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"Transfusi trombosit merupakan tindakan yang dapat menurunkan insiden komplikasi hemoragik pada pasien anemia aplastik. Pasien anemia aplastik memiliki risiko terhadap PTR. PTR dapat terjadi akibat adanya inkompatibilitas transfusi trombosit oleh HPA 1-6 dan 15. Frekuensi alel a dan b pada HPA-3 dan HPA-15 memiliki jumlah yang hampir sama besar, sehingga kedua alel tersebut kemungkinan besar berperan dalam kasus aloimunisasi. Pelayanan transfusi trombosit di Indonesia belum memperhatikan kompatibilitas HPA antara donor dan resipien. Penelitian ini dilakukan untuk menganalisis genotipe HPA-1 hingga HPA-6 dan HPA-15 serta antibodi anti-HPA-3 dan HPA-15 pasien anemia aplastik yang mendapat multitransfusi trombosit. Deteksi alloantibodi HPA dilakukan dengan metode whole platelet ELISA. Hasil positif, dilanjutkan dengan pemeriksaan antibodi anti-trombosit spesifik (anti-β2-mikroglobulin, anti GPIIb/IIIa, dan anti-CD109) dengan metode MAIPA. Genotyping HPA-1 hingga HPA-6 dan HPA-15 dilakukan dengan metode PCR-SSP. HPA-3 dan HPA-15 memiliki frekuensi dengan nilai hampir sama besar pada alel a dan b. Terdapat 17 sampel (58,6%) dari total 29 sampel memiliki antibodi anti trombosit. Dari 17 sampel tersebut, 7 sampel positif terhadap antibodi monoklonal β-2 mikroglobulin (HLA kelas I), 2 sampel positif terhadap antibodi monoklonal GP IIb/IIIa (HPA-3) dan 1 sampel positif terhadap antibodi monoklonal CD109 (HPA-15). Alloimunisasi telah terjadi pada sebagian besar pasien anemia aplastik. Oleh karena itu, pemeriksaan kecocokan antigen HLA kelas I, HPA-3 dan HPA-15 pada pasien anemia aplastik dengan transfusi trombosit berulang perlu dilakukan untuk mengurangi kemungkinan terjadinya aloimunisasi. ......Platelet transfusion is an act that can reduce the incidence of hemorrhagic complications in patients with aplastic anemia. Aplastic anemia patients have a risk to PTR. PTR can occur due to incompatibility of HPA1-6 and 15. The frequency of allele a and b on the HPA-3 and HPA-15 has a number that is almost as large, so that these two alleles are likely to play a role in the case alloimunization. Platelet transfusion service in Indonesia have not notice compatibility HPA alleles between donor and recipient. This study was conducted to analyze genotype HPA-1 to 6 and HPA-15 also HPA-3 and HPA-15 antibody in platelet transfusions in patients with aplastic anemia who received recurrent platelet transfusion. HPA alloantibody detection was conducted using whole patelet ELISA method. The positive results, followed by specific detection of anti platelet antibodies (anti-β2-microglobulin, anti GPIIb/IIIa, and anti-CD109) with MAIPA method. HPA-3 and HPA-15 have almost the same frequency with great value on the allele a and b. There are 17 samples (58,6%) from a total of 29 samples have anti-platelet antibodies. From the 17 samples, 7 samples positive for monoclonal antibody β-2 microglobulin (HLA Class I), 2 samples positive for monoclonal antibody GP IIb/IIIa (HPA-3) and 1 sample positive for monoclonal antibody CD109 (HPA-15). Alloimunization has occurred in the majority of patients with aplastic anemia. Therefore, compatibility checks of HLA class I, HPA-3 and HPA-15 in patiens with aplastic anemia with recurrent platelet transfusion needs to be done to reduce the occurrence of possible alloimunization."

"Latar Belakang: Inkompatibilitas human platelet antigen (HPA) fetomaternal terjadi karena keberadaan antigen pada membran trombosit yang diekspresikan oleh fetus, namun maternal tidak mengekspresikan antigen tersebut. Human platelet antigen yang tidak serasi antara fetus dan maternal dapat memicu respon imun pada masa kehamilan, dan menghasilkan aloantibodi anti-trombosit yang dapat menghancurkan trombosit fetus sehingga mengakibatkan terjadinya trombositopenia pada fetus dan neonatus yang dikenal sebagai fetal/ neonatal alloimmune thrombocytopenia (FNAIT). Deteksi HPA belum dilakukan di Indonesia, sehingga tidak diketahui antigen yang terdapat pada trombosit. Hal ini memungkinkan terjadinya kasus FNAIT dengan salah satu tanda yang dapat dikenali melalui gejala klinis pada neonatus yaitu neonatus mengalami trombositopenia. Tujuan: Mengetahui penyebab imun terjadinya trombositopenia pada neonatus sebagai salah satu upaya dalam memberikan tata laksana yang tepat dan optimal. Metode: Penelitian ini merupakan penelitian deskriptif observasional dengan desain penelitian potong lintang. Subyek pada penelitian ini adalah neonatus dengan trombositopenia sesuai kriteria penelitian. Sampel yang terkumpul dilakukan skrining dan hasil skrining yang menunjukkan keberadaan antibodi trombosit, kemudian dilakukan identifikasi antibodi anti-HPA-3.Hasil dan Diskusi: Hasil skrining pada 30 sampel didapatkan 3 neonatus positif antibodi trombosit, 2 borderline dan 25 negatif antibodi trombosit. Identifikasi antibodi anti-HPA-3 dilakukan pada lima sampel, menunjukkan ke lima sampel negatif terhadap antibodi anti-HPA-3. Skrining antibodi juga dilakukan pada 5 ibu neonatus yang terdeteksi antibodi trombosit dan ke lima nya negatif antibodi trombosit. Terdapat beberapa kemungkinan hasil negatif pada identifikasi antibodi anti-HPA, diantaranya antibodi anti-HPA yang spesifik terhadap glikoprotein lain di membran trombosit atau spesifik HPA lain. Diperlukan penelitian lebih lanjut dalam pembuktian kemungkinan tersebut. Simpulan: Berdasarkan hasil skrining ditemukan lima sampel terdapat antibodi anti-trombosit pada neonatus dengan trombositopenia, namun setelah dilakukan identifikasi pada lima sampel tidak satupun ditemukan antibodi anti-HPA-3. Hasil skrining kelima ibu negatif antibodi anti-trombosit, menunjukkan antibodi trombosit pada neonatus dengan trombositopenia bukan aloantibodi yang berasal dari ibu.......Background: Incompatibility human platelet antigen (HPA) fetomaternal occurs due to the presence of antigens on the platelet membrane expressed by the fetus, but maternal does not express these antigens. Human platelet antigen that is mismatched between the fetus and the maternal can trigger an immune response during pregnancy and produce anti-platelet alloantibodies that can destroy fetal platelets resulting in thrombocytopenia in the fetus and neonate, known as fetal/neonatal alloimmune thrombocytopenia (FNAIT). Human platelet antigen detection has not been carried out in Indonesia, so there is no known antigen on the platelets. This allows the occurrence of FNAIT cases with one of the signs that can be recognized through clinical symptoms in neonates, namely neonates experiencing thrombocytopenia. Aim: Knowing the causes of immunity to neonatal thrombocytopenia is one of the efforts to provide proper and optimal management.Methods: This research is descriptive observational study with a cross sectional design. The subject in this study were neonates with thrombocytopenia according to the study criteria. The collected sample is screened for the presence of platelet antibodies, then identification of anti-HPA-3 antibodies.Result: Screening in 30 samples showed that 3 neonates were positive for platelet antibodies, 2 borderline and 25 were negative for platelet antibodies. Anti-HPA-3 antibody identification was performed in five samples, indicating that all five samples were negative for anti-HPA-3 antibodies. There are several possible negative results on the identification of anti-HPA-3 antibodies, including anti-HPA antibodies that are specific to other glycoproteins on the platelet membrane or the present of platelet antibodies due to specific to other HPA. Further research is needed to prove this possibility.Conclution: Based on the screening result, five samples were found to have platelet antibodies in neonates with thrombocytopenia, after identification none of them were found to be specific anti-HPA-3 antibodies. Screening result of five maternal were negative platelet antibodies, it means platelet antibodies in neonates with thrombocytopenia are not alloantibodies of maternal origin."