Absence Of Hb Research Articles

Detection of e Antigen and Antibody: Correlations With Hepatitis B Surface and Hepatitis B Core Antigens, Liver Disease, and Outcome in Hepatitis B Infections

Testing for e antigen and antibody (anti-e) was performed by immunodiffusion and counterelectrophoresis in patients with polyarteritis nodosa fulminant hepatitis, and chronic active hepatitis (CAH), in 59 asymptomatic carriers of hepatitis B surface antigen (HBsAg) who underwent liver biopsy, and in 150 carriers followed with sequential SGPT determinations. Counterelectrophoresis was more sensitive that immunodiffusion. Neither e antigen nor anti-e was found in the absence of HBsAg. Among HCsAg-positive patients with polyarteritis nodosa and CAH, e antigen was found in 16 of 18 and 13 of 22, respectively. It was not found in any of 43 patients with fulminant hepatitis, of whom 24 were HBsAg-positive. The e antigen was detected in none of 13 biopsied carriers with normal histology, 4 of 28 with nonspecific changes of 11 of 18 with CAH or chronic persistent hepatitis. Conversely, anti-e was present in 9 of 13 with normal biopsy, 7 of 28 with nonspecific changes, and none of 18 with CAH or chronic persistent hepatitis. The e antigen was found more commonly in nonbiopsied carriers with elevated SGPT, and anti-e in those with normal SGPT. Six carriers whose antigenemia terminated spontaneously had anti-e. The presence of e antigen correlated with a high titer of HBsAg, and with immunofluorescent detection of hepatitis B core antigen in the nuclei of hepatocytes. Conversely, anti-e was associated with significantly lower titers of serum HBsAg (P less than 0.001) and lack of detectable hepatitis B core antigen in the liver.

Hb a 2 glu�2 (Hb I) in a Caucasian family: Independent mutation or common origin?

Hemoglobin α16glu (Hb I-Skamania) was confirmed in six persons of a Caucasian family by amino acid analysis of the abnormal tryptic peptide, αT3,4. The confirmation of Hb α16glu in Caucasians and the apparent absence of Hb I in racially unmixed Negroes or in American Indians suggest that Hb α16gly may be of European origin. However, an independent European and African origin can currently not be ruled out. The origin of seven other rare hemoglobin mutants is also uncertain. Independent genetic origin of a rare mutant is confirmed only when a new mutation can be proved.

Brief Report: Absence of Hemoglobin A in a Double Heterozygote for F-Thalassemia and Hemoglobin S

Abstract An adult with minor hematologic abnormalities and hemoglobin electrophoretic pattern characterized by large amounts of hemoglobins S and F together with absent hemoglobin A, was shown to be doubly heterozygous for F-thalassemia and hemoglobin S. Absence of Hb A in this double heterozygote provides further evidence that in F-thalassemia the suppression of the β-chains in cis position is complete.