Low-grade intestinal metaplasia in Indonesia: Insights into the expression of proinflammatory cytokines during Helicobacter pylori infection and unique East-Asian CagA characteristics.

Helicobacter pylori infection is a major cause of intestinal metaplasia. In this study, we aimed to understand the reason underlying the low grade and incidence of intestinal metaplasia in Indonesia, based on the expression of genes encoding proinflammatory cytokines in gastric biopsy specimens. The possible reasons for the lesser virulence of the East-Asian-type CagA in Indonesia than that of the Western-type CagA, which is not common in other countries, were also investigated. The mRNA expression of cytokines was evaluated using real-time PCR. CagA characteristics were analyzed using in silico analysis. The expression of cytokines was typically not robust, among H. pylori-infected subjects in Indonesia, despite them predominantly demonstrating the East-Asian-type CagA. This might partially be explained by the characteristics of the East-Asian-type CagA in Indonesia, which showed a higher instability index and required higher energy to interact with proteins related to the cytokine induction pathway compared with the other types (p < 0.001 and p < 0.05, respectively). Taken together, besides the low prevalence of H. pylori, the low inflammatory response of the host and low CagA virulence, even among populations with high infection rates, may play an essential role in the low grade and low incidence of intestinal metaplasia in Indonesia. We believe that these findings would be relevant for better understanding of intestinal metaplasia, which is closely associated with the development of gastric cancer.

Prognostic value of C-reactive protein-to-albumin ratio in acute pancreatitis: a systematic review and meta-analysis.

Background: Acute pancreatitis (AP) is a common disorder and although most of the cases are mild, the mortality risk is high when it comes to severe AP. It is therefore important to determine the severity of AP as early as possible. This review aimed to determine the prognostic value of C-reactive protein-to-albumin ratio (CRP/alb ratio) in patients with AP. Methods: We performed a systematic search on the electronic databases PubMed, Science Direct, and Cochrane Library up to January 2023. Studies reporting CRP/alb ratio on admission and its association with severity or mortality in AP patients were included. We calculated pooled mean difference (MD) and their 95% confidence intervals (CI) using a random-effects model. Quality assessment of the included studies was appraised using a Newcastle-Ottawa scale. Results: A total of six studies comprising 2244 patients were included in this meta-analysis. Severe AP had higher CRP/alb ratio on admission than mild-moderate AP (pooled MD: 3.59; 95% CI: 2.51-4.68; p<0.00001). CRP/alb ratio was also significantly higher on non-survivor AP patients compared to survivor AP patients (pooled MD: 2.12; 95% CI: 0.43-3.8; p < 0.01). Conclusion: High CRP/alb ratio can be used as an early predictor of poor prognosis in patients with AP.

Diabetes and fatty liver: Involvement of incretin and its benefit for fatty liver management.

Fatty liver disease is defined as liver condition characterized by hepatic steatosis, closely related to pathological conditions in type 2 diabetes and obesity. The high prevalence of fatty liver disease in obese patients with type 2 diabetes reached 70%, reflecting the importance of these conditions with fatty liver. Although the exact pathological mechanism of fatty liver disease, specifically non-alcoholic fatty liver disease (NAFLD) remains not completely revealed, insulin resistance is suggested as the major mechanism that bridged the development of NAFLD. Indeed, loss of the incretin effect leads to insulin resistance. Since incretin is closely related to insulin resistance and the resistance of insulin associated with the development of fatty liver disease, this pathway suggested a potential me-chanism that explains the association between type 2 diabetes and NAFLD. Furthermore, recent studies indicated that NAFLD is associated with impaired glucagon-like peptide-1, resulting in decreased incretin effect. Nevertheless, improving the incretin effect becomes a reasonable approach to manage fatty liver disease. This review elucidates the involvement of incretin in fatty liver disease and recent studies of incretin as the management for fatty liver disease.

Additional treatment of vitamin D for improvement of insulin resistance in non-alcoholic fatty liver disease patients: a systematic review and meta-analysis.

Insulin resistance provides an important role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Several studies already evaluate vitamin D supplementation for NAFLD patients in relation to insulin resistance. The results obtained still carry conflicting results. This study aimed to evaluate the effect of additional treatment of vitamin D for the improvement of insulin resistance in NAFLD patients. Relevant literatures were obtained from PubMed, Google Scholar, COCHRANE, and Science Direct database. The obtained studies were analyzed using fixed effect model or random effect model. Seven eligible studies with a total of 735 participants were included. Vitamin D supplementation improves insulin resistance in NAFLD patients, marked by reduced Homeostatic Model Assessment for Insulin Resistance (HOMA-IR), with pooled mean difference - 1.06 (p = 0.0006; 95% CI - 1.66 to - 0.45). Vitamin D supplementation increase the level of vitamin D serum with pooled mean difference of 17.45 (p = 0.0002; 95% CI 8.33 to 26.56). Vitamin D supplementation decrease ALT levels, with pooled mean difference of - 4.44 (p = 0.02; 95% CI - 8.24 to - 0.65). No effect was observed for AST levels. Vitamin D supplementation provides beneficial effects on the improvement of insulin resistance in NAFLD patients. This supplementation may reduce HOMA-IR in such patients. It may serve as a potential adjunctive treatment for NAFLD patients.

Massive hemobilia caused by rupture of gastroduodenal artery pseudoaneurysm, a delayed complication of laparoscopic cholecystectomy: a case report.

BACKGROUND: Hemobilia is a rare cause of upper gastrointestinal bleeding that originates from the biliary tract. It is infrequently considered in diagnosis, especially in the absence of abdominal trauma or history of hepatopancreatobiliary procedure, such as cholecystectomy, which can cause arterial pseudoaneurysm. Prompt diagnosis is crucial because its management strategy is distinct from other types of upper gastrointestinal bleeding. Here, we present a case of massive hemobilia caused by the rupture of a gastroduodenal artery pseudoaneurysm in a patient with a history of laparoscopic cholecystectomy 3 years prior to presentation. CASE PRESENTATION: A 44-year-old Indonesian female presented to the emergency department with complaint of hematemesis and melena accompanied by abdominal pain and icterus. History of an abdominal trauma was denied. However, she reported having undergone a laparoscopic cholecystectomy 3 years prior to presentation. On physical examination, we found anemic conjunctiva and icteric sclera. Nonvariceal bleeding was suspected, but esophagogastroduodenoscopy showed a blood clot at the ampulla of Vater. Angiography showed contrast extravasation from a gastroduodenal artery pseudoaneurysm. The patient underwent pseudoaneurysm ligation and excision surgery to stop the bleeding. After surgery, the patient's vital signs were stable, and there was no sign of rebleeding. CONCLUSION: Gastroduodenal artery pseudoaneurysm is a rare complication of laparoscopic cholecystectomy. The prolonged time interval, as compared with other postcholecystectomy hemobilia cases, resulted in hemobilia not being considered as an etiology of the gastrointestinal bleeding at presentation. Hemobilia should be considered as a possible etiology of gastrointestinal bleeding in patients with history of cholecystectomy, regardless of the time interval between the invasive procedure and onset of bleeding.