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A CLINICAL STUDY ON THERAPEUTIC MANAGEMENT OF VIRAL HEPATITIS-A IN PAEDITRICS

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About Author:
Kambham Venkateswarlu
1-Final Year Graduate Student
Sri Lakshmi Narasimha College of Pharmacy,
Palluru, Chottoor-517132, Andhra Pradesh, India.
k.v.reddy9441701016@gmail.com

ABSTRACT:
Hepatitis is a general term meaning inflammation of the liver and can be caused by a variety of different viruses such as hepatitis-A, B, C, D, and E. Since the development of jaundice is a characteristic of liver disease, a correct diagnosis can only be made by testing patient’s sera for the presence of specific anti-viral antibiotics. Transmission of HAV is typically by the faecal, oral route. Hepatitis A was formerly called infectious hepatitis, Epidemic hepatitis, Epidemic jaundice, Catarrhal jaundice, type A hepatitis, HA.

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Reference Id: PHARMATUTOR-ART-1616

I.HEPATITIS PRIMARY STUDIES:
Many viruses affect the liver function. But only a few are truly infectious to liver itself leading to clinically significant hepatitis. The term viral hepatitis refers to the diseases caused by this subgroup.

Five human viruses have been identified, including hepatitis A (HAV), B (HBV), C (HCV), D (HDV), E (HEV). All forms of viral hepatitis have a similar pathology, causing an acute inflammation of the entire liver.

1. Hepatitis A:
It is the major cause of acute hepatitis worldwide, accounting for 20-25% of clinical hepatitis in the developed world. Most attacks are mild and often pass unnoticed by the patient. HAV is spread via the fecal-oral route. It has incubation period of 2-7 weeks.

2. Hepatitis B:
The prevalence of hepatitis B (HBV) is low in the USA and Britain, with approximately 0.1-0.2% of the population having markers that indicate that they are chronic carrier. HBV is parentrally transmitted. Acute HBV infection has an incubation period of 3-6 months.

3. Hepatitis C:
It is a blood borne virus with greater infectivity than the human immunodeficiency virus (HIV). The global prevalence of HCV infection is estimated at around 3% in the general population with more than 150 million carriers worldwide. HCV is transmitted parenterally.

4. Hepatitis D:
It can establish infection only in patients simultaneously infected by HBV. It is acquired in the same way as HBV infection, can cause both acute and chronic hepatitis.

5. Hepatitis E:
It is endemic in areas of poor sanitation, where it is transmitted enterically and leads to acute hepatitis. It has an incubation period of 40 days.

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6. Hepatitis F:
Hepatitis F, another distinct non-A, non-B hepatitis virus, is likely to exist. A virus designated as hepatitis F virus was isolated from the stool of a patient with hepatitis. The hepatitis F was develops in persons receiving coagulation factor from pooled blood of the patients who have already recovered from HCV infection.

7. Hepatitis G:
Recently, new blood borne viruses were discovered simultaneously by two investigators and named hepatitis G virus (HGV). These viruses were later determined into the isolates of the same single stranded RNA virus, identified as a members of the flaviviridae family and are now referred to as HGV.

The primary rate of transmission is parental. The virus is often present in 50% of injection drug users, 30% of hemophiliacs and 20% of haemodialysis patients. There is also evidence of a sexual transmission. The site of viral replication has not been identified.

8. Non-A, Non-B, Non-C Hepatitis viruses:
Non-A, Non-C Hepatitis was the term used previously to describe Hepatitis thought to be due to a virus but not HAV or HBV. HCV and HEV are the main hepatitis viruses to emerge from this group. Further such viruses do exists, but the hepatitis viruses described above now accoynt for the majority of Hepatitis virus infections Hepatitis-B virus.

9. JAUNDICE:

Definition:
It is defined as yellowish discoloration of the skin and mucous membrane due to excess amount of bilirubin present in blood.

TYPES:
9.1. Hemolytic jaundice:

If the concentration of bilirubin in the serum rises above normal due to more formation as a result of increased erythrocyte destruction, hemolytic jaundice results. There is lemon-yellow tinge of bulbar conjunctiva.

9.2. Obstructive (Regurgitation) jaundice:
This condition occurs from blockage of the hepatic or common bile ducts. The bile pigment passes from blood to the liver cells as usual. However, failing to be excreted by the bile capillaries, it is absorbed into the hepatic veins and lymphatic.

9.3. Hepatocellular jaundice:
This type of jaundice is caused by liver dysfunction s a result of the damage tom the parenchyma cells by infection, toxins and liver poisons. At a certain stage, the inflammation and damage to liver cells become severe leading to part obstruction to the flow bile. This results in the absorption of conjugated bilirubin and bile into the general circulation cause Orange-Yellow tinge of bulbar conjunctiva

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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.

VI.THE DISEASE:
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.

VII.DIAGNOSIS:
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.

VIII.PREVALENCE:
The highest prevalence of faecal-oral infection occurs is regions where low standards of sanitation promote the transmission of the virus.

IX.PATHOGENESIS:
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.

X.TRANSMISSION:
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

XII.INCIDENCE:
Hepatitis A occurs sporadically and epidemically worldwide, with a tendency to cyclic recurrences.

Worldwide, HAV infections account for 1.4 million cases annually.

XIII.PREVENTION:
*    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.

XIV.TREATMENT:
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.

XV.CONCLUSION:
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.

XVI.REFERENCES:
1.    Eric, T.Herfindal. Dick R. Gourley, Clinical Pharmacy and Therapeutics, 4th edition, P.270-279.
2.    Dipiro, T.Pharmacotherapy, A Pathophysiologic approach, P.622-638.
3.    Speight, M.Avery’s drug treatment, 3rd edition, P.774-776.
4.    Standard Treatment Guidelines, Society of Delhi, P.452-453.
5.    Ghai, O.P.Essential Paediatrics, 4th Edtion, P.153-155.
6.    Saulkrugman et al. Infections disease of children, 8th Edition, P.103-133.
7.    Roger Walker, Clive Edwrds, Clinical Pharmacy and Therapeutics, 3rd Edition, P.209-225
8.    Behrman, Leigman et al. Nelson’s textbook of paediatrics, 16th Edition,1999, P.768-776.
9.    Braunwald, E.Faucias et al, Harrison’s principle of Internal Medicine, 15th Edition, P.1721-1737.
10.    Fiore AE,Hepatitis A transmitted by food. Clin.Infct Dis204; 38(5): 705-715.
11.    Viral hepatitis, pubmed.com
12.    Viral hepatitis who.int
13.    The history of the hepatitis A, globalserve.net
14.    Hepatitis hepnet.com
15.    Hepatology ahealthyme.com
16.    Liver information liverfoundation.org
17.    John T.J. et al. What priority for prevention of hepatitis A in India. Indian Journal of Gastroenterology, 1997, volume 16, Issue 3, Page 109.

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