During the past few decades, particularly since World War II, viral hepatitis has become an increasingly important public health problem throughout the world. Viral hepatitis is one of the commonest causes of jaundice in children and is one of the diseases still unconquered even in the West. In recent years, there has been a better understanding of the epidemiology and clinical picture of the disease which has helped in the formulation of control measures. However, in the absence of isolation of the specific virus and specific serological diagnosis, many lacunae in our knowledge still persist. Infective hepatitis is endemic in most of the urban areas in India. Large number of epidemics have been investigated and reported in recent years. (Mehta and Acharya, 1973). Aurangabad is an area of endemic hepatitis. Dhamahere and Nadkarni (1962) reported water-borne epidemic of infective hepatitis in part of Aurangabad city. As a general rule, infective hepatitis is a mild disease with low mortality. However, the commonest cause of death in this disease is acute liver failure leading to coma and death. In children, its course is usually mild but can lead to post-hepatic cirrhosis, chronic cholestasis, subacute necrosis and hepatic failure. The chances of such complications are high, particularly in our country, where malnutrition is extremely rampant (Rao et al., 1975). Viral hepatitis in children has many interesting facets. Of particular interest is its possible relationship to Indian childhood cirrhosis (Madhavan et al., 1973); a theory of viral aetiology (Achar et al., 1960, Chandra, 1970) is based on a frequent occurrence of jaundice at the onset, history of jaundice and hepatitis - like illness in other family members and clinical resemblance of the acute fulminant variety to submassive necrosis of the liver seen in infective hepatitis.

There is no specific therapy for viral hepatitis and evaluation of any drug in the treatment of infective hepatitis is difficult as it is a variable disease. There are many clinical types having a variable course and prognosis. However, a drug which can restore liver function quickly without producing harmful effects and is reasonably inexpensive is most welcome. Various reports of corticoid therapy are available (Evans et al., 1953; Huber and Willey, 1956; Vakil et al., 1965; Vakil, 1973). However of late, there have been number of reports about the efficacy of Liv.52 in this disease (Arora, 1961. Ramalingam et al., 1971, Sule et al., 1961, Mitra et al., 1974, Rao et al., 1975).

We present a clinical profile of viral hepatitis in children from Aurangabad.

One hundred and thirty cases of viral hepatitis admitted to the Medical College Hospital, Aurangabad, during the period January 1972 to July 1975, were studied. The majority of cases were admitted in the summer months. A detailed clinical history was recorded, physical examination and routine laboratory investigations such as complete blood picture, urinalysis for bile salts, bile pigments, urobilinogen and liver function tests, which included serum bilirubin, serum transaminases etc. were done. Liver biopsy could be done only in 40% of cases on admission and it could not be repeated after treatment in any of the cases.

Infective hepatitis is a systemic viral disease with predominant involvement of the liver. It is a disease of varying severity ranging from mild anicteric hepatitis to acute fulminating hepatitis leading to precoma and coma. The disease is widely prevalent in India. In the Marathwada region it is endemic with periodic outbreaks of epidemics, especially in the summer and early rainy season.

Infective hepatitis is caused by hepatitis virus ‘A’. It occurs endemically and more characteristically in epidemics in institutions, schools and in military camps. The virus is excreted in the faeces and infection follows the ingestion of contaminated food; under conditions of community living, spread is facilitated and epidemics may occur. Viral hepatitis may be caused by hepatitis virus ‘B’ (serum hepatitis) in hospitals and clinics where syringes and needles are used without sterilisation before each inoculation. It has been well proved that serum hepatitis can also be transmitted by the orofaecal route and hepatitis ‘A’ infection by transfusion. Both the types of hepatitis have indistinguishable clinical manifestations which may vary from severe to mild and silent forms. In both, the virus has been shown to be present in the blood in the presymptomatic period. It is therefore apparent that blood from supposedly normal donors who have never had hepatitis may yet contain virus A or virus B or both.

There is strong circumstantial evidence that Australia (Au) antigen is a surface antigen of serum hepatitis (SH) virus which is mildly infectious and which can be transmitted by contagion (Krugman et al., 1967). At present detection of Au (Hepatitis-Associated) antigen is the only simple means available for detecting the SH virus. In the United States, urban endemic hepatitis, particularly in adults, is largely caused by the SH virus (Prince et al., 1970). Data are meagre (Hills et al., 1970); Sehgal and Aikat, 1970; Sama et al., 1971; Sundaravalli, et al., 1971; Kelkar et al., 1973, a, b).

Laboratory acquired infection (Epigastric hepatitis)—endemic hepatitis can occur in laboratory personnel working with materials containing the hepatitis B virus (Sutnick et al., 1971). In India, hepatitis B infection was noted by Baxi (1973) and Mahajan et al., (1974).

Viral hepatitis is often a self-limiting disease, but can have high mortality and morbidity during an epidemic (Melnick, 1957), particularly where malnutrition is endemic. Therapy with an inexpensive and efficient drug is, therefore, welcome. Peak incidence in the present study was in the pre-school age group, an observation made by other workers (Dave et al., 1972; Rao et al., 1975). The higher frequency noted in our study during the summer months also agrees with the observation of other workers (Viswanathan, 1957; Rao et al., 1975; Mitra et al., 1974). Lack of appetite with irritability and fever should alert the physician for the development of jaundice, in a few days and urine examination for bile salts, bile pigments and urobilinogen should be a routine in such cases. Early detection is of importance, to avoid administration of hepatotoxic drugs, such a chlorpromazine, etc. for vomiting, or drugs such as cyprohepatadine hydrochloride for appetite. Abdominal pain was noticed in 42.3 percent; this is in agreement with the observations of Sule et al., (1968). It is attributed to perihepatitis, distension of Glisson’s capsule, phlegmonous enteritis or sudden shrinkage of liver in acute hepatic necrosis (Litchman, 1953).

In the present study Liv.52 was given in the majority of cases in view of our previous experience (Mitra et al., 1974). However, corticosteroids were given a few cases including 5 cases of coma. No control trial of Liv.52 was done in the present study as we have recently reported our experiences from this institution. (Mitra et al., 1974). The efficacy of Liv.52 was observed by several other workers (Arora, 1961, Ramalingam et al., 1971, Dave et al, 1972, Deshpande and Sheth, 1972). We feel from our experiences that the absence of untoward side-effects with even prolonged administration makes this drug safe and effective in the management of viral hepatitis in children.

In the Marathwada region of Maharashtra viral hepatitis is endemic with periodic outbreaks of epidemics, especially in the summer and early rainy season.

One hundred and thirty cases of viral hepatitis in children admitted to Medical College Hospital, Aurangabad were studied. The ages of these children ranged from 5 months to 12 years the highest incidence was in the age group 4-7 years the majority of them (65%) belonged to the poor socio-economic group. Jaundice had lasted for less than 10 days prior to admission in 50% of cases. Mortality rate was 3.8%. Complete biochemical recovery took 8-10 weeks in the majority of the cases.