NASH/ NAFILD ( RACGP article for my personal use ) 

Non-alcoholic fatty liver disease (NAFLD), encompassing both simple steatosis and non-alcoholic steatohepatitis (NASH), is the most common cause of liver disease in Australia.

The non-alcoholic fatty liver disease needs to be considered in the context of the metabolic syndrome, as a cardiovascular disease will account for much of the mortality associated with NAFLD.

more common in the presence of diabetes, obesity, older age and increased inflammation, and is more likely to progress to cirrhosis—— hepatocellular cancer

weight loss remains the only effective treatment for NAFLD.

Simple steatosis— benign but may progress to NASH

when NAFLD occurs in the presence of other features of the metabolic syndrome (MetSy), mortality doubles.

The MetSy

  • elevated serum triglycerides (TG)
  • lowered serum high-density lipoprotein
  • impaired glucose tolerance
  • central adiposity

Metsy + NAFLD = 2X motility

The most common presentation of NAFLD will be an incidental finding of abnormal LFTs. Typical findings in NAFLD are

1 raised ALT and AST, with a preserved ALT: AST ratio of 1.5,

2 raised gamma-glutamyl transferase (GGT) and,

3 occasionally, raised alkaline phosphatase (ALP).

These findings commonly occur in the setting of features of the MetSy.

There are several features on examination and laboratory values that should raise suspicion of cirrhosis,

1 C/F such as spider naevi,

2 low or falling platelets,

3  low albumin

4 reversal in ALT: AST ratio (where AST exceeds ALT),

before the features of portal hypertension and decompensation become obvious

How to diagnose NAFLD

1 evidence of fatty infiltration from( USS/Biopsy)

2 exclusion of significant alcohol consumption

3 exclusion of other causes of hepatic steatosis (eg. medications, surgery, metabolic disorders)

Staging liver disease and detecting cirrhosis is the most important aspect of assessing fatty liver disease.

The traditional gold standard in assessing liver disease is liver biopsy. However, biopsy has an unfavourable cost, safety, availability, sampling error, inter-observer variability and patient acceptance.

A liver biopsy may be considered where cirrhosis is suspected, or where an alternative diagnosis is considered. At this stage, referral to a gastroenterologist is also suggested.

Non-invasive tools for estimating the degree of fibrosis include transient elastography (FibroScan®) etc.

Central adiposity can be assessed using waist circumference measured at the narrowest point mid-way between the lowest rib and the iliac crest at the end of an expiration with the patient standing.

Management

1 Cardiovascular risk factors and lifestyle modification

The cornerstone to managing NAFLD is achieving weight control and reduction in cardiovascular risk factors such as smoking, diabetes, hypertension and dyslipidaemia. This may include referral to a dietician, endocrinologist or cardiologist. Treatment of associated dyslipidaemia is appropriate with either statins or fibrates where required. Moderate elevations in liver enzymes due to the use of statins should be tolerated and treatment continued. However, severe elevations more than 10 times the upper limit of normal should prompt cessation of the medication and reassessment.

Dietary manipulation, such as the adoption of a Mediterranean-type diet, has shown promise. The most important feature appears to be the caloric reduction. Where diet and exercise are unsuccessful in achieving weight reduction, bariatric surgery may be considered.

The presence of normal LFTs does not exclude underlying cirrhosis, nor does a ‘non-cirrhotic’ ultrasound. Monitoring full blood examination (FBE), LFTs, International Normalised Ratio (INR), blood pressure and lipid profile every 6 months is a reasonable approach.

Mild increase in liver enzime – how to investigate

Step1- initial – medications , overthe counter , recreational drugs , screen for alcohol, hepatitis B/C, hemacromatosis , Fatty liver

Step 2- 2nd line –

Autoimmune hepatitis  (ANA ASMA ), < hypothyrodism, celiac disease Wilsons disease, alfga 1 antitripsin ( H/O empesema ) , adrenal insuficiency ( 8AM cortisole, plasma ACTH, High dose ACT stimulation test )

Step 3 – Biopsy

ALT  & AST <2 fold elevated –  observe  otherwise biopsy

AST, ALT, ALP , GGT, Billirubin – marker of liver injury

Albumin prothrombin , billirubin – marker for liver synthetic function

most liver injuries AST<ALT  2:1

Alcohol ALT>AST

History – Right heart failure , Diabetes, skin pigment, IV drugs, Over the counter drugs , Blood transfusion before 1992, travel, contact history of jaundice , obesity , IBD, Emphesema symptoms (alfa 1 antitripsin ), celiac, thyroid symptoms

proximal muscle wasting , CLD signs , Virchow’s signe for malignancy , JVP, Neurological signs for willsons