Case studies Abnormal LFTs
Enoka Gonsalkorala
Caboolture, RBWH
Case 1 – Ms BG
– 19F, Caucasian
– 3/12 of worsening lethargy
– PHMx
– Hay fever, acne
– BMI 30
– Medication – nil
– Work – apprentice hairdresser
– No EtOH
Bloods
– Bili 40, Alb 34, ALT 640, AST 410, ALP 220, GGT 74
– Hb 130 Plt 237 INR 1.7
– Cr 150 Ur 5
What else?
– Previous bloods?
– Other symptoms – joints, skin, pain, weight loss
– Drug history
– Lymecycline – completed 4mths prior to presentation
– No herbs, OCP, over the counter meds, gym supplements, NSAIDs
– Travel
– Camping, ?water ?party drugs ?tattoos
– Returned home 1mth prior to jaundice
– Sexual history
– Not sexually active
– Family history
– Uncle ankylosing spondylitis, great-aunt phemphigoid, uncle scleroderma
Back to bloods…
– Bili 40, Alb 34, ALT 640, AST 410, ALP 220, GGT 74
– Hb 130 Plt 237 INR 1.7
– Cr 150 Ur 5
What are the differentials?
1. Drug Induced Liver Injury (DILI)
2. Infection – biliary, leptospirosis, HBV
3. Autoimmune hepatitis
4. Fatty liver disease
Where to now?
What’s the next step?
Liver ultrasound
Referral pathway
Progress
– ANA 1/640, smooth muscle anti-body positive
– Liver biopsy – autoimmune hepatitis
Normal AIH
Management
– Prednisolone – 40mg daily for two weeks, then wean. Initially weekly blood tests
– Excellent biochemical response
– Commenced 6-mercaptopurine 8 weeks post as steroids sparing agent
Autoimmune Hepatitis
– Multifactorial aetiology – genetics, immune dysregulation, environment
– Insidious onset, F >M
– Diagnostic criteria
– Treatment – Prednisolone
– Taper steroids, add steroid sparing agent – azathioprine, 6-mercaptopurine
– AZA/6MP side effects – Cholestatic hepatitis, pancreatitis, infections, rash, N+V, opportunistic
infections – 10%
– Cytopaenia 5%
Case 3 – Mr ND
– 50M, Caucasian
– New patient to your practice
– PMHx
– T2DM
– Dyslipidaemia
– Ischaemic heart disease
– Medication
– EtOH – 6 units/wk
– Exam – BMI 27, central adiposity
Routine blood tests
– Alb 33, Bili 4, ALT 60, AST 67, GGT 300, ALP 250
– Hb 120, Plt 95, INR 1.1
– HbA1c 8%
– Choles – within normal range
– Concerns?
– Further tests → Health Pathways
– Liver screen negative
Interpretation
1. Alcoholic liver disease
2. Fatty liver disease
3. Advanced liver disease
4. Drug induced liver disease
5. Autoimmune hepatitis
What next?
- Liver US – nodular liver, splenomegaly, 3cm lesion
Low albumin Low platelets
Tertiary management
– Reviewed as Cat 1 pt
– No symptoms of hepatic decompensation (jaundice, ascites, peripheral oedema, variceal bleed, muscle wasting)
– Multi-phase CT confirmed 3cm hepatocellular carcinoma (HCC) without extra hepatic spread
– Discussed at hepatoma MDT
– Not suitable for locoregional curative therapy
– Referred for consideration of liver transplantation – listed
NAFLD
– Definition – hepatic steatosis on imaging or biopsy in the absence of:
– Significant EtOH (<21std for men, <14std for women)
– Medication
– Hereditary disorders
– NASH is a histological diagnosis
– Global prevalence 25%
– Associated conditions – obesity, diabetes, HTN, dyslipidaemia
NAFLD natural history
– Increased mortality – driven by cardiovascular disease
– Cancer related mortality
– Likely to take over as the most common indication for liver transplantation
– Role for bariatric surgery
What to do with the NAFLD patient in the community?
– Lose weight – portion size, exercise
– Control metabolic risk factors
– Diabetes
– HTN
– Lipids (statins can be used safely)
– Cardiovascular health
– Alcohol – limit to safe levels (14units per wk)
– Chronic Disease Management plan
Who to refer with abnormal LFTs?
– ALL patients with cirrhosis (decompensation, bloods, imaging)
– Patients at risk of developing NASH cirrhosis
– High ALT
– Insulin resistance / diabetes
– Metabolic syndrome
– Atypical NAFLD – fatty liver PLUS:
– Drugs – methotrexate, other
– Drug induced liver injury
– Hereditary disorder
Case 3 – Mr ED
– 45M
– General check up
– PMHx – HTN, T2DM
– Medication – perindopril, metformin
– EtOH – 20 units/wk
– Exam unremarkable
Investigations
– Hb 160, WBC 4, Plt 300
– Alb 40, Bili 3, ALT 50, AST 60, ALP 300, GGT 250
– Liver screen
– Ferr 1300, Transferrin saturation 75%
– What is the role of serum iron?
Causes of raised ferritin
– HBV/HCV
– NAFLD
– EtOH
– Hereditary haemachromatosis
– Thalassaemia major
– Non-HFE hereditary iron overload
What would you do next?
– HFE gene test
– Ultrasound liver
– Modify cofactors
– HbA1c
– Reduce/stop alcohol
– Blood pressure
Interpreting HFE results
– HFE Gene panel – which of the following mutations can cause hereditary iron over load? – H63D homozygous
– C282Y : H63D
– C282Y : C282Y
– H63D heterozygous
– Patient – C282Y homozygous
– What next?
– Screen family
– Refer
Hereditary haemochromatosis
– C282Y – homozygous, heterozygous, compound heterozygous (H63D)
– Other organ involvement – Diabetes
– Arthropathy
– Cardiomyopathy
– Hypogonadism
– Hypothyroidism
– 70% of homozygous will have abnormal LFTs, only 10% will have severe liver disease
Management
– Liver biopsy given cofactors – confirmed iron overload, fibrosis stage 2
– Commence venesection (Australian Red Cross, private lab)
– 1 unit 1-2 weekly, check Hb prior – aim <80% drop from baseline
– Check ferritin 3 mthly, aim 50-100
– Avoid vitamin C supplementation
– Do not need to regulate dietary iron intake
Take home…
– Framework to tackle abnormal LFTs – Health Pathways
– Include as much history as possible in referral – CPC guidelines
– Recognise the cirrhotic patient
– Metabolic syndrome and the liver
– Aggressive risk factor modification
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