Complications in viral hepatatis

Complications of interferon therapy include systemic flu like symptoms, marrow suppression, emotional liability (irritability commonly, depression rarely), autoimmune reactions (especially autoimmune thyroiditis), and miscellaneous side effects such as alopecia, rashes, diarrhea and numbness and tingling of the extremities.

With the possible exception of autoimmune thyroiditis, all these side effects are reversible upon dose lowering or cessation of therapy.

No treatment is indicated or available for asymptomatic, nonreplicative hepatitis B carriers, and antiviral therapy should be withheld from patients with decompensated hepatitis B, in whom treatment may be associated with hepatic decompensation.

Such patients should be referred to research centers involved in clinical trials. Other interferons and several nucleoside analogues active against HBV are being evaluated in experimental trials.

For patients with end stage chronic hepatitis B, liver transplantation is the only potential lifesaving intervention. Reinfection of the new liver is almost universal; however, the likelihood of the liver injury associated with hepatitis B in the new liver is variable.

The majority of patients become high-level viremic carriers with minimal liver injury. Unfortunately, an u predictable proportion experience severe hepatitis B – related liver injury, sometimes a fulminant like hepatitis, sometimes a rapid recapitulation of the original severe chronic hepatitis B.

Chronic hepatitis D may follow acute co infection with HBV but at a rate no higher than the rate of chronicity of hepatitis B. That is, although HDV co infection can increase the severity of acute hepatitis B, HDV does not increase the likelihood of progression to chronic hepatitis B.

When, however, HDV super infection occurs in a person who is already chronically infected with HBV, long term HDV infection is the rule and a worsening of the liver disease the expected consequence.

Except for severity, chronic hepatitis B plus D has similar clinical and laboratory features to those seen in chronic hepatitis B alone. Chronic active hepatitis, with or without cirrhosis, is the rule and chronic persistent hepatitis the exception.

A distinguishing serologic feature of chronic hepatitis D is the presence in the circulation of antibodies to liver kidney microsomes (anti- LKM); however, the anti-LKM seen in hepatitis D are designated anti-LKM3 and are distinct from anti-LKM1 seen inpatients with autoimmune chronic active hepatitis and in a subset of patients with chronic hepatitis C.

Management of chronic hepatitis B depends on the level of virus replication. Although progression to cirrhosis is more likely in chronic active than in chronic persistent or lobular hepatitis B, all three forms of chronic viral hepatitis can be progressive.

Randomized, prospective, controlled trials have been established that patients with well compensated chronic replicative hepatitis B, selected to have chronic hepatitis on liver biopsy and aminotransferase elevations, regardless of histologic features, respond to antiviral therapy with interferon-a(alpha).

A four month course of subcutaneous injections, daily at a dose of 5 million units or three times a week at a dose of ten million units, is associated with an approximately 40 percent of seroconversion from replicative (HBeAg and HBV DBA detectable in serum) to non replicative (anti HBe detectable).

HBV infection, with a concomitant improvement in liver histologic features and an approximately ten percent chance of losing detectable HBsAg.

The likelihood of losing HBsAg during therapy is increased in patients with a brief duration disease, followed sufficiently long after successful interferon induced loss of replicative markers, approximately 70 percent of such patients have bee observed to lose HBsAg., i.e, all serologic markers of infection, over a 5 year period.

Immunosuppressed patients with chronic hepatitis B do not appear to be responsive to interferon therapy . Regardless of the epidemiologic mode of acquisition of HCV infection, chronicity follows acute hepatitis C in approximately 50 percent of cases.

What is more, in patients with chronic transfusion associated hepatitis followed for ten years, progression to cirrhosis has been recorded in 20 percent.

Such is the case even for patients with relatively clinically mild chronic hepatitis, including those without symptoms, with only modest elevations of aminotransferase activity, and with chronic persistent hepatitis on liver biopsy.

Even in cohorts of well compensated patients with chronic hepatitis C (no complications of chronic liver disease and with normal hepatic synthetic function), the prevalence of cirrhosis may be as high as 50 percent.

Many cases of hepatitis C are identified in asymptomatic patients who have no history of acute hepatitis C. The source of HCV infection in most of these cases remains a mystery and the natural history of chronic hepatitis C identified under these circumstances in unknown.

| Various complications in viral hepatatis | Different types of viral hepatitis | Treatment process of viral hepatitis | What are the various Causative organisms in viral hepatitis | How to treat & prevent viral hepatitis | What is Prognosis in viral hepatitis | Conceived your First Baby with Hepatitis C in your Blood? | Got Diagnosed for Hepatitis C Infection? | The Difficult Task of Diagnosing Hepatitis C in Aged People | How to deal with Emotionally Disturbed Hepatitis C Infected Persons | How to Handle the Undeterred Hepatitis C Infection Spread | Know the Multiple Entry Routes of Hepatitis C Infection | How to Trap and Fix Eluding Hepatitis C Symptoms in a Person | Correlativity between Hepatitis C and HIV Infection | Varied Treatment Options for Your Hepatitis C Infection | How Young Children Play Safe with Hepatitis C Viral Infection |

What are the various complications in viral hepatatis