Non Alcoholic Fatty Liver Disease

In short presentation About NAFLD

1. Non-Alcoholic Fatty Liver Disease Presented by Dr.Shahadad Hossain Department of Medicine

2. Introduction Non alcoholic fatty liver disease is most common liver disease worldwide. Considered as the hepatic manifestation of metabolic syndrome Excess accumulation of fat >5% of liver weight is NAFLD NASH is the progressive form of NAFLD Average age of NASH patients is 40-50 years 50-60 years for NASH-cirrhosis Common cause of cryptogenic cirrhosis is NASH

3. Incidence and prevalence United States expected to face a NAFLD epidemic by 2030 with a prevalence of 50% ( Olaywi et al. 2013) - Increasing prevalence of obesity and Type 2 DM Prevalence in western countries ranges from 24% to 42% ( Cabelleria et al.2007 ) 10 %-20% of individuals with NAFLD have NASH and 10%-15% of individual with NASH progress to cirrhosis ( Pasumarthy & Srour 2010) NAFLD and NASH are more prevalent in males and Hispanics ( Pan and Falloon . 2014 )

4. Incidence and prevalence About one-third of the population of Bangladesh is affected by NAFLD. Females are predominant sufferer of NAFLD in Bangladesh ( Alam et al.2014 ) Prevalence of NASH is 42% among patients in Bangladesh ( Alam et al.2013)

5. Definition According to AASLD guideline-2018 Nonalcoholic fatty liver disease defined as: A ) there is evidence of hepatic steatosis either by imaging or by histology and B) there are no causes for secondary hepatic fat accumulation such as significant alcohol consumption: Threshold of <20g/day for women and <30g/day for men is adopted use of steatogenic medication or hereditary disorders

6. Working classification of NAFLD Non NASH fatty liver Type 1 ( only steatosis) Type 2 ( steatosis with inflammation ) NASH( non alcoholic steatohepatitis ) Type 3 (steatosis with inflammation with hepatocyte ballooning) Type 4 (steatosis with inflammation with hepatocyte ballooning with fibrosis )

7. Natural history of NAFLD

8. Risk factor associated with NAFLD NAFLD strongly associated with - Obesity- 94% obese, 67% overweight, 25% normal BMI Type 2 diabetes mellitus Dyslipidemia Sedentary life styles Metabolic Syndrome Genetic factor Associated with-- Polycystic ovarian syndrome Hypothyroidism

9. Metabolic Syndrome WHO Definition : Consists of 3 or more of the following FBS > or = 110 mg/dl S. TG > 150 mg/dl S. HDL < 40 mg/dl male , <50 female BP >130/85 mm HG or on Antihypertensive drug Waist girth >102 cm male, >88 cm female

10. Secondary Causes of Hepatic Steatosis Common causes are- Excessive alcohol consumption Medications ( amiodarone, methotrexate, tamoxifen, steroid, valproate, anti-retroviral medicine) Hepatitis C Wilson’s disease Starvation Acute fatty liver of pregnancy

11. Pathophysiology of NAFLD

12. Pathophysiology of NAFLD- video

13. Clinical presentation Frequently asymptomatic May be associated with fatigue mild right upper quadrant discomfort commonly identified as an incidental biochemical abnormality during routine blood tests Occasionally may present lately with- Complications of cirrhosis and portal hypertension, such as variceal haemorrhage , or HCC .

14. Investigation Liver function test : SGPT SGOT Gamma-GT Imaging : USG of abdomen: the liver appears bright due to increase echogenicity Fibroscan of liver with CAP CT scan MRI MR spectroscopy/ Transient elastography . [ Note: In USG,CT scan& MRI cann’t detect <20% fat In that case we do MR spectroscopy /transient elastography] Liver Biopsy

15. Sonographic view of liver in NAFLD

16. CT scan view of liver in NAFLD

17. Liver Biopsy- G old standard investigation Invasive method. Fig: True cut biopsy needle

18. Fibroscan of liver with CAP It is a non-invasive & a newer acceptable method to evaluate the degree of fibrosis and steatosis.

19. Management of NAFLD Non- pharmacological treatment are - Diet: Diet should be less than 25% in calorie of normal diet for the patient age & sex. Avoiding fructose & soft drinks & fast foods Increase intake of omega-3/ omega-6 PUFA( sea fish) in diet Coffee- 2 cups daily beneficial for NAFLD

20. Physical exercise . Moderate exercise maximum 4-5 times weekly for 30-45 minutes each time Strict control of hypertension, diabetes and dyslipidemia. Lifestyle interventions to promote weight loss. [ Sustained weight reduction of 7-10% is associated with significant improvement in histological and biochemical NASH severity]

21. Pharmacological treatment : Vitamin E: Dose 800 IU/ daily improves liver histology in non diabetic adult with biopsy proven NASH. If vitamin E administered at dose 400 IU/day increased the risk of prostate cancer & hemorrhagic stroke in healthy man. 2 . Omega 3 fatty acid: hypertriglyceridemia in patient with NAFLD .

22. Cont … 3. Thiazolidinediones ( P ioglitazole ) used to treat steatohepatitis in patient with biopsy proven NASH but now a days it is not used due to its side effects 4.Ursodeoxycholic acid 5.Metformin 6 . Statin 7 . Orlistat : As an aid to weight loss, this can be given 8 . Silymarin : Herbal products, Hepatoprotective drug

23. Emerging drugs: Obeticholic acid - Farnesoid X receptor (FXR) agonist It is contraindicated in Completely biliary obstruction Elafibrinor experimental medication, PPAR Alpha & delta agonist (Peroxisome proliferator activated receptor) - decrease TG and blood sugar DPP-4 Inhibitor

24. Surgical option of NAFLD Forgut bariatric surgery: It is indicated for obese individual with NAFLD or NASH

25. Management of complication Cirrhosis : Compensated: conservative treatment. Decompensated: liver transplantation indicated Hepatocellular carcinoma: treatment according to HCC management guideline.

26. Acute fatty liver of pregnancy: It affects approximately 1:14000 pregnancies. Onset is usually between (34-36 th ) week. current maternal mortality is (0-18%) and fetal mortality (9-23%) remains high. Death is usually due to extra hepatic causes such as – Disseminated intravascular coagulation with Massive hemorrhage including- sub capsular hematoma and rupture Renal failure

27. Clinical Features : 40% shows sign of eclampsia ad 50% shows signs of pre-eclampsia. Marked nausea , repeated vomiting Abdominal pain followed by jaundice within 2 weeks of onset of symptoms (100%) Hypertension Edema Polydipsia & Polyuria

28. Severe cases marked by- Encephalopathy Renal failure Pancreatitis DIC Investigation: Same as NASH- With some special investigations are: S. Ammonia S. Amino Acid Fibrinogen

29. Management: P rognosis is relatively favorable if intensive care is adequate .