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Introduction and Objectives: Tenofovir Alafenamide (TAF) is a preferred treatment in the most recent EASL and AASLD HBV Guidelines, especially in patients with risk factors for TDF-associated renal and bone effects. In 2 identically-designed double-blind (DB), randomized (2:1), Phase 3 studies (HBeAg-negative patients [N = 425] and HBeAg-positive patients [N = 873]), TAF demonstrated antiviral efficacy non-inferior to that of TDF with superior renal and bone safety. After completing three years of DB treatment, all patients were eligible to receive open-label (OL) TAF through Year eight. Here we present study results for Year five. Materials and Methods: Efficacy was assessed by serial virologic, biochemical, and serologic assessments, while safety data included changes in renal function and changes in hip and spine bone mineral density. Resistance testing and phenotyping were performed annually through Year 5. Results: Of 1298 randomized and treated patients, 1157 (89%; 775 TAF; 382 TDF) entered OL, at year 5, 999 (77%; 675 TAF, 136 TDFTAF OL 3y, 188 TDF-TAF OL 2y) patients remained on treatment. High rates of virologic control were achieved and maintained in patients receiving TAF throughout and for TDF patients who switched to TAF at Weeks 96 or 144. Rates of ALT normalization and serologic responses were also comparable among groups. Eight patients are undergoing phenotypic testing to assess resistance. Adverse events (AEs) leading to discontinuation were low and similar among groups. Renal and bone outcomes were improved following the switch to OL TAF from TDF. Conclusions: After five years of treatment, virologic suppression rates remained high, and TAF was safe and well tolerated, with improved renal and bone safety in patients switching from TDF.

Drug induced liver injury is a common cause of acute liver failure (ALF). While most of these cases are due to dose dependent hepa-totoxicity with acetaminophen, idiosyncratic drug-induced liver injury (DILI) is responsible for about 15% cases of ALF. Antibiotics are the most common cause of idiosyncratic DILI as well as DILI induced ALF. Etodolac is a selective cycloxygenase- 2 (COX -2) inhibitor non-steroidal anti-inflammatory drug used as an analgesic and anti-inflammatory in musculoskeletal diseases. Severe liver impairment is extremely rare. Till date, only 3 cases of ALF related to etodolac have been reported in the literature. Here we report two cases with a unique presentation of ALF occurring due to DILI caused by etodolac, as diagnosed by Roussel Uclaf Causality Assessment Method (RUCAM).

Background. There is sparse literature on the association of adipose tissue with liver histology in patients with nonalcoholic fatty liver disease (NAFLD).Aim. To study the correlation of visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT) and total adipose tissue (TAT) with liver histology in Indian patients with NAFLD.Material and methods. A single slice CT scan at the level of L4-L5 vertebrae was done to assess the abdominal VAT and SAT volumes in 21 patients with histological diagnosis of NAFLD. Adult treatment panel III criteria with modified abnormal waist were used to define metabolic syndrome (MS). Histological grading was done according to the NAFLD activity score (NAS).Results. Twenty-one patients with NAFLD [13 males, median age: 35 years, median BMI: 25.97 kg/m2] were included prospectively. Even though overweight/obese patients had severe liver disease, there was no difference in the volume of VAT adjusted for BMI between 6 (28.5%) lean and 15 (71.5%) overweight/obese patients. Patients with NASH and borderline NASH were older, obese with higher VAT and SAT volumes than no-NASH group. SAT volume (SATV) correlated significantly with hepatic steatosis but none of the adipose tissue volumes had any correlation with other histological variables. Both SATV and TAT volume (TATV) correlated significantly with severity of liver disease as determined by NAS score whereas presence of MS or insulin resistance had no correlation with histological severity.Conclusion. Both subcutaneous and total adipose tissue volume are related to the disease severity as determined by NAFLD activity score in Indian patients with NAFLD.

Primary hepatic anaplastic large cell lymphoma (ALCL) of the liver is a rare entity. We present here two cases of primary hepatic anaplastic large cell lymphoma (ALCL) of the null-cell type. Both the cases had jaundice with “B” symptoms and hepatomegaly. The serum billirubin and liver enzymes were raised in both cases. The liver showed sinusoidal infiltration by atypical lymphoid cells with marked nuclear pleomorphism, dispersed chromatin and prominent nucleoli in both the cases. These cells were positive for CD30, negative for CD3, CD20 and EMA, and diagnosed as ALCL of the null-cell type. We hereby report these cases with the review of literature on primary hepatic ALCL with their possible etio-pathogenesis & diagnostic clues which may help in timely diagnosis & management in such cases.

Background & Aim: Imaging modalities have a role in the diagnosis of patients with nonalcoholic fatty liver disease. Aim of the present study was to evaluate the role of chemical shift magnetic resonance imaging in assessing hepatic steatosis and fibrosis in patients with nonalcoholic fatty liver disease.Methods: Chemical shift magnetic resonance imaging was done in 10 biopsy proven patients (7 females, mean age 41 ± 9.2 years) with nonalcoholic fatty liver disease. Objective measurements of signal intensity (SI) were done and a ratio was calculated (SI out-of-phase liver/ SI out-of-phase kidney)/ (SI in-phase liver/ SI in-phase kidney). A lower ratio indicated a higher signal drop and hence higher fat content. The ratio was correlated with hepatic steatosis on histology (< 33% and > 33%). Patients were classified as having histological NASH or no NASH and MRI was assessed in diagnosing hepatic fi-brosis as seen on liver histology.Results: Six patients had > 33% hepatic steatosis on histology. Five patients (50%) had evidence of histological NASH. MRI was not helpful in differentiating patients with and without his-tological NASH. One patient amongst NASH patients did not have fibrosis, one had stage 1, 2 had stage 2 and one had stage 4 fibrosis. SI ratio ranged between 0.350.69 in 6 patients with steatosis > 33% and was in the range of 0.69-1.20 in four patients with steatosis < 33% on histology. Fibrotic changes seen in 4 patients on biopsy were not detected on MRI.Conclusion: Chemical shift MRI provides objective data on fat infiltration in patients with NAFLD without giving information about hepatic fibrosis.

Background: Insulin resistance plays an important role in the pathogenesis of NAFLD. Pharmacological treatment of patients with NAFLD is still evolving. Insulin sensitizing drugs like metformin may be effective in these patients. Twenty five adult patients with NAFLD who did not achieve normalization of alanine transaminases (ALT) after 6 months of lifestyle interventions and UDCA were treated with metformin 500mg tid for 6 months. Insulin resistance was determined by HOMA-IR. Liver function tests were done monthly and patients were defined having no response, partial response or complete biochemical response depending on the change in ALT. Results were compared with 25 patients with NAFLD from the same cohort treated only with lifestyle interventions (disease controls). Results: Thirteen (52%) patients had class III (n = 5) or class IV (n = 8) disease amounting to histological NASH. Of these 13 patients none had severe inflammation and none had stage 4 fibrosis (cirrhosis). All 25 patients with NAFLD had insulin resistance in comparison to healthy controls. In comparison to disease controls (127.5 ± 41.8 vs. 118 ± 21.6 p = NS), all patients treated with metformin had partial biochemical response (mean ALT 122.2 ± 26.8 vs 74.3 ± 4.2 p < 0.01) and 14 (56%) of them achieved complete normalization of ALT. Conclusions: Metformin is effective to achieve biochemical response in patients with NAFLD who do not respond to lifestyle interventions and UDCA.

Portal vein aneurysms are uncommon incidental imaging findings. They usually do not require any treatment unless symptomatic. Contrast enhanced CT is the imaging modality of choice for depicting its morphology and extension.