Modeling alloantibody formation to highincidence red blood cell antigens in immune responders using genotypic data  

Publications

Share / Export Citation / Email / Print / Text size:

Immunohematology

American National Red Cross

Subject: Medical Laboratory Technology

GET ALERTS SUBSCRIBE

ISSN: 0894-203X
eISSN: 1930-3955

DESCRIPTION

7
Reader(s)
14
Visit(s)
0
Comment(s)
0
Share(s)

SEARCH WITHIN CONTENT

FIND ARTICLE

Volume / Issue / page

Archive
Volume 37 (2021)
Volume 36 (2020)
Volume 35 (2019)
Volume 34 (2018)
Volume 33 (2017)
Volume 32 (2016)
Volume 31 (2015)
Volume 30 (2014)
Volume 29 (2013)
Volume 28 (2012)
Volume 27 (2011)
Volume 26 (2010)
Volume 25 (2009)
Volume 24 (2008)
Volume 23 (2007)
Volume 22 (2006)
Volume 21 (2005)
Volume 20 (2004)
Volume 19 (2003)
Volume 18 (2002)
Volume 17 (2001)
Volume 16 (2000)
Volume 15 (1999)
Volume 14 (1998)
Volume 13 (1997)
Volume 12 (1996)
Volume 11 (1995)
Volume 10 (1994)
Volume 9 (1993)
Volume 8 (1992)
Volume 7 (1991)
Volume 6 (1990)
Volume 5 (1989)
Volume 4 (1988)
Volume 3 (1987)
Related articles

VOLUME 33 , ISSUE 1 (March 2017) > List of articles

Modeling alloantibody formation to highincidence red blood cell antigens in immune responders using genotypic data  

Patricia A.R. Brunker * / Keerthana Ravindran / R. Sue Shirey

Keywords : alloimmunization, high-incidence antigen, genotyping, molecular

Citation Information : Immunohematology. Volume 33, Issue 1, Pages 9-14, DOI: https://doi.org/10.21307/immunohematology-2019-003

License : (Transfer of Copyright)

Published Online: 09-October-2019

ARTICLE

ABSTRACT

Alloimmunization to red blood cell antigens is unpredictable and poorly understood. Patients who are negative for highincidence antigens (HIAs) are at risk for developing the corresponding antibodies. Molecular methods can easily predict the lack of an antigen and thus, the risk of an individual to become immunized. We examined the prevalence and risk factors for HIA alloimmunization in patients at risk based on genotyping results. Genotyping using a molecular method (HEA BeadChip™, Immucor, Warren, NJ) was performed on all patient specimens referred for molecular testing over 45 months; serologic and clinical data were analyzed. We used simple and multiple logistic regression to model the risk factors for alloimmunization to an HIA. Of the 2591 patients genotyped, 32 (1.2%) were homozygous for at least one variant predicting absence of an HIA. Of these 32 patients, prior transfusion or pregnancy history was available for 29 (91%). Four susceptible patients made an antibody to an HIA (12.5% of all, 13.8% of those with a documented exposure). Two of these four patients (50%) had made an alloantibody to another antigen. The odds of forming an antibody to an HIA were not related to the total number of transfusions (p = 0.47), the total number of alloantibodies (p = 0.61), or diagnosis of sickle cell disease (p = 0.77) in simple logistic regression. Adjustment for the other two variables in a multiple logistic regression was also not significant for each variable (p = 0.6, p = 0.7, and p = 0.7, respectively). Although they had a known exposure to alloantigens through transfusion or pregnancy, 86.2 percent of patients (25 of 29) at risk for alloantibody formation to an HIA in fact did not mount an immune response to that antigen. Possible risk factors including the number of transfused units or the total number of alloantibodies made were not predictors of making an alloantibody to an HIA in our sampling. Our results suggest that other patient-specific risk factors for alloimmunization exist.

You don't have 'Full Text' access of this article.

Purchase Article Subscribe Journal Share