Hepatitis C is an infection caused by the hepatitis C virus (HCV), which attacks liver cells and causes liver inflammation.

1. HEPATITIS C
DR ASIF ALI KHAN

2. PATIENT DATA
 Age: 26
 Sex: Female
 Ethnicity: Asian
 Height: 5’8’’
 Weight: 125 lbs
 Diagnosed with Hepatitis C, 3 years ago
 Complaints: fatigue, anorexia, pale skin and weakness.

3. ASSESSMENT
 Had no appetite for the past few weeks
 Only juice, water, diet coke in the past 2 days
 About 1200 cal intake per day
 Lost 10# in 6 months
 Doesn’t like liver or lima beans
 200 mg of milk thistle twice daily
 3 grams chicory
 500 mg ginger at least twice daily
 Daily multivitamin/mineral supplements
 Treated with Alpha-interferon and ribavirin
Food and nutrition related history:

4. BIOCHEMICAL DATA

5. LAB DATA INTERPRETATION
 High BUN: indicates kidney disease or dehydration
 High Creatinine: indicates kidney disease or dehydration as well
 Slightly high glucose: pre-diabetes
 High Bilirubin: confirms that the liver is the cause of jaundice
 Low total protein: caused from the liver disease, malnutrition and
protein-loss enteropathy
 High Alkaline Phosphatase: suggests cholestasis
 High ALT and AST: increase with liver damage

6. LAB DATA INTERPRETATION
 High triglycerides: because of the decreased bile salts. And in Cirrhosis, the
body prefers lipids for energy in the fasting state
 High PT: indicates vitamin K deficiency and decreased synthesis of clotting
factors
 Low RBC, hemoglobin, and hematocrit: anemia
 Protein in urine: a sign of kidney disease
 Stool is light brown: Fat malabsorption

7. NUTRITION FOCUS PHYSICAL FINDINGS
 Dry skin and mucus because of the dehydration
 Bruises because of the liver disease and vitamin K deficiency
 Weight loss due to loss of appetite
 Enlarged esophageal veins; hypertension
 Pale skin is a sign of anemia

8. BRUISING RELATED TO VITAMIN K DEF.

9. CLIENT HISTORY
 The patient was in a good health until 3 years ago when she was diagnosed with Hepatitis
C.
 Mother(living) – HTN, diverticulitis, cholecystitis, carpal tunnel syndrome.
 Father(deceased) – diabetes mellitus, peptic ulcer disease.
 Maternal grandmother – cholecystitis, bilateral breast cancer.
 Maternal grandfather – leukemia
 Parental grandfather – cirrhosis
 Parental grandmother – amyotrophic lateral sclerosis
 The previous nutrition therapy was 3 years ago: small, frequent meals, plenty of liquids.
 Previously treated with alpha-interferon and ribavirin.
 Seasonal allergies treated with antihistamines.
 Live with a roommate who is a law student.

10. HEPATITIS C SUMMARY
 Hepatitis C is an infection caused by the hepatitis C virus (HCV), which attacks liver cells
and causes liver inflammation. The virus is mainly transmitted parenterally, especially
through IV drug use or needlestick injuries in healthcare settings.
 Most patients are asymptomatic in the acute phase, but may develop fever, malaise,
fatigue, or jaundice. Transition to chronic infections occurs in up to 85% of cases since
asymptomatic patients are rarely diagnosed and treated.
 Chronic infection is associated with increased mortality due to cirrhosis and hepatocellular
carcinoma. Suspicion of HCV infection due to exposure, clinical presentation, or elevated
aminotransferase levels should be followed up with HCV antibody and HCV RNA testing to
confirm the diagnosis.
 Acute HCV infection is treated with interferon-α, while a combination of two direct-acting
antivirals (e.g., Ledipasvir, Sofosbuvir ) is recommended in cases of chronic infection. More
than 90% of patients are cured with adequate treatment.
 Viral Hepatitis: Comparing Hepatitis A, B, C, D, and E

11. DEFINATIONS
Acute hepatitis C:
 HCV infection that develops during the first 6 months following the
exposure
Chronic hepatitis C:
 HCV infection that persists beyond 6 months following the exposure.

12. EPIDEMIOLOGY
 Prevalence: up to 2% of the US population has chronic HCV infection
 Incidence: 1 cases per 100,000 population, > 40,000 new infections per
year in the US
 Clinical progression: 75–85% of individuals with HCV infection go on to
develop chronic disease

13. PATHOGENSIS
 Hepacivirus C (Hepatitis C virus): RNA virus of the Hepacivirus genus and Flaviviridae
family
 The risk of chronic infection is multifactorial and depends on the host's ability to
clear the pathogen through activation of multiple innate immunity pathways against
the viral envelope.
 Flawed proofreading capability of RNA-dependent RNA polymerase (no 3'-5' exonuclease
activity) introduces mutations into genes encoding viral glycoprotein envelope and
enabling novel antigen production.
 Rapid replication rate produces many antigenically unique viral envelopes.
 Infection persists because the production rate of new mutant virions exceeds the
production rate of host antibodies.
 There are six genotypes: In the US, the main ones are genotype 1 (65–80%) and
genotype 2 (10–15%).
 Reinfection with another HCV genotype is possible.

14. TRANSMISSION
 Parenteral
1. Needle sharing among IV drug users
2. Needlestick injury (e.g., health care workers)
3. Blood transfusion
4. Dialysis
 Organ transplantation
 Sexual: rare (in contrast to HBV and HIV)
 Perinatal (vertical)

15. High-risk groups for HCV infection
 IV drug users (especially long-time users)
 Hepatitis B virus (HBV) or HIV-positive individuals
 Prison inmates
 Individuals born between 1945–1965
 Recipients of blood transfusions or organ transplants before 1992

16. CLINICAL FEATURES
Incubation period:
 2 weeks to 6 months
Acute course
 Asymptomatic in 80% of cases
 Symptomatic as features of Acute viral hepatitis
1. Malaise, fever, myalgias, arthralgias
2. RUQ pain, tender hepatomegaly
3. Nausea, vomiting, diarrhea
4. Jaundice, possibly pruritus

17. Chronic course
 Seen especially in asymptomatic individuals (up to 85%), as the
disease may go undiagnosed and treatment may be delayed or
never initiated (carrier state).
 Findings often mild, nonspecific (e.g., fatigue)
 Liver cirrhosis (up to 25% of cases) within 20 years of infection
 Extrahepatic features (common)
 Hematological
 Mixed cryoglobulinemia
 Lymphoma (especially B-cell non-Hodgkin lymphoma)
 ITP
 Autoimmune hemolytic anemia
 Monoclonal gammopathies

18.  Renal: Membranoproliferative glomerulonephritis (more common), Membranous
glomerulonephritis
 Rheumatological: Polyarteritis nodosa, Sjogren syndrome, Dermatological,
Porphyria cutanea tarda, Lichen planus
 Endocrine: Diabetes mellitus, Autoimmune thyroiditis (may lead to
hypothyroidism)
 Vascular: leukocytoclastic Vasculitis
 Others: sialadenitis

19. DIAGNOSTICS
 Detection of antibodies
 EIA/ELISA : standard immunoassay tests for anti-HCV antibodies; (positive in cases of acute, chronic, and
previous HCV infection)
 PCR for HCV RNA if antibodies are positive.
 If positive PCR: active HCV infection (may be acute or chronic)
 If negative PCR: no active infection, but prior infection
 Determines HCV genotype and virus titer assists in treatment planning and monitoring
 Liver function tests
 ↑ Transaminases with AST/ALT ratio (Ratio < 1: acute hepatitis , Ratio ≥ 1: chronic hepatitis)
 ↓ Total protein/albumin, coagulation (particularly ↑ prothrombin time), ↓ cholinesterase
 Cholestasis parameters: ↑ γ-GT, ↑ alkaline phosphatase, ↑ bilirubin
 Inflammation markers: leukocytosis, ↑ ferritin
 Liver biopsy indications: If diagnosis is inconclusive, For evaluating fibrosis in patients with chronic hepatitis
C, Evaluation of response to therapy
 Ultrasound: detection of cirrhosis and neoplasia, e.g., HCC
 Rule out coinfections: HIV, hepatitis A virus (HAV), hepatitis B virus (HBV) serology necessary

20. PATHOLOGY
Acute Phase
 Focal areas of macrovesicular steatosis
 Bile duct injury
 Sinusoidal inflammation of hepatic cells
 Lobular involvement in the form of eosinophilic single-cell necrosis
Chronic phase
 Lymphoid follicles in portal triad
 Necroinflammation of periportal liver cells
 Variable degree of fibrosis
 Severe hepatocyte injury
 Without treatment, the disease will ultimately progress to liver fibrosis, cirrhosis,
and hepatocellular carcinoma.

21. TREATMENT
General recommendations
 Avoid hepatotoxic drugs (e.g., acetaminophen) and alcohol use.
 Refer to an addiction specialist to treat substance use.
Acute hepatitis C
 Treatment goal: prevent transition to chronic infection
 Antiviral therapy
 The same regimens as for chronic HCV infection
 Monitoring for 12–16 weeks is recommended before initiation.
 Treatment should be started if HCV is not cleared.
 No treatment is necessary if HCV is cleared.
 Monitoring: regular monitoring of HCV RNA every 4–8 weeks for 6–12 months

22. Treatment Chronic hepatitis C
Treatment goals
 Complete cure
 Eradication of HCV RNA in serum as defined by SVR (sustained virologic response)
Treatment regimens
 Chosen based on viral genotype (the most important predictive factor for response to
therapy), viral load, history of antiviral treatment, and degree of liver fibrosis
 Chronic HCV infection is always treated with a multidrug approach (no antivirals are approved
as monotherapy).
 Combination of two direct-acting antivirals (DA): Antivirals target and inhibit HCV-encoded
proteins that are essential for the HCV replication cycle.

23. Combination of two direct-acting antivirals (DAAs)
 Ledipasvir PLUS Sofosbuvir for 8–12 weeks (genotypes 1, 4, 5, and 6)
 Sofosbuvir PLUS velpatasvir for 12 weeks (all 6 genotypes)
 Sofosbuvir PLUS daclatasvir
 Elbasvir PLUS grazoprevir
 Glecaprevir PLUS pibrentasvir (all genotypes)
 Sofosbuvir PLUS simeprevir
 Ombitasvir/ paritaprevir /ritonavir PLUS dasabuvir

24. Interferon PLUS ribavirin
 May be used to in the treatment of all genotypes
 Interferon -based treatment is still used as a last resort in cases of treatment failure.
 Ribavirin on its own may be combined with DAAs to increase antiviral activity.
In addition to any treatment regimen, vaccinations for hepatitis A and B
should be given.
Interferon and ribavirin are associated with severe side effects (e.g., arthralgias,
thrombocytopenia, leukopenia , depression, and anemia) and teratogenicity.

25. COMPLICATIONS
 Rarely fulminant hepatitis (liver failure)
 Liver cirrhosis
 Hepatocellular carcinoma
 Secondary hemochromatosis

26. PREVENTION
 Screening recommendations
 Universal hepatitis C screening
 All individuals aged 18–79 years should be screened at least once in their lifetimes.
 All women should be screened at each pregnancy.
 Periodic testing is indicated in individuals with ongoing high-risk of exposure
 IV drug users
 Long-term hemodialysis patients
 One-time testing is indicated in individuals exposed to (potentially) HCV-positive blood,
especially: [23]
 Infants born to HCV -positive mothers
 Healthcare personnel with percutaneous or parenteral exposure to blood with known HCV-positive or
unknown HCV status
 Screening protocol
 Anti-HCV antibody test
 Confirmatory PCR for HCV RNA

27. THANK YOU