Abnormal liver blood profile.

  • AST
  • ALT
  • GGT
  • ALK PHOS
  • T PROTEIN
  • ALBUMIN
  • GLOBULIN
  • PT TIME
  • PARTIAL THROMBOPLASTIN

HSE Document

We should be investigating nearly all abnormal LFTs further and shouldn’t use the duration or the degree of the abnormality to decide whether to investigate further.

  • Severe liver disease can present despite normal LFTs.
  • 84% of abnormal LFTs will still be abnormal in 1 months time.
  • 50% of abnormal LFTs found in GP are not further investigated. It is thought that this leads to late presentations for lots of people.
  • 20% of LFTs come back abnormal and less than 10% of these are caused by pre-existing liver disease. 

Transient elastography (FibroScan) is a non-invasive method proposed for the assessment of hepatic fibrosis in patients with chronic liver disease by measuring liver stiffness.

  • Abnormal LFTs have often not been investigated adequately- 50% of patients presenting with end stage liver disease without a previous diagnosis of liver disease were noted to have previous abnormal liver tests
  • Mild rises should not be overlooked – The extent of the liver blood test abnormality is not necessarily a guide to clinical significance (e.g. chronic Hep C with a lower ALT may be more significant than acute Hep A with an ALT over 1000)
  • Patients should be considered for investigation irrespective of the duration of the abnormality –Single unexplained abnormal liver tests (e.g. by drugs, infection etc.) warrant further investigation in the absence of a cause.It is important to note that liver tests may appear to return to normal but the underlying cause will still be there (e.g. fatty liver).

Common causes of abnormal liver blood tests

  • Alcohol related liver disease (ARLD)
  • Non alcohol related liver disease (NAFLD)
  • Chronic viral hepatitis (HBV/HCV)
  • - Medication

RED FLAGS: (urgent referral/2ww HBP) (admit if acutely unwell)

  • Jaundice – Refer to jaundice clinic 
  • Low albumin/raised INR
  • Ascites
  • Encephalopathy
  • Weight Loss/marked cholestasis (refer 2ww HBP)


SPECIFIC POSTIVE LIVER AETIOLOGY SCREEN RESPONSES TO AID DIAGNOSTIC PATHWAY

  • NAFLD suspected – If USS shows fatty liver disease or raised AST:ALT ratio follow NAFLD guidelines

(Note patients with a raised ALT/GGT who are obese may still have NAFLD despite a normal USS)

Raised ALT/AST ratio is only relevant in fatty liver disease (ie ignore if normal BMI)
 

  • RAISED BILIRUBIN:

No haemolysis, mostly unconjugated bilirubin (>70%) = Gilbert’s (no referral needed)

Haemolysis +unconj. Bilirubin = Refer haematology

Mostly conjugated bilirubin (>50%) = ?drugs, ?Dubin-Johnson Rotor syndrome.

  • Hep B serology +ve – Refer hepatology with HIV/HCV serology
  • Hep C antibody +ve - Perform Hep C viral load & request Genotype
    • HIV /HBV serology
    • If HCV PCR positive – refer hepatology
    • If negative – repeat 3m later and if still negative reassure patient infection has cleared, no need to refer
       
  •  Positive anti-mitochondrial antibody – refer Hepatology
  •  Anti-smooth muscle antibody or anti-nuclear antibody positive with raised IgG - refer to Hepatology (A&G if antibody positive with normal IgG)
  •  RAISED FERRITIN:
    • Exclude common causes – alcoholism, inflammation, metabolic syndrome/fatty liver, cell necrosis, malignancy.
    • If not explained by common causes and normal FBC – request ‘Haemochromatosis: Investigation’ on ICE (contains: LFT, Ferritin, Iron Saturation and HFE Gene).
    • see Genetic Haemochromatosis Clinical Guideline
    • HFE gene +ve – refer hepatology
    • No HFE gene - hepatology A&G.
    • (Genetic haemochromatosis is a common condition, affecting around 1 in 150 people, characterised by iron overload. The majority of patients with genetic haemochromatosis are homozygotes for the C282Y polymorphism. Early treatment with venesection is effective in preventing irreversible complications and improving mortality.*consider iron loading anaemia if FBC abnormal.)