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Viral hepatitis–induced acute liver failure (ALF) is a preventable cause for liver-related mortality worldwide. Viruses are the most common cause for ALF in developing nations in contrast to the west, where acetaminophen is largely responsible. Viruses may be hepatotropic or affect the liver secondary to a systemic infection. In tropical countries, infections such as leptospirosis, scrub typhus and malaria can mimic the symptoms of ALF. Differentiating these ALF mimics is crucial because they require etiology-specific therapy. Treatment of viral hepatitis-induced ALF is two-pronged and directed towards providing supportive care to prevent organ failures and antiviral drugs for some viruses. Liver transplantation (LT) is an effective modality for patients deteriorating despite adequate supportive care. Early referral and correct identification of patients who require a transplant are important. Liver support devices and plasma exchange have evolved into "bridging modalities" for LT. Preventive strategies such as hand hygiene, use of clean and potable water and inclusion of vaccines against viral hepatitis in the national program are simple yet very effective methods focusing on the preventive aspect of this disease. [ABSTRACT FROM AUTHOR]

Summary: Background: In cirrhosis patients with acute variceal bleeding (AVB), the optimal duration of vasoconstrictor therapy after endoscopic haemostasis is unclear. Aims: We aimed to compare efficacy of 1‐day versus 3‐day terlipressin therapy in cirrhosis patients with AVB post‐endoscopic intervention. The primary objective was to compare rebleeding at 5 days between the two arms. Secondary objectives included rebleeding and mortality rates at 6 weeks. Methods: In this open‐label, randomised controlled trial, cirrhosis patients with AVB were randomised to either 1‐day or 3‐day terlipressin therapy. Results: A total of 150 cirrhosis patients with AVB were recruited to receive either 1 day (n = 75) or 3 days (n = 75) of terlipressin therapy. One patient from 1‐day arm was excluded. Modified intention‐to‐treat analysis included 149 patients. Baseline characteristics were comparable between the two groups. Rebleeding at 5 days: 3 (4.1%; 95% confidence interval [CI]: 0.4–9.0) versus 4 (5.3%; 95% CI: 2.0–10.0), risk difference (RD) p = 0.726 and 5‐day mortality rates: 1 (1.4%; 95% CI: 0–7.3) versus 1 (1.3%; 95% CI: 0.2–7.0), RD p = 0.960 were similar. Rebleeding at 42 days: 9 (12.2%; 95% CI: 7.0–20.0) versus 10 (13.3%; 95% CI: 7.0–20.0), RD p = 0.842 and mortality at 42 days: 5 (6.8%; 95% CI: 3.0–10.0) versus 4 (5.3%; 95% CI: 2.0–10.0), RD p = 0.704 were also similar. Patients in the 1‐day terlipressin therapy arm experienced significantly fewer adverse effects compared with those receiving 3 days of terlipressin therapy: 28 (37.8%) versus 42 (56%), p = 0.026. Conclusions: Our results suggest that 1 day of terlipressin therapy is associated with similar 5‐day and 42‐day rebleeding rates, 42‐day mortality and an overall superior safety profile compared with 3‐day of terlipressin therapy. These findings require to be validated in double‐blinded, larger, multiethnic and multicentre studies across the various stages of cirrhosis (CTRI/2019/10/021771). [ABSTRACT FROM AUTHOR]

Background: Acute‐on‐chronic liver failure (ACLF) is associated with a high short‐term mortality rate in the absence of liver transplantation. The role of therapeutic plasma exchange (TPE) in improving the outcomes of ACLF and acute decompensation (AD) is unclear. In this retrospective analysis, we aimed to determine the impact of TPE on mortality in patients with ACLF. Methods: ACLF patients receiving TPE with standard medical treatment (SMT) were propensity score matched (PSM) with those receiving SMT alone (1:1) for sex, grades of ACLF, CLIF C ACLF scores, and the presence of hepatic encephalopathy. The primary outcomes assessed were mortality at 30 and 90 days. Survival analysis was performed using Kaplan Meier survival curves. Results: A total of 1151 patients (ACLF n = 864 [75%], AD [without organ failure] n = 287 [25%]) were included. Of the patients with ACLF (n = 864), grade 1, 2, and 3 ACLF was present in 167 (19.3%), 325 (37.6%), and 372 (43.0%) patients, respectively. Thirty‐nine patients received TPE and SMT, and 1112 patients received only SMT. On PSM analysis, there were 38 patients in each group (SMT plus TPE vs SMT alone). In the matched cohort, the 30‐days mortality was lower in the TPE arm compared to SMT (21% vs 50%, P =.008), however, the 90‐day mortality was not significantly different between the two groups (36.8% vs 52.6%, P =.166); HR, 0.82 (0.44‐1.52), P =.549. Conclusion: TPE improves short‐term survival in patients with ACLF, but has no significant impact on long‐term outcomes. Randomized control trials are needed to obtain a robust conclusion in this regard. [ABSTRACT FROM AUTHOR]

Arsenic toxicity is a major health issue that also threats male reproductive system leading to impairment of fertility. The antioxidant capacity of casein and pea enriched formulated high-protein diet (FHPD) is found to be effective in different toxicity management. The present study was endeavored to investigate the mitigatory aspect of FHPD on arsenic stimulated testicular apoptosis. Adult male rats were maintained on either normal diet as control (Gr I, n = 8) and arsenic (As2O3) treated at a dose of 3 mg/kg/rat/day (Gr II, n = 8) or on isocaloric FHPD as supplemented (Gr III, n = 8) with same dose of arsenic for 30 consecutive days. Testicular histomorphometry, spermatokinetics, testicular functional marker enzymes, serum gonadotrophins, oxidative stress markers, testicular deoxyribonucleic acid (DNA) damage, and apoptosis markers were evaluated to assess the reprotoxicity of arsenic and subsequent protection by FHPD. FHPD protected the histopathological alterations and also restored normal spermatogenesis. Altered enzymatic activities of testicular functional markers like lactate dehydrogenase, γ-glutamyl transferase, acid phosphatase, and alkaline phosphatase were also regularized. FHPD also reinstated the normal level of follicle stimulating hormone (FSH), luteinising hormone (LH), and also normalized the enzymatic activities of testicular glutathione peroxidase and glutathione reductase. Testicular DNA damage was also prevented by FHPD supplementation. Testicular apoptosis marked by the altered messenger ribonucleic acid and protein expression of apoptotic markers like Bax, Bcl-2, caspase 9, and caspase 3 were also attenuated upon FHPD supplementation along with diminution of arsenic accumulation in testicular tissues. FHPD not only mitigated the adverse effects of arsenic induced gonadotoxicity but also helped in sustaining the normal reproductive functions. [ABSTRACT FROM AUTHOR]

Background: The role of hepatic venous pressure gradient (HVPG) in predicting further decompensation in cirrhosis patients with acute variceal bleeding (AVB) is not known. We aimed to evaluate the role of HVPG in predicting further decompensation in cirrhosis patients with AVB Methods: In this prospective study, 145 patients with cirrhosis with esophageal or gastric AVB were included. HVPG was measured on the day of the AVB. Decompensating events occurring after 42-days of AVB were considered further decompensation. Results: The median age of the study cohort was 44 years; 88.3% males. The predominant etiology of cirrhosis was alcohol (46.2%). Overall, 40 (27.6%) patients developed further decompensation during median follow-up of 296 days following AVB. Gastro intestinal bleeding n = 27 (18.6%) and new-onset/worsening ascites n = 20 (13.8%) were the most common decompensating events. According to the multivariate model, HVPG was an independent predictor of any further decompensation in esophageal AVB patients but not in gastric variceal bleeding patients. HVPG cut-off of ≥16 mmHg predicted further decompensation in the esophageal AVB. However, HVPG was not an independent predictor of mortality. Conclusion: HVPG measured during an episode of acute variceal hemorrhage from esophageal varices predicts further decompensating events in cirrhosis patients. [ABSTRACT FROM AUTHOR]

Editorial: The tip of the non-alcoholic fatty liver disease iceberg - the more we know, the smaller it gets? Another important clinical aspect that adds to the complexity of managing NAFLD is the slow rate of disease progression coupled with the risk of extrahepatic events (cardiac, cerebrovascular, etc.) in this patient group. Hepatic steatosis (HS) is defined as an intrahepatic fat content of more than 5%.[1] While the clinical entity of non-alcoholic fatty liver disease (NAFLD) is based on a diagnosis of intrahepatic steatosis, it was initially considered a benign disease without much clinical significance. The role of imaging to identify HS is developing rapidly with the widespread use of computerized tomography (liver attenuation index) and magnetic resonance imaging (proton density fat fraction-MRI-PDFF). [Extracted from the article]

Viral infections are among the major causes of acute liver failure (ALF) worldwide. While the role of agents such as hepatitis A, B, C, D and E viruses in precipitating ALF are well known, improvements in serological assays have led to the detection of viral agents such as Epstein Barr virus, cytomegalovirus etc. as atypical causes of ALF. Despite the plethora of literature available on viral hepatitis and ALF, there is very limited large-scale epidemiologic data on the prevalence, risk factors of progression and outcomes in ALF of viral causes. This is important as viral infections remain the leading cause of ALF in the East and in developing countries, while the impact of viral ALF in the West has largely been ameliorated by effective vaccination and sanitization programs. This review focuses specifically on the available prognostic scores that aid in the management of ALF of viral etiologies while also briefly reviewing the current literature on newer viral agents known to cause ALF, risk factors of progression, outcomes and how management algorithms can be developed by incorporation of prognostic scoring systems for referral and transplant listing. [ABSTRACT FROM AUTHOR]