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Original Article
PMID: 17642821

Hepatic involvement and hepatitis B surface antigen (Hbs Ag) in leprosy

PK Nigam, GB Gupta, A Khare
 Department of Skin & STD, JNM Medical College, Raipur - 492 001, Chattisgarh, India

Correspondence Address:
P K Nigam
Katora Talab, Raipur - 492 001
How to cite this article:
Nigam P K, Gupta G B, Khare A. Hepatic involvement and hepatitis B surface antigen (Hbs Ag) in leprosy. Indian J Dermatol Venereol Leprol 2003;69:32-34
Copyright: (C)2003 Indian Journal of Dermatology, Venereology, and Leprology


Hepatic involvement and hepatitis B surface antigenemia was studied in 80 leprosy patients and results were compared with 50 normal healthy controls. HbsAg was detected in 7.54% of lepromatous leprosy patients as compared to 2% of the normal healthy controls. There was a decrease in albumin and increase in globulin levels with significant decrease in A: G ratio. SGPT levels were significantly raised in lepromatous leprosy patients. Histopathological changes were present in 57.1 % of lepromatous leprosy and 23.8% of tuberculoid leprosy patients.
Keywords: Leprosy, HbsAg


Liver is the most frequently affected visceral organ in leprosy particularly in the multi-bacillarytype.[12] Administration of hepatotoxic drugs may further deteriorate the liver functions.[2] Therefore monitoring of liver function tests (LFT) is very important to assess the metabolic status of the liver before administration of MDT. Several investigators have reported an increased prevalence of hepatitis B surface antigen (HbsAg) in patients with lepromatous leprosy[3],[4] (LL) attributed either to the genetic susceptibility[3] or to the impaired cell mediated immune response[4] of the leprosy patients. Besides this, other investigators found no increase in the prevalence of HbsAg in LL patients as compared to patients with tuberculoid leprosy or normal healthy individuals[5] suggesting that the prevalence of HbsAg in leprosy patients simply followed the pattern prevalent in normal healthy population in that environment. Lenka et al,[6] reported small but significant rise in SGPT levels in patients of LL with HbsAg as compared to those without antigen indicating a form of chronic anicteric hepatitis.

The present study was undertaken to detect the incidence of Australia antigen and evaluated the hepatic status by studying the various liver function tests and histopathological examination of leprosy patients.

Materials and Methods

Eighty leprosy patients attending the skin and leprosy department of Pt. J.N.M. Medico College and leprosy hospital, Raipur were randomly selected and classified according tc criteria of Ridly and Jopling.[7] These patient consisted of 53 cases of lepromatous leprosy (42 males, 11 females) (Group II), 24 cases o tuberculoid leprosy (11 males, 13 females) (GrouF III), and 3 cases of borderline leprosy (Group IV) Fifty normal healthy individuals (32 males, 1f females) (Group I) without any past history a jaundice served as control.

HbsAg was detected b) immunoelectrophoresis method.[8] LFT includec serum proteins, bilirubin, SCOT, SGPT, alkalinE phosphatase, and cholesterol by the methods o Wooten.[9] Bleeding time, clotting time anc prothrombin time were also measured. Livei biopsy was performed using Vim Silverman′s needle.


The range of the values (with mean value in parenthesis) of total serum proteins (TSP) gm/ dl), serum bilirubin (mg/dl), SGOT (I.U./L), alkaline phosphatase (K.A. unit/dl), cholesterol (mg/dl) are shown in [Table - 1].


An interesting association betweer HbsAg and leprosy has been reported by various workers.[3],[9] Although, by and large, the infectior is believed to occur by parenteral transmission, c faeco-oral contamination by hepatitis B virus car not be ruled out as most of the leprosy patients belong to the lower socio-economic groups Besides this, leprosy itself could act as or immunosuppressant and give way to further lodgement of HBV resulting in the carrier state." After infection with HBV, the first virologic market detec[Table - 1] serum is HbsAg.[12]

In our study, the incidence of HbsAg it normal healthy controls was 2% and is it accordance with the incidence of HbsAg in norma population in different studies from our country.[13],[14]

HbsAg was detected in 7.54% of lepromatous leprosy patients. A similar high incidence of HbsAg ranging from 6.1%-10% in lepromatous leprosy patients was also reported by other workers.[13] Some workers have reported the prevalence of HbsAg in 2-5% of cases with tuberculoid leprosy." However, none of our patients with tuberculoid or borderline leprosy showed the presence of HbsAg in his blood, a finding consistent with that of Saha and Dutta.[4] Besides HbsAg, hepatitis B surface antibody was also detected in 2(3.7%) cases of lepromatous leprosy showed the presence of this antibody. Presence of this antibody indicates previous Australia antigenemia.

The mean serum protein levels were normal in all the groups. However, a decrease in albumin and an increase in globulin levels with lowering of A:G ratio, which was significant statistically (p< .001), was observed in them. This hyperglobulinemia is attributed to antigenic stimulation, immunological phenomenon and hepatic involvement in leprosy.[16]

The mean SGOT, SGPT and alkaline phosphatase levels were normal in patients with borderline and tuberculoid leprosy. The lepromatous leprosy patients also showed normal levels of SCOT and alkaline phosphatase, however the SGPT levels were significantly raised (p< .005) in them as compared to controls. Nigam et al[17] also observed similar changes in SCOT, SGPT and alkaline phosphatase levels in their leprosy patients.

The bleeding time, clotting time, prothrombin time, serum bilirubin and cholesterol levels were normal in all the groups, consistent with the other studies.[1],[17]

Histopathological changes in the liver were observed in 57.1 % of cases with lepromatous leprosy and in 23.8% cases of tuberculoid leprosy. Primarily, the fatty changes, granulomatous changes or infiltration with mononuclear cells were observed. The changes were more predominant in disease of more than 3 years duration.

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