AIM:To describe the pathophysiology, clinical presentation, natural history, and therapy of portal hypertensive gastropathy (PHG) based on a systematic literature review. METHODS:Computerized search of the literature was performed via PubMed using the following medical subject headings or keywords: "portal" and "gastropathy"; or "portal" and "hypertensive"; or "congestive" and "gastropathy"; or "congestive" and "gastroenteropathy". The following criteria were applied for study inclusion: Publication in peer-reviewed journals, and publication since 1980. Articles were independently evaluated by each author and selected for inclusion by consensus after discussion based on the following criteria: Well-designed, prospective trials; recent studies; large study populations; and study emphasis on PHG. RESULTS:PHG is diagnosed by characteristic endoscopic findings of small polygonal areas of variable erythema surrounded by a pale, reticular border in a mosaic pattern in the gastric fundus/body in a patient with cirrhotic or non-cirrhotic portal hypertension. Histologic findings include capillary and venule dilatation, congestion, and tortuosity, without vascular fibrin thrombi or inflammatory cells in gastric submucosa. PHG is differentiated from gastric antral vascular ectasia by a different endoscopic appearance. The etiology of PHG is inadequately understood. Portal hypertension is necessary but insufficient to develop PHG because many patients have portal hypertension without PHG. Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy PHG increases in frequency with more severe portal hypertension, advanced liver disease, longer liver disease duration, presence of esophageal varices, and endoscopic variceal obliteration. PHG pathogenesis is related to a hyperdynamic circulation, induced by portal hypertension, characterized by increased intrahepatic resistance to flow, increased splanchnic flow, increased total gastric flow, and most likely decreased gastric mucosal flow. Gastric mucosa in PHG shows increased susceptibility to gastrotoxic chemicals and poor wound healing. Nitrous oxide, free radicals, tumor necrosis factor-alpha, and glucagon may contribute to PHG development. Acute and chronic gastrointestinal bleeding are the only clinical complications. Bleeding is typically mild-to-moderate. Endoscopic therapy is rarely useful because the bleeding is typically diffuse. Acute bleeding is primarily treated with octreotide, often with concomitant proton pump inhibitor therapy, or secondarily treated with vasopressin or terlipressin. Nonselective β-adrenergic receptor antagonists, particularly propranolol, are used to prevent bleeding after an acute episode or for chronic bleeding. Iron deficiency anemia from chronic bleeding may require iron replacement therapy. Transjugular-intrahepaticportosystemic-shunt and liver transplantation are highly successful ultimate therapies because they reduce the underlying portal hypertension. SYSTEMA...

Amyloidosis is a common complication of patients with monoclonal gammopathy of undetermined significance (MGUS), smoldering multiple myeloma (SMM), and multiple myeloma (MM). This proteinaceous material can be deposited intercellularly in any organ system, including the gastrointestinal (GI) tract. In the GI tract, amyloidosis affects the duodenum most commonly, followed by the stomach and colorectum. Gastric amyloidosis causes symptoms of nausea, vomiting, early satiety, abdominal pain, and GI bleeding. A case of upper GI bleeding from gastric amyloidosis is presented in a patient with SMM. Esophagogastroduodenoscopy (EGD) revealed a gastric mass. Endoscopic biopsies revealed amyloid deposition in the lamina propria, consistent with gastric amyloidosis. Liquid chromatography tandem mass spectrometry performed on peptides extracted from Congo red-positive microdissected areas of paraffin-embedded stomach specimens revealed a peptide profile consistent with AL- (lambda-) type amyloidosis. Based on this and multiple other case reports, we recommend that patients with GI bleeding and MGUS, SMM, or MM undergo EGD and pathologic examination of endoscopic biopsies of identified lesions using Congo red stains for amyloidosis for early diagnosis and treatment.

Analyze efficacy, safety of endoscopic therapy for duodenal duplication cysts (DDC) by comprehensively reviewing case reports.Tandem, independent, systematic, computerized, literature searches were performed via PubMed using medical subject headings or Keywords “cyst” and “duodenal” and “duplication”; or “cyst”, and “endoscopy” or “endoscopic”, and “therapy” or “decompression”; with reconciliation of generated references by two experts. Case report followed CARE guidelines.Literature review revealed 28 cases (mean = 1.3 ± 1.2 cases/report). Endoscopic therapy is increasingly reported recently (1984–1999: 3 cases, 2000–2015: 25 cases, P = 0.003, OR = 8.33, 95%-CI: 1.77–44.5). Fourteen (54%) of 26 patients were men (unknown-sex = 2). Mean age = 32.2 ± 18.3 years old. Procedure indications: acute pancreatitis-16, abdominal pain-8, jaundice-2, gastrointestinal (GI) obstruction-1, asymptomatic cyst-1. Mean maximal DDC dimension = 3.20 ± 1.53 cm (range, 1–6.5 cm). Endoscopic techniques included cyst puncture via needle knife papillotomy (NKP)/papillotome-18, snare resection of cyst-7, cystotome-2, and cyst needle aspiration/ligation-1. Endoscopic therapy was successful in all cases. Among 24 initially symptomatic patients, all remained asymptomatic post-therapy without relapses (mean follow-up = 36.5 ± 48.6 months, 3 others reported asymptomatic at follow-up of unknown duration; 1 initially asymptomatic patient remained asymptomatic 3 years post-therapy). Two complications occurred: mild intraprocedural duodenal bleeding related to NKP and treated locally endoscopically.A patient is reported who presented with vomiting, 15-kg-weight-loss, and profound dehydration for 1 month from extrinsic compression of duodenum by 14 × 6 cm DDC, underwent successful endosonographic cyst decompression with large fenestration of cyst and endoscopic aspiration of 1 L of fluid from cyst with rapid relief of symptoms. At endoscopy the DDC was intubated and visualized and random endoscopic mucosal biopsies were obtained to help exclude malignant or dysplastic DDC.Study limitations include retrospective literature review, potential reporting bias, limited patient number, variable follow-up.In conclusion, endoscopic therapy for DDC was efficacious in all 29 reported patients including current case, including patients presenting acutely with acute pancreatitis, or GI obstruction. Complications were rare and minor, suggesting that endoscopic therapy may be a useful alternative to surgery for nonmalignant DDC when performed by expert endoscopists.

Background: Bariatric surgery leaks result in significant morbidity and mortality. Experts report variable therapeutic approaches, without uniform guidelines or consensus.Objective: To review the pathogenesis, risk factors, prevention, and treatment of gastric sleeve leaks, with a focus on endoscopic approaches. In addition, the efficacy and success rates of different treatment modalities are assessed.Design: A comprehensive review was conducted using a thorough literature search of 5 online electronic databases (PubMed, PubMed Central, Cochrane, EMBASE, and Web of Science) from the time of their inception through March 2020. Studies evaluating gastric sleeve leaks were included. MeSH terms related to "endoscopic," "leak," "sleeve," "gastrectomy," "anastomotic," and "bariatric" were applied to a highly sensitive search strategy. The main outcomes were epidemiology, pathophysiology, diagnosis, treatment, and outcomes.Results: Literature search yielded 2418 studies of which 438 were incorporated into the review. Shock and peritonitis necessitate early surgical intervention for leaks. Endoscopic therapies in acute and early leaks involve modalities with a focus on one of: (i) defect closure, (ii) wall diversion, or (iii) wall exclusion. Surgical revision is required if endoscopic therapies fail to control leaks after 6 months. Chronic leaks require one or more endoscopic, radiologic, or surgical approaches for fluid collection drainage to facilitate adequate healing. Success rates depend on provider and center expertise. Conclusion:Endoscopic management of leaks post sleeve gastrectomy is a minimally invasive and effective alternative to surgery. Their effect may vary based on clinical presentation, timing or leak morphology, and should be tailored to the appropriate endoscopic modality of treatment.

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Introduction The optimal colonoscopy withdrawal time is still a controversial topic. While several studies demonstrate that longer withdrawal time improves adenoma detection rate, others have contradicted these findings. Methods Three independent reviewers performed a comprehensive review of all original articles published from inception to January 2021 and included studies reporting comparison of the two cohorts—(i) ≥ 6 but less than 9 min of colonoscopy withdrawal time (CWT) and (ii) ≥ 9 min of CWT. The outcome measures were the following: (i) adenoma detection rate (ADR), (ii) advanced ADR, and (iii) sessile serrated adenoma detection rate (SDR). The meta‐analysis was performed, and the statistics were two‐tailed. Results A total of seven studies met the inclusion criteria after a thorough search of the literature was completed. The analysis revealed that ≥ 9 min of CWT had significantly higher odds of adenoma detection as compared with 6–9 min of CWT (odds ratio [OR] 1.54, 95% confidence interval [CI] 1.30–1.82; I2 = 93.7). Additionally, a significantly higher odds of sessile serrated adenoma detection (OR 1.68, 95% CI 1.28–2.22; I2 = 0) and a trend towards higher odds of advanced adenoma detection (OR 1.38, 95% CI 0.98–1.95, I2 = 90) were seen with CWT of at least 9 min when compared with 6–9 min of CWT. Conclusion This systematic review and meta‐analysis analysis provides further evidence that at least 9 min of CWT cohort had significantly higher ADR and SDR as compared with the at least 6 min but less than 9 min of cohort.

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