Viral hepatitis


* Hepatitis fulminant: is defined by a prothrombin time (PT) <50% with clinical signs of hepatic encephalopathy.

If the time between jaundice and encephalopathy is> 2 weeks (<3 months) we speak of sub-fulminant hepatitis.

The principal offending virus are viruses A, B, D.

* Severe Hepatitis: n is defined as prothrombin time (PT) <50% without clinical signs of hepatic encephalopathy.

* Chronic viral hepatitis: is defined as a persistent elevation of transaminases more than 6 months after acute viral hepatitis.

* Hepatitis B HBV is a DNA virus (family: hepadnavirus) formed of a capsid (HBcAg) and a casing (HBsAg); HBeAg is a soluble form of the HBcAg and reflects a viral multiplication.

It has no direct CPE.

Lysis of hepatocytes is caused by the immunogenic reaction of the virus.

* Hepatitis C: HCV is an RNA virus (family: flavivirus).

It is cytopathic and the immune response directed against the VDC seems low.

Hepatitis A, B and C
Hepatitis A, B and C


– The forms jaundiced represent 10% of cases.

– Elevation frank transaminases; between 10 times and 100 times normal

– Acute hepatitis B: Incubation long (6 weeks to 4 months); asymptomatic in 90% of cases; severe forms represents a case in 1000. acute infection becomes chronic 1 out of 10 times the diagnosis relies on the presence of HBsAg and / or anti-HBc IgM.

– Acute hepatitis C: incubation (4 to 6 weeks);transaminase elevation is usually moderate (<10N).

The appearance of anti-HCV is often late (serology is positive in 50% of cases) => PCR.

Never severe form; chronicity in 50% of cases.

– Prognostic factors: TP (<50%); Hepatic encephalopathy (asterixis, confusion …)

– We do not treat acute hepatitis B

– In case of acute hepatitis C jaundiced: no immediate treatment; realization of a PCR at 12 weeks and treatment with INFpeg + ribavirin 24 weeks if positive.

If hepatitis C non jaundiced, performing PCR rapidly and treating the same pattern if positive.

– Histology: ballooning, acidophilic degeneration, maximum body Councilmann


– There is an elevation of aminotransferases for more than 6 months; usually moderate (between 1-5 xN); ALT> AST (a report AST> ALT evokes cirrhosis).

PAL are usually normal.

– An elevated bilirubin and decreased TP reflect liver failure (cirrhosis)

– Serology Hepatitis B: HBsAg +; HBcAg +; Ac anti-HBs –

– The diagnosis of chronic viral hepatitis can not be said by liver biopsy

– Piecemeal necrosis lesions interesting hepatocytes bordante periportal blade (piece-meal necrosis) are an essential histological evidence.

– The Knodell appreciate the 4 elements (periportal necrosis, intralobular necrosis, portal inflammation fibrosis).

The score of Metavir appreciate two things: the activity and fibrosis.


– Infection with HBV becomes chronic in 10% of cases.

– The chronic carrier of the virus B is defined by the presence of HBsAg for more than 6 months.

The Ac IgM anti-HBc is generally absent.

– There are 3 types of chronic carrier B virus:

* Portage healthy HBsAg

* Chronic hepatitis is active

* Chronic active hepatitis

– The viral replication results in the presence of replication markers: HBeAg and HBV DNA in the absence of Ac anti-HBe.

In some cases there is a chronic active hepatitis B mutagenic with negative HBeAg.

It is infection by a mutant B virus which is unable to synthesize HBeAg.

– Chronic infection with B virus evolves in 3 phases:

* Replicative phase: strong viral replication with insufficient immune response (HBeAg +, Ac anti-HBe -; low transaminases)

* Seroconversion phase: strong increase in transaminases and decreased viral DNA; biopsy showed chronic active hepatitis; negativity of HBeAg and appearance of HBeAb.

* Non-replicative phase: HBeAg -; Anti-HBe + Ac; Viral DNA -; two events can occur to stage (HBs seroconversion: healing; reactivation of the virus B).

– The treatment is indicated in cases of active viral replication; it is based on interferon, lamivudine and adefovir.


– Around 60-90% of subjects infected with the virus C become chronic carriers

– Chronic hepatitis C is often asymptomatic

– The evolution of transaminases is very capricious with significant fluctuations

– Played in 20 to 30% of cases of cirrhosis (10 to 20 years) (mainly concern the active forms = 40%).

– The risk of hepatocellular carcinoma is important to cirrhosis

– A liver biopsy is essential (activity of hepatitis and therapeutic indication)

– You have to treat subjects with chronic hepatitis: with Metavir score of ≥ F2 whatever the activity; without decompensated cirrhosis; with an increase in transaminases.

– Treatment is indicated in patients with cirrhosis (unlike hepatitis B): F4. objective: reduction of HCC risk and regression of fibrosis.