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Acute kidney injury in ACLF carries a high mortality. Infusion of terlipressin gives earlier and higher response than noradrenaline with improved survival in ACLF patients with HRS-AKI. This article is protected by copyright. All rights reserved.

Thromboelastography (TEG) provides a more comprehensive global coagulation assessment than routine tests (international normalized ratio [INR] and platelet [PLT] count), and its use may avoid unnecessary blood component transfusion in patients with advanced cirrhosis and significant coagulopathy who have nonvariceal upper gastrointestinal (GI) bleeding. A total of 96 patients with significant coagulopathy (defined in this study as INR >1.8 and/or PLT count < 50 × 109/L) and nonvariceal upper GI bleed (diagnosed after doing upper gastrointestinal endoscopy, which showed ongoing bleed from a nonvariceal source) were randomly allocated to TEG‐guided transfusion strategy (TEG group; n = 49) or standard‐of‐care (SOC) group (n = 47). In the TEG group, only 26.5% patients were transfused with all three blood components (fresh frozen plasma [FFP], PLTs, and cryoprecipitate) versus 87.2% in the SOC group (P < 0.001). Although 7 (14.3%) patients in the TEG group received no blood component transfusion, there were no such patients in the SOC group (P = 0.012). Also, there was a significantly lower use of blood components (FFP, PLTs, and cryoprecipitate) in the TEG group compared with the SOC group. Failure to control bleed, failure to prevent rebleeds, and mortality between the two groups were similar. Conclusion: In patients with advanced cirrhosis with coagulopathy and nonvariceal upper GI bleeding, TEG‐guided transfusion strategy leads to a significantly lower use of blood components compared with SOC (transfusion guided by INR and PLT count), without an increase in failure to control bleed, failure to prevent rebleed, and mortality.

Severe alcoholic hepatitis (SAH) is often a progressive disease with high mortality and limited steroid responsiveness. Management options of steroid nonresponsive SAH (day 7 Lille score > 0.45) are limited. We assessed the efficacy and safety of granulocyte colony‐stimulating factor (G‐CSF) in steroid nonresponders. A randomized, double‐blind, single‐center trial (NCT01820208) was conducted between March 2013 and June 2016 in patients with histologically proven SAH, nonresponsive to 40 mg/day of prednisolone were randomized to G‐CSF (12 doses, 300 μg each in 28 days) or placebo. Responders were continued with prednisolone. Of the 430 patients with SAH, 132 received steroid therapy. Of these, 33 (25%) were nonresponders and were randomized to G‐CSF or placebo (14 in each group after exclusions). The baseline characteristics of both groups were comparable. The 28‐day mortality was comparable between the groups (21.4%, G‐CSF; 28.6%, placebo; P = 0.69). At 90 days, in the G‐CSF but not in the placebo group, the Model for End‐Stage Liver Disease reduced from 24.6 ± 3.9 to 19.4 ± 3.7 (P = 0.002) and Maddrey’s discriminant function from 74.8 ± 22.8 to 57.4 ± 31 (P = 0.26). Infections were less common (28% versus 71%; P < 0.001) with lower 90‐day mortality (35.7% versus 71.4%; P = 0.04) in the G‐CSF than in the placebo group. On Cox regression analysis, receiving G‐CSF (hazard ratio, 0.37; SD, 0.14‐0.98; P = 0.04), and high baseline serum creatinine (hazard ratio, 4.12; SD, 1.7‐10.3; P = 0.002) predicted day‐90 outcomes in steroid nonresponsive SAH. Patients tolerated G‐CSF without any major adverse events. Conclusion: Approximately one‐quarter of patients with SAH do not respond to corticosteroid therapy. Administration of G‐CSF is safe and helps to reduce the disease severity and 90‐day mortality in these patients.

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