A Study of Liver Function Tests in leprosy.

Leprosy is a chronic progressive granulomatous disease caused by Mycobacterium leprae. Hepatic involvement is seen in early stages of the disease. Administration of the hepatotoxic drugs like Rifampicin and Dapsone may further deteriorate the liver function. The present study was undertaken to evaluate hepatic status by studying the various liver function tests in leprosy patients and compared to healthy controls. Thirty untreated leprosy patients (18 Multibacillary, 12 Paucibacillary) with duration of illness varying from one month to three years were selected as cases. Twenty healthy age and sex matched persons were taken as controls. Hepatic functional status was evaluated by estimation of serum total bilirubin, alanine transaminase, aspartate transaminase, alkaline phosphatase, total protein, albumin and globulin. Independent sample 't' test was used to compare the data. P < 0.05 was considered as significant. Except for serum total protein, there was a statistically significant difference between the mean values of all the parameters in cases when compared to controls. The present study revealed minimal derangement in hepatic function in leprosy patients. Therefore monitoring of liver function tests is very important to assess the functional status of the liver before administration of therapy in leprosy.

Hepatic involvement in lepromatous leprosy.

Hepatic involvement in a lepromatous leprosy (LL) patient is reported. The serum concentrations of aminotransferases were much higher than previously described in the leprosy literature. Other causes for hepatic damage were ruled out. Such hepatic involvement and elevation of aminotransferases have never been described in leprosy.

Hepatitis C virus antibody, viral RNA and genotypes in leprous patients in Japan.

BACKGROUND/METHODS: Markers of hepatitis C virus infection were tested for in 229 patients with leprosy (male 154, female 75) in Japan. RESULTS: Antibody to hepatitis C virus by a second-generation enzyme immunoassay was detected in 68 patients (30%), and RNA of hepatitis C virus in 41 (18%), in prevalence rates much higher (p < 0.001) than those in matched controls (11/923 or 1.2% and 9/923 or 1.0%, respectively). Hepatitis C virus genotypes were II/1b in 37 (90%), III/2a in three (7%) and IV/2b in one (2%), in which II/1b was more frequently (p < 0.003) represented than in hepatitis C virus carriers without leprosy in Japan (520/767 or 68%). The 41 patients with hepatitis C virus viremia had serum transaminase levels significantly higher than those in the other 188 patients without viremia (p < 0.01). CONCLUSIONS: These results indicate that leprous patients confined in institutions are at high risk of hepatitis C virus infection, and that patients infected with hepatitis C virus should be monitored for liver function and placed on interferon therapy whenever required.

Does isoniazid increase the hepatotoxicity of the combination prothionamide-dapsone? Isoprodian Study Group.

In order to assess the potential additive liver toxicity of isoniazid to that of a thioamide-containing treatment, a prospective, randomized, double-blind trial of 24 weeks' duration involving 772 adult patients was conducted in four leprosy centers--two in India, one in Madagascar, and one in the Ivory Coast. Patients with multibacillary leprosy were given daily 100 mg dapsone (DDS) and 350 mg prothionamide (PTH) plus monthly 600 mg rifampin (RMP) in combination either with 350 mg isoniazid (INH) or with a placebo. After clinical and laboratory (including HBs-Ag testing) examinations on admission, the side effects (especially gastrointestinal disturbances and liver toxicity) were assessed at regular intervals during treatment by laboratory testing (aminotransferases, bilirubin, alkaline phosphatase) and by recording spontaneous complaints. Analysis of the frequency and seriousness of the side effects was made before breaking the code (with or without INH). Although 10% of the patients had liver toxicity leading to stopping treatment, no significant difference in the occurrence of side effects was observed between patients treated with or without INH. Most (75%) of the observed side effects occurred during the first 4 weeks of treatment, and the time of their onset was not related to INH. Body weight and age were factors related to the frequency of side effects [the higher the body weight, the lesser the rate of side effects (p = 0.03)] and the rate of serious side effects increased with age (p = 0.02). But, again, the frequency of the side effects was not related to INH administration. Therefore, from the present study it can be concluded that INH does not increase the toxicity of the thioamide-containing treatment.

Hepatic ultrasonography in patients with lepromatous leprosy.

Hepatic Sonography was done in 36 patients with lepromatous Leprosy and 3 patients with borderline lepromatous leprosy with the view to assess abnormalities of size, changes in the echotexture and to observe the presence of any nodules and calcification in the liver. Routine liver function tests were also done in these patients. No definite abnormal sonographic findings were seen in the liver in a large majority of these patients. One patient, however, showed nodular changes in the liver.

A study of incidence of Australia antigen and derangements in liver function tests in leprosy.

The present study was conducted in 50 patients of various subtypes of leprosy (Lepromatous, Tuberculoid, Borderline borderline) and 25 healthy control, for detection of Australia antigen and various liver function tests (serum protein, cholesterol, alkaline phosphates, SGOT, SGPT, bilirubin and liver biopsy) to see incidence of Australia Antigen and derangement in liver function. It was concluded that incidence of Australia antigen in study and control group was zero. Total serum protein and serum globulin was increased in lepromatous leprosy. A/G ratio was reversed in 34.3% and 50% in lepromatous and tuberculoid leprosy respectively. Granulomatous hepatitis was seen in 66.66% and 50% cases of lepromatous and tuberculoid leprosy respectively. No relationships was established between hepatic lesion, Australia antigen and liver function test.

The effect of clofazimine on liver function tests in lepra reaction (ENL).

Twenty patients with suspected DDS resistance and repeated attacks of lepra reactions were selected for the study. Clofazimine was administered in different doses over a period of 12 months. Elevated levels of transaminases and Alkaline phosphatase prior therapy attained values to near normalcy. Progressive fall in serum Bilirubin and Proteins with normal A/G ratio at the end of therapy was also observed. Clofazimine by its anti-inflammatory and antibacterial action could inhibit the process of liver damage and happened to have minimal deleterious effect on liver by studying the liver function tests.

Hepato-protective role of indigenous drug Liv-52 in lepromatous leprosy.

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 1.6 mg% 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.

Hepatic structure and function in Papua New Guineans with leprosy.

Hepatic function, including plasma bromsulphthalein (BSP) clearance was studied in 20 Papua New Guineans with leprosy: 11 lepromatous (LL) (6 had erythema nodosum leprosum (ENL)) (group A), and 9 tuberculoid or borderline (BT or BB) (group B); 12 controls (group C) were also studied. Four of five with abnormal BSP results had significant complicating or additional factors (hepatic amyloidosis, pustular ENL, hepato-cellular carcinoma and a pyogenic abscess), compared with two of 15 with normal results (tuberculous osteitis and pyogenic osteomyelitis). In nine (five from group A, and four from group B) needle liver biopsy histology was assessed: foci of vacuolated phagocytes and histiocytes, and tuberculoid granulomata were the most frequent lesions; none had cirrhosis. Leprosy is not associated with impaired hepatocellular function unless a severe complication or coincident disease is concurrently present. In this limited study therapeutic agents were not associated with abnormal liver structure or function. When liver function is abnormal in leprosy, another cause (e.g. secondary amyloidosis, sepsis or malignancy) should be searched for.

[Hepatic function in the clinical spectrum of Hansen's disease]. / La función hepática a través del espectro clínico de la hanseniasis.

The liver function was studied in 100 hanseniasis patients. They were classified in the following 10 groups: quiescent LL (20 patients), quiescent BL (13 patients), quiescent BB (7 patients), quiescent BT (9 patients), quiescent TT (12 patients), reactional LL (12 patients), reactional BL (10 patients), reactional BB (7 patients), reactional BT (5 patients), reactional TT (5 patients); a comparison was made with a control group (10 healthy individuals). It was found a hyperproteinemia with high levels of globulin and normal levels of albumin in the serum of all clinical forms, and a typical pattern of "light damage hepatic cells" with raised in the enzymatic activity of GOT, GPT and alkaline phosphatase with no changes in turbidity tests and bilirrubinemia, in all reactional patients. The physiopathology of this problem and the types III and IV hypersensitivity phenomena are discussed.

Liver in leprosy--I. Functional changes.

Liver function tests were carried out in 79 leprosy patients, out of which 28 patients were being treated and 42 patients were not receiving any treatment. The rest 9 patients were clinically quiescent. In the untreated group there were 28 tuberculoid and 14 lepromatus cases. The 28 patients receiving treatment were composed of equal number of lepromatus and tuberculoid groups. The liver function tests of 10 of the untreated tuberculoid patients were repeated after six months of specific therapy with D.D.S. The values of liver function tests of these patients were compared with that of 20 normal adults. The most important abnormality observed in the patients were a reversal of albumin/globulins ratio which was more common in the lepromatus group than in the tuberculoid group. Treatment with D.D.S. has resulted in the reduction of the serum globulin. There were no changes in transaminases and alkaline phosphatase activities in the untreated patients. But however a rise in the above enzymes were observed in patients on treatment. The mean serum cholesterol values of the patients were lower than that of the controls.

Liver function in leprosy.

Thirty eight patients of leprosy were classified on the basis of clinical and biopsy findings into 10 lepromatous (all reactional), 20 tuberculoid (7 in reaction) and 8 dimorphic (5 in reaction). The liver function tests--serum proteins, albumin/globulin ratio, fractions in paper electrophoresis, serum glutamic pyruvic transaminase (SGPT) and thymol turbidity tests--and the serum cholesterol was estimated in each patient. The abnormalities were a reversal of the albumin/globulin ratio in all the three groups and an increase in beta/globulin fraction in the lepromatous group, but total proteins were within normal limits. The thymol turbidity test showed moderately elevated levels in all three groups. SGPT was slightly raised in a few cases. Only a single patient with tuberculoid leprosy showed serum cholesterol to be over 250 mg per 100 ml.

Androgenic status of lepromatous leprosy patients with gynecomastia.

The androgenic status of 24 lepromatous leprosy male patients, 12 with and 12 without gynecomastia, was studied in comparison with that of 12 normal healthy males. Plasma testosterone levels were significantly diminished in the gynecomastia group as compared to levels in either of the control groups. The patients without gynecomastia showed values not significantly lower than those of normal males. Histopathologic examination of the leprous testes showed a variable admixture of inflammatory, degenerative anf fibrotic changes which were more severe and more frequent in the patients with gynecomastia than in those without it. Parenchymatous liver function tests showed greater derangement in the gynecomastia group as compared to the controls Histopathology of the liver showed lepromatous infiltration in patients with and without gynecomastia though the changes in liver were minimal in patients who showed total testicular degeneration in the biopsies.

Hepatic granulomas in leprosy. Their relation to bacteremia.

A clinicopathologic study of liver disease was conducted on 28 patients with leprosy who lived in Taiwan. None of the patients exhibited symptoms or signs of liver disease. Hepatic granulomas were found in 21 patients. Histologically, the infiltrates were epithelioid, foam cell, and histiocytic in type. Hepatic dysfunction was absent, except for mild sulfobromophthalein elevations in the severely infected cases. Hepatic granulomas correlated with the cutaneous reactions in lepromatous leprosy, but the association was poor for other stages of disease. Hepatic involvement varied with the severity of cutaneous infection and with the frequency and intensity of bacteremia. An estimated 1,000 to 10,000 acid-fast bacilli/ml of blood was required to generate the hepatic infiltrates.