Abnormal LFTs
GP CME 2014Workshop Fri 55 mins
Dr Alasdair Patrick
Macmurray Center
GP CME 2014
Dr Alasdair Patrick
Gastroenterologist
Overview
• Liver Function Tests
– Cholestasis
– Hepatocellular / Hepatitic
• Tests of Liver Synthetic Function
– Bilirubin, Albumin & INR
• Clinical aspects
• Cases
• Cirrhosis
– Middlemore Cirrhosis Audit
Normal Liver Anatomy
Portal Vein
Hepatic Artery
Bile Duct
Central Vein
Liver Function Tests (ULN)
Nature of liver disease
Cholestasis
ALP (110)
GGT (60)
Hepatitis
ALT (45)
AST (45)
Synthetic Function
Bilirubin (<24)
Albumin (35-47)
Prothrombin ratio (<1.2)
Patterns of raised LFT’s
A purely cholestatic or purely hepatitic picture is uncommon
Cholestatic ALT / ALP < 2
Mixed ALT / ALP 2 - 5
Hepatitic ALT / ALP > 5
[ Ratio = ALT (x ULN) / ALP (x ULN)]
Cholestatic Enzymes –
Alkaline phosphatase (ALP)
• Produced in many tissues
• Raised levels usually come from the biliary
epithelium, bones, or placenta
• If GGT normal unlikely hepatic source
• Cholestasis causes increased synthesis of ALP
and “leakage” of ALP in to the circulation
Cholestatic Enzymes –
Gammaglutamyl transpeptidase (GGT)• Found in cell membranes throughout the body including
hepatocytes and biliary epithelium
• Levels are not raised in bone disease or pregnancy
• Raised serum levels almost always have a liver origin (usually relating to cholestasis or fatty liver)
• Serum levels can be elevated in the absence of liver disease due to enzyme induction by anticonvulsants (phenytoin) or EtOH
Causes of Cholestasis
• Bile duct obstruction– Stones, tumour, surgery, parasites
• Drugs– Clavulanic acid, Flucloxacillin, Erythromycin
• Liver congestion / heart failure
• Sepsis / systemic inflammatory disorders
• Hormonal– Pregnancy, OCP
• Chronic biliary disorders– Primary Biliary Cirrhosis, Primary Sclerosing Cholangitis
• Inherited conditions– Biliary atresia, Cystic fibrosis
Cholestasis
Normal Stones & dilated CBD
Cholestasis
Normal
PSC
Hepatocellular –
Alanine Aminotransferase (ALT)• Catalyses the formation of pyruvate in the
cytosol
• Found in many tissues but by far the highest levels are in the liver
• Elevated levels are relatively specific for liver disease
• More sensitive marker of liver disease in chronic viral hepatitis than the AST
Hepatocellular –
Aspartate Aminotransferase (AST)• Catalyses the formation of oxaloacetate in the
cell cytosol and mitochondria
• Found in many tissues but high levels in liver and muscle (cardiac & skeletal)
• Elevated levels are not as specific for liver disease as an elevated ALT
• Less sensitive marker of hepatic inflammation than ALT
Hepatocellular Damage
Acute
• Viral hepatitis– EBV, HAV, HBV
• Drugs & herbal remedies– Paracetamol OD
• Ischaemic / hypoxic
Rare:
• Autoimmune (AIH)
• Wilson’s disease, Budd Chiari Syndrome, AFLP
Chronic (> 6 months)
• Viral hepatitis– HBV, HCV
• Fatty liver (NALFD)
• EtOH (AFLD)
• Drugs
• Haemochromatosis
• Autoimmune
• Wilson’s
Transaminases – Rules of thumb
• Chronic liver disease - ALT & AST are usually only mildly elevated ( typically 1.5 - 3 x ULN) - May be normal
• Ratio AST / ALT ratio is < 1 in most liver disease– Alcohol related hepatitis is the exception where the ratio is
usually > 2
• The degree of elevation of the does not correlate well with the degree of histological damage in the liver
• Levels may go in to the many thousands acutely and the liver recover completely
• Falling levels usually denote recovery but are an ominous sign if the liver synthetic function is worsening
• Levels < 10x ULN are non-specific
Causes: Transaminases > 1000 IU / L
• Ischaemic hepatitis (shock)
• Acute viral hepatitis
– HAV, HBV
• Drugs
– Paracetamol OD, halothane, Carbemazepine
[Alcoholic hepatitis ALT & AST < 300 IU/L]
Bilirubin
Two primary sources
Indirect (unconjugated): old red cells, removed by the spleen, sent to the liver
Liver “adds” glucuronic acid, making these cells water soluble for excretion; now called direct (or conjugated)
Synthetic Function –
Bilirubin• 80% comes from breakdown of haemoglobin
– Taken up by hepatocytes and conjugated with glucuronic acid and excreted in bile
• Normally > 95% of serum bilirubin is unconjugated (indirect); if conjugated - hepatobiliary diseases
• Only conjugated (direct) bilirubin can be excreted in the urine
• Unconjugated hyperbilirubinaemia may occur due to over production of bilirubin (haemolysis) or inherited disorders of bilirubin conjugation (Gilbert’s syndrome)
Bilirubin and Prognosis
• Poor sensitivity for detecting liver dysfunction
– Large reserve capacity of the liver to remove bilirubin without the development of hyperbilirubinaemia
• In acute cholestatic disease (stone disease) hepatocyte synthetic function is normal and the degree of hyperbilirubinaemia does not influence prognosis
• In viral hepatitis, alcoholic hepatitis and PBC the serum bilirubin does correlate with the degree of injury on biopsy and the prognosis
Synthetic Function –
Albumin
• Made in the liver (30g/day)
• Quantitatively the most important protein in the
blood (500g in body fluids), important role in
maintaining colloid osmotic pressure
• Serum albumin level is determined by the rate of
synthesis, rate of loss / degradation and the
volume of distribution
Albumin
• A low serum albumin is a good indicator of
liver synthetic failure in the presence of
chronic liver disease, however other
causes of hypoalbuminaemia need to be
considered:
• Renal loss (Nephrotic syndrome)
• Protein-calorie malnutrition
• Haemodilution (raised)plasma volume
Synthetic Function –
PR/INR
• Most clotting factors are synthesised in the liver
– Liver transplantation is a surgical cure for
haemophilia!
• In the setting of both acute and chronic liver
failure the INR is a very useful indicator of liver
synthetic function and prognosis, however other
causes of a raised INR need to be excluded: • Vitamin K deficiency (prolonged cholestasis)
• Increased clotting factor consumption (DIC)
• Warfarin therapy
PR/INR
• In chronic liver failure INR rarely rises above 2.0
• In acute or fulminant liver failure the INR may rise rapidly to very high levels (>10), this is associated with a very poor prognosis and liver transplanation should be considered
• Even an INR of 1.3 in the setting of an acute severe hepatitis is of concern and should be repeated after 6-8 hrs
LFT’s & Liver Failure
Acute (FHF)• ALT & AST usually >
1,000
• INR & Bilirubin rise rapidly
• Alb falls rapidly
• Patient unwell for hours or days
• Death within days of cerebral oedema, sepsis or multi-organ failure
Chronic (Cirrhosis)• ALT & AST usually < 200
• INR & Bilirubin rise slowly
• Alb falls slowly
• Patient unwell for months or years
• Death from variceal haemorrrhage, sepsis, encephalopathy or other complications
Clinical aspects
Please call out what these signs are!!
Examination Findings
Dupytrons Contracture
Examination Findings
Palmar Erythema
Examination Findings
Gynaecomastia
Examination Findings
Spider Naevi
Patient with abnormal LFTs
• History
– Alcohol: try to quantify
– Blood products or IVDU
– Past history
• Diabetes, hyperlipidaemia
– Medications– Including OTC
– Paracetamol, Amoxicillin-clavulanic acid, erythromycin, HMGCoA reductase inhibitors, NSAIDS
– Family history
– Travel history
Questions to ask yourself
• Is the illness a primary liver disorder or is it secondary to another condition?
• Clue can be in the LFTs
– Is the source of the “liver test” extra-hepatic? An abnormality of a single test may be due to a non hepatic cause
• Is this an acute illness or chronic? If chronic, is it compensated or decompensated?
• Do the tests signify a serious illness? What is the diagnosis and prognosis?
Suggested work up
Screen
• Fasting lipids and glucose
• Viruses HBV HCV (EBV CMV)
• Auto immune markers• ANA, AMA, SMA
• Immunoglobulins
• Coeliac serology, Iron studies, Thyroid function tests
• USS –focal lesions, fatty liver, portal hypertension
Second run
• Alpha one anti-trypsin, Copper and ceruloplasmin in pt <40, Anti LKM, SLA
Case 1: AS23♀
• Unwell 2 days
• Abdominal pain and lethargy
• Depressed but otherwise well
• OE: Jaundiced, No signs of CLD
• LFTs Bil 250
ALP 160
GGT 200
ALT 2380
AST 1960
• Thoughts?
Case 1: AS23♀
• Other Bloods:– INR 2.3, Cr 85, pH 7.40, Paracetamol 120
• Liver Screen– Negative (HAV and HBcoreIgM – Negative)
• Imaging– USS: Normal
• Pattern of LFT Disturbance– Hyperbilirubinaemia, Hepatitic Picture ALT>1000
• Diagnosis– Paracetamol Overdose
Case 1: AS23♀
x
Paracetamol Treatment Nomogram
Paracetomol overdose
• Liver Transplant Criteria (Kings College)
• Paracetamol– Arterial pH < 7.3; or
– All three: INR>6.5, Cr>300, G3-4 Encephalopathy
• Non Paracetamol– INR >6.5; or
– Three of the following five criteria• Patient age <11 or >40;
• Bilirubin >300;
• Time from onset of jaundice to enceph. greater than 7 days;
• INR >3.5; or,
• Drug toxicity
Paracetomol overdose
• Follow up
– Gradual improvement of LFT’s and synthetic
function
• Treatment
– Close Observation
– Frequent Blood test repeat
– Rx – n-acetyl cysteine (NAC)
– Psychiatry
Case 2: GH66♀
• Gradual Itch
• Previous autoimmuine thyroid disease
• OE: Normal apart from scratch marks
• LFT’s Bil 15
ALP 502
GGT 438
ALT 65
AST 48
Thoughts?
Case 2: GH66♀
• Other Bloods:– INR 1.0, Alb 40
• Liver Screen– AMA Positive, ANA 1:80
• Imaging– USS: Normal
• Pattern of LFT Disturbance– Choleststatic picture with preserved synthetic function
• Diagnosis– Primary Biliary Cirrhosis
Primary biliary cirrhosis
• Auto-immune disease of the liver
– Slow progressive destruction of small bile
ducts
• Female to male ratio 9:1
• Prevalence 1:4000
Primary biliary cirrhosis
• Treatment
– Ursodeoxycholic acid
• Reduce the cholestasis - improves LFT’s results
• Minimal effect on symptoms
• Whether it improves prognosis is controversial
– Cholestyramine (bile acid sequestrant)
• Absorb bile acids in the gut
• Alternative agents: Naltrexone & Rifampicin
– Ongoing follow up
Case 3: GF 56♂
• Heavy alcohol consumption – Many years
• Stopped 4 weeks ago
• Gradual jaundice, confusion and lethargy
• OE: Jaundiced, Spider Naevi, Small liver
• LFTs Bil 406
GGT 198
ALP 137
AST 126
ALT 52
Thoughts?
Case 3: GF 56♂
• Other Bloods:– INR 1.8, Albumin 30
• Pattern of LFT Disturbance– Mixed, significant hyperbilirubinaemia, AST>ALT
• Liver Screen– Negative
• Imaging– USS: Coarse Liver Echotexture
• Diagnosis– Alcoholic Hepatitis
Alcoholic hepatitis
Alcoholic hepatitis
• Treatment
– Abstinence from Alcohol
– Monitor for withdrawal
– Vitamin K
– In Hospital 3 weeks
• Good improvement
– Prednisone 30mg Daily for 4 weeks
– Cirrhosis follow up
Case 4:
• 22 Chinese lady who says she has Hep B
– ALT normal
– sAg +ve, eAg +ve, anti HBE –ve
• HBV DNA 10*9
• What would you do?
• Watch 6/12ly and get flare and
seroconverts
Case 5
• 47 year old Indian man
– Ex boozer
• ALT 55
• What else would you check?
– HBsAg positive• HBe Ag-ve, anti HBe +ve
– What would you do now?
• Rpt 6/12 ALT 127
• What would you do now?
– Fibroscan- cirrhosis
Viral Hepatitis
Viral Hepatitis : Hepatitis A
• Food, water borne; heat labile
• Faecal - oral contamination; contagious
• Usually self limited, lasting days to weeks
• 99% spontaneous recovery, no treatment
• Tests: HAV IgM antibody = acute infection
• HAV total antibody (IgM & IgG) = exposure
• only, could be post infection or vaccination
Viral Hepatitis : Hepatitis B
• Blood, semen, saliva, vaginal secretions
• Highly contagious; sexually transmitted
• 90-95% self limited over 6 months
• Chronic infection: >6 months
• DNA virus: incorporates into host with chronic infection
Viral Hepatitis : Hepatitis B
• HBV at risk groups (who to test)
– Maori, Pacificans, Asians, contacts of those
with HBsAg patients, IVDU, MSM
– Abnormal liver function tests
HBV Serology
• HBV s Ag: surface antigen; +
infection
• HBV s Ab: surface antibody; -
infection
• HBV c Ab: core antibody IgM,
IgG; only + with infection,
not vaccination
• HBV e Ag: envelope antigen;
if + actively replicating virus
• HBV DNA: actual viral load in
blood
Serologic markers of infection
and their significance
(in some
cases)
Recovery
from acute
hepatitis B
DNA (PCR if
required)
Anti-HBe
HBeAg
Anti-HBc
IgG
Anti-HBc
IgM
Anti-HBs
HBsAg
Successful
vaccination
Chronic
HBeAg –
disease
Chronic
HBeAg +
disease
Acute
hepatitis B
HBV Treatment Decision
• E- Antigen Status
• Likelihood of progression ie significant fibrosis
now
• Likelihood of adhering to treatment
– Lamivudine (not first line)
– Entecavir
– Adefovir (Lam Resistant)
– Tenofovir
– Pegylated interferon
Why treat Hepatitis B ?
• To prevent complications of cirrhosis ie
decompensated cirrhosis and its
complications eg HCC
• Ultimate Goal – cure, permanent
suppression, roadmap concept
• Once decision made, more or less life long
Viral Hepatitis : Hepatitis C
Blood borne, not in
food or water; not
highly sexually
transmitted*
Not highly contagious
20% self clearing;
80% chronicity
RNA virus: does not
incorporate into host
Viral Hepatitis: Hepatitis C
HCV Ab: + means past exposure; can take 3-6 months to form; not found if acute
ELISA: used to confirm Ab; + rules out false positives
HCV PCR RNA: confirms actual viral presence in blood; can be +/- or a viral count (qualitative vs. quantitative)
HCV Genotype: there are at least six (6) different (geno)types of HCV virus
Viral Hepatitis : Hepatitis C
HCV Genotypes: different mutations of same virus (different branches, same tree)
Can vary by global geography
Not predicative of damage or symptoms
Can predict response to treatment
Can be used to determine who is the best treatment candidate
G1 & 4: most stubborn; G2 & 3: most responsive; G5 & 6: most rare
HCV: When to refer to a
specialist
• HCV Ab +
• RNA +
• Suitability for treatment – alcohol use,
ongoing drug use, motivation, mental state
eg depression (consider SSRI at the time
of referral)
• Treatment improving all the time
• Expect 70-90% cure with new drugs
Case 5
• Asymptomatic 40 year old man
• Screening LFTs
– Bili 38
– ALT 15 IU/ml
– ALP 85
– GGT 30
– Alb 36
• What other information would be helpful?
Case 5
• Otherwise well
– No alcohol
– No family history
• What bloods would you check?
• Diagnosis: Gilberts syndrome
• How could you confirm this?
– unconjugated hyperbilirubinaemia
• Often increases in infections but also on starving
Case 6
• 46 year old European man– Feeling tired
– Gaining weight• Wt 120kg, BMI 32
– Occasional alcohol
• LFTs– T bili 20
– GGT 198
– ALP 88
– AST 40
– ALT 65
Thoughts?
Non-alcoholic fatty liver disease
(NAFLD)
• Spectrum of severity
– Mild fatty infiltration
– Non-alcoholic steatohepatitis
– Fibrosis, cirrhosis
• Most common cause of abnormal LFT’s in primary care
• Hepatic manifestation of metabolic syndrome
NAFLD
• Associated with
– Obesity - central
– Type-2 diabetes
– Hypertension
– Hypertriglyceridaemia
– FHx of type-2 DM common in absence
NAFLD
• Thought to affect up to 24% population
• 70% of obese
• 50% of type-2 DM
• Mostly benign….
– Cirrhosis and hepatocellular carcinoma?
• Cirrhosis risks - age, obesity, DM
NAFLD - Clinical
• Symptoms
– Usually none
– Fatigue, RUQ discomfort
• Laboratory
– Elev GGT and ALT
• If AST > ALT suspect ETOH, or cirrhosis if denied
– Elev TG/Chol, glucose
– USS (CT also)
Ultrasound
• Hepatomegaly
• Altered echogenicity
• Can’t distinguish mild form from
steatohapatitis/cirrhosis
Differential• Should exclude other causes
– Viral hepatitis
– Drugs - esp alcohol
– Autoimmune (ANA, SMA)
– Metabolic (iron, copper)• High ferritin with normal transferrin saturation common in
NAFLD
• If saturation >45% ---> HH studies in Caucasians
• Investigate for metabolic syndrome if not known– Almost always assoc with insulin resistance
• High risk of type 2 diabetes
Role of liver biopsy
• Not clearly elucidated
• Consider in
– Pts at risk severe disease
– Concerning lab studies
• AST>ALT, low platelets
Management
• Not really known
• Evidence accumulating that reducing BMI
and improving insulin resistance with
diet/exercise can reverse
• Some evidence that there are promising
drugs coming
• Bariatric surgery?
Weight loss
• Aim 0.5-1kg/wk
• Faster can precipitate steatohepatitis or
gallstones
• Decrease refined sugars
• Increase fibre
• Cholesterol improving and DM diet
Exercise
• Increases oxidative capacity of myocytes
• Increases insulin sensitivity
• Check LFTs monthly
• Should see improvements in 2-3/12
Insulin resistance
• Metformin
– Improves insulin sens of all tissues
– Improves transaminases in NASH
– Reverses fatty liver in mice
• Glitazones
• Other classes under investigation
Lipids
• Statins
– Reduce LDL and TG
– Improves LFTs in NASH
• Fibrates
– Gemfibrozil
• Increases HDL, decreases TG
• Modest effect only on NASH
Helpful points
• Fatty liver can lead to cirrhosis
• Females and elderly do worse
• Often asymptomatic
• USS usually sufficient for diagnosis
• No established treatment
– Steady weight loss first line if obese
– Rapid weight loss may be dangerous
Cirrhosis
Normal
Cirrhosis
Liver Cirrhosis
• May be the end result of chronic cholestatic or hepatitic disease
• Liver synthetic function may be impaired or normal
• The enzymes may be of any pattern or may be normal if the underlying aetiology is inactive or no longer present
Cirrhosis - Importance
• Why Important?– Hepatoma 1-2% per annum
– Variceal Bleeding
– Decompensation – Risk of Liver Failure
• Suggested By– Bloods
• ↓Platelets, ↓Albumin, ↑INR, ↑Bilirubin
– Clinical Examination
• Liver Specific / Other Organ injury
– Imaging: USS / CT
• Irregular contour, ↑PV size, Splenomegaly, Varices
– Endoscopy
• Varices, Portal Hypertensive Gastropathy (PHG)
Survival according to Child-
Pugh Score
Grade Score 1 year 5 year 10 year
A 0 – 6 84% 44% 27%
B 7 – 9 62% 20% 10%
C 10 - 15 42% 21% 0%
POINTS 1 2 3
Encephalopathy None Grade 1, 2 Grade 3, 4
Ascites None Mild Moderate
Bilirubin < 35 35 - 50 > 50
Albumin > 35 28 - 35 < 28
INR < 1.3 1.3 – 1.5 > 1.5
Pugh et al. Br J Surg, 1973
Middlemore Hospital Audit - Cirrhosis
New patients presenting each year
0 20 40 60 80 100
Before 2001
2001
2002
2003
2004
2005
2006
2007
2008
2009
2010
2011
Number
Linear (Number)
Gerred et al. 2012
Cirrhosis: Patients removed from
the database
0 2 0 4 0 6 0 8 0
p r e 2 0 0 1
2 0 0 1
2 0 0 2
2 0 0 3
2 0 0 4
2 0 0 5
2 0 0 6
2 0 0 7
2 0 0 8
2 0 0 9
2 0 1 0
2 0 1 1
D e c e a s e d
L o s t o r m o v e d
T ra n sp la n ted
C a s e s w ith d ra w n fro m F o llo w -u p
Ye
ar
Gerred et al. 2012
Cirrhosis: Number of patients under
Follow-up
0 100 200 300 400 500
2001
2003
2005
2007
2009
2011
Number
Linear (Number)
Gerred et al. 2012
Cirrhosis – New Case Aetiology
N u m b e r o f N e w C a s e s
Ye
ar o
f p
re
se
nta
tio
n
0 5 0 1 0 0 1 5 0
2 0 0 1
2 0 0 2
2 0 0 3
2 0 0 4
2 0 0 5
2 0 0 6
2 0 0 7
2 0 0 8
2 0 0 9
2 0 1 0
2 0 1 1
A L D
H B V
H C V
N A F L D
O th e r
Gerred et al. 2012
Cirrhosis: Primary Aetiology and
Gender
Primary Aetiology of Cirrhosis
Nu
mb
er
of
pati
en
ts
HBV HCV ALD NAFLD Other0
50
100
150
200
250
Male
Female
M ale
F emale
35% 20% 18% 14% 12%
Gerred et al. 2012
Cirrhosis: Age of presentation &
Aetiology
A e tio lo g y
Ag
e
AL
D
HB
V
HC
V
NA
FL
D
3 0
4 0
5 0
6 0
7 0
8 0
P <0.001
Gerred et al. 2012
Cirrhosis: Race
E th n ic ity
Ag
e
Asia
n
Eu
rop
ean
Ind
ian
Mao
r i PI
2 0
4 0
6 0
8 0
5 2 y rs 5 6 y rs5 7 y rs5 9 y rs5 5 y rs
Gerred et al. 2012
Aetiology of Cirrhosis and Ethnicity
N u m b e r o f c a s e s
Eth
nic
ity
0 1 0 0 2 0 0 3 0 0 4 0 0 5 0 0
As ia n
E u r o p e a n
In d ia n
M a o r i
P I
A L D
H B V
H C V
N A F L D
O th e r
Gerred et al. 2012
Cirrhosis: Survival & AetiologyC h a r t-5 : S u r v iv a l & A e tio lo g y
0 5 1 0 1 5
0
2 0
4 0
6 0
8 0
1 0 0
A L D
H B V
H C V
N A F L D
Y e a rs o f F o llo w -u p
Pe
rc
en
t s
urv
iva
l
P<0.001
Gerred et al. 2012
Cirrhosis: Survival & EthnicityC h a r t-4 : S u rv iv a l & E th n ic it ie s
0 5 1 0 1 5
0
2 0
4 0
6 0
8 0
1 0 0
A s ia n
E u ro p e a n
In d ia n
M a o ri
P a c if ic
Y e a rs o f F o llo w -u p
Pe
rc
en
t s
urv
iva
l
P=0.002
Gerred et al. 2012
Cirrhosis: Complications - 4yr FU
ALD HBV HCV NAFLD
Variceal
bleed
24% 6% 10% 18%
SBP 12% 6% 7% 6%
Ascites 57% 24% 21% 34%
Encephalop
athy
35% 11% 13% 14%
HCC 11% 25% 13% 13%
Transplant and death - 4yr FU
ALD NAFLD HBV HCV
OLT 2% 3% 7% 6%
Liver
Death
22% 17% 20% 12%
Other
Death
26% 18% 7% 7%
Total
Death
48% 35% 27% 19%
HCC Surveillance
Period (-1:1st 6 months, -2:2nd 6 months)
Cirrhosis Middlemore - Conclusions
• Number of Cirrhotic patients under follow-up has quadrupled in the last 10 years
• HCV and NAFLD are driving rising numbers of new cases in recent years
• Generally patients with cirrhosis are living longer but death and complications remain common
• Poor prognosis in Maori despite predominantly HBV and young
• Poor prognosis in ALD and NAFLD - older and sicker at presentation
Take home messages: Patient care
• Jaundice and evidence of liver failure– Immediate discussion and consider admission
• Jaundice, no liver failure– Immediate discussion ?admission
– Urgent USS, (haemolysis screen)
• Major elevation ALT/ AST (10 X ULN)– Immediate discussion ?admission
– Repeat and review within 24 hours with synthetic function
Take home messages: Patient care
Moderate elevation LFTs (5 X ULN)
– INR, Bilirubin, early
– Repeat with 48 hours with liver screen
– Early referral
• Evidence of cirrhosis, no liver failure
– Abnormal LFTs, abnormal USS, low platelets
– Early referral with liver screen
Take home messages: Patient care
• Mild Elevation of LFTs (2-3x ULN)
– Repeat
– Liver screen
– USS
– Referral
• A methodical approach will usually yield
the diagnosis!
Dr Alasdair Patrick
Gastroenterologist