This document discusses non-alcoholic fatty liver disease (NAFLD), the most common liver disease worldwide. NAFLD refers to excess fat accumulation in the liver not caused by alcohol consumption. It ranges from simple fatty liver to non-alcoholic steatohepatitis (NASH), which can progress to cirrhosis. Risk factors include obesity, diabetes, and metabolic syndrome. Diagnosis involves imaging and blood tests, while biopsy is the gold standard. Treatment focuses on lifestyle changes like diet and exercise, while emerging drugs target specific mechanisms. Without treatment, a minority of NASH cases may progress to complications like liver failure and cancer.

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-
Gold 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 :
1. 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 ( Pioglitazole)
 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 (34-36th ) week.
current maternal mortality is (0-18%) and
fetal mortality (9-23%) remains high.
 Death is usually due to extra hepatic causes such as –
1. Disseminated intravascular coagulation with
2. Massive hemorrhage including- sub capsular hematoma and rupture
3. Renal failure

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

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

29. Management:
Prognosis is relatively favorable if intensive care
is adequate.