Immunohematology and Genetic Testing (red cells, leukocytes and platelets)
Keán A. Thompson, BHSc (he/him/his)
Western Cape Blood Service
Worcester, Western Cape, South Africa
HDFN is a pregnancy related complication, whereby the red cells of fetus cross the placental barrier; resulting in alloimmunisation of primarily, but not limited to, Rhesus (Rh) antigens. It has symptoms of fetal red cell destruction for subsequent fetae, causing jaundice. Most commonly, HDFN results from the Rh antigen, which is entirely preventable if the Rh antigen status of the mother is known. However, in the case of CEK antigen phenotyping is not practiced at the Western Cape Blood Service (WCBS). Although, CEK antigen alloimmunisation for the most part, it can be prevented. The red blood cell products patients receive can be responsible for alloimmunisation, but many factors play a role.
The aim of this study was: To determine the rate of alloimmunisation of females of child bearing age; & Compare alloimmunisation rate among age groups.
Study
Design/Methods:
A retrospective descriptive study was performed. A list of all records from 2012 to 2022 was obtained from the IT department at the WCBS. Criteria included female patient with at least one record at WCBS, between the ages of 16 and 50 years old (y/o). The patients DOB, ABO and Rh group, antibody status was retrieved. Duplicate records and records not matching criteria were removed. Total and CDE or Kell antigen alloimmunisation rate was performed. Additionally, patients were divided among ages 16-25; 26-35; 36-50 and alloimmunisation rates were compared.
Results/Findings:
In total 41507 patient records were retrieved from the database. Of these patients, alloimmunised rate was 10% (n = 4151). Alloimmunisation rate for CDE or Kell antigens was 5.39% (n = 2239).
Among age groups, 16 to 25 [total: 0.31% (n = 129); CDEK: 0.10% (n = 43)], 26 to 35 [total: 2.75% (n = 1142); CDEK: 1.18% (n = 489)] & 36 to 50 [total: 6.94% (n = 2880); CDEK: 4.12% (n = 1709)]
The patient population mean ages was 39.15 (SD ± 7.35 y/o). The total alloimmunised population, 38.9 (SD ± 6.0 y/o).
Conclusions:
Upon comparing the alloimmunisation rate, 53.94% (n = 2239) of the total alloimmunised patients had antibodies to CDE or Kell antigens. Interestingly, in both the total and CDE or Kell alloimmunised group majority of the patients were between the ages of 26 and 50. Which could be a result of higher possibility of receiving blood products as they age or exposure to fetal antigens during placental rupture at child birth. A limitation of this study is lack of transfusion history comparison. Further studies could elucidate the potential likelihood of alloimmunisation source. Many western countries have adopted further antigen typing requirements on the female patients of child bearing age. However, in resource constricted areas, especially Africa, extended phenotyping may not be feasible.