Autoimmune gastritis as an unexpected cause of diarrhea in a young adult with type I diabetes: a case report.

BACKGROUND: Type 1 diabetes mellitus (T1DM) is a lifelong diagnosis that involves immune-mediated damage of pancreatic beta cells and subsequent hyperglycemia, manifesting as: polyuria, polydipsia, polyphagia, and weight loss. Treatment of type 1 diabetes centers on insulin administration to replace or supplement the body's own insulin with the goal of achieving euglycemia and preventing or minimizing complications. Patients with T1DM are at risk for developing other autoimmune conditions, most commonly thyroid or celiac disease. CASE PRESENTATION: A 20-year-old African American female with T1DM was referred by her endocrinologist to pediatric gastroenterology for 2 months of nocturnal, non-bloody diarrhea, left lower quadrant pain, and nausea; she was also being followed by neurology for complaints of lower extremity paresthesias and pain. The patient's initial lab-workup was remarkable for a low total Immunoglobulin A (IgA) level of < 6.7 mg/dL. As IgA deficiency is associated with an increased risk of celiac disease, the patient underwent upper and lower endoscopy, which was grossly unremarkable; however, histology revealed a pattern consistent with autoimmune gastritis. Subsequent serum evaluation was remarkable for an elevated fasting gastrin level and an elevated parietal cell antibody level without macrocytic anemia, iron deficiency, or vitamin B12 depletion. The patient was diagnosed with autoimmune gastritis (AIG) and subsequently initiated on parenteral B12 supplementation therapy with improvement in her neurologic and gastrointestinal symptoms. CONCLUSION: This case illustrates the importance of recognition of red flag findings in a patient with known autoimmune disease. Following well-established health maintenance recommendations for individuals with T1DM ensures that common comorbidities will be detected. Autoimmune gastritis, while a rarer pathology in the pediatric population, deserves consideration in patients with pre-existing autoimmune conditions and new gastrointestinal or neurologic symptoms, as AIG can be associated with poor outcomes and risk of malignancy. Initial lab findings associated with an eventual diagnosis of AIG typically include anemia, iron deficiency, or Vitamin B12 deficiency. However, as demonstrated in this case, symptoms of AIG can rarely present before anemia or Vitamin B12 deficiency develops. To prevent permanent neurological damage, parenteral Vitamin B12 therapy must be considered even in the absence of Vitamin B12 deficiency, especially in those patients already experiencing neurological symptoms.

Association of Helicobacter pylori Positivity With Risk of Disease and Mortality.

INTRODUCTION: Helicobacter pylori colonizes the human stomach. Infection causes chronic gastritis and increases the risk of gastroduodenal ulcer and gastric cancer. Its chronic colonization in the stomach triggers aberrant epithelial and inflammatory signals that are also associated with systemic alterations. METHODS: Using a PheWAS analysis in more than 8,000 participants in the community-based UK Biobank, we explored the association of H. pylori positivity with gastric and extragastric disease and mortality in a European country. RESULTS: Along with well-established gastric diseases, we dominantly found overrepresented cardiovascular, respiratory, and metabolic disorders. Using multivariate analysis, the overall mortality of H. pylori -positive participants was not altered, while the respiratory and Coronovirus 2019-associated mortality increased. Lipidomic analysis for H. pylori -positive participants revealed a dyslipidemic profile with reduced high-density lipoprotein cholesterol and omega-3 fatty acids, which may represent a causative link between infection, systemic inflammation, and disease. DISCUSSION: Our study of H. pylori positivity demonstrates that it plays an organ- and disease entity-specific role in the development of human disease and highlights the importance of further research into the systemic effects of H. pylori infection.

Collagenous gastritis in children: A national cohort.

BACKGROUND: Collagen gastritis is a rare disease that manifests in children mainly as isolated gastric involvement associated with martial deficiency anemia. There are no recommendations for the management and follow-up of these patients. We aimed to describe the clinical data, endoscopic findings, and treatments deployed in France's children with collagenous gastritis. METHODS: All French pediatric gastroenterology centers and pediatric centers for rare digestive diseases (Centres de Maladies Rares Digestives) were contacted to collect cases of collagenous gastritis, defined on gastric biopsies and diagnosed before 18 years of age. RESULTS: A total of 12 cases diagnosed (4 males and 8 females) between 1995 and 2022 could be analyzed. The median age at diagnosis was 12.5 years (7-15.2). The most frequent clinical presentation was abdominal pain (6/11) and/or nonspecific symptomatology attributed to anemia (8/10). Anemia was present in all children (11/11; Hb 2.8-9.1 g/dL). Nodular gastritis was present in 10 patients (antrum: 2; fundus: 4; in antrum and fundus: 4). All patients had a basement membrane thickening (from 19 to 100 µm). The treatments received were PPI (11), oral or intravenous martial supplementation (12), budesonide (1), and prednisone (1). Martial supplementation improved anemia in all cases. At discontinuation, nine of 10 patients had a recurrence of anemia. CONCLUSION: Collagenous gastritis is an exceptional condition, clinically manifested in children as abdominal pain and iron deficiency anemia probably of hemorrhagic origin. Patients require long-term follow-up and monitoring of their disease to describe the risk of progression better.

Collagenous Gastritis Is an Underdiagnosed Cause of Anemia and Abdominal Pain: Systematic Scoping Review.

BACKGROUND: Collagenous gastritis (CG) is a rare disease characterized by infiltration of the lamina propria with mononuclear cells and subepithelial deposition of collagen. Due to its nonspecific presentation, it is often misdiagnosed. The clinical characteristics, endoscopic, and histopathologic features, and treatment outcomes of CG have not been well defined. AIMS: We aim to summarize the existing evidence of CG. METHODS: According to the PRISMA Extension for Scoping Reviews, we performed a search on MEDLINE and EMBASE for articles with keywords including "collagenous gastritis" and "microscopic gastritis" from the inception of these databases to August 20, 2022. RESULTS: 76 Articles, including nine observational studies, and 67 case reports and series were included. There were 86 cases of collagenous colitis in the final analysis. Most patients presented with anemia (61.4%), followed by abdominal discomfort (60.5%), diarrhea (25.3%), and nausea/vomiting (23.0%). While 60.2% had gastric nodularity on endoscopy, erythema or erosions (26.1%) were also common, as well as normal findings (12.5%). 65.9% of histopathologic findings included subepithelial collagen bands, and 37.5% had mucosal inflammatory infiltrates. Common treatments employed were iron supplementation (42%), followed by PPI (30.7%), prednisone (9.1%), and budesonide (6.8%). Clinical improvement was seen in 64.2%. CONCLUSION: This systematic review summarizes the clinical characteristics of CG. Further studies to establish clear diagnostic criteria and identify effective treatment modalities of this less-recognized entity are needed.

Iron pill-induced gastritis: an unrecognized side effect of iron-deficiency anemia.

Iron-deficiency anemia is a prevalent condition usually treated with iron supplementation. Iron pill-induced gastritis is an under-recognized, albeit serious potential complication of iron pill ingestion in the upper gastrointestinal tract. This entity must be identified by healthcare providers who prescribe iron. The diagnosis of this unusual drug-induced disease is based on endoscopic findings and histopathological examination, because the clinical symptoms are vague and non-specific. Herein we report a case of a 79-year-old woman with iron-deficiency anemia taking oral ferrous sulfate with multiple congestive and eroded polypoid lesions. Histology showed an H. pylori-negative erosive gastritis with iron deposition, confirming the diagnosis of iron pill-induced gastritis. The aim of this report is to highlight that iron pill-induced gastritis is an under-diagnosed entity that must be kept in mind when patients undergo chronic iron-pill therapy because it can lead to serious complications of the upper gastrointestinal tract.

Pediatric Collagenous Gastritis: Clinical and Histologic Outcomes in a Large Pediatric Cohort.

OBJECTIVE: The aim of the study was to present the clinical characteristics, treatment, and outcomes of pediatric collagenous gastritis (CG). METHOD: This is a retrospective cohort study. Patients were identified via query of the institutional pathology database. Clinical data was obtained by review of medical records. RESULTS: Forty patients (57.5% female) were identified, mean age 11.3 ±â€Š3.7 years (2-16years). Isolated CG was present in 66.7%, coexisting collagenous duodenitis (CD) in 17.5%, collagenous colitis (CC) in 7.5%, and collagenous ileitis in 2.5%. Atopic comorbidities were found in 25%, autoimmune comorbidities in 12.5%. PRESENTING SYMPTOMS: Abdominal pain (77.5%), vomiting (65%), anemia (57.5%), nausea (55.5%), diarrhea (32.5%), anorexia (25.0%), weight loss (25%), gastrointestinal bleed (22.5%), poor growth (20%), poor weight gain (12.5%). ENDOSCOPIC FINDINGS: All had abnormal endoscopic findings on esophago-gastro-duodenoscopy (EGD), most commonly gastric nodularity (77.5%), visible blood (20%), erosions/superficial ulcerations (10%), ulcers (7.5%). Histologically, all patients had increased subepithelial collagen deposition. TREATMENT: A variety of medications aimed towards inflammation and symptomatic treatment were used. Patients with anemia received iron supplementation and responded. Otherwise, there was no significant association of clinical or histologic improvement with specific treatments. CLINICAL AND HISTOLOGIC OUTCOMES: 87.5% reported improvement or resolution of symptoms at the last follow-up (34.8 ±â€Š27.0 months). Persistent sub-epithelial collagen was noted in 73.1% on the last EGD. CONCLUSIONS: Despite persistent findings of increased sub-epithelial collagen deposition during the follow-up period, most patients with CG show remission or resolution of clinical symptoms. Anemia responds to iron supplementation in all patients.

Autoimmune gastritis concomitant with gastric adenoma and subacute combined degeneration of the spinal cord.

A 62-year-old woman was referred to our department for further investigation of anaemia. Blood test showed macrocytic anaemia. Oesophagogastroduodenoscopy (OGD) revealed proximal-predominant gastric atrophy and flat elevated lesion in the gastric body. Several days after OGD, she complained of gait disturbance and was diagnosed with subacute combined degeneration of the spinal cord. Furthermore, laboratory tests showed positive for both anti-parietal cell and anti-intrinsic factor antibodies, as well as increased serum gastrin level and decreased pepsinogen I level, which confirmed the diagnosis of autoimmune gastritis (AIG). Anaemia and neurological symptoms were improved after vitamin B12 supplementation. Subsequently, the patient underwent gastric endoscopic submucosal dissection; histopathological examination revealed gastric adenoma. AIG can cause gastric neoplasms and vitamin B12 deficiency, with the latter resulting in pernicious anaemia and neurological disorders. These diseases are treatable but potentially life-threatening. This case highlights the importance of early diagnosis of AIG and proper management of its comorbidities.

Subacute Combined Degeneration of the Spinal Cord Caused by Autoimmune Gastritis.

A 68-year-old woman presented with a 2-year history of worsening unsteady gait. Her neurological examination revealed peripheral neuropathy with lower limb sensory dominance. T2-weighted imaging revealed a disorder of the posterior cervical cord. Blood test findings revealed vitamin B12 deficiency, and gastroscopy revealed typical findings of autoimmune gastritis. She received vitamin B12 supplementation, but some peripheral neuropathy symptoms persisted due to longstanding vitamin B12 deficiency. Asymptomatic patients should undergo gastroscopy to detect autoimmune gastritis, as chronic vitamin B12 deficiency causes irreversible peripheral neuropathy.

Iron deficiency anemia: clinical and etiological features.

BACKGROUND: Iron deficiency is the most common nutritional deficiency worldwide and its resulting anemia appears as a public health problem. Iron deficiency anemia is rather a symptom than a disease in itself, and the identification of its etiology is of paramount importance. AIM:   to study the clinical and etiological features of iron deficiency anemia in an Internal Medicine department. METHODS: We conducted a retrospective descriptive study between 2001 and 2015 at an internal medicine department including patients presenting with iron deficiency anemia and having at least one etiological investigation. RESULTS: The average age was 45.6  16,3 years. Three main mechanisms of iron deficiency anemia were noted: repeated blood loss (94.4%), digestive malabsorption of iron (17.8%) and lack of dietary iron intake (6.6%). The digestive origin dominated the etiologies of iron deficiency anemia with a leading frequency of gastritis (32.2%). An underlying cancer was discovered in six cases. The average duration of follow-up was 9.1 months. An unfavorable outcome (persistence or recurrence of iron deficiency anemia) was associated with an absence or insufficiency of etiological treatment (p << 10-3) and with a duration of iron treatment inferior to 4 months (p = 0.034). CONCLUSION: In case of iron deficiency anemia, the prognosis depends on the quality of the etiological investigation. It can allow the discovery of an underlying cancer. The management of iron deficiency anemia relies on a well-led iron supplementation and an optimal treatment of the incriminated cause.

Helicobacter pylori Multidrug Resistance Due to Misuse of Antibiotics in Iran.

BACKGROUND: Helicobacter pylori might become highly resistant to antibiotics taken through the life time of patients. This study examined the change in antibiotic resistance of H. pylori by time. METHODS: Out of 985 dyspeptic patients who were referred to the endoscopy unit of Shariati hospital during 2010-2017, 218 patients with gastric biopsies positive for rapid urease test (RUT) and H. pylori culture were recruited in the study. H. pylori isolates were examined for resistance to 8 currently used antibiotics by the disc diffusion method. Results were compared with those from our three previous studies. The frequency of multidrug resistance (MDR) was also assessed. RESULTS: The highest resistance rate was to metronidazole (MTZ) (79.4%) followed by ofloxacin (OFX) (58.7%), ciprofloxacin (CIP) (46.8%), levofloxacin (LVX) (45%), tetracycline (TET) (38.5%), clarithromycin (CLR) (34.4%), amoxicillin (AMX) (27.1%) and furazolidone (FRZ) (23.9%). No significant difference was found between resistance of H. pylori isolates from male and female <40 and >40 years old and patients with gastritis and peptic ulcer. The highest rates of MDR were to MTZ+OFX (4.6%), MTZ+OFX+TET (2.8%), MTZ+OFX+CIP+LVX (6.4%) and MTZ+OFX+TET+ CIP+LVX (5%). CONCLUSION: Resistance to MTZ increased from 33%-55.6% in previous studies to 79.4% by time, to CLR increased from 1.4-7.3% to 34.4%, to TET increased from 0-38.1% to 38.5%, to AMX increased from 1.4%-7.3% to 27.1% and to FRZ increased from 0%-4.5% to 23.9%. Resistance to FQs was 45%-58.7%. Increase in H. pylori antibiotic resistance indicates antibiotic misuse. In Iran, with a considerable number of H. pylori- infected patients, antibiotic therapy should be saved for high risk patients and according to local antibiotic resistance patterns.

Supplementation of Caricol®-Gastro reduces chronic gastritis disease associated pain.

OBJECTIVE: Papaya and oats are natural food and used in traditional medicine in many parts of the world. Papaya has a high content of enzymes supporting digestive function. Oats are a source of minerals, beta-glucan fibres, immunmodulatory and antiinflammatory probiotic substances. Caricol®-Gastro combines both constituents, it was designed as vegan organic preparation for intestinal inflammatory diseases. We performed a randomized, double blind placebo controlled clinical trial to investigate the potential of Caricol®-Gastro as add on therapy in patients with diagnosed chronic gastritis. METHODS: 60 Patients with endoscopically confirmed mild chronic disease were recruited. A structured interview documented the baseline data. Then the patients were allocated to the verum or placebo group by handing out a numbered study package with the study substance for the daily intake at home. A single dose was 20 g, taken twice per day. After 30 days the participants were interviewed again. RESULTS: After the intake phase the disease related symptoms were found improved in both groups, indicating a strong placebo effect. However, the pain load reduction in the Caricol®-Gastro group was significantly larger (p=0.048). DISCUSSION: Due to the inherent biological activities of ingredients of papaya and of oats and their known effects (anti-inflammatory, epithelial integrity), the observed beneficial effects may be owed to the constituents synergisms to reduce chronic inflammation. We conclude, that the regular intake is a safe add on therapeutic option for patients with chronic gastritis to support standard medical care.

World trends for H. pylori eradication therapy and gastric cancer prevention strategy by H. pylori test-and-treat.

Helicobacter pylori-associated gastritis leads to the development of gastric cancer. Kyoto global consensus report on H. pylori gastritis recommended H. pylori eradication therapy to prevent gastric cancer. To manage H. pylori infection, it is important to choose the appropriate regimen considering regional differences in resistance to clarithromycin and metronidazole. Quinolones and rifabutin-containing regimens are useful as third- and fourth-line rescue therapies.

Protein losing enteropathy caused by eosinophilic gastroenteritis: A case report.

Protein losing enteropathy (PLE), a very rare disease with hypoproteinemia and edema as its characteristics, is caused by various diseases resulting in protein depletion from the gut. The diagnosis is relatively difficult due to its complex pathogeneses. The present paper reported a case whose symptom started with acute diarrhea and hypoproteinemia. Gastrointestinal endoscopies showed digestive ulcers and colon polyp. The treatments contained albumin infusion, Chinese herbal decoction and other symptomatic therapies. The hypoproteinemia become even worse and edema occurred after 4 days' treatment. A larger dose of albumin infusion (40-60 g/d) and modified herbal decoctions were prescribed. A final diagnosis of eosinophilic gastroenteritis (EG) complicated with PLE was confirmed by histopathological examination of a repeated gastroscopy. After three weeks' treatment, the serum albumin level was raised and the edema subsided gradually. In conclusion, herbs may have an effect on PLE patients, but PLE resulting from EG is very complex and easy to misdiagnose, especially in atypical conditions. Further studies are required to find the exact mechanisms.

Aspirin treatment exacerbates oral infections by Trypanosoma cruzi.

Oral transmission of the protozoan parasite Trypanosoma cruzi, the etiological agent of Chagas disease, has been documented in Latin American countries. The reported cases of infection were due to the ingestion of contaminated fresh fruit, juices, or sugar cane juice. There have been few studies on the physiopathology of the disease in oral transmission cases. Gastritis is a common ailment that can be caused by poor dietary habits, intake of alcohol or other gastric irritants, bacterial infection, or by the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs). This study investigated in a mouse model whether gastric mucosal injury, induced by aspirin, would affect the course of disease in animals infected with T. cruzi by the oral route. The CL14 and G strains of T. cruzi, both of low infectivity, were used. To this end, groups of BALB/c mice were treated during 5 days with aspirin (100 mg kg(-1)) before oral infection with T. cruzi metacyclic forms (4 × 10(5) or 5 × 10(7) parasites/mouse). Histological analysis and determination of nitric oxide and TNF-α were performed in gastric samples obtained 5 days after infection. Parasitemia was monitored from the thirteenth day after infection. The results indicate that aspirin treatment of mice injured their gastric mucosa and facilitated invasion by both CL14 and G strains of T. cruzi. Strain CL14 caused more severe infection compared to the G strain, as larger numbers of amastigote nests were found in the stomach and parasitemia levels were higher. Our study is novel in that it shows that gastric mucosal damage caused by aspirin, a commonly used NSAID, facilitates T. cruzi infection by the oral route.

Treatment of hemorrhagic gastritis by Ankaferd blood stopper versus Omeprazole: experimental randomized rat models.

BACKGROUND: Ankaferd blood stopper (ABS) is a herbal extract that enhances mucosal healing. It has therapeutic potential in the management of external hemorrhage and controlling gastrointestinal bleeding associated with various benign lesions refractory to conventional antihemorrhagic measures. The aim of this experimental study was to assess the effects of ABS on hemorrhagic lesions and compare them with omeprazole. METHODS: The study was conducted on 30 rats. Rats were divided into five groups: group A (only indomethacin), group B (ABS administration 60 min before indomethacin-induced injury), group C (ABS administration 30 min after indomethacin-induced injury), group D (omeprazole administration 60 min before indomethacin-induced injury), group E (omeprazole administration 30 min after indomethacin-induced injury). Gastric mucosal lesions were produced by indomethacin in all three groups. The effect was studied morphologically 6 h after oral administration of the drug. Subsequently, affected tissue was examined histologically. RESULTS: Based on the number and the total size of hemorrhagic lesions, the hemorrhagic lesion scores were significantly better in Group C compared to other groups (p < 0.05). The hemorrhagic lesion score of Group B was significantly better than Group D and Group A (p < 0.05). Omeprazole groups (Group D, Group E) did not show significant improvement as indicated by macroscopic scores. There was no significant difference between the groups with respect to microscopic scores. CONCLUSION: These results indicate that ABS has a potent inhibitory action on indomethacin-induced gastric bleeding and mucosal lesions and it is useful in the treatment of acute gastric mucosal lesions.

Dietary prevention of Helicobacter pylori-associated gastric cancer with kimchi.

To prove whether dietary intervention can prevent Helicobacter pylori-induced atrophic gastritis and gastric cancer, we developed cancer preventive kimchi (cpKimchi) through special recipe and administered to chronic H. pylori-initiated, high salt diet-promoted, gastric tumorigenesis mice model. H. pylori-infected C57BL/6 mice were administered with cpKimchi mixed in drinking water up to 36 weeks. Gross and pathological gastric lesions were evaluated after 24 and 36 weeks, respectively and explored underlying molecular changes to explain efficacies. Cancer preventive actions of anti-inflammation and anti-mutagenesis were compared between standard recipe kimchi (sKimchi) and special recipe cpKimchi in in vitro H. pylori-infected cell model. The erythematous and nodular changes, mucosal ulcerative and erosive lesions in the stomach were noted at 24th weeks, but cpKimchi administration significantly ameliorated. After 36th weeks, scattered nodular masses, some ulcers, and thin nodular gastric mucosa were noted in H. pylori-infected mice, whereas these gross lesions were significantly attenuated in cpKimchi group. On molecular analysis, significant expressions of COX-2 and IL-6, activated NF-κB and STAT3, increased apoptosis, and marked oxidative stresses were noted in H. pylori-infected group relevant to tumorigenesis, but these were all significantly attenuated in cpKimchi group. cpKimchi extracts imparted significant selective induction of apoptosis only in cancer cells, led to inhibition of H. pylori-induced proliferation, while no cytotoxicity through significant HO-1 induction in non-transformed gastric cells. In conclusion, daily dietary intake of cpKimchi can be an effective way either to rejuvenate H. pylori-atrophic gastritis or to prevent tumorigenesis supported with the concerted actions of anti-oxidative, anti-inflammatory, and anti-mutagenic mechanisms.

Practical selection of antiemetics in the ambulatory setting.

Nausea and vomiting are mediated primarily by three neurotransmitter pathways: visceral stimulation releases dopamine and serotonin; vestibular and central nervous system activation release histamine and acetylcholine; and chemoreceptor trigger zone activation releases dopamine and serotonin. Clinicians can improve the effectiveness and cost-effectiveness of treatments by targeting the appropriate pathways. Antihistamines and anticholinergics are most effective in patients with vestibular-mediated nausea secondary to vertigo. Serotonin antagonists block serotonin in the intestines and chemoreceptor trigger zone, and are most effective for treating gastroenteritis. Dopamine antagonists block dopamine in the intestines and chemoreceptor trigger zone; indications for these agents are similar to those for serotonin antagonists. For treatment of mild pregnancy-induced nausea, pyridoxine with or without doxylamine is recommended, and ginger may also be effective. In patients with migraine headache-associated nausea, metoclopramide improves response to oral anti-migraine agents. Ondansetron reduces nausea and vomiting in children with acute gastroenteritis and in women with hyperemesis gravidarum.

Fecal microbiota transplantation and prednisone for severe eosinophilic gastroenteritis.

Eosinophilic gastroenteritis is a rare disease of unknown etiology. It is characterized by patchy or diffuse eosinophilic infiltration of the bowel wall to a variable depth and various gastrointestinal manifestations. We describe a case of severe eosinophilic gastroenteritis presenting as frequent bowel obstruction and diarrhea in a 35-year-old man. The patient was misdiagnosed and underwent surgery because of intestinal obstruction when he was first admitted to a local hospital. Then he was misdiagnosed as having Crohn's disease in another university teaching hospital. Finally, the patient asked for further treatment from our hospital because of the on-going clinical trial for treating refractory Crohn's disease by fecal microbiota transplantation. Physical examination revealed a slight distended abdomen with diffuse tenderness. Laboratory investigation showed the total number of normal leukocytes with neutrophilia as 90.5%, as well as eosinopenia, monocytopenia and lymphocytopenia. Barium radiography and sigmoidoscopy confirmed inflammatory stenosis of the sigmoid colon. We diagnosed the patient as having eosinophilic gastroenteritis by multi-examinations. The patient was treated by fecal microbiota transplantation combined with oral prednisone, and was free from gastrointestinal symptoms at the time when we reported his disease. This case highlights the importance of awareness of manifestations of a rare disease like eosinophilic gastroenteritis.

Metagenomic analysis of the gastric microbiota cultivable from a patient with gastritis concomitant with Barrett's esophagus.

Barrett's esophagus is a distal metaplasia characterized by the transformation of squamous mucosa into columnar mucosa. This esophageal phenotype is a product not only of the chronic reflux of gastric acids, but also by microorganisms that colonize the oral cavity and stomach. Two classes of microbiota can be identified in Barrett's esophagus; microbiota type I is associated with the normal esophagus and type II with an inflamed esophagus. The present study describes the gastric microbiota of a patient with antral gastritis concomitant with Barrett's esophagus absent infection with Helicobacter pylori. Gastric biopsies were obtained following the protocol of Sydney and following ethical practices. The isolates were cultivated under microaerophilic conditions on Columbia Agar supplemented with IsoVitaleX™ and 7% sterile blood. Extracted DNA was sequenced using 454-GS and the results analyzed on the MG-RAST server. Gram negative isolates were found and bacteria resistant to levofloxacin, amoxicillin, tetracycline, erythromycin, and clarithromycin. The phyla Bacteroidetes, Firmicutes, Fusobacteria and Proteobacteria, the genus Bacteroides and the species group Bacteroides fragilis were most abundant. Functionally, the metabolism of carbohydrates, amino acids, and to a lesser extent, the metabolism of cofactors and vitamins were most dominant, and of which the enzymes ß-glucosidase (EC 3.2.1.21), ß-galactosidase (EC 3.2.1.23) and ß-N-acetylhexosaminidase (EC 3.2.1.52) were most dominant. The findings of this study, because they are of only one case may probably suggest a possible pathogenic role, previously undescribed for Bacteroides fragilis, associated with human gastritis when concomitant esophageal pathology exists.

Metagenomic analysis of the gastric microbiota cultivable from a patient with gastritis concomitant with Barrett´s esophagus / Análisis metagenómico de la microbiota gástrica cultivable a partir de un paciente con gastritis concomitante con esófago de Barrett

Barrett’s esophagus is a distal metaplasia characterized by the transformation of squamous mucosa into columnar mucosa. This esophageal phenotype is a product not only of the chronic reflux of gastric acids, but also by microorganisms that colonize the oral cavity and stomach. Two classes of microbiota can be identified in Barrett’s esophagus; microbiota type I is associated with the normal esophagus and type II with an inflamed esophagus. The present study describes the gastric microbiota of a patient with antral gastritis concomitant with Barrett’s esophagus absent infection with Helicobacter pylori. Gastric biopsies were obtained following the protocol of Sydney and following ethical practices. The isolates were cultivated under microaerophilic conditions on Columbia Agar supplemented with IsoVitaleX™ and 7% sterile blood. Extracted DNA was sequenced using 454-GS and the results analyzed on the MG-RAST server. Gram negative isolates were found and bacteria resistant to levofloxacin, amoxicillin, tetracycline, erythromycin, and clarithromycin. The phyla Bacteroidetes, Firmicutes, Fusobacteria and Proteobacteria, the genus Bacteroides and the species group Bacteroides fragilis were most abundant. Functionally, the metabolism of carbohydrates, amino acids, and to a lesser extent, the metabolism of cofactors and vitamins were most dominant, and of which the enzymes β-glucosidase (EC 3.2.1.21), β-galactosidase (EC 3.2.1.23) and β-N-acetylhexosaminidase (EC 3.2.1.52) were most dominant. The findings of this study, because they are of only one case may probably suggest a possible pathogenic role, previously undescribed for Bacteroides fragilis, associated with human gastritis when concomitant esophageal pathology exists.

El esófago de Barrett es una metaplasia distal caracterizada por la transformación de la mucosa escamosa a mucosa columnar. Este fenotipo esofágico es producto no solo de la exposición crónica al reflujo de ácidos gástricos sino también a microbios colonizantes de la cavidad oral y del estómago. El esófago Barrett presenta 2 clases de microbiotas; la microbiota tipo I asociada con esófago normal y la tipo II a fenotipos esofágicos inflamatorios. En el presente estudio se describió la microbiota gástrica de una paciente con gastritis antral concomitante con esófago de Barrett sin infección por Helicobacter pylori y se obtuvieron biopsias gástricas siguiendo el protocolo de Sydney y estándares bioéticos. Los cultivos se hicieron en condiciones microaerofílicas en agar Columbia suplementados con isovitalex y sangre estéril al 7%. El ADN extraído fue sometido a secuenciación empleando 454 GS y las lecturas fueron analizadas en el servidor MG-RAST. Se obtuvieron aislamientos gram-negativos y resistentes a levofloxacina, amoxicilina, tetraciclina, eritromicina y claritromicina. Los Phylum Bacteroidetes, Firmicutes, Fusobacteria y Proteobacteria, el género Bacteroides y las especies de grupo Bacteroides fragilis fueron los más abundantes. Funcionalmente, el metabolismo de carbohidratos, aminoácidos y en menor grado el metabolismo de cofactores y vitaminas fueron los más dominantes; de los cuales las enzimas la β-glicosidasa (EC 3.2.1.21), β-galactosidasa (EC 3.2.1.23) y la β-N-acetilhexosaminidasa (EC 3.2.1.52) fueron las más dominantes. Estos resultados, por ser de un solo caso, solo podrían sugerir un posible papel patogénico no descrito para Bacterioides fragilis asociado con gastritis humana cuando existe patología esofágica concomitante.