Hepatitis B virus and primary hepatocellular carcinoma: treatment of HBV carriers with Phyllanthus amarus.

A viricide capable of eliminating hepatitis B virus (HBV) from chronic carriers should, theoretically, decrease the risk of primary hepatocellular carcinoma. Extracts of Phyllanthus amarus have been shown to inhibit the DNA polymerase of HBV and woodchuck hepatitis virus (WHV) in vitro. Three of four recently infected WHV carriers treated i.p. with P. amarus extract lost WHV, animals infected for greater than or equal to 3 months showed a decrease in virus levels. Preliminary results in human carriers treated orally with P. amarus for 1 month indicated that approximately 60% of the carriers lost HBV during the observation period.

A study of HTLV-I and its associated risk factors in Trinidad and Tobago.

Seroprevalence of human T-lymphotropic virus type 1 (HTLV-I) among a sample of persons selected from a government register of businesses in Trinidad was 3.2% in 1,025 persons of African descent compared to 0.2% among 487 persons of Asian descent and 0% among 46 persons of European-descent. In Tobago, from a coastal village, among persons of African ancestry ascertained as part of a cardiovascular survey, the rate was 11.4%, which was significantly higher when corrected for age and race than the rate in Trinidad. The seroprevalence rate of antibodies to hepatitis A and B was also significantly elevated in Tobago compared to Trinidad. HTLV-I seroprevalence rates were higher in females than males while hepatitis A and B rates were not significantly different in the two sexes. For males, age was a significant determinant of HTLV-I seropositivity, while for females, age, markers of poor sanitation, and hepatitis B were each independently linked to HTLV-I seropositivity. The frequent occurrence of multiple infectious exposures in persons of lower socioeconomic circumstances in this tropical environment may result in immune activation that heightens susceptibility to HTLV-I infection.

Increased serum ferritin in chronic liver disease: a risk factor for primary hepatocellular carcinoma.

Previous studies from this laboratory support the view that increased serum ferritin levels are associated with an increased risk of primary hepatocellular carcinoma (PHC). We have tested this hypothesis in a population of Korean patients with chronic liver disease followed for development of PHC. Serum ferritin levels were measured over time in 249 patients with liver diseases (mostly chronic) followed for 2 to 17 years in Seoul, Korea. Most of the patients were chronically infected with hepatitis B virus. During the first 8 months of follow-up, there were no cases of PHC and no deaths. During this same period, no patient had a serum ferritin level initially below 300 ng/ml and rising above 300 ng/ml, but some patients with ferritin levels above 300 ng/ml experienced decreases to below 300 ng/ml. Therefore, patients were grouped by ferritin level during the first 8 months of follow-up into 3 categories according to the above criteria. Multivariate analysis showed that consistently elevated ferritin levels (category 3) were significantly associated with the development of PHC. Men were more likely to have elevated ferritin levels than women and were at higher risk of developing PHC. Men who were chronically infected with HBV and had ferritin levels above 300 ng/ml had a 50% chance of developing PHC during the follow-up period, compared with a 20% risk of PHC for men with lower ferritin levels (categories 1 and 2). This elevated risk of PHC in men with elevated ferritin levels was confined to the first 3 years of follow-up.

Lack of perinatal transmission of hepatitis B virus infection in Senegal, West Africa.

Between 1977 and 1980, 1442 pregnant women in Thies, Senegal, were tested for serologic markers of hepatitis B virus (HBV) infection. Of these, 9.8% were HBsAg(+), 59.9% were anti-HBs(+), and 15.6% had anti-HBc alone. Of 116 HBsAg(+) pregnant women, only 19.8% were HBeAg(+), a much lower proportion of infectious carriers than seen in Asian populations. Cord blood from 1353 babies was HBsAg(-), implying that the babies were not infected prior to birth. Four hundred sixty-two babies, including 88 born to HBsAg(+) mothers, were observed for 2 weeks to 38 months after birth. In contrast to observations in Asia, none of the babies became HBsAg(+) before 5 months of age, and only three of the 16 born to HBeAg(+) mothers became HBsAg(+) within the first year of life; all three developed chronic infections (i.e., HBsAg(+) for greater than or equal to 6 months. In the second year of life, six of 34 babies born to HBsAg(+), HBeAg(-)/anti-HBe(-) mothers became infected with HBV, and four of the six developed chronic infections. During the first 3 years of life, infections occurred at a higher rate in infants born to HBsAg(+) (17%) than to HBsAg(-) (4%) women. The latter group of infants included 4.0% of those born to anti-HBs(+) mothers, 4.6% born to anti-HBcAg(+), and 3.2% born to uninfected women. These observations indicate that HBV infections in Senegal usually do not occur perinatally, but do occur at high incidence later in infancy and childhood. Such infections can be prevented by the use of hepatitis B vaccine alone; administration of hepatitis B immune globulin should not be needed.

Localization of the amino acid substitution site in a new variant of human serum albumin, albumin Mexico-2.

Using an electrophoretic screening procedure, we have discovered that two species of human serum albumin Mexico occur that are indistinguishable by conventional electrophoretic methods. We suggest that these species be referred to as albumins Mexico-1 and Mexico-2. Isolation and determination of the partial sequence of the cyanogen bromide fragment of albumin Mexico-2 that differs from the corresponding fragment of the common albumin A revealed this variant to arise from at least a glycine/aspartic acid substitution at position 550. This region of the albumin molecule is involved in the binding of the fatty acid, palmitate.

Distribution of albumin variants Naskapi amd Mexico among Aleuts, Frobisher Bay Eskimos, and Micmac, Naskapi, Mohawk, Omaha, and Apache Indians.

In order to help define the boundaries of the distribution of the albumin variants Naskapi and Mexico which are polymorphic among several American Indian groups, we examined sera from Micmac, Mohawk, Northwest River Naskapi, Omaha and Apache Indians, and from Aleuts and Eskimos. Sera from a total of 1,524 individuals were examined. Using a cellulose acetate membrane electrophoretic system with Tris-Citric acid at pH 5.4 we were able to distinguish normal albumin and both variants in the same run. Naskapi and Mexico variants were absent from Aleut, Eskimo, Micmac, Mohawk and Omaha samples. The albumin Naskapi variant was present in an allele frequency of 0.03 in the Naskapi Indian sample. Albumin variants Naskapi and Mexico were found in the Apache sample at frequencies of 0.016 and 0.037, respectively. This report supersedes that previously published by Schell and Agarwal ('76). Generally, within an area there is a correspondence between changes in the frequency of albumin variants and changes in the ethnic background and history of the area's populations. At the same time, when viewing widely separated areas, relationships between distant groups based on linguistic and cultural similarities are paralleled on a biologic level by the distribution of normal albumin and variant albumins.

The Australia antigen in Brazilian healthy persons and in leprosyand leukaemia patients.

The distribution of the Australia antigen was investigated in 633 white and negroid healthy persons, 218 white and negroid leprosy patients, and 50 white leukaemia patients. The subjects were living at the time of the investigation in two southern Brazilian cities. Two of the patients with leukaemia showed the antigen, as also did three out of 358 negro subjects, but no reactors were found among the healthy white subjects and leprosy patients.