Therapeutic Effects of Liv.52 in Post-Necrotic Hepatitis

Prof. Gupta, S., F.R.C.P., D.C.H., Head of the Department of Pediatrics, Gastroenterology Unit, Khatri, R.L., D.C.H., Resident Medical Officer, Pediatrics, and Srivastava, G., M.D., Pediatrician. Maulana Azad Medical College, New Delhi, India.

Infectious hepatitis is encountered in paediatric practice either during an epidemic or as sporadic cases. Clinically it may present in mild, moderate or severe forms. Varying degrees of destruction of the liver cells, degeneration, necrosis, autolysis have been reported chiefly in the centre of the lobule. Damage is limited to hepatic cells and does not involve the reticulum stroma, portal canals or intralobular vasculature. The lesion is widespread and diffuse in the whole parenchyma of the liver.

The liver has manifold functions and is intimately connected with various metabolic processes closely connected with growth and development. Its proper functioning has a great effect on the physiological functioning of the whole body. Hepatic injury leads to derangement of its functions. The liver has great reserve powers and also powers of regeneration; this being so, it is very difficult to correlate the clinical findings with biochemical and laboratory tests and even biopsy studies to determine the degree and extent of liver damage.

Aspiration biopsy studies of the liver offer a very reliable and certain method of assessing the structural and histopathological changes in the liver during the progress of the disease and it can also indicate the effects of therapy. A needle biopsy specimen, though small in size, can pick up a large number of pathological conditions as it gives the correct cytological picture and changes therein, especially in a disease like infectious hepatitis which is characterised by diffuse and widespread lesions.

Hepatic cells function in a constant state of portal anoxia and their characteristic reaction is necrosis, the extent of which depends on the nature of the injury. The condition may advance rapidly to hepatocellular failure, or may gradually show a picture of mild or moderate cirrhosis of liver.

The present paper reports a study of two patients suffering from infectious hepatitis who were treated and followed up for a year and a half each. Clinical, biochemical and laboratory studies were repeatedly carried out and the transthoracic needle biopsy study was done before and after the therapy. The findings are presented below:

Case I :

A.S., three-year-old male, came with fever and jaundice for 10 days. Diagnosis of infectious hepatitis was made. he was put on supportive therapy, but his condition deteriorated and he was admitted after 10 days with a diagnosis of subacute hepatitis and impending coma. On admission, his serum bilirubin was 4.6 gm%. Total blood proteins 6.5 gm%, serum albumin being 4.3 gm% and serum globulin 2.3 gm%. S.G.O.T. was 140 units ml. and S.G.P.T. 123 units ml., Prothrombin time 26 seconds, urobilinogen was present in urine and stools were clay coloured. The child was put on steroids and other supportive measures. Steroids were gradually tapered off after six weeks of therapy. He recovered on this regimen and was discharged after one month’s stay in the hospital. At this time his liver was soft and 6 cm below costal margin in the midclavicular line and spleen 3 cm below the costal margin. Liv.52 tablets were given, one tablet t.i.d., after stopping the steroids.
He was called for laboratory studies and liver biopsy after a period of four months after his discharge from the hospital. The findings were serum bilirubin 0.6 mg%, total proteins 7.2 gm%, serum albumin 4.3 gm%, serum globulin 2.9 gm%, S.G.O.T. 36 units/ml, S.G.P.T. 30 units/ml prothrombin time 20 seconds (control 15 sec.), liver was soft and measured 3 cm below the costal margin in the midclavicular line and the spleen 1 cm below the left costal margin showing marked regression in the size of both the organs.
Case I: Microphotograph 1(Before treatment) Case I: Microphotograph 2(Before treatment)
Liver biopsy showing necrosis and fibrosis H.E. stain Reticulin to show extensive stainfibrosis and necrosis
Liver biopsy showed a post-necrotic cirrhosis on histopathological examination (Microphotographs 1 and 2). Liv.52 therapy was continued for almost 10 months. His liver became soft and spleen was just palpable. His clinical condition improved remarkably. Repeat liver biopsy was performed after one year of Liv.52 and the histopathological studies of the biopsy material revealed normal liver structure. (Microphotograph 3). He is under continuous observation till today. Case I: Microphotograph 3 (After treatment)

After Liv.52 for 1 year, 1 tablet,t.i.d. normal liver

Case II:

Varsha, eleven-year-old girl, was admitted with a provisional diagnosis of post-hepatitis cirrhosis. She gave a history of distension of abdomen for 3 months. Oedema of feet for one month, anorexia for one month, yellow colour of urine for two weeks and occasional vomiting. There was no history of having taken drugs or of a bleeding tendency. There was a history of jaundice – 18 days’ duration – three months ago. She was moderately nourished, with pallor and icterus and generalised anasarca. There was no cyanosis or dyspnoea. The liver was 4 cm palpable in the mid-clavicular line, firm to the feel but not tender. The spleen was 4.5 cm, palpable and firm Blood showed haemoglobin 8 gm%, total white cell count 7600, polymorph 64%, lymphocytes 32%, large monocytes 3%, eosinophils 1%, urine showed bile pigments. Serum bilirubin 4.8 mg%, zinc sulphate turbidity 8 units. Prothrombin time 36 seconds, S.G.O.T. 128 units, S.G.P.T. 142 units, total blood proteins 6.4 gm%, albumin 2.6 gm%, globulin 3.8 gm%, ascitic fluid proteins 1.8 gm%.

The child was treated with routine treatment along with Prednisolone 2 mg/kg/day and Liv.52, 2 tablets t.i.d. for six weeks. After six weeks, icterus decreased considerably, ascites disappeared, the liver and the spleen regressed to 2 cm and there was marked improvement of appetite. Prednisolone was gradually tapered off and stopped after a total period of three months of therapy. Liver function tests at this stage (after three months) were normal but liver biopsy revealed post-necrotic cirrhosis. (Microphotographs 4-7). The liver was just palpable and the spleen not palpable. There was weight gain of 2 kg.

The child was subsequently given Liv.52 tablets for two years after initial admission and the liver and spleen at the last observation were not palpable. The patient was followed up in liver clinic and was given 2 tablets of Liv.52 t.i.d. and the liver biopsy and revealed normal hepatic parenchyma. (Microphotographs 8-9).

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