The present study incorporates a study of 42 cases of lepromatous leprosy for hepatic involvement and role of indigenous herbal preparation in protecting the liver in leprosy. Liver was enlarged in 32 cases, which was tender in 8 patients. Alteration in liver function irrespective of extent and duration of the illness (3 months to 10 years with mean duration of illness = 2 years 5 months) was mainly seen as uniform elevation of serum proteins (6.2-9.2 gms%, mean = 7.5 gms%) with hypoalbuminaemia (2.0-4.4 gms%, mean = 2.9 gms%). Highest level of serum bilirubin of 1.6mg% was detected in 6 cases, emphasising the presence of leprous hepatitis. Raised level of serum transaminases (SGOT=65.2 IU, SGPT = 78.7 IU) were proportionate to the liver and muscle involvement. Presence of characteristic granulomata in the liver around the central vein, periportal area and even distribution at various locations in the liver lobules were the most significant changes in 12 out of 15 liver tissues. Acid fast M. leprae were demonstrated in 12 patients. The present work emphasises the detection of hepatic involvement in the early stage of the disease and hepato-protective, role of indigenous drug Liv.52 in lepromatous leprosy which usually lead to dreaded mutilated complications in the body.

Key words: Lepromatous leprosy, Liver, Herbs.

Forty two patients of lepromatous leprosy were included in this study, who were diagnosed on clinical, histological and bacteriological grounds5,12,13. All patients were thoroughly scrutinised to exclude any other overt cause which is known to produce derangement in liver function and such cases were not included in this study.

Biochemical liver function tests were performed by standard techniques before and after 6 and 12 weeks of therapy. These included serum proteins, albumin, globulin, bilirubin, thymol turbidity, serum transaminases, LDH, alkaline phosphatase and prothrombin time. Percutaneous liver biopsy was performed under aseptic technique wherever possible. Hematoxyline and eosine stained sections were examined. Acid fast bacilli were demonstrated by Fite Faraco's modified technique17.

Patients were grouped into two groups:

Group I: Control group of 20 cases treated with Dapsone etc., but without Liv.52.

Group II: Clinical trial group of 22 cases getting Liv.52, 2 tablets three times a day for at least 12 weeks along with antileprotic drugs.

Follow-up was made for first two months every week then monthly for the 12 months. The clinical assessment of recovery of patients regarding protective role of Liv.52 was judged by the clinical improvement, biochemical tests and histopathological changes in the liver12,16,19.

Forty two cases of lepromatous leprosy were divided into two groups:

Group I (20 cases) and Group II (22 cases) for studying the therapeutic response of the drug. Their ages varied from 8 to 62 years with the mean age of 30.2 years and male to female ratio of 3.6:1 (Table 1). The duration of illness varied from 3 months to 10 years and the mean duration of illness was 2 years 5 months. Hepatomegaly was noted in 32 patients, which was tender in 8 of them.

Biochemical changes: Liver functions were deranged in proportion to the liver involvement (Table 2). Hepatic damage and dysfunction was manifested as raised serum levels of transminases, LDH and alkaline phosphatase. There is uniform elevation of serum proteins with lowered level of serum albumin leading to reversal of albumin globulin ration. This alteration was irrespective of the extent and duration of the disease.

Therapeutic Response: The average period of therapy pertaining to hepatic dysfunction was 12 weeks in Group II cases but were followed to a maximum period of 12 months and Liv.52 was repeated as and when indicated (5 cases). The findings are summarised in Table 4 and Table 5. The mean fall of enzymatic levels after scheduled therapy was better and quick in Group II cases as compared to Group I. Serum albumin was raised from 2.84 gms% to 4.6 gms% in Group II cases. This rise in serum albumin was significant as compared to Group I cases.

Histology of the liver showed decreased stellate fibrosis in Group II cases along with earlier and quick clearance of lymphocytic infiltration. Liver cell necrosis was checked in clinical trial group cases.

Lepromatous leprosy is considered to be a systemic disease and pathologically it is a reticuloendothelial disease. The alteration in hepatic function in the present series of cases is the testimony of involvement and affection of hepatobiliary system.

There is significant rise in serum transaminases, alkaline phosphatase and LDH, which might be due to combination of hepatic dysfunction and muscular involvement^7,12,13, whereas Mohanty and Murty¹¹ stressed mainly on muscular involvement. Gupta et al⁹ and Lodha et al¹⁰ reported normal values. There is uniform rise in serum proteins with hypoalbuminaemia (serum albumin = 2.0-4.4 gms%) which was irrespective of extent and duration of the disease. This is the result of deranged hepatocyte function and hyperplasia of reticuloendothelial cells^7,10,12,13.

The typical histological lesions of the liver have been reported by various workers^4,13,14,21. Two types of lesions have been encountered i.e., granulomata specific of leprosy and non-specific collection of mononuclear cells, both types of lesions progressed to portal scarring in due course of time which might be due to drug, nutritional factors or end result of the disease itself. The predominance of histiocytes containing multiple M. leprae and lipoid material was the important feature of its being a disease of reticuloendothelial system. The presence of M. leprae all along the sinusoids evidently showed that the spread of infection occurs through blood stream and the body tissue reacts to this insult by proliferation of reticulo-endothelial cells in the form of histocytes in the liver and other organs²¹.

Amyloidosis was seen in one patient who had extensive disease for the prolonged period (10 years). Its incidence has been variously reported ranging from 5.9% to 50%²². The higher incidence of it from Western countries was due to the fact of dietary and/or environmental factors.

It is observed in the present series of cases that patients of Group II who were on indigenous drug, had speedier clinical as well as biochemical improvement as compared to patients of Group I who were not on Liv.52. The period required for improvement is cut short in Group II cases and thereby helping in overcoming the morbidity of the disease. It has been reported that many indigenous plants have beneficial effects on liver disease and act as hepato-protective^2,3,16,19. Liv.52 is a preparation from indigenous herbs of The Himalaya Drug Co., which accelerates the clinical as well as biochemical recovery²⁰. It stimulates mitotic activity¹⁵ of the hepatic cells and thus stimulates the regeneration of liver cells, which will correct all secondary abnormalities consequent to liver parenchymal necrosis and degeneration. Liv.52 presumably improves the function of hepatocytes and promotes the regeneration of the necrosed cells, thereby improving the protein synthesis. It diminishes the activity of serum transaminases and arrests the cell necrosis and inflammation. It is observed histologically in Group I cases the persistence of necrotic changes, granulomata formation progressing to stellate fibrosis, which is not seen in Group II cases. Therefore it can be said that Liv.52 restores normal liver functions earlier and in shorter duration, improves appetite, gives sense of well being, is anti-inflammatory and effectively contributes to healthy repair and regeneration of liver cells which proves its hepato-protective role.

We express our sincere gratitude to The Himalaya Drug Company, Shivsagar 'E', Dr. A.B. Road, Bombay-18 for the generous supply of Liv.52.