A CLINICAL STUDY ON THERAPEUTIC MANAGEMENT OF VIRAL HEPATITIS-A IN PAEDITRICS
II.WHAT CAUSES THE DISEASES?
Hepatitis A is caused by infection with the hepatitis A virus (HAV) , a non-enveloped, positive stranded RNA virus, first identified by electron microscopy in 1973, classified within the genus hepatovirus of the picornavirus family.
The virus interferes with the liver’s functions while replicating in hepatocytes.
III.HOW IS HAV SPREAD?
* Transmission of HAV is typically by the faecal- oral route.
* Occasionally, HAV is also acquired through sexual contact (anal-oral) and blood transfusions.
IV.WHO IS SUSCEPTIBLE TO INFECTION?
People who have never contracted HAV and who are not vaccinated against hepatitis A are at risk of infection.
In areas where HAV is highly endemic, most HAV infections occur during early childhood.
V.WHERE IS HAV A PROBLEM?
The virus is present worldwide and the risk of infection is proportional to levels of sanitation and personal hygiene. Nearly all the children are infected with HAV before the age of 9.
Patient with unapparent or subclinical hepatitis have neither symptoms nor jaundice. Children generally belong to this group. These asymptomatic cases can only be recognised by detecting biochemical or serologic alternations in the blood.
Since both clinically and biochemically, acute hepatitis due to HAV cannot be distinguished from that due to the other hepatitis virus, serologic tests are necessary for a virus specific diagnosis.
Diagnosis of hepatitis is made by biochemical assessment of liver function. The specific routine diagnosis of acute hepatitis A is made by finding anti-HAV IgM in the serum of patients. A second option is the detection of virus and/or antigen in the faeces.
Virus and antibody can be detected by commercially available RIA, EIA or ELISA kits. These commercially available assays for anti-HAV IgM and total anti-HAV (IgG) for assessment of immunity are below detection level. At the onset of disease, the presence of IgG anti HAV persists lifelong after acute infection, detection of IgG anti-HAV alone indicates past infection.
The highest prevalence of faecal-oral infection occurs is regions where low standards of sanitation promote the transmission of the virus.
Virus-induced cytopathology may not be responsible for the pathologic changes seen in HAV infection as liver disease may result primarily from immune mechanisms. Antigen-specific Lymphocytes are responsible for the destruction of infected hepatocytes.
HAV is generally acquired by the faecal-oral route by either person-to-person contact or ingestion of contaminated food or water. Hepatitis A is an enteric infection spread by contaminated excreta.
Hepatitis A may be acquired from faecally contaminated food or water.
XI.SURVEILLANCE AND CONTROL:
* Providing safe drinking watervand proper disposal of sanitary waste.
* Monitoring water beds where shellfish are harvested.
* Monitoring disease incidence
* Determining sources of infection.
* Detecting outbreaks
* Containing spread
Hepatitis A occurs sporadically and epidemically worldwide, with a tendency to cyclic recurrences.
Worldwide, HAV infections account for 1.4 million cases annually.
* Almost all infections are spread by the faecal-oral route, good personal hygiene, high quality standards for public water supplies and proper disposal of sanitary waste have resulted in a low prevalence of HAV infections in many well developed societies.
* Proper hand washing after bowel movement and before food preparation are important measures to reduce the risk of transmission from infected individuals.
* For pre exposure protection, the use of hepatitis A vaccine instead of IG is now highly recommended. Immunization should be a priority for persons at increased risk of acquiring hepatitis A.
* Post exposure prophylaxis of non-vaccinated people, the passive administration of IG can modify the symptoms of infection, provided it is given within 2 weeks of exposure.
* No special precautions are demanded for vaccinated persons.
* Universal immunisation would successfully control hepatitis A although at present, high costs and limited availability of vaccines preclude such a recommendation.
* Eradication can only be achieved through universal vaccination policies as long as HAV is not endemic in primates.
As no treatment exists for hepatitis A, prevention is the most effective approach against the disease.
Therapy should be supportive and aimed at maintaining adequate nutritional balance (1 g/kg protein, 30-35 cal/kg). There is no good evidence that restriction of fats has any beneficial effect on the course of the disease. Eggs, milk and butter may actually help provide a correct caloric intake. Alcoholic beverages should not be consumed during acute hepatitis because of the direct hepatotoxic effect of alcohol.
Adrenocortical steroids and IG are of no value in acute, uncomplicated hepatitis A, since they have no effect on the resolution of the underlying disease.
Patients who are taking oral contraceptives do not need to discontinue their use during the course of disease.
Referral to a liver transplant center is appropriate for patients with fulminate hepatitis A, although the identification of patients requiring liver transplantation is difficult. A good proportion of patient (60%) with grade 4 encephalopathy will still survive without transplantation. Temporary auxiliary liver transplantation for sub acute liver failure may be a way to promote native live regeneration.
This review contains detailed information regarding viral hepatitis A. This will act as tool to understand viral hepatitis and to create awareness among society.
This review is to be continued for coming days for further developments.
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