Endoscopic and histopathological assessment of individuals undergoing one anastomosis gastric bypass: a 2-year follow-up.

BACKGROUND: There is much debate over the occurrence of biliary reflux to the gastric pouch after one anastomosis gastric bypass (OAGB) and its potential risks. OBJECTIVE: To assess endoscopic and histopathological findings following a standardized protocol of biopsy collection two years after OAGB. METHODS: A historical cohort study was conducted, based on a prospectively collected database, which involved 39 participants who underwent OAGB. Participants underwent clinical evaluation and esophagogastroduodenoscopy at the time of surgery and 24 months afterward. Post-operatively, biopsy specimens in esophagogastric junction, pouch, and anastomosis were systematically collected. RESULTS: 92.3% of the participants were female and the mean age was 37 ± 8.5 years. The mean body mass index (BMI) significantly decreased from 37.6 ± 5.7 kg/m2 to 27 ± 4.1 kg/m2 after 2 years (p < 0.001). The mean %TWL was 27.2 ± 10.5%. The prevalence of non-erosive gastritis significantly increased from 25.6 to 51.3% (p = 0.02). Erosive gastritis significantly decreased from 28.2 to 10.3% (p = 0.04). Four cases of marginal ulcers were identified (10.3%). The commonest histopathological finding was mild inflammation in 74.3% (esophagogastric junction), 58.9% (pouch), and 71.8% (anastomosis). There was one case of focal intestinal metaplasia in each site of interest and no cases of dysplasia or severe inflammation. CONCLUSIONS: Using a standardized protocol of post-operative biopsy collection, low rates of severe endoscopic and histopathological abnormalities were observed two years after OAGB. Nevertheless, as most patients have histologically proven inflammation, bile in the gastric pouch, and endoscopic gastritis, long-term surveillance is essential because of the uncertain risk of these abnormalities.

Assessment of Gastritis and Gastric Cancer Risk in the Chilean Population Using the OLGA System.

Gastric cancer (GC) is the first cancer-related cause of death in Chile; however, no plan for GC early detection has been implemented in this country. The OLGA system characterizes gastritis from stages 0 to IV according to the risk of developing GC based on H. pylori infection, atrophy, metaplasia and GC. In this study, the performance of the OLGA system was evaluated in 485 Chilean patients receiving routine endoscopy to improve the detection of early GC or preneoplastic lesions. The results showed that OLGA scores, atrophy, metaplasia and GC increased significantly with age (p < 0.001). Conversely, H. pylori infection was higher in younger groups (p < 0.05). All gastric lesions were more frequent in men than women. The majority of patients with atrophy also had metaplasia (99%, p < 0.0001). Patients with H. pylori infection had more gastric atrophy and metaplasia than those without infection (p < 0.05). Of the 485 patients, 21 (4.3%) had GC, being 2.3 times more frequent among men than women and about 2/3 (14) were in OLGA stage ≥2. In addition, 19 (90%) GC patients had atrophy and 18 (85%) had metaplasia (p < 0.001). In conclusion, the OLGA system facilitated the evaluation of GC precursor lesions particularly in patients with an OLGA score > 2 between 45 and 56 years old, because this group showed atrophy and intestinal metaplasia more frequently. Therefore, biennial endoscopic surveillance of patients with an OLGA >2 can be an important health policy in Chile for diagnosing GC in its early stages and reducing mortality over the next two decades.

[Effect on medical practices after health insurance application for "H. pylori gastritis"].

Eradication therapy for H. pylori infected gastritis became the health insurance application in Japan in 2013. It will seem that the conception of "the chronic gastritis" greatly changes from now on in Japan. "The chronic gastritis" will be classified in H. pylori gastritis and functional dyspepsia in the near future. On the other hand, it is expected that the process of the gastric cancer detection survey greatly changes too. It seems that the ABC checkup using the blood will be carried out in place of Barium examination. A decrease in gastric cancer mortality is expected as things mentioned above from now on.

Additional value of upper GI tract endoscopy in the diagnostic assessment of childhood IBD.

OBJECTIVES: For the choice of treatment in children with inflammatory bowel disease (IBD), it is important to make a distinction between Crohn disease (CD) and ulcerative colitis (UC). To look for pathognomonic features of CD, upper gastrointestinal tract (UGT) endoscopy has become part of the routine evaluation of children with suspected IBD; however, pathological changes can also be found in the UGT in patients with UC. The aims of the present study were to establish the role of UGT involvement in the diagnostic assessment of suspected IBD in children and to detect histopathological changes in the UGT mucosa, which can distinguish CD from non-CD (UC and non-IBD). METHODS: Biopsies (colon, ileum, duodenum, stomach, esophagus) from children suspected of having IBD who underwent endoscopy between 2003 and 2008 were reassessed by a blinded, expert pathologist. The histological findings of the UGT were compared with the diagnosis based on ileocolonic biopsies and the final diagnosis. RESULTS: In 11% of the children with CD, the diagnosis was based solely on the finding of granulomatous inflammation in the UGT. Focal cryptitis of the duodenum and focally enhanced gastritis were found significantly more frequently in children with CD compared with children with UC and non-IBD, with a specificity and positive predictive value of 99% and 93% and 87.1% and 78.6%, respectively. CONCLUSIONS: Histology on ileocolonic biopsies alone is insufficient for a correct diagnosis of CD or UC in children. UGT endoscopy should, therefore, be performed in the diagnostic assessment of all children suspected of having IBD.

Assessment of systemic matrix metalloproteinase and their regulator response in children with Helicobacter pylori gastritis.

BACKGROUND: Helicobacter pylori causes gastritis and is the most important risk factor of peptic ulcer disease and gastric cancer. In chronic adulthood H. pylori infection some matrix metalloproteinases (MMPs), which are proteolytic metalloendopeptidases regulated by tissue inhibitors of metalloproteinases (TIMPs), are upregulated. Our aim was to determine circulating levels of MMPs and their regulators TIMP-1, human neutrophil elastase (HNE) and myeloperoxidase (MPO) in childhood H. pylori infection. DESIGN AND METHODS: Twenty-six H. pylori positive and 34 H. pylori negative children whose H. pylori status was verified by histological examination of gastric biopsies were included. Serum samples were analysed by enzyme-linked immunosorbent assay. RESULTS: Significantly decreased serum levels of TIMP-1 were detected in H. pylori-infected children (median, 97.50 ng/mL) as compared to H. pylori-negative children (median, 118.5 ng/mL, p = 0.003). However, there were no significant differences in serum levels of MMP-2, -7, -8, -9, and their regulators HNE and MPO between H. pylori-positive and -negative children. CONCLUSIONS: Differing from the recent findings in adulthood H. pylori infection, only circulating TIMP-1 levels were significantly different between H. pylori-positive and -negative children. Whether this reflects the first sign of a proteolytic cascade later leading to increased levels of MMPs remains to be shown.

[Helicobacter pylori. I. Morphology, biochemistry, antigenic profile and correlated diseases]. / Helicobacter pylori. I. Parte: Morfologia, biochimica, profilo antigenico e patologie correlate.

Infection by Helicobacter pylori (HP) occurs all over the world and is related to the socio-economic development of the subject's country of residence and age. Various strains of HP can be identified on the basis of the microbiological characteristics of the bacterium and, in particular, or its antigenic profile, while the virulence factors are responsible for the damage that HP can cause. The virulence factors include components (flagellum and adhesin) and substances produced by bacterium (enzymes and cytotoxins), the most important among which are urease and the cytotoxins, CagA and VacA. It is the association of these virulence factors that is responsible for the different pathologies to which HP-positive subjects are prone. The link between HP and gastritis, peptic ulcer and gastric cancers (adenocarcinoma and lymphoma) is now proven. Whether there is a link between HP and RAP in young children is still a matter for debate; some Authors claim that there is, while others refute it.

Infección por helicobacter pylori y daño gástrico en niños de nivel socioeconómico bajo / Helicobacter pylori infection and gastric damage in children of low socioeconomical status

Objetivo: establecer relaciones entre los hallazgos histológicos y endoscópicos en la mucosa gástrica y la identificación de H. pylori en niños en que se realizó endoscopía digestiva por distintas razones. Pacientes y método: Se estudiaron retrospectivamente los antecedentes clínicos, el aspecto endoscópico de la mucosa gástrica y los informes del examen histológico de la misma en 100 niños (59 varones) de baja condición socioeconómica, de 2 a 17 (promedio 11) años de edad en que, por diferentes motivos, fue necesario realizar endoscopia digestiva alta para fines diagnósticos y se cotejaron con la presencia o ausencia de H. pylori registrada mediante prueba de la ureasa o en el examen histológico de los muestras obtenidas. Resultados: En 69 por ciento de los niños de la serie se identificó H. pylori, cuya prevalencia aumento con la edad (X2 11,97 p= 0,0025), llegando a 78 por ciento entre los 13 a 17 años. El agente se detectó en 30 por ciento de los niños sin lesiones histológicas y en 88 por ciento de los que tenían signos de gastritis. En 16 por ciento de los niños infectados no se registraban síntomas de la afección a pesar de estar contaminados y tener lesiones gástricas. Conclusión: estos resultados sugieren una fuerte asociación causa a efecto (X2 = 34,5, p= 0,00001) entre colonización de la mucosa gástrica con el agente y la existencia de signos endoscópicos e histológicos de gastritis

Optimal therapy for stress gastritis.

OBJECTIVE: The authors compared the results of sucralfate versus H2 blocker +/- antacid as prophylaxis for stress ulceration in an intensive care unit patient population. SUMMARY BACKGROUND DATA: Stress ulceration carries high morbidity and mortality for the patient who is critically ill. Gastric acid neutralization is an effective prophylaxis. The impact of increased gastric colonization with bacterial pathogens on nosocomial pneumonia after acid neutralization is unclear. The efficacy of sucralfate prophylaxis for stress ulceration and its the effect on the nosocomial pneumonia rate is controversial. The financial implications of sucralfate prophylaxis versus H2 blocker-based acid neutralization therapy has not been studied. METHODS: Ninety-eight injured patients who were critically ill and who required intubation and intensive care unit (ICU) support for at least 72 hours without gastric feeding were randomized and received either maximal H2 blocker infusion therapy (continuous infusion of ranitidine at 0.25 mg/kg/hr after a loading dose of 0.5 mg/kg) plus antacids (for persistent pH < 4) or sucralfate (1 g every 6 hours via nasogastric tube) for stress ulcer prophylaxis. Efficacy in preventing stress ulcer complications was determined. The impact of each therapeutic approach on development of nosocomial pneumonia was evaluated. The charges/cost for each approach was analyzed. RESULTS: Heme-positive gastric aspirates occurred in 99% of the patients, whereas 12 (7 in the H2 blocker group and 5 in the sucralfate group) were grossly positive for blood. However, only one from each group required transfusion, and one in the H2 blocker group required operation. Gastric colonization preceded tracheobronchial colonization in five patients in the H2 blocker group and one patient in the sucralfate group; simultaneous gastric/oropharyngeal colonization preceded positive tracheobronchial growth in six patients who received H2 blocker and one patient who received sucralfate. The overall pneumonia rate was 27.5% in the H2 blocker group and 20.8% in the sucralfate group (p = 0.48). Days on ventilator were 13.5 versus 9.1, (p = 0.06), ICU lengths of stay were 14.7 versus 10.2 (p = 0.06), and hospital lengths of stay were 27.8 versus 20.0 (p = 0.029) for the H2 blocker group and sucralfate group, respectively. Based on current charges and protocols for optimal H2 blocker and sucralfate prophylaxis, use of sucralfate rather than H2 blockers would decrease the annual cost by more than $30,000 per bed. CONCLUSIONS: Sucralfate is as efficacious as maximal H2 blocker therapy for stress ulceration prophylaxis, and may have a beneficial effect on the incidence of nosocomial pneumonia. Sucralfate has a major reduction on nursing requirements for stress ulcer prophylaxis and would save approximately $30,000 per ICU bed per year in patient charges.

Amoxycillin plus tinidazole for Campylobacter pylori gastritis in children: assessment by serum IgG antibody, pepsinogen I, and gastrin levels.

32 children (mean age 12 years, range 6-18) with non-specific abdominal pain and Campylobacter pylori positive gastritis received a six week course of daily oral amoxycillin (50 mg/kg) and tinidazole (20 mg/kg). Before treatment and one month after stopping treatment, endoscopic biopsy samples were taken from the antral mucosa and serum C pylori IgG antibody, pepsinogen I, and gastrin levels were measured in fasting blood samples. One month after treatment 30 children (94%) were cleared of C pylori and gastritis had resolved in 27 (84%) and was improved in the remaining 5. Serum IgG, pepsinogen I, and gastrin levels were significantly decreased after treatment. Of 12 children assessed at six months, 9 remained free of C pylori. Increases or decreases in IgG level indicated clearance or recurrence, respectively, of C pylori.

Assessment of the 'mucus-bicarbonate' barrier in the stomach of patients with chronic gastric disorders.

The composition of gastric mucus and the amount of gastric bicarbonate secretion have been investigated in 26 subjects including healthy controls, duodenal ulcer patients and subjects with chronic gastric disorders (benign gastric ulcer or chronic superficial gastritis). Qualitative changes in gastric mucus (expressed as a reduction in the values of 'mucoprotective index') were found in the gastric ulcer group, but not in patients with chronic superficial gastritis. Basal bicarbonate secretion was significantly reduced (p less than 0.01) in subjects with gastric ulcer and chronic gastritis, compared with healthy controls. Mucus secretion and bicarbonate production proved to be normal in duodenal ulcer patients. Our results support the concept that impairment of the 'mucus-bicarbonate' barrier is an important pathogenetic factor in gastric ulcer and chronic gastritis.

Assessment of the upper gastrointestinal tract in hemodialysis patients awaiting renal transplantation.

Seventy-five dialysis patients awaiting renal transplantation were studied. Investigations included single contrast barium meal, serum gastrin assay, gastric acid studies, and fiberoptic gastroduodenoscopy with multiple biopsies. Radiological studies revealed five duodenal ulcers and one gastric ulcer. Endoscopy showed gastroduodenal lesions in 57 patients (49%). Superficial gastritis was present in 50 patients (66.7%), atrophic gastritis in 11 (14.6%), and duodenitis in 30 (40%). Hypergastrinemia was observed in 48 patients (64%). Maximum acid output was markedly elevated in 33 patients. Acid hypersecretion was found to be correlated with the presence of endoscopic lesions and histological evidence of gastritis. Nine of the 11 patients with atrophic gastritis were acid hyposecretors and had low gastrin levels. Pretransplant gastric assessment identified a relevant number of gastroduodenal lesions in these patients. The increased risk of severe posttransplant ulceration justifies thorough gastric assessment and prophylactic antiulcer therapy in all renal transplant candidates.

Alkaline reflux gastritis. An objective assessment of its diagnosis and treatment.

The hypothesis that reflux of upper intestinal content, particularly of bile acids (BA), is responsible for a unique postgastrectomy syndrome, alkaline reflux gastritis, was tested on 28 occasions in 21 postoperative patients (14 symptomatic patients, 7 controls). Parameters evaluated: recumbent (rec.), upright, p.c. intragastric pH, {BA}, net BA reflux per hour, specific BA fractions, fasting and p.c. gastrin, maximal acid output (MAO), gastric emptying of solids by delta-scintigraphy), and the severity of nonstomal histologic gastritis, the "gastritis score," graded 0-15 by an independent senior pathologist. For the entire group, gastritis severity correlated positively with intragastric {BA} and net BA reflux per hour, both in recumbency and p.c. Five symptomatic patients demonstrated rec. and p.c. {BA} and net BA reflux per hour greater than two standard deviations from comparable mean values in control patients. They differed significantly from the remaining symptomatic patients as follows: increased intragastric {BA} and net BA reflux per hour, increased intragastric pH and decreased MAO. They also demonstrated a more severe grade of gastritis. Lithocholic acid was present in their reflux content significantly more often. Bilious vomiting was also more frequent. No other differences could be identified, either objectively or clinically, between the symptomatic groups. Four patients with excessive reflux underwent Roux-en-Y revision and restudy 6-22 months later. BA reflux was completely abolished, histologic gastritis improved, hematocrit rose, MAO increased, and gastric emptying slowed. Burning pain, bilious vomiting, and symptoms of esophageal reflux were eliminated. Vomiting and nausea were improved. Diarrhea was unchanged. The objective criteria outlined can identify symptomatic postgastrectomy patients with a greater than normal reflux and gastritis. Clinical criteria alone cannot. Revisional surgery in these patients eliminates reflux, improves gastritis, and produces symptomatic improvement. The hypothesis under consideration is strengthened but not proven.

[A safe alternative for the diagnosis of pernicious anemia--a contribution to medical economics (proceedings)]. / Sichere Alternative für die Perniziosa-Diagnostik--ein Beitrag zur Kostensenkung.

Mucosal biopsies of corpus and antrum were performed in 17 patients with pernicious anemia. In all patients the corpus mucosa showed atrophic gastritis, while in 16 the antrum was normal or showed only superficial gastritis. This combination is conclusive for pernicious anemia. Over 80% of megaloblastic anemias are caused by pernicious anemia. It is therefore proposed that endoscopy and biopsy be performed as the first examination in these patients. In this way the diagnosis is simple, rapid and economical.