Narendra S. Choudhary

Excellent outcome of living donor liver transplantation in patients with hepatopulmonary syndrome: a single centre experience.

Hepatopulmonary syndrome (HPS) worsens the prognosis of cirrhosis and liver transplantation is only definitive treatment. There is paucity of data about role of living donor liver transplantation (LDLT) in HPS.

Sarcopenic obesity with metabolic syndrome: a newly recognized entity following living donor liver transplantation

There are limited data about sarcopenic obesity in liver transplant recipients.

Treating morbid obesity in cirrhosis: A quest of holy grail.

The problem of obesity is increasing worldwide in epidemic proportions; the situation is similarly becoming more common in patients with cirrhosis which negatively affect the prognosis of disease and also makes liver transplantation difficult especially in the living donor liver transplantation setting where low graft to recipient weight ratio negatively affects survival. Treatment of obesity is difficult in cirrhosis due to difficulty in implementation of lifestyle measures, limited data on safety of anti-obesity drugs and high risk of surgery. Currently approved anti-obesity drugs have limited data in patients with cirrhosis. Bariatric surgery remains an option in selected compensated cirrhotic patients. Endoscopic interventions for obesity are emerging and are quite promising in patients with cirrhosis as these are minimally invasive. In present review, we briefly discuss various modalities of weight reduction in obese patients and their applicability in patients with cirrhosis.

High MELD score does not adversely affect outcome of living donor liver transplantation: Experience in 1000 recipients

In countries where deceased organ donation is scarce, there is a big gap between demand and supply of organs and living donor liver transplantation (LDLT) plays an important role in meeting this unmet need. This study was conducted to analyze the effect of pretransplant Model for End‐stage Liver Disease (MELD) score on outcomes following LDLT.

Estimation of normal values of serum transaminases based on liver histology in healthy Asian Indians.

Liver biopsy‐based studies have shown that serum levels of aminotransferases are lower than conventional cut‐off of 40 IU/mL in persons with normal histology. There is no such study in Indian population based on liver histology. This study aims to estimate normal values of serum aminotransferases in healthy Indian population with normal liver histology.

Low-dose short-term hepatitis B immunoglobulin with high genetic barrier antivirals: the ideal post-transplant hepatitis B virus prophylaxis?

Low‐dose hepatitis B immunoglobulin (HBIG) and nucleos(t)ides analogs (lamivudine/adefovir) used for the prevention of hepatitis B virus (HBV) recurrence after liver transplantation (LT) are associated with some risk of HBV recurrence and antiviral resistance.

Terbinafine Induced Liver Injury: A Case Report

Drug induced liver injury (DILI) is a cause of significant morbidity; timely diagnosis is important and requires a high index of suspicion. Terbinafine induced liver injury is rare. We report a case of Terbinafine induced hepatitis-cholestatic injury. The patient had a prolonged recovery phase lasting 3 months after discontinuation of drug.

Effect of Empagliflozin on Liver Fat in Patients With Type 2 Diabetes and Nonalcoholic Fatty Liver Disease: A Randomized Controlled Trial (E-LIFT Trial)

OBJECTIVE Sodium–glucose cotransporter 2 (SGLT-2) inhibitors have been shown to reduce liver fat in rodent models. Data regarding the effect of SGLT-2 inhibitors on human liver fat are scarce. This study examined the effect of empagliflozin (an SGLT-2 inhibitor) on liver fat in patients with type 2 diabetes and nonalcoholic fatty liver disease (NAFLD) by using MRI-derived proton density fat fraction (MRI-PDFF). RESEARCH DESIGN AND METHODS Fifty patients with type 2 diabetes and NAFLD were randomly assigned to either the empagliflozin group (standard treatment for type 2 diabetes plus empagliflozin 10 mg daily) or the control group (standard treatment without empagliflozin) for 20 weeks. Change in liver fat was measured by MRI-PDFF. Secondary outcome measures were change in alanine transaminase (ALT), aspartate transaminase (AST), and γ-glutamyl transferase (GGT) levels. RESULTS When included in the standard treatment for type 2 diabetes, empagliflozin was significantly better at reducing liver fat (mean MRI-PDFF difference between the empagliflozin and control groups −4.0%; P < 0.0001). Compared with baseline, significant reduction was found in the end-of-treatment MRI-PDFF for the empagliflozin group (16.2% to 11.3%; P < 0.0001) and a nonsignificant change was found in the control group (16.4% to 15.5%; P = 0.057). The two groups showed a significant difference for change in serum ALT level (P = 0.005) and nonsignificant differences for AST (P = 0.212) and GGT (P = 0.057) levels. CONCLUSIONS When included in the standard treatment for type 2 diabetes, empagliflozin reduces liver fat and improves ALT levels in patients with type 2 diabetes and NAFLD.

Liver Transplantation for Alcohol-Related Liver Disease.

Alcoholic liver disease (ALD) is a common indication for liver transplantation. It is a much debated indication for deceased donor liver transplantation due to organ shortage and potential of alcohol relapse after liver transplantation. A six-month abstinence before liver transplantation is required at most centers to decrease chances of alcohol relapse after liver transplantation. However, this rule is not relevant for patients with severe alcoholic hepatitis or severely decompensated patients who are unlikely to survive till 6 months. Long-term care of these patients after liver transplantation includes assessment of relapse, smoking, and surveillance of de novo malignancies. Current review discusses role of abstinence, factors affecting alcohol relapse, liver transplantation for alcoholic hepatitis, role of living donor liver transplantation, and long-term care of ALD patients who undergo liver transplantation.

Eosinophilic gastroenteritis mimicking as a malignant gastric ulcer with lymphadenopathy as shown by computed tomography and endoscopic ultrasound.

10.4103/2303-9027.151373 A 44-year-old male presented with a history of occasional epigastric pain over a 1 year period. A gastroscopy was performed by another hospital, it was diagnosed as a gastric ulcer. He had received proton pump inhibitors for a period of 3 months with no relief to the symptoms. He had no history of appetite or weight loss, and there was no history of any co-morbidity or allergy. There was no history of alcohol intake, smoking, medications intake or peripheral eosinophilia. Undergoing a further gastoscopy revealed a deep ulcer without raised margins at the lesser curve near antrum and thickened folds in surrounding area [Figure 1], biopsies were suggestive of dense eosinophilic infiltration. A computed tomography (CT) scan was performed as he had deep ulcer and thickened gastric folds, it showed eccentric mural thickening of antro-pyloric region along the greater curvature, as well as ulceration and enlarged peri-antral and gastro hepatic ligament lymph nodes [Figure 2]. The possibility of malignancy was still a possible outcome and at this point could not be ruled out. Endoscopic ultrasound (EUS) was perform with FNA from lymph nodes and for better characterization of thickened folds. EUS showed a 5 mm deep ulcer, thickened gastric wall (up to 11 mm) in the area surrounding ulcer with the loss of wall layer pattern. The opposite wall was of normal thickness and wall layer pattern of the stomach [Figure 3] with perilesional lymph nodes measuring 5 mm to 1 cm [Figure 4]. EUS guided FNA of the lymph nodes was negative of malignancy. Repeat biopsies from the ulcer edges showed dense eosinophilic infiltrate [80-100 eosinophils per high-power field as shown in Figure 5]; Helicobacter pylori was negative. A diagnosis of eosinophilic gastroenteritis (EG) was made. He was given steroids in tapering doses, and he became asymptomatic at 2 months.