Randomized Controlled Trial of Intravenous Ferric Carboxymaltose vs Oral Iron to Treat Iron Deficiency Anemia After Variceal Bleed in Patients With Cirrhosis.

INTRODUCTION: Limited evidence exists on the optimal strategy to correct iron deficiency anemia after variceal bleeding (VB) in cirrhosis. This trial compared the efficacy and safety of intravenous ferric carboxymaltose (IV-FCM) with those of oral iron therapy in this cohort. METHODS: In this open-label, single-center, randomized controlled trial, eligible patients with hemoglobin <10 g/dL and iron deficiency (ferritin <100 ng/mL) after VB received either IV-FCM (1,500-2,000 mg) divided into 2 doses (n = 48) or oral carbonyl iron (100 mg elemental iron/day) (n = 44) for 3 months. The primary outcome was change in hemoglobin at 3 months. Secondary outcomes included improvement in anemia (last hemoglobin >12 g/dL), normalization of iron stores (ferritin >100 ng/mL), liver-related adverse events, adverse drug reactions, and changes in quality of life (CLDQOL questionnaire). RESULTS: Baseline characteristics, including median Child-Turcotte-Pugh score 7 (interquartile range [IQR] 6-9), Model for End-Stage Liver Disease score 12 (IQR 10-17), blood hemoglobin (8.25 ± 1.06 g/dL), and ferritin (30.00 ng/mL [15.00-66.50]), were comparable in both arms. The median increase in hemoglobin at 3 months in the IV and oral arms was 3.65 g/dL (IQR 2.55-5.25) and 1.10 g/dL (IQR 0.05-2.90 g/dL) ( P < 0.001), respectively. Iron stores normalized in 84.6% and 21% of the IV and oral arms, respectively ( P < 0.001). Anemia improved in 50% and 21.9% in the IV and oral arms, respectively ( P < 0.009). Patients in the IV arm showed a significant improvement in all domains of CLDQOL. Liver-related adverse events were comparable in both arms. Transient mild/moderate hypophosphatemia developed in 43% of patients receiving IV-FCM. DISCUSSION: Intravenous iron replacement is efficacious and safe to treat iron deficiency anemia after VB in patients with cirrhosis.

Assessing the Risk of Further Decompensation and Survival in Patients With Cirrhosis With Variceal Bleeding as Their First Decompensation Event.

INTRODUCTION: Limited data exist on long-term outcomes of patients with compensated cirrhosis presenting with acute variceal bleeding (AVB) as an index and lone decompensating event. This study aimed to evaluate the incidence of further decompensation, survival, and risk factors of mortality in these patients. METHODS: Patients with otherwise compensated cirrhosis presenting with AVB as their index decompensating event (n = 463) were analyzed in this single-center retrospective study. The incidence of individual decompensation events and survival was estimated using competing risk analysis. Risk factors for poor outcomes were identified. RESULTS: The mean age was 47.4 (13.2) years, with most patients (86.5%) being males. Alcohol-related liver disease (42.3%) and viral cirrhosis (22.4%) were the main etiologies with a median Model for End-Stage Liver Disease score of 14 (11-15) at baseline. Over a median follow-up of 42 (24-62) months, 292 patients experienced further decompensations: ascites (n = 283; 96.9%), rebleeding (n = 157; 53.8%), and hepatic encephalopathy (n = 71; 24.3%). Most events occurred with similar frequency across different etiologies, except acute-on-chronic liver failure, which was more common in nonviral cirrhosis (Gray test, P = 0.042). Patients with viral and nonviral cirrhosis had similar survival (5-year survival: 91% and 80.1%, respectively; P = 0.062). Patients with early further decompensations (onset <6 weeks of index AVB event) (n = 40) had a higher mortality (52.5% vs 20.2% for late decompensations; P < 0.001). Active alcohol consumption (hazard ratio [HR]: 9 [5.31-15.3], P < 0.001), high white blood cell count at presentation (HR: 2.5 [1.4-4.4], P = 0.001), and early decompensation (HR: 6.2 [3.6-10.6], P < 0.001) predicted poor survival. DISCUSSION: Despite a high incidence of further decompensation, 5-year survival of patients at this stage of cirrhosis is more than 80% across all etiologies in the absence of early further decompensation and active alcohol consumption.

Distinct course of portal hypertension in patients with cirrhosis with gastric variceal bleeding as their first decompensation: a propensity score-matched study.

BACKGROUND AND AIMS: Limited data exist on course of portal hypertension in patients with cirrhosis with gastric variceal (GV) bleeding as their index decompensation. We evaluated long-term outcomes in this subgroup and compared them with a propensity score-matched cohort of patients with esophageal variceal (EV) bleeding. METHODS: Patients with cirrhosis with GVs (IGV-1 and GOV-2) bleeding as their index decompensation were analyzed in this retrospective study. Incidence of new-onset clinical decompensations and survival were estimated and compared with a cohort of patients with EVs bleeding matched for etiology and disease severity using competing risk analysis. RESULTS: Baseline characteristics of patients with GVs related bleeding (n = 51) (mean age-48.1 ± 12.9 years, 80% males, non-viral cirrhosis: 80.3%) were similar to the cohort of EVs bleeding (n = 51) (mean age-45.9 ± 14.2, 88% males, non-viral cirrhosis: 78.4%). The 1-year and 3-year rates of new-onset ascites were (17.9%, 34.2%) and (23.9%, 49%) in patients with GVs and EVs related index bleeding, respectively (Gray's test, p = 0.035). The 1-year and 3 year rate of rebleed was (35.6%, 46.3%) and (13.9%, 35.7%) in patients with GVs and EVs related index bleeding, respectively (Gray's test, p = 0.1). While overall survival was similar across both the groups (GV: 29.6% vs EV: 21.6%, p = 0.495), rebleeding-related deaths occurred exclusively in patients with GV (rebleeding-related deaths: GV: 40% vs EVs: 0%; non-bleeding liver-related deaths: GV: 60% vs EV: 100%; p = 0.048). CONCLUSIONS: Rebleeding predominates the course of portal hypertension in patients with cirrhosis presenting with GVs related bleeding, whereas ascites is the most significant event on follow-up in those with EVs related bleeding.

Evaluating the Practice of Prescribing Beta-blockers in Compensated Cirrhosis by Gastroenterologists in the Asia Pacific Region.

Non-selective beta-blockers (NSBBs) have a role in the management of portal hypertension. They are currently advocated in patients with clinically significant portal hypertension (CSPH) based on Baveno-VII consensus. Current survey aimed to evaluate the practice and perceptions of prescribing NSBBs in portal hypertension by gastroenterologists and hepatologists in Asia-Pacific region in patients with compensated cirrhosis. Out of 1500 gastroenterologists approached in the region, 328 gastroenterologists responded and completed the survey. 75% of the respondents were found not to be following practice of evaluating CSPH as they prescribed NSBBs in patients of compensated cirrhosis with high-risk varices only. Major concerns raised were non-availability of hepatic venous pressure gradient and reliable non-invasive tests as surrogate of CSPH to adapt PREDESCI methodology. While 56.7% used carvedilol as the preferred NSBB to treat patients with compensated cirrhosis, 43.3% used propranolol. This survey assessed the real-world scenario of prescribing NSBBs among practicing gastroenterologists/hepatologists in patients with compensated cirrhosis.