Background: Splanchnic venous system thrombosis is a well recognized local vascular complication of acute pancreatitis (AP). It may involve thrombosis of splenic vein (SplV), portal vein (PV) and superior mesenteric vein (SMV), either separately or in combinations, and often detected incidentally, indeed some cases present with upper gastrointestinal bleed, bowel ischemia and hepatic decompensation. Incidence is variable depending on study subjects and diagnostic modalities. Pathogenesis is multifactorial centered on local and systemic inflammation. Management involves treatment of underlying AP and its complications. Universal use of anticoagulation may lead to increased risk of bleeding due to frequent need of interventions (radiologic/endoscopic/surgical). Literature on anticoagulation in setting of AP is sparse and at present there is no consensus guideline on it. Current article details our experience on splanchnic venous thrombosis (SVT) in AP in a well defined cohort of patients at a tertiary care center. Methods: Hospitalized patients with AP from January 2018 to December 2018 were included in the study. Detailed information on demographic, clinical, laboratory, radiologic features, and indication of anticoagulation use were collected prospectively during the index admission. Outcome variables were analyzed at the end of 6 months. Results: Twenty four out of 105 (22.85%) patients with AP develop SVT. Etiology of AP was alcohol use in 21/24 (87.5%) subjects. Most common vessel involved was isolated SplV in 11/24 (45.8%) patients followed by SplV along with PV and SMV 9/24 (37.50%, P < 0.001). Bowel ischemia 4/12 (33.3%), hepatic decompensation 3/12 (25%), triple vessel involvement 4/12 (33.3%) and pulmonary embolism 1/12 (8.3%) were reasons for anticoagulation. There was no statistical difference with respect to development of varices, collateral formation, recanalization, bleeding and mortality with use of anticoagulation (P > 0.05 with respect to all above variables). Conclusions: SVT is commonly seen in alcohol-induced AP. Anticoagulation does not affect outcomes of SVT. Subset of patients may benefit with anticoagulation.

Background/AimsThe existence of non-celiac gluten sensitivity has been debated. Indeed, the intestinal and extra-intestinal symptoms of many patients with irritable bowel syndrome (IBS) but without celiac disease or wheat allergy have been shown to improve on a gluten-free diet. Therefore, this study set out to evaluate the effects of gluten on IBS symptoms.MethodsWe performed a double-blind randomized placebo-controlled rechallenge trial in a tertiary care hospital with IBS patients who fulfilled the Rome III criteria. Patients with celiac disease and wheat allergy were appropriately excluded. The participants were administered a gluten-free diet for 4 weeks and were asked to complete a symptom-based questionnaire to assess their overall symptoms, abdominal pain, bloating, wind, and tiredness on the visual analog scale (0-100) at the baseline and every week thereafter. The participants who showed improvement were randomly assigned to one of two groups to receive either a placebo (gluten-free breads) or gluten (whole cereal breads) as a rechallenge for the next 4 weeks.ResultsIn line with the protocol analysis, 60 patients completed the study. The overall symptom score on the visual analog scale was significantly different between the two groups (P<0.05). Moreover, the patients in the gluten intervention group scored significantly higher in terms of abdominal pain, bloating, and tiredness (P<0.05), and their symptoms worsened within 1 week of the rechallenge.ConclusionsA gluten diet may worsen the symptoms of IBS patients. Therefore, some form of gluten sensitivity other than celiac disease exists in some of them, and patients with IBS may benefit from gluten restrictions.

The authors studied the relationship of endoscopic esophagitis and gastroesophageal flap valve (GEFV) in patients with symptomatic gastroesophageal reflux (GER). On endoscopy, the GEFV was graded as I to IV in 138 patients with acid regurgitation and heartburn relieved by antacids, and in 54 control subjects without symptoms suggestive of GER. Grade of GEFV was correlated with the grade of esophagitis, response to medical treatment, duration of symptoms, obesity, smoking, sex, and age of the patient. Abnormal GEFV (grades III and IV) was more frequent in patients with symptomatic GER, both with and without esophagitis, compared with control subjects (p = 0.000001. p = 0.03). Abnormal GEFV was significantly more common in patients with GER with esophagitis compared with those without (p < 0.00001). There was no significant difference in the distribution of normal and abnormal GEFV in patients with grade I esophagitis. However, grade 2 and grade 3 esophagitis were associated more commonly with an abnormal GEFV (p < 0.00001, p < 0.02 respectively). Hiatal hernia is always associated with an abnormal GEFV. Abnormal GEFV correlated significantly with age (more frequent when older than 40 years). Sex, duration of symptoms (>3 years), response to medical therapy, smoking, and obesity (body mass index > 30 kg/m2) did not correlate significantly with abnormal GEFV. We conclude that endoscopic esophagitis is usually associated with abnormal GEFV. It is more frequent in grades 2 and 3 but not grade 1 esophagitis. It is also encountered more commonly after the age of 40 years.

Approximately 24% of patients with AIH have severe-AIH. Conventional autoantibodies are often absent in severe-AIH; however, it does not alter the outcome. Immunosuppressants should be given expediently in patients with severe-AIH.

Present study shows that although diastolic dysfunction is a frequent event in cirrhosis, it is usually of mild degree and does not correlate with severity of liver dysfunction. There are no significant differences in echocardiographic parameters between alcoholic and non-alcoholic cirrhosis. HRS is not correlated to diastolic dysfunction in cirrhotic patients. There is no difference in survival at one year between patients with or without diastolic dysfunction. Diastolic dysfunction in cirrhosis is unrelated to circulatory dysfunction, ascites and HRS.