the cirrhotic patient on HCV therapy
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Transcript of the cirrhotic patient on HCV therapy
THE CIRRHOTIC PATIENT ON HCV THERAPY
Dr. David PearsonGastroenterology, Victoria
Disclosures
None relevant to this presentation
Why is Fibrosis/Cirrhosis Important?
Progressive fibrosis may lead to debility and death from liver failure or cancer
Advanced fibrosis (F3-4) means reduced response to Hepatitis C therapies
Successful treatment of Hepatitis C infection will halt the progression of liver disease in these patients at high risk of symptomatic decompensation
When to treat?
Before the onset of advanced fibrosis Better response in early disease: F0-2 Treatment better tolerated if patient is
healthier Fatigue and other symptoms Anemia No risk of decompensation from loss of
functioning liver mass Best response to therapy:
Younger age Less fibrosis Elevated ALT Female
What is cirrhosis?
What is cirrhosis?
Architectural description of the liver after long term injury and regeneration with replacement of functioning liver tissue by fibrosis.
Is partially reversible if the noxious agent is removed and the liver is able to regenerate.
Eventually leads to functional liver impairment.
How do we know the patient is cirrhotic?
History Alcohol excess Male sex Longer duration of infection (>20 years) Steatosis
Physical exam Liver contour (enlarged left lobe, rounded,
firm) Splenomegally, ascites, caput: portal HTN Spider angiomas, gynecomastia: estrogenic Jaundice Asterixis
How do we know the patient is cirrhotic?
Imaging Nodular contour, altered shape Enlarged spleen, abdominal varices Ascites
Lab Thrombocytopenia, anemia, leukopenia INR, albumin, bilirubin AST/ALT ratio (often normal ALT) Biopsy
Fibroscan: Transient elastography Fibrotest/FibroSure
Pretreatment evaluation of the cirrhotic patient
Education and preparation are important Vaccinations (CDC)
HBV, HAV, Strep pneumonia (Pneumovax) Influenza, varicella, MMR, tetanus, diptheria
Screening Gastroscopy Abdominal U/S
Portal Hypertension Portal vein thrombosis Hepatocellular carcinoma
Pretreatment evaluation of the cirrhotic patient
Contraindications to treatment Pregnancy/contraception advice Auto-immune hepatitis Renal insufficiency Severe cardiopulmonary disease Uncontrolled affective disorder/psychosis Hepatocellular carcinoma
Is there a history of liver decompensation?
Potential drug interactions
Pretreatment evaluation of the cirrhotic patient
Is there an opportunity for improvement? Alcohol/smoking cessation Other comorbidities to optimize?
Diabetes, cardiac, pulmonary Relative contraindications to treatment
Decompensated cirrhosis Ascites, encephalopathy, jaundice
Albumin <35 Bilirubin >25 Platelets <75, 000 Anemia: Hg <130 male; <120 female
Pretreatment evaluation of the cirrhotic patient
What about non medical factors? Housing Disability coverage/income replacement Drug coverage Preparing patient expectations for the
experience on therapy
Cirrhosis: Implications for treatment
48 wks therapy for G1; 24 wks for G2/3 More likely to need medications tapered,
more frequent measurement of hematology recommended.
Less able to tolerate therapy: need closer follow up and reassessment
Higher rate of drop out due to adverse effects, esp G1’s
Cirrhosis: Implications for treatment
Recent French report treating cirrhotics with triple therapy: 35-45%signficant adverse events (anemia, infection, renal failure, decompensation) 1% death from infection, bleeding 50% significant anemia and EPO use 5% significant neutropenia and
thrombocytopenia Esp age>65, female, low initial Hg
A practical approach
Anticipate trouble! Identify the fragile cirrhotic: Thorough work up
before treatment should identify those most at risk
4 week lead in may be illuminating…. How bad is a patient’s liver disease
Compensated Previously decompensated: “Recompensated” Currently decompensated Abnormal liver functions: bilirubin, albumin,
INR Abnormal hematology at baseline predicts
cytopenias on therapy
How do you know you’re in trouble?
Symptomatic decompensation Variceal bleeding, ascites, encephalopathy Treatment of symptoms Is there an identifiable precipitant?
Alcohol, new medication, infection Does therapy need to be stopped?
Infection Low threshold for antibiotic use with bacterial
infection; patient are immune compromised Respiratory, urinary, skin
How do you know you’re in trouble?
Treatment related issues Cytopenias: dose reductions; growth factors Symptoms: Fatigue, mucositis Other organ systems: cardiac, skin rash,
diarrhea
What to do when you’re in trouble
Limited options Anemia: taper Riba/IFN; NOT DAA’s
?role of EPO Platelets/WBC: taper IFN Diarrhea Rash
When to stop
Futility rules Decompensation Medication intolerance
Fatigue, Rash, Diarrhea Low doses, regression to single agent IFN
The case
54 yr old man; G1a, start Pegasys Sept 2010
Cirrhosis: ex-IVDU/Alcohol; compensated 2007 Thoracic aortic aneurysm repair 2009 Aortic valve endocarditis Baseline: WBC 3.8/Hg121/plt 68
INR 1.1, ALT 94, alb 40, bili 25 IFN 1000 mg/ IFN 180 mcg
Week 5 Hg 95, plt 30 Hold riba a week, restart at 600
The case
Week 12 Hg 80-95, plt 30-40; fatigue – off work Riba 400-600, IFN 2/3 – PCR 2 log drop
Week 26 Riba stopped, had been interrupted and dose
reduced IFN 2/3 dose Week 24 PCR negative
Week 30 ascites, increased fatigue, 25 lb wt loss then 12 lb gain Stop all Rx
The case
PCR negative at wk 30 = end treatment PCR relapsed 12 weeks later Ascites slow to resolve; issues with
congestive failure and required urgent aortic valve replacement May 2011
Now wants to be retreated!
Role of the Hepatitis Nurse
Educator Advisor Coach Confidant
ThePlan
An Individual Effort
Inspiration
Encouragement
Motivation
Thank you for your attention
Questions?