dr derek luo dr alasdair patrick - gp cme north/fri_room11_1402_lft cases.pdf · •reduce the...
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Dr Derek LuoConsultant Gastroenterologist
Director
Greenlane Medical Specialists
Auckland
14:00 - 14:55 WS #37: Interpreting LFTs
15:05 - 16:00 WS #49: Interpreting LFTs (Repeated)
Dr Alasdair PatrickGastroenterologist and General Physician
Middlemore Hospital
Auckland
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The only fully comprehensive
Gastroenterology center in Auckland
Opened in 2009
Largest Gastro practice in NZ
12 Gastroenterologists
1 Paediatric Gastroenterologist
1 Hepatologist
4 Surgeons
Dietician
Full diagnostic facilities on site
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Dr Alasdair PatrickGastroenterologist
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Case 1: AS23♀
• Unwell 2 days• Abdominal pain, Jaundiced and drowsy• Depressed otherwise well• OE: Jaundiced, No signs of CLD• LFTs Bil 250
ALP 160GGT 200ALT 2380AST 1960
• Thoughts?
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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
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Case 1: AS23♀
x
Paracetamol Treatment Nomogram
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Paracetomol overdose
• More than 250mg/kg likely severe liver damage
• 12g total potentially fatal– Less if low glutathione or p450 induction
• When taken in excessive amounts conjugation becomes inundated giving rise to alternate metabolism and toxic metabolite– Gives liver and renal tubule necrosis
• NAC 100% effective in first 8 hours
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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
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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
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Case 2: GH66♀
• Gradual Itch• Previous autoimmuine thyroid disease• Abnormal LFT’s on routine GP testing• OE: Normal apart from scratch marks• LFT’s Bil 15
ALP 502GGT 438ALT 65AST 48
Thoughts?
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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 (Cholangitis)
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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
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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• T bili best indicator of prognosis
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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 198ALP 137AST 126ALT 52
Thoughts?
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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
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Alcoholic hepatitis
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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
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Case 4:
• 22 lady Chinese 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
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Case 5
• 47 year old Indian man– Ex boozer
• ALT 55
• What else would you check?– HBsAg positive
• HBe Ag-ve, anti HBe +ve
• Rpt 6/12 ALT 127
• What would you do now?– Fibroscan- cirrhosis
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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?
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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
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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?
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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
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NAFLD
• Associated with
– Obesity - central
– Type-2 diabetes
– Hypertension
– Hypertriglyceridaemia
– FHx of type-2 DM common in absence
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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
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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)
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Ultrasound
• Hepatomegaly
• Altered echogenicity
• Can’t distinguish mild form from steatohapatitis/cirrhosis
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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
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Role of SWE
• Not clearly elucidated
• Consider in
– Pts at risk severe disease
– Concerning lab studies
• AST>ALT, low platelets
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Management
• Not really known
• Evidence accumulating that reducing BMI and improving insulin resistance with diet/exercise can reverse
• Endoscopic weight loss options or Bariatric surgery?
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Weight loss
• Aim 0.5-1kg/wk
• Faster can precipitate steatohepatitis or gallstones
• Decrease refined sugars
• Increase fibre
• Cholesterol improving and DM diet
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Exercise
• Increases oxidative capacity of myocytes
• Increases insulin sensitivity
• Check LFTs monthly
• Should see improvements in 2-3/12
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Weight Loss in NASH
• Randomized 2:1 ratio to receive intensive lifestyle intervention (LS) or structured education (control) for 48 weeks.
• LS group lost an average of 9.3% TBW versus 0.2% in the control group (p=0.003).
• LS group reduction of NAS of at least 3 points or had post treatment NAS ≤ 2 compared with the control group (72% versus 30%, p=0.03).
• Participants who achieved the study weight loss goal (>7%), had significant improvements in NAS (P < 0.001).
Pomrat et al. Hepatology 2010
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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
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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
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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
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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!
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Dr Alasdair Patrick
Gastroenterologist