Patient: Female, 56Final Diagnosis: Colonic MALT lymphomaSymptoms: Epigastric painMedication: —Clinical Procedure: Colonoscopy and biopsySpecialty: Gastroenterology and HepatologyObjective:Rare diseaseBackground:Non-Hodgkin lymphoma (NHL) is a well-known hematologic malignancy. The gastrointestinal (GI) tract is the most commonly involved extra nodal site. MALT lymphomas are uncommon, accounting for 5% of all NHL. Gastric mucosa-associated lymphoid tissue (MALT) lymphoma is the prototype seen in association with Helicobacter pylori. Colonic MALT lymphoma is rare and comprises only 2.5% of the MALT lymphomas. Its etiology and treatment is not well established.Case Report:A 56-year-old Hispanic woman presented to the clinic with symptoms of chronic epigastric pain for the past three years and a 13-pound weight loss over the past two months. The patient did not have any prior medical conditions. Her systemic examination was unremarkable, while her routine labs revealed mild anemia. An upper endoscopy and colonoscopy for colorectal cancer screening were performed revealing erosive gastropathy with duodenal ulcers and a 5 cm broad based polypoid mass in the hepatic flexure respectively. Computed tomography (CT) of the abdomen revealed a round, well demarcated mass at the hepatic flexure of the colon. The histopathology and immunophenotyping were consistent with extra nodal marginal zone of MALT lymphoma. Stool testing for H. pylori was positive. The patient received two weeks of H. pylori eradication therapy and four cycles of rituximab. Repeat colonoscopy after completion of chemotherapy showed complete resolution of the MALT lymphoma.Conclusions:Unlike gastric MALT lymphoma, treatment of colonic MALT lymphoma is not standardized. Chemotherapy and surgical resection have been utilized to successfully treat it. Only a handful of cases have reported successful treatment of colonic MALT lymphoma with rituximab monotherapy.

The incidence of cirrhosis is rising, and identification of these patients prior to undergoing any surgical procedure is crucial. The preoperative risk stratification using validated scores, such as Child-Turcotte-Pugh (CTP) and Model for End-Stage Liver Disease, perioperative optimization of hemodynamics and metabolic derangements, and postoperative monitoring to minimize the risk of hepatic decompensation and complications are essential components of medical management. The advanced stage of cirrhosis, emergency surgery, open surgeries, old age, and coexistence of medical comorbidities are main factors influencing the clinical outcome of these patients. Perioperative management of patients with cirrhosis warrants special attention to nutritional status, fluid and electrolyte balance, control of ascites, excluding preexisting infections, correction of coagulopathy and thrombocytopenia, and avoidance of nephrotoxic and hepatotoxic medications. Transjugular intrahepatic portosystemic shunt may improve the CTP class, and semielective surgeries may be feasible. Emergency surgery, whenever possible, should be avoided.

Irritable bowel syndrome (IBS) is the most common functional gastrointestinal disorder characterized by presence of abdominal pain or discomfort associated with altered bowel habits. It has three main subtypes - constipation predominant IBS (C-IBS), diarrhea predominant IBS (D-IBS) and IBS with mixed features of both diarrhea as well as constipation (M-IBS). Its pathophysiology and underlying mechanisms remain elusive. It is traditionally believed that IBS is a result of multiple factors including hypersensitivity of the bowel, altered bowel motility, inflammation and stress. Initial studies have shown familial aggregation of IBS suggesting shared genetic or environmental factors. Twin studies of IBS from different parts of world have shown higher concordance rates among monozygotic twins than dizygotic twins, and thus suggesting a genetic component to this disorder. Multiple studies have tried to link single-nucleotide polymorphisms (SNPs) to IBS but there is little evidence that these SNPs are functional. Various molecules have been studied and investigated by the researchers. Serotonin, a known neurotransmitter and a local hormone in the enteric nervous system, has been most extensively explored. At this time, the underlying gene pathways, genes and functional variants linked with IBS remain unknown and the promise of genetically-determined risk prediction and personalize medicine remain unfulfilled. However, molecular biological technologies continue to evolve rapidly and genetic investigations offer much promise in the intervention, treatment and prevention of IBS.

BACKGROUND There is little evidence about the association of pre-existing hepatitis C infection (HCV) with outcomes in patients with coronavirus disease 2019 (COVID-19). AIM To assess the prevalence of history of HCV among patients with COVID-19 and to study the relationship of in-hospital mortality in relation with other predictors of poor outcomes in the presence or absence of COVID-19 induced acute liver injury. METHODS In a retrospective single-center study design, 1193 patients with COVID-19 infection were studied. Patients were then classified into those with and without a history of HCV, 50 (4.1%) and 1157 (95.9%) respectively. RESULTS Multivariate cox-regression models showed that age, HCV, D-Dimer, and ferritin were the only predictors of in-hospital mortality. Acute liver injury and fibrosis score (Fib-4 score) were not different between both groups. Multivariate cox-regression model for liver profile revealed that aspartate aminotransferase/ alanine aminotransferase ratio, Fib-4 score, and HCV were predictors of in-hospital mortality. After propensity score matching HCV was the only predictor of mortality in the multivariate cox-regression model. A model including HCV was found to add predictive value to clinical and laboratory parameters. CONCLUSION In patients with COVID-19, history of HCV infection leads to an accentuated severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virulence, irrespective of baseline comorbidities, admission laboratory variables, or COVID-19-induced liver injury, which may be related to extrahepatic effects of HCV leading to enhanced ACE-2/TMPRSS mechanisms of SARS-CoV-2 viral entry, baseline cytokine-mediated pro-inflammation, and endothelial dysfunction.

Disturbances in iron metabolism can be genetic or acquired and accordingly manifest as primary or secondary iron overload state. Organ damage may result from iron overload and manifest clinically as cirrhosis, diabetes mellitus, arthritis, endocrine abnormalities and cardiomyopathy. Hemochromatosis inherited as an autosomal recessive disorder is the most common genetic iron overload disorder. Expert societies recommend screening of asymptomatic and symptomatic individuals with hemochromatosis by obtaining transferrin saturation (calculated as serum iron/total iron binding capacity × 100). Further testing for the hemochromatosis gene is recommended if transferrin saturation is >45% with or without hyperferritinemia. However, management of individuals with low or normal transferrin saturation is not clear. In patients with features of iron overload and high serum ferritin levels, low or normal transferrin saturation should alert the physician to other - primary as well as secondary - causes of iron overload besides hemochromatosis. We present here a possible approach to patients with hyperferritinemia but normal transferrin saturation.