Hepatitis C Virus Infection
A curable viral liver disease transmitted via blood that causes silent liver damage, cirrhosis, and cancer over decades.
- Hematemesis indicating variceal hemorrhage in undiagnosed cirrhosis.
Emergency Management: Hepatic encephalopathy. Treat with Lactulose 30 mL PO q1-2h until bowel movement.
Hepatitis C is a blood-borne viral infection caused by the Hepatitis C virus (HCV), a positive-sense single-stranded RNA virus. It causes chronic liver inflammation in 75-85% of acutely infected patients, leading to progressive fibrosis and cirrhosis.
Detailed Overview
HCV is highly insidious, often remaining asymptomatic for decades. Unlike HBV, it is highly curable with short courses of direct-acting antivirals (DAAs) that target viral proteins (NS3/4A, NS5A, NS5B). Widespread screening is essential to identify infected individuals before irreversible liver damage or hepatocellular carcinoma (HCC) occurs.
Epidemiology & Demographics
About 58 million people globally have chronic HCV. Incidence in the US is highest among baby boomers (1945-1965) and younger adults via injection drug use.
Etiological Mechanism
Hepatitis C virus (Genotypes 1-6).
Primary Causes
Hepatitis C virus (HCV)
- Intravenous drug use: Sharing needles/syringes is the most common current transmission route.
- Blood transfusion before 1992: Prior to widespread HCV blood screening.
HCV enters hepatocytes and translates its RNA into a polyprotein, cleaved by viral proteases into structural and non-structural proteins (e.g., NS5A). The virus replicates in the cytoplasm. The host immune system attempts to clear infected cells via CD8+ T-cells, but HCV's high mutation rate leads to immune evasion. Chronic inflammation drives hepatic stellate cell activation and collagen deposition.
Characteristic Clinical Presentation
- Fatigue: Common and often debilitating.
- Arthralgia: Joint pain associated with immune complex deposition.
- Brain fog: Mild cognitive impairment.
Physical Examination Signs
- Often normal until advanced cirrhosis.
- Palpable purpura in patients with secondary cryoglobulinemia.
- Splenomegaly in portal hypertension.
- Hepatocellular Carcinoma: 1-4% annual risk in patients with HCV cirrhosis.
- Mixed Cryoglobulinemia: Systemic vasculitis affecting kidneys and skin.
Diagnostic Criteria & Guidelines
Positive HCV antibody followed by detectable quantitative HCV RNA PCR.
Differential Diagnosis
- Hepatitis B
- Alcoholic liver disease
- Hemochromatosis
Laboratory Tests & Biomarkers
- Anti-HCV Antibody: Positive.
- HCV RNA PCR: Detectable (confirms active infection).
- Platelets: < 150,000/mcL suggests advanced fibrosis/cirrhosis.
Imaging Modalities & Findings
- Transient Elastography:
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Chronic Hepatitis C
Persistent viremia > 6 months, F1-F3 fibrosis.
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Compensated Cirrhosis
F4 fibrosis, no clinical signs of liver failure.
Glecaprevir/Pibrentasvir 300/120 mg PO daily for 8 weeks OR Sofosbuvir/Velpatasvir 400/100 mg PO daily for 12 weeks.
Second-Line & Adjunctive Therapy
Sofosbuvir/Velpatasvir/Voxilaprevir 400/100/100 mg PO daily for 12 weeks (for DAA failures).
Surgical & Procedural Management
Liver transplantation for end-stage liver disease (MELD > 15).
Recommended Lifestyle Changes
- Strict alcohol avoidance.
Patient Counseling & Advice
DAAs have >95% cure rates but do not grant immunity; reinfection is possible. Assess for drug interactions (e.g., PPIs, statins).
Follow-Up & Monitoring Schedule
Check HCV RNA 12 weeks post-treatment to confirm Sustained Virologic Response (SVR12). If cirrhosis present, life-long ultrasound every 6 months for HCC.
Preventive Strategies
Harm reduction programs (needle exchange). No vaccine available.
>95% cure rate with DAAs, drastically reducing mortality.
Frequently Asked Questions
View Official Guideline