Viral Hepatitis in Children
Sudhakar Rao, V., Reddi, Y.R. and Rohini, K. Institute of Child Health, Niloufer Hospital, Hyderabad, India. (Paper read at the XII National Conference of Indian Academy of Paediatrics, Manipal, Karnataka)
ABSTRACT
One hundred and twenty cases of viral hepatitis were randomised into four equal groups, viz., A, B, C and D. Group A received Liv.52 alone; Group B received prednisone alone; Group C received a combination of Liv.52 and prednisone and Group D received only supportive therapy without either Liv.52 or steroids. Liver biopsies were performed before commencement of therapy and repeated during and after treatment along with other relevant biochemical investigations. Though all cases recovered completely, recovery was earliest in Liv.52 treated cases. Addition of steroids to Liv.52 did not show any extra advantage. Cases treated with steroids alone took longer time for histopathological recovery than those treated with Liv.52 alone. The mean recovery period for Liv.52 treated cases with or without prednisone was 5 weeks, while cases receiving prednisone alone recovered in a mean period of 10 weeks. Those with only supportive treatment took about 14 weeks for complete recovery.
INTRODUCTION
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 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 great, particularly in our country, where malnutrition is extremely rampant1. There is no specific therapy for viral hepatitis, and therefore a drug, which can restore liver function quickly without producing harmful effects, and is reasonably inexpensive, is most welcome. Of late, there have been a number of reports about the efficacy of Liv.52 in this disease2,3.
The purpose of this paper is to review our experiences with 120 cases of viral hepatitis on whom controlled studies have been made, with special reference to therapy with Liv.52 and steroids.
MATERIAL AND METHODS
One hundred and twenty cases of viral hepatitis admitted to the Paediatric Wards of the Institute of Child Health, Niloufer Hospital, during the 2½ year period from January 1972 to August 1974, consecutively, were randomised into four groups, 30 in each group and designated as Groups A, B, C and D. A proforma was designed for the purpose of study which included a detailed history and physical examination and routine investigations, such as complete blood picture, urinalysis for bile salts, bile pigments and urobilinogen and liver function tests, which included serum bilirubin, Vanden Bergh, thymol turbidity, thymol flocculation, total serum proteins, albumin/globulin ratio, serum transaminase, etc. Liver biopsy was done on admission and repeated during and after treatment at intervals varying from 3 to 12 weeks. Treatment for Group A cases consisted of Liv.52 alone, for Group B, prednisone alone, while Group C received a combination of Liv.52 and prednisone and Group D received only placebo with supportive treatment (Table 1). The results of treatment were analysed at the end of the study.
OBSERVATIONS
Infective hepatitis accounted for 1.4 per cent of total hospital admissions, with a slight preponderance for males, the male-female ratio being 65:55. Peak incidence was observed during the late summer and winter months, although cases were encountered throughout the year.
Table 1: Dosage schedule of Liv.52 |
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Age in years |
Group A |
Group B |
Group C |
Group D |
Upto 20 years |
Liv.52, 2 teaspoons, twice a day |
Prednisone, 2 mg/kg for 2 weeks |
Liv.52 |
Placebo |
2-10 years |
Liv.52, 2 teaspoons, thrice a day |
Prednisone 1 mg/kg for 1 week |
Prednisone |
|
10-12 years |
Liv.52, 2 tablets, thrice a day |
Prednisone, ½ mg/kg for one week |
|
|
Socio-economic status: Seventy two per cent belonged to the poor socio-economic group, 15 per cent to the middle-income group and the rest to the high income group.
Duration of jaundice: Jaundice lasted for less than 10 days prior to admission in the majority of cases (60 per cent). It was detected after admission in 3 per cent (Table 3).
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Symptoms: Lack of appetite of sudden onset was the most frequent complaint, and jaundice was noticed by mothers in 70 per cent cases, the time of appearance of jaundice varying from 2-8 days after the loss of appetite. Fever was present in 88 per cent and yellow urine was noticed by the mother in 86 per cent cases. Clav coloured stools were present in 55 per cent. Intense pruritus was the presenting symptom in 6 per cent cases, in whom enlarged tender liver and jaundice were detected by the examining doctor in the outdoor department. Four per cent cases presented with fever with chills and rigors and were mistaken for malaria on admission. In 3 per cent, jaundice appeared after admission. None of the cases presented with hepatic coma, although altered sensorium was noticed in 2 cases (Table 4).
Signs: Seventy three per cent had mild jaundice, while 21 per cent had what could be called moderate jaundice. Rest 6 per cent had very severe jaundice and presented with severe pruritus. Liver was enlarged in 98 per cent, the hepatomegaly ranging from 1-6 cm below the costal margin in the midclavicular line. Tenderness was discernible in 68 per cent, although it was difficult to appreciate tenderness in infants below 1 year. There was no hepatomegaly but only discomfort on pressing the subcostal region in 2 per cent. Lymph nodes were enlarged in 34 per cent. Ascites was seen in 2 per cent and bradycardia was detected in 2 per cent. These children had oedema of legs also. Electrocardiogram showed only sinus bradycardia.
Laboratory investigations: The serum bilirubin levels ranged from 2-15 mg% and alkaline phosphatase levels from 10-25 King Armstrong units. Thymol turbidity ranged from 1-10 units. Elevated levels of serum glutamic oxalo acetic and pyruvic transaminase (SGOT and SGPT) were found in 87 per cent cases.
The histopathologic changes in liver included vacuolation of hepatocytes in varying degrees with scanty and granular cytoplasm. The portal tracts were infiltrated with mononuclear cells and segmented leucocytes. Focal areas of necrosis were noticed in 48 per cent and there was destruction of limiting plate in 32 per cent. Cholestasis with bile pigment in hepatocytes and biliary canaliculi was found in only 5 per cent. The glycogen content of the liver cells was found to be reduced in sections stained with Periodic acid Schiff. The reticulin framework was found to be disturbed in all cases.
Refference: http://www.himalayahealthcare.com/pdf_files/liv227.pdf
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