Leprosy and hepatitis B coinfection in southern Brazil

To investigate the association of leprosy with hepatitis B virus (HBV) infection, as yet unknown for South Brazil, we assessed hepatitis B virus coinfection in 199 South Brazilian leprosy patients (119 lepromatous, 15 tuberculoid, 30 borderline, 12 undetermined and 23 unspecified) and in 681 matched blood donors by screening for the hepatitis B virus markers HBSAg and anti-HBc, using ELISA. Positive samples were retested and anti-HBc+ only samples were tested for the hepatitis B surface antibody (anti-HBs). There was a strong association between leprosy and hepatitis B virus infection (OR = 9.8, 95% CI = 6.4–14.7; p = 0.004·E−30), as well as an association between HBV infection and lepromatous leprosy, compared to other forms (OR = 2.4, 95% CI = 1.2–4.8; p = 0.017). We also found that confinement due to leprosy was associated with hepatitis B virus infection (OR = 3.9, 95% CI = 2.1–7.4; p = 0.015·E−3). Leprosy patients are susceptible to develop hepatitis B virus infection, especially lepromatous. Institutionalized patients, who probably present a stronger Th2 response, have higher risk of being exposed to hepatitis B virus. This clearly emphasizes the need for special care to leprosy patients in preventing hepatitis B virus coinfection in South Brazil.

Leprosy and hepatitis B coinfection in southern Brazil.

To investigate the association of leprosy with hepatitis B virus (HBV) infection, as yet unknown for South Brazil, we assessed hepatitis B virus coinfection in 199 South Brazilian leprosy patients (119 lepromatous, 15 tuberculoid, 30 borderline, 12 undetermined and 23 unspecified) and in 681 matched blood donors by screening for the hepatitis B virus markers HBSAg and anti-HBc, using ELISA. Positive samples were retested and anti-HBc+ only samples were tested for the hepatitis B surface antibody (anti-HBs). There was a strong association between leprosy and hepatitis B virus infection (OR=9.8, 95% CI=6.4-14.7; p=0.004 · E(-30)), as well as an association between HBV infection and lepromatous leprosy, compared to other forms (OR=2.4, 95% CI=1.2-4.8; p=0.017). We also found that confinement due to leprosy was associated with hepatitis B virus infection (OR=3.9, 95% CI=2.1-7.4; p=0.015 · E(-3)). Leprosy patients are susceptible to develop hepatitis B virus infection, especially lepromatous. Institutionalized patients, who probably present a stronger Th2 response, have higher risk of being exposed to hepatitis B virus. This clearly emphasizes the need for special care to leprosy patients in preventing hepatitis B virus coinfection in South Brazil.

Primary hepatocellular carcinoma in intertropical Africa: relationship between age and hepatitis B virus etiology.

Clinical observations of patients with primary hepatocellular carcinoma (PHC) at Le Dantec Hospital, Dakar, Senegal, were studied to determine a correlation with hepatitis B virus (HBV) infection. Of the 103 patients with PHC, 80 had an active HBV infection (HBsAg and/or anti-HBc); 23 showed signs of previous HBV infection (anti-HBs and anti-HBc). The two groups were similar in the detection of alpha-fetoprotein (approximately 60%) and in the major clinical findings: hepatomegaly, 76.25% and 86.96%, respectively; and ascites, 57.50% and 47.83%, respectively. Jaundice, however, was three times more frequent (P < 0.01) in the group of patients with signs of active HBV replication. Distribution of HBV markers as a function of age at onset of PHC revealed that the presence of HBsAg was primarily confined to the sera of the younger patients (< 50 yr old). When compared with leprosy patients and blood donors, the younger PHC patients differed in the frequency of detection of HBsAg and anti-HBs. The older people (> 50 yr old) in the three groups (PHC patients, leprosy patients, and blood donors) had identical HBV markers.

Australia antigen and antibody in British patients with leprosy.

Seventy-five sera collected from leprosy patients in England were tested for Australia antigen and antibody. Australia antigen was detected in only two patients with lepromatous leprosy and in one patient with borderline pure leprosy. Antibody to Australia antigen was found in one patient with lepromatous leprosy. These findings differ from previous reports and it is suggested that the frequency of Australia antigen in lepromatous leprosy is a function of the incidence of this antigen in the general population rather than increased genetic susceptibility to chronic infection.

Current concepts in viral hepatitis.

A great deal of interest and speculation has arisen from the discovery of a specific antigen, Australia antigen, in the serum of a high proportion of patients with viral hepatitis. This antigen has been found also in the serum of some patients with other conditions, including Down's syndrome, leukemia, leprosy, chronic renal disorders, and chronic active liver disease. It is not found in the serum of normal persons. Australia antigen has been postulated as the causative agent of viral hepatitis. In most patients the antigen can be detected for less than two weeks during the acute phase of the disease. Its persistence in other conditions may be due to an impairment of the immune response. The course of acute viral hepatitis is usually uncomplicated, full recovery of liver function taking place within four to six weeks, with restoration of normal liver histology within three to four months. Follow-up studies of patients in whom hepatitis has developed during epidemics have failed to reveal evidence of subsequent chronic progressive liver disease. This suggests that most cases of chronic active hepatitis are not the result of preceding acute viral hepatitis. However, the recent finding of Australia antigen in the serum of a small number of patients raises the possibility that sporadic viral hepatitis may be one of the causes of the chronic active hepatitis. Alternatively, the presence of the antigen may be interpreted as being due to an altered immune response. The treatment of acute hepatic coma remains unsatisfactory. Several new forms of therapy have been tried in recent years in an uncontrolled way. These include multiple exchange blood transfusions, isolated pig liver perfusion, human cross-circulation, and cross-circulation with baboons. Transient improvement may follow any of these procedures, but evidence that they influence the final outcome of the disease is lacking. The rapid fluctuations in the neurological status of individual patients makes it difficult to interpret the effects of therapy. Also, until satisfactory objective criteria of degrees of coma are universally accepted it will be impossible to compare one mode of therapy with another.