Lifestyle interventions, namely optimizing nutrition and increasing physical activity, remain the cornerstone of therapy for non-alcoholic fatty liver disease (NAFLD), as this can lead to the significant improvement or resolution of disease. The optimal nutritional approach to treat NAFLD remains unclear. The aim of this systematic review is to evaluate the effectiveness of different nutritional patterns on hepatic, metabolic, and weight-loss endpoints. MEDLINE via PubMed, Embase, Scopus, and Google Scholar were searched. Randomized trials of dietary interventions alone for adults with NAFLD were selected. Two authors independently reviewed articles, to select eligible studies, and performed data abstraction. Six studies, representing 317 patients, were included. The participants had a median age of 46, mean body mass index (BMI) 31.5 and were 64.3% male. The mean study duration was 16.33 ± 8.62 weeks. Reduction in hepatic steatosis (HS) was statistically significant in 3/5 Mediterranean Diet (MD), one low-carbohydrate, one intermittent fasting (IF) and 1/2 low fat (LF) diet interventions. A total of 3/5 studies using MD, 1/2 LF interventions, and the one IF intervention demonstrated significant reductions in weight. In conclusion, there appears to be most data in support of MD-based interventions, though further randomized trials are needed to assess comparative effectiveness for NAFLD.

Introduction. Acute pancreatitis (AP) is the most common cause of gastroenterological hospitalization in the USA, with a mortality ranging from 5 to 20%. Up to 80% of cases are caused by cholelithiasis and alcohol abuse. Less common etiologies that need to be explored include hypertriglyceridemia, trauma, ERCP, infections, and drugs. A number of medications are known to cause acute pancreatitis, with 0.3-1.4% of all cases of pancreatitis being drug induced (DIP). Here, we present a case of metronidazole-induced acute pancreatitis. Case Summary. A 60-year-old female presented with constant severe epigastric pain associated with nausea, vomiting, and anorexia for one day. She had no past medical history of alcohol use or hypertriglyceridemia and was s/p cholecystectomy in the distant past. Symptoms had begun three days after starting metronidazole for Clostridium difficile colitis. Lipase was > 396, and CT abdomen revealed peripancreatic fat stranding. She was diagnosed with AP, metronidazole was suspected to be responsible and hence stopped, and supportive management initiated. Her symptoms improved rapidly, and pancreatic enzymes normalized within 2 days. Of note, she had had an episode of acute pancreatitis 3 years ago, also following metronidazole use, with resolution at discontinuation of the drug. She had concurrently been on omeprazole during both episodes. Discussion. Metronidazole is a commonly used antibiotic and is infrequently reported as a cause of DIP. Our review suggests the possibility of a dose-response and duration-response effect between metronidazole use and occurrence of pancreatitis. The most common presenting symptom and sign was moderate to severe epigastric pain and tenderness, accompanied by nausea/vomiting. Symptoms usually start within 2-7 days of starting the medication and usually resolve 2-5 days after discontinuation of therapy and pancreatitis treatment. The most common causative dose was 1-1.5 g/day. Our review also supports findings by Norgaard et al. suggesting that concurrent use of omeprazole potentiates the risk of metronidazole-induced pancreatitis. Conclusion. Metronidazole is a commonly used antibiotic that may cause metronidazole-induced pancreatitis, especially if patients are concurrently taking PPIs. Awareness needs to be raised amongst clinicians regarding this association, in order to correctly identify etiology of pancreatitis and discontinue metronidazole promptly when suspected as the causative factor.

Hepatitis C virus (HCV) is known to cause chronic hepatitis C, and its sequelae of cirrhosis and hepatocellular carcinoma. Hepatitis C genotype 3 (HCV-3) in particular is notorious for causing accelerated liver fibrosis, cardiovascular, and metabolic effects, thus increasing morbidity and mortality. It is the commonest variant in Asian countries like India and Pakistan. It is also one of the hardest-to-treat genotypes, especially among treatment-experienced and cirrhotic patients. Due to limited health care affordability and accessibility in these areas, many patients remain untreated. Until recently, the established therapy for HCV had been a combination of pegylated interferon + ribavirin. However, it was only effective in about half of patients and had severe adverse effects; hence a more efficacious option needed to be found. Recent advances have led to the development of sofosbuvir, an NS5B inhibitor that is fast becoming the standard of care, in combination with other novel drugs. It was initially marketed at $1,000 per pill, a cost that was too high for most. Thus, it has not been utilized as a global therapy as yet. Formulation of effective interferon-free regimens is a huge milestone, and awareness needs to be raised regarding these new highly effective options in both the physician and the patient population. This article discusses the newest drugs and combinations that have been developed in the fight against HCV-3, as a treatment outline for HCV-3-dominant areas. It also highlights recent breakthroughs in cost reductions of these drugs and the effort to make them globally accessible. Saeed N, Gurakar A. Tackling HCV-3 in Asia: Breakthroughs for Efficient and Cost-effective Treatment Strategies. Euroasian J Hepato-Gastroenterol 2016;6(1):35-42.