INTRODUCTION
Viral 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 of Maharashtra it is endemic with periodic outbreaks of epidemics, especially in the summer and early rainy season.
The mortality rate of hepatic coma (deep) due to viral hepatitis is as high as 90 percent (Sherlock, 1978). Even today there is no specific treatment of viral hepatitis and its complications. The role of steroids is questionable. Corticosteroids have been advocated in acute fulminating hepatitis by many authors (Ducci and Katz, 1951; 1955; Katz and Evans, 1953; and Evans et al, 1953). But the mortality rate in cases of hepatic coma due to viral hepatitis remains high. In quest of a drug to treat these cases we were prompted to undertake a controlled clinical trial of Liv.52, an indigenous herbal preparation (The Himalaya Drug Co.).
Liv.52 has been used in various hepatic disorders with encouraging results. (Sule et al, 1968; Mukerjee and Dasgupta, 1971; Arora, 1969; Jaffari and Shyam Raj, 1969; Dayal et al, 1970; Patel et al, 1972).
The exact mode of action of this drug is not very clear. It has been shown to stimulate hepatic functions possibly by reducing intra-hepatic congestion and relieving cholestasis. The drug has diuretic, anabolic, choleretic, stomachic and regenerative properties (Damle and Deshpande, 1966; Kale et al, 1966 and Patel et al, 1972). It contains extracts of various plants.
Capparis spinosa 23%
Cichorium intybus 23%
Solanum nigrum 12%
Cassia occidentalis 6%
Terminalia arjuna 12%
Achillea millefolium 6%
Tamarix gallica 6%
Mandur bhasma 12%
MATERIAL AND METHODS
A study of 100 cases of viral hepatitis was instituted between the period February 1973 to September 1973. The results obtained were compared with an earlier series of 50 cases treated with corticosteroids. The cases were randomised into two groups: control, on standard supportive therapy without Liv.52; and trial, on standard supportive therapy plus Liv.52. Cases selected for the study were:
1. Cases with serum bilirubin of more than 10 mg/100 ml.
2. Cases with pregnancy having elevated serum bilirubin level (antenatal).
3. Cases of viral hepatitis falling in the immediate post-natal period.
4. Cases of viral hepatitis with precoma and coma.
The patients were classified as:
1. Uncomplicated cases.
2. Cases complicated by precoma and coma.
In both the groups treatment was identical and symptomatic except that cases in the trial group were given Liv.52 in doses of 3 tablets three times a day, crushed and fed through a nasal tube in comatose patients. Paediatric age group patients received Syrup Liv.52 four teaspoonful three times a day. None of the patients in these two groups received corticosteroids. Blood transfusions in both groups were given on the following criteria:
1. Prothrombin time more than twice the control value.
2. Presence of occult gastrointestinal bleeding as detected by Benzidine test.
3. Presence of frank gastrointestinal bleeding.
Cases of precoma and coma received the following additional treatment.
1. Protein-free diet.
2. Bowel wash 8 hourly.
3. Oral Neomycin 6-8 g. a day.
4. Dose of Liv.52 was increased to 4 tablets every 6 hours.
The following investigations were carried out in the present study:
1. Routine haemogram
2. Urine examination for urobilinogen, bilirubin, sugar, albumin and microscopic examination.
3. Urine cultures were done routinely in all cases of viral hepatitis with pregnancy.
4. Bleeding time and clotting time (B.T., C.T.)
5. Biochemical tests:
(a) Serum bilirubin
(b) S.G.O.T.
(c) One stage prothrombin time.