विवरण
Non-alcoholic fatty liver disease is the most common liver disease worldwide, affecting up to 25% of the global population. The exact cause is unknown, but it is often associated with obesity, insulin resistance, high blood pressure, and high cholesterol levels. It is divided into two types: simple fatty liver and non-alcoholic steatohepatitis (NASH). NASH is a more severe form of NAFLD that can lead to liver damage and cirrhosis. It is typically diagnosed through blood tests, imaging tests (such as ultrasound or MRI), and sometimes a liver biopsy. Treatment involves lifestyle changes such as losing weight, exercising regularly, and eating a healthy diet. In some cases, medications may be prescribed.
सारांश
- Non-alcoholic fatty liver disease (NAFLD) is defined as fat accumulation in the liver exceeding 5% of hepatocytes, in the absence of significant alcohol consumption (≤20g/day). It can be primary (NAFLD itself) or secondary to other conditions like hepatitis C or metabolic disorders.
- NAFLD encompasses a spectrum from simple steatosis to non-alcoholic steatohepatitis (NASH), characterized by inflammation and potential fibrosis, which can progress to cirrhosis and hepatocellular carcinoma. Definitive NASH diagnosis requires a liver biopsy.
- The global prevalence of NAFLD ranges from 13-30%, with concerns that India reaches 30%. Risk factors include obesity, metabolic syndrome, sedentary lifestyle, and Western diets, making it a significant health issue in Asia. The new nomenclature "metabolic-associated fatty liver disease" (MAFLD) considers metabolic risk factors alongside steatosis.
- Etiology of fatty liver includes metabolic disorders, inborn errors, post-surgery conditions, and drugs like amiodarone, methotrexate, and estrogens. A thorough drug history is crucial.
- Pathogenesis involves a "two-hit" process. The first hit (steatosis) results from lifestyle factors, while the second hit (NASH) is driven by oxidative stress, inflammation, gut dysbiosis, and endotoxins. Around 20% of NAFLD progresses to NASH, potentially leading to cirrhosis and hepatocellular carcinoma.
- Routine liver function tests are poor predictors of steatosis or fibrosis severity in NAFLD. While elevated transaminases or GGT might be observed, many patients have normal results. Additional tests are needed for metabolic parameters and to exclude other liver diseases.
- Fibrosis assessment is crucial. Transient elastography (FibroScan) measures liver stiffness but can be unreliable in obese individuals. Non-invasive scoring systems like the NAFLD Fibrosis Score and FIB-4 score are used. MRI liver multi-scan provides an alternative to biopsy with good accuracy but is costly.
- Evaluation involves imaging to detect fatty liver, excluding alcohol and other causes, and using risk markers to categorize patients as low or high risk. Low-risk patients need lifestyle management, while high-risk patients require further investigation (MRI, FibroScan, or biopsy) to identify NASH.
- Chemical predictors of NASH include age, postmenopausal status, Asian ethnicity, hypertension, obesity, dyslipidemia, insulin resistance, and elevated AST/ALT ratio. Treatment is indicated for progressive NASH, high-risk NASH, or active NASH on biopsy.
- Liver biopsy reveals steatosis, hepatocyte ballooning, and inflammatory cells (neutrophils) in zone 3. These histological parameters guide diagnosis and follow-up.
- Management's cornerstone is lifestyle modification: minimum 45 minutes of exercise five days a week achieving 60-70% of maximum heart rate, and 10% body weight reduction in 6-8 months. Dietary changes include low-fat, low-carb (preferably Mediterranean), coffee inclusion, and alcohol abstinence.
- Weight loss significantly improves histological parameters. Three percent loss reduces steatosis, five percent reverses ballooning, seven percent resolves NASH, and 10 percent may regress fibrosis. FibroScan is crucial for routine follow-up.
- Pharmacological treatments target metabolic pathways (e.g., saroglitazar, obeticholic acid), inflammation (e.g., vitamin E), and fibrosis. Several drugs are in development. Saroglitazar, a PPAR agonist, addresses lipids, insulin sensitivity, and fibrosis.
- Recent advances include duodenal mucosal resurfacing, a procedure showing promise in improving NASH and diabetes markers by ablating and regrowing the duodenal mucosa to reduce insulin sensitivity. This procedure is still under investigation and not yet FDA-approved.
नमूना प्रमाण पत्र
वक्ताओं के बारे में
Dr Siddharth Dhande MD
Gastroenterologist Hepatologist and Interventional Endoscopist, Mumbai
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