Viral hepatitis, HDV symptoms, Treatment of acute HCV, Occult hepatitis C and HEV

Hepatitis D is a kind of viral hepatitis caused by the hepatitis delta virus (HDV), HDV is one of five known hepatitis viruses: A, B, C, D, and E, HDV complications such as liver failure in acute infections and a rapid progression to liver cirrhosis, with an increased risk of developing liver cancer in chronic infections, In combination with the hepatitis B virus, hepatitis D has the highest fatality rate of all the hepatitis infections.


Hepatitis D is also known as “delta hepatitis,” It is a liver infection caused by the hepatitis D virus (HDV), Hepatitis D only takes place in people who are infected with the hepatitis B virus.

  • RNA virus.
  • Blood borne infection.
  • Coinfection with acute HBV infection or as a superinfection in patients with Pre-existing chronic HBV infection.
  • Incubation period: 1 to 4 months.
  • Diagnosis: anti-HDV Abs (IgM, IgG) & HDV RNA.
  • Treatment: Pegylated interferon 48 weeks.


  • RNA virus.
  • Blood borne.
  • 7 genotypes.
  • Incubation period: 15 to 150 days.
  • Acute cases are usually asymptomatic.
Viral hepatitis

Hepatitis C

Acute HCV

The classic diagnosis of acute HCV:

  1. The patient comes with acute hepatitis.
  2. HCV-RNA is positive.
  3. Anti-HCV is negative.

Spontaneous clearance

  • Of persons recently infected with HCV, approximately 27% clear infection spontaneously.
  • Predictors of spontaneous clearance: Symptomatic patients (jaundice), IL28B CC genotype.

Treatment of acute HCV

  • Monitoring for Spontaneous Clearance: All patients with acute HCV should have.
  • HCV RNA monitoring every 4 to 8 weeks for a minimum of 16 weeks. (6 months).
  • If the decision is made to treat a patient with acute HCV infection, the same regimens should be used as recommended for the initial treatment of patients with chronic hepatitis C.

Factors that accelerate the progression

  • Male gender.
  • Older age at infection.
  • Duration of infection.
  • Alcohol use.
  • Insulin-resistant diabetes mellitus.
  • Steatosis.
  • HIV infection and other immunosuppressive states.

Treatment of chronic HCV


  1. Interferon (regular, pegylated).
  2. Ribavirin.
  3. DAAs (protease inhibitors, polymerase inhibitors, NS5A inhibitors).

Key Data for HCV treatment decisions:

HCV treatment history:

  • Interferon and ribavirin regimen?
  • Protease inhibitor? Sofosbuvir?

Fibrosis stage? Options for fibrosis assessment.


  • Sofosbuvir (Sovaldi).
  • Simeprevir (Olysio).
  • Daclatasvir (daklinza).
  • Paritaprevir/ritonavir Ombitasvir (Qurevo).
  • Sofosbuvir + Ledipasvir (Harvoni).
  • Sofosbuvir + velpatasvir (epclusa).

General rules

  • The treatment duration is 3 to 6 months.
  • Drug combinations using different groups are given, and monotherapy is contraindicated.
  • The response rate is generally > 90%.
  • Sofosbuvir cannot be used in severe renal impairment.
  • Protease inhibitors cannot be used in decompensated cirrhosis.

Extra-Hepatic Manifestation

  • Mixed cryoglobulinemia.
  • Non-Hodgkin lymphoma.
  • DM, type II, and insulin resistance.
  • Cardiovascular disease.
  • Fatigue.
  • Cognitive impairment.
  • Reduced health-related quality of life.
  • Renal disease.

Mixed cryoglobulinemia

  • Is a systemic vasculitis caused by the deposition of circulating immune complexes in the small vessels.
  • Characterized by the presence of circulating Igs that precipitate at low temperatures.
  • (under 37 °C) and can solve by serum re- warming.
  • Type II (MC-II):(Polyclonal IgG and monoclonal IgM with rheumatoid factor (RF) activity.
  • Patients with joint pain and positive rheumatoid factor may be true rheumatoid arthritis or chronic HCV with mixed cryoglobulinemia.
  • We differentiate between them by Anti-CCP which is positive in rheumatoid arthritis and negative in chronic HCV with mixed cryoglobulinemia.

Clinical picture

  • The most common symptoms are weakness, arthralgias, and orthostatic palpable purpura (Meltzer and Franklin triad).
  • Peripheral neuropathy represents the most frequent clinical feature after the triad, followed by sicca syndrome & renal involvement.


Serum-mixed CGs, high RF values, and reduced C4 values are the most frequent laboratory data.


Antiviral therapy is considered, when feasible, the mainstay of treatment for most HCV-linked extrahepatic diseases.

Occult hepatitis C (OCI):

  • Elevated transaminases.
  • – ve HCV antibodies.
  • +ve HCV RNA in low levels detected by Amplification techniques in: Serum, PBMCs (Peripheral Blood Mononuclear Cells), and liver biopsy.

A patient with HCV

HCV-RNA is positive and Anti-HCV is negative and the patient is known to have hepatitis C, in this case, we have different possibilities:

  1. 1. The patient is in the acute stage (high transaminase more than 10 times upper normal).
  2. 2. The patient is in occult hepatitis C (the enzymes will be much less as it is a form of chronic hepatitis C).


  • RNA virus, 8 genotypes.
  • Only G 1-4 infect humans. IP 15-60 days.
  • Acute infection is usually silent & self-limited.
  • <5% may develop symptoms of acute hepatitis, Jaundice mainly cholestatic (in 90% to 100% ).
  • Progression to ALF is rare, particularly with pregnant women.
  • Diagnosis by HEV Abs IgM & HEV RNA.
  • In immunocompromised patients, PCR is the most reliable test for diagnosis because serologic testing may be negative.
  • Acute HEV infection does not usually require antiviral therapy. Most infections are spontaneously cleared.
  • Ribavirin ( 600 mg/day) for 3-6 months in acute severe & chronic cases.

Extrahepatic manifestations

  • Meningitis.
  • Neuralgic amyotrophy.
  • Guillain-Barre syndrome.
  • Cryoglobulinemia.
  • Glomerulonephritis.
  • Myocarditis.
  • Pancreatitis.

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