Newly diagnosed type 1 diabetes in a 93 year old

Type 1 diabetes is typically a disease of young but can present at any age. We present a case of a 93-year-old woman who presented with 10 days history of feeling lethargic, polydipsia and decreased appetite. Her capillary blood glucose was raised at 25 mmol/L with significant ketonaemia and venous blood gas showing metabolic acidosis. She had a background of primary hypothyroidism and vitamin B12 deficiency with weakly positive parietal cell antibodies. Laboratory investigations confirmed diabetes with HbA1c of 117 mmol/mol (12.9%). In view of high clinical suspicion of type 1 diabetes, her diabetes autoantibodies were checked which showed strongly positive anti-GAD antibody with titre of >2000 IU/mL (range<10) confirming our diagnosis. She was treated with diabetic ketoacidosis protocol with intravenous fluids and intravenous insulin. On recovery, she was discharged home on once daily insulin with aim to self-manage diabetes with support from district nurses and to avoid hypoglycaemia.

Histologic features in an autoimmune gastritis patient with hypergastrinemia: Call for a grading system for G cell hyperplasia

Introduction/Objective Autoimmune gastritis (AG) is characterized by oxyntic glands destruction, metaplasia, enterochromaffin-like endocrine cell abnormality and G-cell hyperplasia with hypergastrinemia. The gastrin level can be extraordinarily high in certain cases to justify suspicion of Zollinger-Ellison syndrome. We herein report one such case and discuss clinical implication of a grading system for G-cell hyperplasia to correlate histology with gastrin levels. Methods/Case Report The patient was a symptomatic 65 year-old female with hypergastrinemia (2,068 pg/mL), negative abdomen/pelvis CT scan, positive anti-intrinsic factor and anti-parietal cell antibodies. Under esophagogastroduodenoscopy, biopsies were obtained from gastric cardia, fundus, corpus, incisura angularis, and antrum. Morphology and immunostains confirmed autoimmune gastritis. Diffuse linear pattern G-cell hyperplasia was evident in antrum and incisura angularis, counting up to 200 G-cells per linear millimeter. One study defined G-cell hyperplasia as &gt;140 gastrin-positive cells per linear millimeter while another proposed a 2-tier stratification, i.e., simple hyperplasia (4-5 cells for each gland) and linear hyperplasia (continuous chain-like distribution of G-cells). Such scoring, however, was largely qualitative and fell short in delineating the extent of G-cell hyperplasia and correlation with gastrinemia. Results (if a Case Study enter NA) NA Conclusion Lack of G-cell grading system hindered our unequivocal determination of the G-cell hyperplasia as underlying or contributing cause of hypergastrenemia. The unique features of our case highlighted the necessity for installing a practical grading system that incorporates G-cell density, pattern (linear vs. nodular), extent of involved areas, other features of AG to correspond to gastrin level. With accumulation of clinical information, one such grading system is feasible and will improve our knowledge and patient care.

Dose-dependent association of proton pump inhibitors use with gastric intestinal metaplasia among Helicobacter pylori-positive patients

Background Gastric intestinal metaplasia is a pre-cancerous condition associated with multiple factors. Objective We evaluated whether cumulative proton pump inhibitor dose is associated with the diagnosis of gastric intestinal metaplasia while controlling for multiple variables. Methods We retrospectively identified patients who underwent upper endoscopy with gastric biopsy between 2005 and 2014. Covariate data retrieved included age, sex, ethnicity, smoking status, Helicobacter pylori status (based on clarithromycin–amoxicillin–proton pump inhibitor issued), cumulative proton pump inhibitor issued within 10 years (quartiles (PPI-Q1–4) of daily drug dose), anti-parietal cell antibodies, body mass index and comorbidity index. Results Of the 14,147 included patients (median age 63.4 years; women 54.4%; Helicobacter pylori-positive 29.0%), 1244 (8.8%) had gastric intestinal metaplasia. Increasing age, Helicobacter pylori infection, smoking, anti-parietal cell antibodies and proton pump inhibitor use were all associated with the diagnosis of gastric intestinal metaplasia. Upper quartiles of cumulative proton pump inhibitor doses (PPI-Q4 and PPI-Q3 vs. PPI-Q1) were associated with the diagnosis of gastric intestinal metaplasia: adjusted odds ratios 1.32 (95% confidence interval (CI) 1.11–1.57) and 1.27 (95% CI 1.07–1.52), respectively, for the whole cohort ( Ptotal 0.007, Ptrend 0.013), 1.69 (95% CI 1.23–2.33) and 1.40 (95% CI 1.04–1.89), respectively, for Helicobacter pylori-positive patients ( Ptotal 0.004, Ptrend 0.005) and 1.21 (95% CI 0.98–1.49) and 1.20 (95% CI 0.96–1.49), respectively, for Helicobacter pylori-negative patients ( Ptotal 0.288, Ptrend 0.018). Upper quartiles of proton pump inhibitor dose were associated with a 5–10-fold increased risk of low-grade dysplasia. Conclusions Among Helicobacter pylori-positive patients, proton pump inhibitor use appears to be associated with a dose-dependent increased likelihood of gastric intestinal metaplasia.

Anti-parietal cell antibodies seroconversion in patients with autoimmune atrophic gastritis: a prospective study

The purpose of the study was to evaluate the atrophic changes of body and antrum gastric mucosa, the occurrence of Helicobacter pylori infection and the possibility of seroconversion in patients with autoimmune gastritis throughout 10 years. Material and methods. 203 Chernobyl nuclear power plant accident recovery workers were included in the prospective study. Blood levels of anti-parietal cell antibodies, basal gastrin-17, pepsinogens I and II were evaluated in all the patients to diagnose autoimmune gastritis and to assess gastric mucosa non-invasively. Results. Anti-parietal cell antibodies were found in 34.5% of the patients. Eradication rates were low (32.850.0%) in the patients with atrophy of gastric mucosa in the first 3 years of observation. Statistically significant decrease in pepsinogen I and gastrin-17 serum levels was observed in the patients with H. pylori-associated autoimmune gastritis throughout first 46 years. In the next 710 years pepsinogen I and gastrin-17 serum levels were increasing possibly due to positive effect of H. pylori eradication therapy. Successful eradication leads to disappearance of anti-parietal cell antibodies in 33.4% of the patients by the 10th year of the observation. Conclusion. The obtained results show that H. pylori eradication therapy is effective in reducing atrophic changes of gastric mucosa in the patients with autoimmune gastritis. Against the background of successful treatment the levels of pepsinogen I and gastrin-17, the markers of body and antrum gastric mucosa atrophy, were increasing. In the patients with autoimmune gastritis but without H. pylori infection the following trend was not noticed.

The etiology of chronic gastritis in children with celiac disease

Study objective. To investigate the etiology of chronic gastritis in children with various forms of coeliac disease. Patients and methods. 176 children with various forms of coeliac disease and morphologically verified chronic gastritis (CG) were examined. The first group consisted of 58 children with CG and newly diagnosed CD who did not adhere to a gluten-free diet (GFD), the second group included 49 children with CG and CD on a GFD. The comparison group (group 3) consisted of 69 children with CG but without CD. Morphological examination of the gastric and duodenal mucous membrane was performed. Verification of Helicobacter pylori infection for all participants was carried out by the rapid urease test (RUT) and the histological detection of the rod forms of H. pylori in any part of the gastric mucosa. Serological examination included determination of tissue transglutaminase IgA и IgG antibodies and deamidated gliadin peptide IgG antibodies; anti-parietal cell antibodies, IgG. Results. H. pylori was equally often detected in children with CD and in the control group: in group 1 – 63.8%, in group 2 – 53.1%, in group 3 – 68.1% (p1-2 = 0.387; p1-3 = 0.954; p2-3 = 0.420). Anti-parietal cell antibodies were equally common in groups 1 and 3, but were not detected in group 2: in group 1 – 14.9%, in group 3 – 10.1% (p1-2 = 0.002; p1-3 = 0.562; p2-3 = 0.012). Most often, the etiology of CG remained undetermined in group 2, among children with CD, who adhere to the GFD: group 1 – 19%, group 2 – 40.8%, group 3 – 15.9% (p1-2 = 0.025; p1-3 = 0.776; p2-3 = 0.012). CG associated with bile reflux was found in all groups without statistically significant differences: in group 1 – 5.2%, in group 2 – 6.1%, in group 3 – 5.8% (p1-2 = 0.877; p1-3 = 0.916; p2-3 = 0.960). The level of antibodies to Castle’s factor correlated with the level of antibodies to tissue transglutaminase r = 0.483; p = 0.002. Conclusion. The study data are suggestive of a systemic effect of celiac disease on the gastric mucosa. The stomach, along with the small intestine, is a target organ for celiac disease. The coexistence of primary immune-mediated lesion of the gastric mucosa and the H. pylori-induced inflammatory and autoimmune proсess is also possible. The prevalence of H. pylori in CD does not depend on a gluten-free diet and does not differ from the prevalence of H. pylori in CG. Key words: celiac disease, chronic gastritis, children