Non-alcoholic fatty liver disease (NAFLD) is commonly diagnosed in obese subjects; however, it is not rare among lean individuals. Given the absence of traditional risk factors, it tends to remain under-recognised. The metabolic profiles of lean NAFLD patients are frequently comparable to those of obese NAFLD patients. Though results from several studies have been mixed, it has been generally revealed that lean subjects with NAFLD have minor insulin resistance compared to that in obese NAFLD. Several genetic variants are associated with NAFLD without insulin resistance. Some data suggest that the prevalence of steatohepatitis and advanced fibrosis do not differ significantly between lean and obese NAFLD; however, the former tend to have less severe disease at presentation. The underlying pathophysiology of lean NAFLD may be quite different. Genetic predispositions, fructose- and cholesterol-rich diet, visceral adiposity and dyslipidaemia have potential roles in the pathogenic underpinnings. Lean NAFLD may pose a risk for metabolic disturbances, cardiovascular morbidity or overall mortality. Secondary causes of hepatic steatosis are also needed to be ruled out in lean subjects with NAFLD. The effectiveness of various treatment modalities, such as exercise and pharmacotherapy, on lean NAFLD is not known. Weight loss is expected to help lean NAFLD patients who have visceral obesity. Further investigation is needed for many aspects of lean NAFLD, including mechanistic pathogenesis, risk assessment, natural history and therapeutic approach.

Amoebic peritonitis secondary to rupture of amoebic liver abscess (ALA) has been reported to occur in 2.4 to 13% of cases with a high fatality rate. There is still no consensus as to how a ruptured ALA associated with diffuse amoebic peritonitis be optimally managed. The mortality rates following surgical therapy in patients with ruptured ALA freely into the peritoneum have ranged from 20%‐ to 50%. The introduction of percutaneous catheter drainage (PCD) has opened a new therapeutic possibility for this group of patients and emerging data suggest that PCD should be the preferred option in such group of patients.

Obstructive jaundice caused by periampullary duodenal diverticulum in absence of choledocholithiasis or tumor is known as Lemmel syndrome. This is a rare cause of obstructive jaundice. We report here a patient of blunt trauma abdomen who underwent emergency laparotomy whose sequelae was a controlled external biliary fistula which healed and led to obstructive jaundice. What appeared to be a clear cut diagnosis of benign biliary stricture or bilioma gave a surgical surprise on opening the pandoras box. The uniqueness of this case lies in its etiopathogenesis as well as the dearth of available literature related to post traumatic Lemmel syndrome. This case provides us with a insight into an easy to be overlooked cause of obstructive jaundice in the absence of duodenal diverticula.

Cases and Techniques Library (CTL) E355Rai Praveer et al. EUS-guided thrombin injection in splenic artery aneurysm … Endoscopy 2014; 46: E355-E356

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