Background and Aims: COVID-19 is a dominant pulmonary disease, with multisystem involvement, depending upon co morbidities. Its profile in patients with pre-existing chronic liver disease (CLD) is largely unknown. We studied the liver injury patterns of SARS-Cov-2 in CLD patients, with or without cirrhosis. Methods: Data was collected from 13 Asian countries on patients with CLD, known or newly diagnosed, with confirmed COVID-19. Result: Altogether, 228 patients [185 CLD without cirrhosis and 43 with cirrhosis] were enrolled, with comorbidities in nearly 80%. Metabolism associated fatty liver disease (113, 61%) and viral etiology (26, 60%) were common. In CLD without cirrhosis, diabetes [57.7% vs 39.7%, OR=2.1(1.1-3.7), p=0.01] and in cirrhotics, obesity, [64.3% vs. 17.2%, OR=8.1(1.9-38.8), p=0.002) predisposed more to liver injury than those without these. Forty three percent of CLD without cirrhosis presented as acute liver injury and 20% cirrhotics presented with either acute-on-chronic liver failure [5(11.6%)] or acute decompensation [4(9%)]. Liver related complications increased (p<0.05) with stage of liver disease; a Child-Turcotte Pugh score of 9 or more at presentation predicted high mortality [AUROC-0.94, HR=19.2(95CI 2.3-163.3), p<0.001, sensitivity 85.7% and specificity 94.4%). In decompensated cirrhotics, the liver injury was progressive in 57% patients, with 43% mortality. Rising bilirubin and AST/ALT ratio predicted mortality among cirrhosis. Conclusions: SARS-Cov-2 infection causes significant liver injury in CLD patients, decompensating one fifth of cirrhosis, and worsening the clinical status of the already decompensated. The CLD patients with diabetes and obesity are more vulnerable and should be closely monitored.

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.

Pseudocysts of the pancreas are not rare, but spontaneous perforation and/or fistulization occurs in fewer than 3% of these pseudocysts. Perforation into the free peritoneal cavity, stomach, duodenum, colon, portal vein, pleural cavity and through the abdominal wall has been reported. Spontaneous rupture of the pancreatic pseudocyst into the surrounding hollow viscera is rare and, may be associated with life-threatening bleeding. Such cases require emergency surgical intervention. Uncomplicated rupture of pseudocyst is an even rarer occurrence. We present a case of spontaneous resolution of a pancreatic pseudocyst with gastric connection without bleeding. A 67-year-old women with a large pancreatic pseudocyst resulting from a complication of chronic pancreatitis was referred to our institution. During hospital stay, there was sudden decrease in the size of epigastric lump. Repeat computed tomography (CT) revealed that the size of the pseudocyst had decreased significantly; however, gas was observed in stomach and pseudocyst along with rent between lesser curvature of stomach and pseudocyst suggestive of spontaneous cystogastric fistula.The fistula tract occluded spontaneously and the patient recovered without any complication or need for surgical treatment. After 5 wk, follow up CT revealed complete resolution of pseudocyst. Esophagogastroduodenoscopy revealed that the orifice was completely occluded with ulcer at the site of previous fistulous opening.

Gastric schwannomas are rare mesenchymal tumors that arise from the nerve plexus of gut wall. They present with nonspecific symptoms and are often detected incidentally. Preoperative investigation is not pathognomic and many are therefore misdiagnosed as gastrointestinal stromal tumors. We report a rare case of a 37-year old woman who underwent laparotomy for complex bilateral ovarian cyst with resection of gastric-gastrointestinal stromal tumor preoperatively, but confirmed to have a gastric schwannomas postoperatively. This case underscores the differential diagnosis of submucosal, exophytic gastric mass as schwannoma.

Growth retardation by anthropometry was documented in a quarter of patients with EHPVO. All patients had significantly low IGF-1 and IGFBP-3 levels in comparison with controls despite normal anthropometry in majority of patients (75%).