to and mimicked normal skin., Conclusions: All 3 grafts (autograft, allograft, and xenograft) have the potential to reconstitute epithelial defects. This approach can overcome the limitation of autologous skin donor sites, especially in burn cases.

Background: Helicobacter pylori (H.pylori) is associated with chronic gastritis, peptic ulcers, gastric adenocarcinomas and mucosa associated tissue lymphomas. Cytotoxin associated gene A (CagA) is one of the virulence factors of H.pylori. It is hypothesized that reactive oxygen species (ROS) play roles in H.pylori associated disease especially in development of gastric adenocarcinoma. Individuals infected with H.pylori bearing CagA produce more ROS than others. 8-hydroxydeoxyguanosine (8OHdG) is an in vitro marker of DNA damage and oxidative stress. The aim of this study was to investigate the relationship between 8OHdG level, H.pylori infection and CagA and alterations of serum 8OHdG level after H.pylori eradication., Materials and Methods: Patients admitted with dyspeptic complaints and upper gastrointestinal endoscopy were assessed. H.pylori was determined from histopathology of specimens. Serum 8OHdG levels of three groups (H.pylori negative, H. pylori positive CagA negative and H.pylori positive CagA positive) were compared. Patients with H.pylori infection received eradication therapy. Serum 8OHdG levels pretreatment and posttreatment were also compared., Results: In total, 129 patients (M/F, 57/72) were enrolled in the study. Serum 8OHdG level of H.pylori negative, H. pylori positive CagA negative and H.pylori positive CagA positive groups were significantly different (5.77±1.35 ng/ml, 5.43±1.14 ng/ml and 7.57±1.25 ng/ml respectively, p=0.05). Furthermore, eradication therapy reduced serum 8OHdG level (6.10±1.54 ng/ml vs 5.55±1.23 ng/ml, p=0.05)., Conclusions: Individuals infected with H.pylori bearing CagA strains have the highest serum 8OHdG level and eradication therapy decreases the serum 8OHdG level. To the best of our knowledge this is the first study that evaluated the effect of CagA virulence factor on serum 8OHdG level and the effect of eradication therapy on serum 8OHdG levels together. Eradication of CagA bearing H.pylori may prevent gastric adenocarcinoma by decreasing ROS. 8OHdG level may thus be a good marker for prevention from gastric adenocarcinoma.

Helicobacter pylori infection is an established risk factor for gastritis, gastric ulcer, peptic ulcer and gastric cancer. CagA +ve H. pylori has been associated with oxidative DNA damage of gastric mucosa but their combined role in the development of gastric cancer is still unknown. Here we compare the combined expression of cagA and 8-hydroxy-2'-deoxyguanosine (8-OHdG) in normal, gastritis and gastric cancer tissues. Two hundred gastric biopsies from patients with dyspeptic symptoms, 70 gastric cancer tissue samples and 30 gastric biopsies from non-dyspeptic individuals (controls) were included in this study and 8-OHdG was detected by immunohistochemistry (IHC). Histological features and the presence of H. pylori infection were demonstrated by Hematoxylin and Eosin (HE), Giemsa and alcian blue-periodic acid-Schiff ± diastase (AB-PAS ± D) staining. DNA was extracted from tissues and polymerase chain reaction (PCR) performed to determine the presence of ureaseA and cagA genes of H. pylori. The results showed the presence of H. pylori in 106 (53 %) gastric biopsies out of 200 dyspeptic patients, including 70 (66 %) cases of cagA + ve H. pylori. The presence of cagA gene and high expression of 8-OHdG was highly correlated with severe gastric inflammation and gastric cancer particularly, in cases with infiltration of chronic inflammatory cells (36.8 % cagA + ve, 18 %), neutrophilic activity (47.2 %, 25.5 %), intestinal metaplasia (77.7 %, 35.7 %) and intestinal type gastric cancer (95 %, 95.4 %) (p ≤ 0.01). In conclusion, H. Pylori cagA gene expression and the detection of 8-OHdG adducts in gastric epithelium can serve as potential early biomarkers of H. Pylori-associated gastric carcinogenesis.

The extended monitoring (up to 1 year 11 months) of PCR markers was implemented concerning viral infections: cytomegalovirus, Epstein-Barr virus, simple herpes virus type I and II, hepatitis B virus, hepatitis C virus and bacterial infection of Helicobacter pylori in bioassays (blood, biopsy material of mucous coat of stomach and inferior third of esophagus) from children with different types of chronic gastritis. In biological samples from patients with gastritis type A and type A + B DNA of hepatitis B virus (87% and 71% of patients correspondingly) and DNA of Epstein-Barr virus (63% and 67% of patients) were detected with high rate. Under gastritis type B and C these markers were detected significantly rarely (20-36%). Among patients with gastritis type A, B and A + B, the positive results on DNA of cytomegalovirus consisted 13-17%. In patients with gastritis type C DNA of cytomegalovirus was not detected. In any of analyzed samples no DNA of simple herpes virus type I and II was detected. The control of DNA of H. pylori demonstrated its presence in biological materials of 67% and 84% of patients with gastritis type B and A +B. This type of DNA was absent in patients with gastritis type A and C. Under gastritis type A, B and A+B, DNA of Epstein-Barr virus and DNA of hepatitis B virus detected more often in biological materials of mucous coat of stomach (71%-100%) and out of them simultaneously in blood in 33%-60% of examined patients and only in blood up to 29%. DNA of Epstein-Barr virus was detected in leukocytes of peripheral blood and DNA of hepatitis B virus both in plasma and leukocytes of peripheral blood. Under gastritis type C DNA of Epstein-Barr virus was always detected in leukocytes of peripheral blood (in 20% out of these patients simultaneously in biological material) and DNA of hepatitis B virus just as much in blood (plasma and/or leukocytes of peripheral blood) and biological materials. The lower concentrations (less than 700 copies/ml) DNA of hepatitis B virus in most samples were detected in absence of markers of hepatitis B virus. In patients with autoimmune gastritis and in absence of bacterial infection H. pylori (group I) or against its background (group III) PCR-markers of hepatitis B virus and Epstein-Barr virus were detected quite often. The evidence of persistence (in superior sections of digestive organs) of Epstein-Barr virus nad hepatitis B virus is detection of DNA of these viruses under their extended monitoring (up to 1 year 11 months) in biological samples from patients with autoimmune forms of gastritis type A and type A+B.

Introduction: The reactivation of varicella-zoster virus occurs in immunocompromised patients, especially in cases of hematological malignancy. Disseminated reactivation could involve digestive tract with life-threatening condition., Case Report: A 76-year-old woman, with a history of chronic lymphocytic leukemia, presented with left hypochondrium pain, and a vesicular rash with hemorrhagic shock that revealed an hemorrhagic gastritis due to varicella-zoster virus. The literature review identified 28 additional cases of gastrointestinal mucosal damage during reactivation of varicella-zoster virus. Mortality is 40%. We report here the first case in the course of low-grade lymphoid malignancy., Conclusion: Acute gastrointestinal symptoms in immunocompromised patients should evoke a varicella-zoster virus reactivation with gastrointestinal involvement. This clinical manifestation, although rare, should not be ignored because of its severity., (Copyright © 2013 Société nationale française de médecine interne (SNFMI). Published by Elsevier SAS. All rights reserved.)

Introduction: Ulcerative colitis (UC) has been recognised as a systemic immune disorder that is not as restricted as colitis. UC-related gastrointestinal lesions with bleeding can develop soon after colectomy and can progress rapidly. Therefore, we considered the clinical features and treatment of these UC-related lesions., Methods: We reviewed the patient data in our UC surgery database to evaluate its prevalence and features., Results: We found 7/1,100 patients with UC-related lesions between January 2000 and April 2013. These lesions developed at a mean of 24 (range 8-480) days after colectomy. Six of the seven patients suffered from gastrointestinal bleeding as an initial symptom that rapidly developed into massive bleeding or perforations. All of the patients were diagnosed with pancolitis; at the time of colectomy, fulminant, severe, moderate, and mild colitis were presented by four, one, one, and one patients, respectively. All patients with enteritis had consecutively developed other infectious complications, including anastomotic leakage, pyoderma gangrenosum, wound infection, and pneumonia. Although patients with bleeding did not respond to treatment with corticosteroids, they responded well to infliximab soon after its administration. Although six of the seven patients showed cytomegalo virus re-activation in blood or pathological examinations, ganciclovir was not effective in its elimination., Conclusion: Although UC-related lesions with an unknown aetiology can occur after colectomy, immediate examination and treatment are required if gastrointestinal bleeding is found after surgery. Because gastrointestinal bleeding from UC-related lesions can worsen rapidly and may be related to mortality, early potent immunosuppressive therapy should be considered.

Different lines of evidence support an association between Epstein-Barr virus (EBV) and gastric cancer (GC). The main understood risk factor to develop GC is infection by Helicobacter pylori (H. pylori), which triggers a local inflammatory response critical for progression from gastritis to GC. The role of EBV in early inflammatory gastric lesions has been poorly studied. A recent study proposed a cutoff value of 2000 EBV particles to identify patients with increased chances of infection of the gastric epithelium, which may favor the inflammatory process. To better understand the role of EBV in cancer progression, we analyzed 75 samples of GC, 147 control samples of non-tumor gastric tissue derived from GC patients and 75 biopsies from patients with non-atrophic gastritis (NAG). A first-round PCR was used for EBV detection in tumor and non-tumor controls and a more sensitive nested PCR for gastritis samples; both PCRs had lower detection limits above the proposed cutoff value. With this strategy 10.67% of GC, 1.3% of non-tumor controls and 8% of gastritis samples were found positive. An EBER1 in situ hybridization showed EBV infection of epithelial cells in GC and in a third of NAG samples, while in the other NAGs infection was restricted to the mononuclear cell infiltrate. EBV-positive GCs were enriched in lace and cribriform patterns, while these rare patterns were not observed in EBV negative samples. Our results support a role for EBV in GC and early precursor lesions, either as directly oncogenic infecting epithelial cells or indirectly as an inflammatory trigger.

Background: Gastritis and gastric cancer are the most common diseases in the Kazakh population. Polymorphisms in genes coding of cytokines have been played important role with gastric disease risk. The risk alleles of cytokines in patients with gastritis can predict the risk of developing gastric cancer. The aim of this study was to investigate cytokine gene polymorphisms as risk factors for the development of gastritis in a case-control study with gastritis patients and healthy individuals from the Kazakh ethnic group, living in North Kazakhstan., Materials and Methods: The polymerase chain reaction followed by direct sequencing were used for detection of two functional polymorphisms in the IL1 gene family, and TaqMan SNP Genotyping Assay Sets were applied for three potentially functional polymorphisms in the IL10 gene, and one in the TNFA promoter., Results: Association analysis of studied allelic variants and the development of gastritis in H. pylori- positive patients showed that IL1B -31C/C, IL1B -511T/T and IL1RN -2/2 allelic variants were associated with development of gastritis (OR=1.8 (1.07-3.16), p=0.025; OR=1.7 (1.04-2.99), p=0.035, and OR=4.92 (2.45-9.85), p<0.001) respectively. Haplotype C-T that combines both homozygous allelic variants of IL1B gene also had a statistically significant association with slightly higher OR (OR: 1.43, 95% CI: 1.08-1.88)., Conclusions: The data from the current study showed that the genotype IL-1B -511T/-31C-IL1-RN-2 and H. pylori infection increase risk of gastritis in the Kazakh population. That genotype combination might be a factor increasing the risk of developing gastric cancer.

The article describes a clinical case of chronic gastritis associated with Helicobacter pylori infection and Epstein-Barr virus. The authors draw attention to the peculiarities of dyspepsia syndrome, on the characteristics of this disease in the endoscopic and morphological study.

Objective: To establish the diagnostic value of the determination of leukocyte composition of inflammatory infiltrate in chronic gastroduodenite in childhood., Patients and Methods: We examined 103 patients aged 8-17 with chronic gastroduodenitis associated with Helicobacter pylori. To detect Hp and Epstein-Barr viral infections we used esophagogastroduodenoscopy, quick urease test, bacterioscopy of gastrobiopsies. We performed the analysis of the cellular composition of the inflammatory infiltrate., Results: It was found that the number of lymphocytes and neutrophils located in the lamina and intraepithelial increases, which is associated with the degree of inflammation. Increased to the maximum was the number of intraepithelial lymphocytes, both in the body, and in the antrum. Intensity of leukocyte infiltration is directly correlated with the increased prevalence of inflammation. Persistence of Epstein-Barr virus (35.9% of patients) is followed by more severe intraepithelial lymphocytic infiltration in the stomach. In 4-6 months after treatment 18 patients with severe gastritis were repeatedly studied for the inflammatory infiltrate. A significant decrease in the number of intraepithelial neutrophils was found., Conclusion: Cellular composition of the infiltrate is an objective characteristic of chronic inflammation in the gastric mucosa. Persistence of Epstein-Barr virus is accompanied by an increase in the amount of intraepithelial lymphocytes and neutrophils.

Objective: Our aim was to reveale the features of histological mucosa with different composition of the microflora of stomach and duodenum in children with chronic gastroduodenitis., Methods: The study included 122 children with chronic gastroduodenitis from 5 to 17 years old. All patients underwent endoscopy with histology of biopsy specimens of gastric and duodenal mucosa in 94 patients and in 48 patients among them with morphometry of biological material. Identification of herpes simplex virus 1, 2 types, cytomegalovirus, human papilloma virus 16, 18 types, Helicobacterpylori was carried out using polymerase chain reaction in biopsies of gastroduodenal mucosa and gastric juice., Results: Children with chronic gastroduodenitis depending on the identified microorganisms were divided into groups: 1st (n = 51)--without detectable microorganisms, 2nd (n = 28)--with associations of H. pylori and viruses, 3rd (n = 15)--only with viruses, 4th (n = 28)--with H. pylori. Thus, in patients with H. pylori inflammation was noted mainly in the antral mucosa and dystrophic changes--in the duodenal mucosa. In the presence of viruses the inflammation was expressed more in the fundal stomach and duodenum. When viral-bacterial associations were observed most pronounced inflammatory-dystrophic process was localized throughout the gastroduodenal mucosa., Conclusion: In children with chronic gastroduodenitis in the presence of bacterial, viral and mixed microflora in the stomach and duodenum identified characteristic histological features of the mucosa, manifested in a different localization and severity of inflammatory and dystrophic changes.

The efficiency of immunomodulating therapy with cycloferon in children aged from 10 to 16 years with verified chronic gastroduodenitis was estimated. It was shown that the cycloferon treatment provided reliable increase of T- and B-cellular populations in mucous membranes of the stomach and duodenum, normalization of the number of CD8-lymphocytes, higher titers of IgG antibodies to herpes viruses 1 and 2. It also promoted reduction of inflammation in the mucous membranes along with reduction of the disease clinical signs.

The article contains the results of studies of clinical and morphological features of chronic gastritis of viral and bacterail etiology in age aspects. Chronic gastritis when infected with Epstein-Barr virus in elderly patients has clinical and morphological differences from chronic gastritis associated with Helicobacter pylori infection, consisting in significantly lower severity of regenerative changes in the cervical epithelium of the mucous membrane of the body and antrum of the stomach, cervical mucosal epithelium of the body, antrum, bottom mucosal epithelium of the stomach body; and significantly more rare intestinal metaplasia in the stomach and the absence of stromal fibrosis antrum.

The study included 120 patients with pre-cancer conditions of the stomach and 30 patients with gastric cancer stage II-IV. The ELISA method in the blood serum was used to determine the markers of the infection caused by Herpes simplex virus (HSV) types 1 and 2, Cytomegalovirus (CMV), and Epstein-Barr virus (EBV). The majority of the patients exhibited high titers of markers of Herpesvirus mixed infection. These data allow recommending the determination of IgG antibodies to antigens of herpesviruses in patients with the diseases of the stomach and assigning the appropriate antiviral drugs.

Introduction: Singapore had its first case of pandemic influenza A (H1N1) 2009 on 26 May 2009. As of 3 August 2009, 440 children with confirmed H1N1were admitted to KK Women's and Children's Hospital (KKH)., Materials and Methods: This is a retrospective case control study of children admitted from 26 May 2009 to 19 July 2009 with H1N1infection. Cases and controls were first differentiated by whether they were complicated or non-complicated in nature, and subsequently analysed with regards to possible independent risk factors., Results: We analysed 143 admitted children; 48 cases and 95 controls (1: 2 ratio). Significant comorbidity was found in 20.3% (n = 29) of patients with the majority having asthma (n = 18, 12.6 %) followed by obesity (n = 7, 4.9%). Binary logistic regression analysis showed risk factors for complicated disease were comorbidity (adjusted OR 6.0, 95% CI, 2.5 to 14.6, P < 0.0001) and age <2 years (adjusted OR 9.8, 95% CI, 2.4 to 40, P = 0.001). Age less than 5 years was not found to be a risk factor., Conclusion: In the early stages of an evolving influenza epidemic when oseltamivir stocks are low, oseltamivir treatment for influenza can be streamlined and offered to those at highest risk who are under 2 years old or have significant comorbidity to prevent complicated disease.

Background: H. pylori infection is acquired during childhood and causes a chronic inflammatory response in the gastric mucosa, which is considered the main risk factor to acquire gastric cancer (GC) later in life. More recently, infection by Epstein-Barr virus (EBV) have also been associated with GC. The role of EBV in early inflammatory responses and its relationship with H. pylori infection remains poorly studied. Here, we assessed whether EBV infection in children correlated with the stage of gastritis and whether co-infection with H. pylori affected the severity of inflammation., Methodology/principal Findings: 333 pediatric patients with chronic abdominal pain were studied. From them, gastric biopsies were taken and inflammation graded according to the Sydney system; peripheral blood was drawn and antibodies against EBV (IgG and IgM anti-VCA) and H. pylori (IgG anti-whole bacteria and anti-CagA) were measured in sera. We found that children infected only by EBV presented mild mononuclear (MN) and none polymorphonuclear (PMN) cell infiltration, while those infected by H. pylori presented moderate MN and mild PMN. In contrast, patients co-infected with both pathogens were significantly associated with severe gastritis. Importantly, co-infection of H. pylori CagA+/EBV+ had a stronger association with severe MN (PR 3.0) and PMN (PR 7.2) cells than cases with single H. pylori CagA+ infection., Conclusions/significance: Co-infection with EBV and H. pylori in pediatric patients is associated with severe gastritis. Even single infections with H. pylori CagA+ strains are associated with mild to moderate infiltration arguing for a cooperative effect of H. pylori and EBV in the gastric mucosa and revealing a critical role for EBV previously un-appreciated. This study points out the need to study both pathogens to understand the mechanism behind severe damage of the gastric mucosa, which could identified children with increased risk to present more serious lesions later in life.

The varicella zoster virus (VZV) is a very rare cause of gastritis. Gastritis caused by VZV can be presented as abdominal pain, vomiting. Most of the cases reported with varicella gastritis in the literature are immunocompromised patients with various kinds of malignancy, and most of these patients are adults. Here we report an adolescent girl with acute abdominal pain. The girl was immunocompetent. Her endoscopically taken biopsy material revealed varicella, and her gastritis was healed with acyclovir therapy. This is a very rare condition and not frequently reported in the literature. The authors want to drive attention to the fact that varicella gastritis can be seen in immunocompetent children, the presentation can be nausea, vomiting and/or (severe) abdominal pain. Serological studies may be less helpful than tissue studies, so interventional procedures should be done., (Copyright © 2012 Elsevier B.V. All rights reserved.)

The article assesses the effectiveness of administering immunomodulating drug cycloferon in patients aged 10 to 16 years with chronic gastroduodenitis. It is established that the use of cycloferon in children with virus-associated chronic gastroduodenitis leads to a significant increase in T- and B-lymphocyte populations in mucous membranes of the stomach and duodenum, and contributes to the elimination of viruses. This results in reduced severity and activity of inflammation in the mucous membranes and decreases clinical manifestations of the disease.

A 58-year-old male developed epigastric discomfort and high fever in 2010. Complete blood count showed leukocytosis and a small number of atypical lymphocytes. Gastric endoscopy revealed multiple gastroduodenal erosions and ulcers. Biopsy specimens were obtained and pathological examination demonstrated cytomegalic inclusion bodies. Cytomegalovirus (CMV) IgM antibody was positive and CMV DNA was detected with PCR in his blood, leading to the diagnosis of CMV gastroduodenitis. He was treated with intravenous ganciclovir and his symptoms resolved rapidly. It is recognized that CMV gastroduodenitis is extremely rare in immunocompetent hosts but sometimes shows a severe clinical course in elderly patients. The results from our present patient suggest that we should consider CMV infection in the differential diagnosis of multiple gastroduodenal erosions and ulcers. Our data also suggested that anti-CMV medications could be important treatment options for CMV gastroduodenitis, especially in elderly patients.