Transfusion medicine (Oxford, England) · 2013
Human platelet-specific antigen frequencies in Indonesian population.
Клиническое исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Asmarinah, Dharma R, Ritchie N K, Rahayu S, Putricahya E, Santoso S
Аннотация
BACKGROUND: Alloantibodies against human platelet antigens (HPAs) are responsible for the development of alloimmune thrombocytopenia including platelet transfusion refractoriness (PTR) and neonatal alloimmune thrombocytopenia (NAIT). Therefore, transfusion of HPA-compatible platelets is of importance for the management of these diseases.
AIM: Determination of the allele frequency of the major HPA systems for Indonesian blood donors and the development of the first HPA-typed donor registry in Indonesia.
METHODS: DNA derived from 500 Indonesian healthy blood donors was genotyped for HPA-1 to HPA-6 and HPA-15 alleles by the use of polymerase chain reaction sequence-specific primer method.
RESULTS: The gene frequencies of the rare allelic variants HPA-1b, -2b, -3b, -4b, -5b, -6b and -15b were 0·023, 0·060, 0·493, 0·052, 0·032, 0·044 and 0·049, respectively. However, donors homozygous for the HPA-1b, -2b and -6b were not found in this cohort, indicating that the risks of alloimmunisation caused by incompatibility of these three HPA systems are extremely low. In contrast, alloimmunisation against HPA-3, -4, -5 and -15 systems is anticipated.
CONCLUSION: The development of an HPA-genotyped registry for donors homozygous for HPA-1b, -2b and -6b is desired for the optimum management of PTR patients and children with NAIT.
AIM: Determination of the allele frequency of the major HPA systems for Indonesian blood donors and the development of the first HPA-typed donor registry in Indonesia.
METHODS: DNA derived from 500 Indonesian healthy blood donors was genotyped for HPA-1 to HPA-6 and HPA-15 alleles by the use of polymerase chain reaction sequence-specific primer method.
RESULTS: The gene frequencies of the rare allelic variants HPA-1b, -2b, -3b, -4b, -5b, -6b and -15b were 0·023, 0·060, 0·493, 0·052, 0·032, 0·044 and 0·049, respectively. However, donors homozygous for the HPA-1b, -2b and -6b were not found in this cohort, indicating that the risks of alloimmunisation caused by incompatibility of these three HPA systems are extremely low. In contrast, alloimmunisation against HPA-3, -4, -5 and -15 systems is anticipated.
CONCLUSION: The development of an HPA-genotyped registry for donors homozygous for HPA-1b, -2b and -6b is desired for the optimum management of PTR patients and children with NAIT.