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Biomedical subjects

E D Lustbader

Publications and source records attributed to E D Lustbader.

7 recordsLinked to original sources
PubMed1979

Serum iron levels and response to hepatitis B virus.

Response to hepatitis B virus (HBV) infection [HBV surface antigen (HBsAg) and antibody to HBsAg (anti-HBs)], serum iron, total iron-binding capacity, hematological status (erythrocytes, Hb, and hematocrit), and evidence of liver damage (serum glutamic pyruvic transaminase; aspartate aminotransferase, L-aspartate:2-oxoglutarate aminotransferase, EC 2.6.1.1) were determined for 201 patients on chronic renal dialysis. Four factors-serum iron level, transminase level, sex, and HBV response [i.e., infected-HBsAg(+) (HBsAg positive), anti-HBs(+) (anti-HBs positive), or no response]-were analyzed simultaneously to test the hypothesis that serum iron is higher in those with HBsAg in their serum than in those without HBsAg, independent of the transaminase level. Four independent, statistically significant two-factor interactions were identified. (i) Serum iron is higher in those HBsAg(+). (ii) Serum iron is higher in those with increased transaminase. (iii) Transaminase is higher in those HBsAg(+). (iv) Males are more likely to be HbsAg(+) and females are more likely to be anti-HBs(+). Also, those who are HBsAg(+) have significantly higher percent iron saturation (serum iron/total iron-binding capacity). That is, the hypothesis was supported by the findings. Several additional biological hypotheses are suggested, including a possible role of increased iron levels in susceptibility and response to HBV infection and the possible relationship between higher iron levels and the likelihood of HBV infection progressing to primary hepatocellular carcinoma. In addition, further tests of the initial hypothesis in nonhospitalized populations with endemic HBV infection are proposed.

Alanine Transaminase↗
PubMed1977

Host responses to hepatitis B infection in patients in a chronic hemodialysis unit.

Host responses to hepatitis B infection were studied in 222 patients in a chronic hemodialysis unit. From 1970 to 1976, patients were monitored monthly for development of hepatitis B surface antigen (HBsAg), antibody to hepatitis B surface antigen (anti-HBs), and serum transaminase (SGPT) elevations. Five categories of patients were identified as: 1) chronic carriers of HBsAg; 2) transiently HBsAg(+), who developed anti-HBs; 3) HBsAg(-) on admission, who developed anti-HBs without becoming HBsAg(+); 4) anti-HBs(+) on admission; 5) uninfected who remained HBsAg(-) and anti-HBs(-). For a patient who became HBsAg(+) in this clinic, the probability of becoming a chronic carrier was 62-8% and rose to 88.5% if he or she had been HBsAg(+) for five consecutive months. Males were more likely to become chronic carriers, and females were more likely to develop anti-HBs. Neither age, race, nor type of underlying kidney disease was associated with particular host responses to hepatitis B virus. No effect of hepatitis B infection on mortality was detected. Variation in host response to hepatitis B infection among renal dialysis patients may affect the usefulness of hepatitis B hyperimmune globulin and hepatitis B vaccine and be related to the outcome of kidney transplantation.

Antibodies, Viral↗
PubMed1977

Forecasting the development of primary hepatocellular carcinoma by the use of risk factors: studies in West Africa.

An association between hepatitis B virus (HBV) and primary hepatocellular carcinoma (PHC) has been found in several studies in Africa, Asia, and elsewhere. In this paper we considered the interrelations between several events related to HBV infection, which include the presence of: 1) hepatitis B surface antigen (HBsAg), 2) antibody to hepatitis B core antigen (anti-HBc), 3) antibody to the surface antigen (anti-HBs), 4) chronic liver disease, 5) elevated alpha-fetoprotein, and 6) PHC. With the use of preliminary epidemiologic data, risk factors related to these events were calculated. We suggested that the interactions between these events and HBV infection in parents be used to estimate the risk of PHC for an individual in this environment.

Adolescent↗
PubMed1976

Host responses to hepatitis-B infection in patients with primary hepatic carcinoma and their families. A case/control study in Senegal, West Africa.

A case/control study of patients with primary hepatic carcinoma (P.H.C.) and their families was carried out in Dakar, Senegal. 28 P.H.C. cases were matched by age,sex, and ethnic group with 28 controls. Serum was collected from cases, controls, parents (28 mothers, 27 fathers) of cases, parents of controls, 71 siblings of cases, and 58 siblings of controls. Assays of their sera for hepatitis-B surface antigen (HBsAg), antibody to HBsAg (anti-HBs) and antibody to hepatitis-B core antigen (anti-HBc) produced the following results. (1) Nearly all P.H.C. cases (97%) and controls (93%) had some evidence of infection with hepatitis-B virus (H.B.V.), but the cases were more likely to be anti-HBc(+) and less likely to be anti-HBs(+) than the controls. (2) Most of the mothers of the cases were HBsAg(+) (71%), whereas only 14% of the mothers of controls were HBsAg(+). Lover titres of anti-HBs were less common in the mothers of the cases. (3) None of 27 fathers of cases had detectable anti-HBs, but 13 (48%) of the fathers of controls were anti-HBs(+). (4) Siblings of the P.H.C. cases were more likely to have anti-HBs than either their sibs with P.H.C. or the sibs of the controls. However, sibs of P.H.C. cases had lower titres of anti-HBs than the sibs of the controls. These data are consistent with the hypothesis that the P.H.C. cases were infected with H.B.V. by their mothers and that there was an environmental factor which affected the immunological response of all family members to H.B.V. Infection with H.B.V. and the mode of response to that infection among members of families appear to be major factors in the aetiology of P.H.C. in West Africa.

Adult↗
PubMed1976

Study design for a hepatitis B vaccine trial.

A short-time trial of small sample size for an evaluation of the hepatitis B vaccine is proposed and designed. The vaccine is based on the premise that antibody to the surface antigen of the hepatitis B virus is protective against viral infection. This premise is verified by using the presence of the surface antigen as the marker of infection and comparing infection rates in renal dialysis patients who had naturally acquired antibody to patients without antibody. Patients with antibody have an extremely low risk of infection. The probability of remaining uninfected decreases at an exponential rate for patients without antibody, implying a constant risk of infection at any point in time. The study design described makes use of this time independence and the observed infection rates to formulate a clinical trial which can be accomplished with a relatively small number of patients. This design might be useful if, in preliminary studies, it is shown that the vaccine produces antibody in the patients and that protection against hepatitis B virus would be beneficial to the patients.

Antibodies, Viral↗