Abstract

NAFLD characterized by steatosis, when NASH by steatosis, lobular inflammation or steatosis with fibrosis. NAFLD increasingly recognized today as hepatic manifestation of systemic 'metabolic complex also in India and in province like West Bengal with BMI greater than equal 30kg/m 2 , 67% of overweight patients in which BMI greater than or equal to 25 kg/m 2 and even in 25% normal weight population or with uncontrolled type 2- NIDDM. NAFLD/NASH today one of most common liver diseases in USA, Australia, Europe, Asian countries like china, Dallas, India, and West Bengal with emerging epidemic of obesity due to DM, consumption of fast food and rich food habits in people of industrialized cities and towns even in rural villages of West Bengal . NASH a progressive form of the disease finally leads to cryptogenic cirrhosis of liver even HepatoCellular Carcinoma requires liver transplant for cure. In most cases of NASH, Insulin resistance is found. The responsible gene is fetuin-A (FetA), ethnicity, Familial clustering in first degree relatives (20% of NASH). Natural history of NAFLD variable, although most patients experience an indolent course, some others progress to cirrhosis and liver related death. Paired liver biopsy data of predominantly NASH patients shows that over a follow up period of 2-5 years 18% - 29% patients improved with life style modification and treatment, 34% to 53% remain stable and 26% to 37% develop Cirrohosis and 9% of Cirrohosis from NASH within short time, The two hit hypothesis is widely accepted theory to explain progression of NAFLD from benign steatosis towards NASH. Diagnosis of NASH is challenging before clinicians, Radiologists by USG, with fibroscan devices, MRI, PET scan unless live needle biopsy is done and final diagnosis of NASH remains in clinical knowledge of combined Hepatologists and Hispatothologists. Liver enzymes, several biomarkers for NASH availble like TNF- alpha, Adiponectin- TNF/adiponectin ratio, serum leptin, C reactive protein.

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