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