Ravi, Sujan

INTRODUCTION: Alcohol-associated hepatitis (AH) is a severe condition with high short-term mortality. Identifying key predictors of poor outcomes is critical for guiding therapeutic strategies. Mean arterial pressure (MAP), a key determinant of tissue perfusion and systemic hemodynamics, may play a pivotal role in prognosis. METHODS: We analyzed a multicenter, prospective cohort of 323 patients hospitalized with AH, with validation in an independent cohort of 290 patients. Survival was evaluated using Kaplan-Meier curves and compared with the log-rank (Mantel-Cox) test. Cox proportional hazards models were used to estimate hazard ratios for mortality, adjusted for Model for end stage liver disease score. Mechanistic insights were explored through assessment of cardiovascular biomarkers. RESULTS: A baseline MAP <80 mm Hg was associated with significantly higher mortality at both 28 days (27.3% vs 8.0%) and 90 days (40.3% vs 15.6%; P < 0.001 for both). This association persisted after adjusting for Model for end stage liver disease score, age, and baseline hepatic encephalopathy. The incidence of infections during follow-up was similar across MAP groups (27.6% vs 22.8%), but acute kidney injury occurred more frequently in the MAP <80 mm Hg group (62% vs 38%, P < 0.001). In the validation cohort, patients with MAP <80 mm Hg also demonstrated significantly lower 28-day transplant-free survival. Although B-type natriuretic peptide and plasma renin levels were altered in patients with AH, they did not correlate with MAP values. DISCUSSION: A baseline MAP <80 mm Hg is an independent predictor of short-term and mid-term mortality in patients with AH. Strategies aimed at restoring hemodynamic stability may improve outcomes in this high-risk population.

INTRODUCTION: We present a case of idiopathic varices in the small bowel and colon discovered after extensive work up for iron-deficiency anemia and portal hypertension. CASE DESCRIPTION/METHODS: 41-year-old with no known medical history underwent esophagogastroduodenoscopy (EGD) and colonoscopy for evaluation of iron-deficiency anemia. EGD was normal. Colonoscopy revealed diffuse colonic varices extending from the cecum to the rectum (Figure 1). Computed tomography enterography showed numerous varices of the mid jejunum. Magnetic resonance imaging of the abdomen showed patent portal circulation and no other abnormalities. Echocardiogram did not show any evidence of right heart failure. Transjugular liver biopsy showed a portosytemic pressure gradient of 4 mm of Hg indicating the absence of portal hypertension. Liver biopsy only showed mild steatosis and no fibrosis. A direct measurement of portal pressure was 3 mmof Hg again indicating the absence of portal hypertension. DISCUSSION: Given the extensive workup with no evidence of portal hypertension, patient is thought have idiopathic varices in the small bowel and colon. Ectopic varices, especially in the colon are rare and are usually associated with portal hypertension. Idiopathic colonic varices in association with small bowel varices are even more infrequently described in existing literature. Clinical presentation has been reported with massive hemorrhage, recurrent bleeds and even as incidental findings in endoscopies and imaging performed for other reasons. Management options include conservative frequent follow up or surgery if there is evidence of recurrent bleeds or massive hemorrhage.

Abstract Identifying patients at high risk for acute kidney injury (AKI) during hospitalization among patients admitted with severe alcoholic hepatitis (AH) is an unmet clinical need. We performed a multicentric prospective cohort study using data from 4 different cohorts on well‐characterized patients hospitalized with severe AH. Data collected on 773 AH patients from 4 cohorts across the globe were randomly split into test (n = 390) and validation (n = 383) cohorts. We found that 32% of the patients developed inpatient AKI in the test cohort. Approximately 60% of patients met criteria for systemic inflammatory response syndrome (SIRS) at admission. Hepatic encephalopathy, SIRS, and Model for End‐Stage Liver Disease score at admission predicted inpatient AKI with odds ratios of 3.86, 2.24, and 1.14, respectively. The AKI risk score developed using these predictors stratified risk of inpatient AKI to low (score <3), moderate (3‐4), and high (>4). These findings were replicated in the validation cohort. In the whole study cohort, patients with AKI had a lower 90‐day survival (53% versus 77%; P < 0.001). Those with AKI risk score of >4 had significantly lower 90‐day survival as compared with those with risk scores between 3 and 4 and <3 (47% versus 68% versus 88%; P < 0.001). In conclusion, AKI occurs frequently in AH patients and negatively impacts short‐term mortality. The AKI risk score is useful in identifying patients at high risk for inpatient AKI and may be useful for developing new therapeutic strategies to prevent AKI in patients with AH.