Patients with liver cirrhosis frequently experience rectal variceal bleeding subsequent to portal hypertension. Unlike gastroesophageal variceal bleeding, a well-established guideline does not exist in terms of management of bleeding rectal varices. A 75-year-old male with non-alcoholic-steatohepatitis induced cirrhosis presented with a 3-day history of severe rectorrhagia. Considering patient\'s clinical history, TIPS was not performed and thus, a novel endovascular technique termed balloon-occluded antegrade transvenous obliteration was considered. Under conscious sedation, an occlusion was made through balloon catheter by sclerotic agents including air/sodium tetradecyl sulfate/Lipiodol. After the procedure, and in the 6 months follow up period the patient\'s hemodynamic status was stable and he recovered without any serious complications. Balloon-occluded antegrade transvenous obliteration is a feasible and safe modality for treating rectal varices bleeding and could be used as an alternative approach in patients with contraindications to traditional treatments.

Among the large population of patients with non-alcoholic fatty liver disease (NAFLD), identifying those with advanced disease remains challenging. Many patients are diagnosed late, following the development of liver-related complications, leading to poor clinical outcomes. Accumulating evidence suggests that using non-invasive tests for liver fibrosis in patients with metabolic risk factors improves the detection of patients in need of specialised management and is cost-effective. Because of the vast number of patients requiring evaluation, the active participation of general practitioners and physicians who manage patients with metabolic disorders, such as diabetologists, is crucial; this calls for the increased awareness of NAFLD beyond liver clinics. Non-invasive case-finding strategies will need to be further validated and generalised for upcoming drug therapies to have the required impact on the worldwide burden of NAFLD.

OBJECTIVE: NAFLD has today emerged as the leading cause of liver disorder. There is scanty data on risk factors associated with NAFLD emanating from India. The present study was conducted to identify the risk factors associated with NAFLD.
METHODS: 464 consecutive NAFLD patients and 181 control patients were subjected to detailed questionnaire regarding their lifestyle and dietary risk factors. Anthropometric measurements were obtained and biochemical assays were done. Comparison of different variables was made between NAFLD patients and controls using principal component analysis (PCA).
RESULTS: NAFLD patients had higher BMI [26.25 ± 3.80 vs 21.46 ± 3.08 kg/m(2), P = 0.000], waist-hip ratio [0.96 ± 0.12 vs 0.90 ± 0.08, P = 0.000] and waist-height ratio [0.57 ± 0.09 vs 0.50 ± 0.06, P = 0.000] compared to controls. Fasting blood sugar [101.88 ± 31.57 vs 90.87 ± 10.74 mg/dl] and triglyceride levels [196.16 ± 102.66 vs 133.20 ± 58.37 mg/dl] were significantly higher in NAFLD group. HOMA-IR was also higher in NAFLD group [2.53 ± 2.57 vs 1.16 ± 0.58, P = 0.000]. Majority (90.2%) of NAFLD patients were sedentary. Family history of metabolic syndrome (MS) was positively correlated with NAFLD. Dietary risk factors associated with NAFLD were non-vegetarian diet [35% vs 23%, P = 0.002], fried food [35% vs 9%, P = 0.000], spicy foods [51% vs 15%, P = 0.001] and tea [55% vs 39%, P = 0.001]. Diabetes, hypertension, snoring and sleep apnoea syndrome were common factors in NAFLD. On multivariate PCA, waist/height ratio and BMI were significantly higher in the NAFLD patients.
CONCLUSIONS: The risk factors associated with NAFLD are sedentary lifestyle, obesity family history of MS, consumption of meat/fish, spicy foods, fried foods and tea. Other risk factors associated with NAFLD included snoring and MS.

A 45 year old female with a body mass index (BMI) of 24 underwent successful liver transplantation (LT) for alcoholic cirrhosis using a donor liver from an obese woman with microvesicular steatosis (80%) and minimal macrovesicular steatosis (5-10%) on liver biopsy. Ascites and hepatosplenomegaly developed soon after LT with progressive increase of serum alkaline phosphatase to 1340 IU/L while aspartate aminotransferase (AST), and alanine transaminase (ALT), and total bilirubin remained normal. Imaging showed marked hepatomegaly, extensive fatty infiltration of the liver, and compression of the hepatic veins with narrowing of the intrahepatic inferior vena cava (IVC). Liver biopsy on post-operative day 39 revealed 90-100% macrovesicular steatosis, steatohepatitis, and portal fibrosis. A hepatic venogram showed a 10 cm segment of intrahepatic IVC stenosis that was stented, improving portal venous pressure measurements. However, portal hypertension requiring diuretic therapy and multiple paracenteses remained. By 3 months after LT, her liver had grown to 22 cm, transaminases increased 2-4 times the upper limit of normal with a 2:1 AST to ALT ratio. Liver biopsy at post-LT day 82 showed no change in steatosis and steatohepatitis despite corticosteroid withdrawal and interval periportal and perisinusoidal fibrosis. 12 weeks after LT, the patient was found to have low apolipoprotein B (65 mg/dL), high-density lipoprotein (HDL) (<10 mg/dL), low-density lipoproteins (LDL) (9 mg/dL), and total cholesterol (<50 mg/dL) levels. Therapy was started for NASH with high dose (800 IU daily) vitamin E and pioglitazone 15 mg daily, and she received topical vegetable oil and oral essential fatty acid supplements. Liver enzymes normalized after 3 months and her lipid profile improved markedly (HDL 27 mg/dL, total cholesterol 128 mg/dL), with progressive decrease in liver size and resolution of ascites after 5 months of therapy. At 2 years post-LT, the liver enzymes remain normal and lipids have normalized.