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

by Heba Soffar · Published July 4, 2023 · Updated May 9, 2024

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.

HDV

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.

HCV

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

Acute HCV

The classic diagnosis of acute HCV:

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

Hepatitis C

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

Drugs:

Interferon (regular, pegylated).
Ribavirin.
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.

Drugs

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.

Lab

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

Treatment:

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

HEV

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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