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"ABSTRAKLatar belakang: Patomekanisme trombositopenia pada infeksi Dengue hingga saat ini masih belum jelas. Cheng dkk mendapatkan adanya mimikri molekul antara protein disulfida isomerase permukaan trombosit dengan protein NS1 virus Dengue, sehingga anti-NS1 mengenali PDI. Penelitian ini bertujuan untuk mengetahui adanya korelasi antara anti-NS1 dan anti-PDI permukaan trombosit sebagai salah satu mekanisme trombositopenia pada infeksi Dengue.Metode: Penelitian dengan disain potong lintang terhadap darah 19 pasien infeksi Dengue yang diambil pada demam hari ke 3, 5 dan 7. Jumlah trombosit dicatat, anti-NS1 dideteksi menggunakan metode ELISA phase padat, anti-PDI dideteksi menggunakan metode MAIPA direk, dan eksplorasi pengenalan antibodi serum pasien terhadap protein trombosit menggunakan western blot.Hasil: Didapatkan korelasi lemah antara OD anti-NS1 dengan jumlah trombosit. Pada analisis kinetika anti-NS1 dan anti PDI secara individual didapatkan pola yang bervariasi. Analisis pada 2 kelompok sampel didapatkan korelasi positif lemah yang kemudian menjadi korelasi negatif lemah pada demam hari ke5 dan ke7. Pada eksplorasi antibodi pada serum pasien ditemukan adanya kemungkinan pengenalan antibodi terhadap GPIIb, GPIIIa, dan ERp57.Kesimpulan: Terdapat korelasi negatif lemah antara OD anti-NS1 dan jumlah trombosit, ada korelasi positif lemah antara OD anti-NS1 dan anti-PDI trombosit, serta adanya kemungkinan pengenalan antibodi serum pasien terhadap GPIIb, GPIIa dan ERp57.

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ABSTRACT

Background: Patomechanism thrombocytopenia in Dengue infection still not clear. Cheng et all demonstrated molecular mimicry mechanism between PDI on platelet and region protein NS1-DV, so anti-NS1 recognize PDI on platelet and act like anti-PDI. In this study, we observed the correlation of anti-NS1 and anti-PDI on platelet as one of the mechanism of trombositopenia in Dengue infection

Materials and Method : We observed nineteen patients with Dengue infection by a cross sectional study. Patients blood were collected on day 3, 5 and 7 after the onset of fever. We collected data of platelet count, anti-NS1 were determined by using solid phase ELISA method, anti-PDI platelet were determined by using Direct MAIPA method, and the exploration of antibody activities in patient sera against PDI platelet were done using Western Blot method.

Result : There was no significant weak correlation between OD anti-NS1 and platelet count. In individually analysis of the kinetics of anti-NS1 and anti-PDI shows variation of patterns. Correlation analysis between 2 sampel group (>1x105/µl and ≤1x105/µl) we have weak correlation, but on 5th day after fever onset the correlation become weak negative correlation on 5th day and on 7th day after fever onset. Western blot analysis shows antibodies activity in patient serum that recognized GP IIb, GP IIIa, dan ERp 57, which is moleculer that content PDI.

Conclusion : We have weak negative correlation between OD anti-NS1 with platelet count that stronger in day 5th after the onset of fever. There was weak positive correlation between OD anti-NS1 and OD anti-PDI that the correlation change to negative correlation in day 5th after the onset of fever in IgG anti-Dengue positive (+) group. The recognize antibody in patient serum to GP IIb, GP IIIa, dan Erp 57, still not clear yet."

"ABSTRAKLatar belakang : Etiologi trombositopenia sangat beragam sehingga sulit untukdiidentifikasi. Sangat penting mengetahui penyebab terjadinya trombositopeniakarena berhubungan erat dengan rencana penatalaksanaan yang diberikan. Belumtersedia tes diagnostik sederhana, cepat dan mudah untuk mengetahui aktivitastrombopoiesis. Immature platelet merupakan trombosit muda yang berhubunganerat dengan aktivitas trombopoiesis. Diharapkan pengukuran persentase immatureplatelet dapat membedakan etiologi trombositopenia yang terjadi karenagangguan produksi megakariosit di sumsum tulang atau karena meningkatnyadestruksi di perifer sehingga dapat menghindari tindakan pemeriksaan aspirasisumsum tulang.Tujuan : Penelitian ini bertujuan menilai pemeriksaan IPF sebagai penandaaktivitas trombopoiesis pada pasien trombositopenia. Mendapatkan nilai rujukanparameter IPF pada orang dewasa normal di Jakarta menggunakan alat sel hitungotomatik Sysmex XE-5000. Mendapatkan nilai cutt-off IPF untuk membedakantrombositopenia yang disebabkan oleh gangguan produksi atau gangguandestruksi.Metode : Desain penelitian adalah potong lintang. Menggunakan 256 orangpeserta medical check up di RS MMC dan 203 pasien trombositopenia yangberasal dari RSCM dan RS MMC.Hasil : Nilai rujukan IPF orang dewasa di Jakarta menggunakan Sysmex XE-5000 sebesar 0.64-3.20%. Nilai cutt-off IPF untuk membedakan trombositopeniadengan aktifitas trombopoiesis meningkat atau trombositopenia dengan aktifitastrombopoiesis normal atau rendah sebesar 7.65% dengan sensitivitas 91% danspesifisitas 92%.Kesimpulan : Kami menyimpulkan bahwa IPF dapat dijadikan salah satupenanda aktivitas trombopoiesis pada pasien trombositopenia sehingga dapatmembedakan penyebab trombositopenia karena gangguan produksi trombosit disumsum tulang atau gangguan destruksi perifer.

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ABSTRACTBackground: It is difficult to identify the etiology of thrombocytopenia due to itsvarious types. A simple, fast and easy diagnostic test is not available yet toidentify thrombopoiesis activity. Immature Platelet Fraction is anevaluation/assessment of immature platelet, which represents the state ofthrombopoiesis. It is expected that the immature platelet measurement will be ableto distinguish the etiology of current thrombocytopenic caused by defectmegakaryocytic production in the bone marrow or by the increased peripheralplatelet destruction, thereby avoiding the need for bone marrow aspirationexamination.Aims: The IPF examination is a marker of thrombopoiesis activity on patientswith thrombocytopenia. This study was performed to establish reference rangeof IPF on healthy adults in Jakarta and its cut-off values to distinguishthrombocytopenia caused by production disturbance or destruction by usingSysmex XE-5000 automated hematology analyzer.Method: Cross-sectional study in thrombocytopenic patients. We have analyzedIPF in 256 people who undergo medical check-up at MMC Hospital and 203thrombocytopenia patients from RSCM and MMC Hospital.Results: The reference range of adult IPF was 0.64-3.20%. The IPF cut-off todistinguish thrombocytopenia caused by increasing thrombopoiesis activity orthrombocytopenia with normal or low thrombopoiesis activity was 7.65% and itssensitivity and specificity were 91% and 92% respectively.Conclusions: We conclude that IPF can be used as thrombopoiesis activitymarker in thrombocytopenic patients; hence, it can distinguish the cause ofthrombocytopenia caused by platelet production disorder in the bone marrow orperipheral destruction."

"[ABSTRAKLatar Belakang: Angka kejadian trombositopenia pada neonatus dilaporkan antara 22-35%, dan salah satu komplikasinya adalah perdarahan intraventrikular (PIV). Penelitian sebelumnya di Rumah Sakit Cipto Mangunkusumo (RSCM) Jakarta melaporkan angka kejadian PIV masih tinggi pada bayi usia gestasi < 35 minggu sebesar 43,47%. Perdarahan intraventrikular menyebabkan dampak yang berat pada perkembangan neurologis dan mortalitas. Di Indonesia, belum ada penelitian mengenai hubungan trombositopenia dan PIV. Tujuan: Mengetahui hubungan trombositopenia dengan PIV pada bayi usia gestasi < 35 minggu dan korelasi antara derajat berat trombositopenia dan derajat berat PIV. Metode: Penelitian potong lintang dengan penelusuran rekam medis dilakukan di Divisi Neonatologi Departemen Ilmu Kesehatan Anak Fakultas Kedokteran Universitas Indonesia RSCM pada subjek yang dirawat pada bulan Januari 2012 sampai Desember 2014 dengan diagnosis PIV. Subjek dibagi menjadi kelompok PIV ringan sedang (derajat ≤ 2) dan berat (derajat > 2). Nilai trombosit dicatat pada hari yang sama dengan diagnosis PIV. Digunakan uji Pearson?s chi-square, Fischer, analisis multivariat, dan korelasi untuk analisis data. Hasil: Angka kejadian PIV berat dengan trombosit < 100.000/uL sebesar 28,2% dibanding 10,4% pada nilai trombosit ≥ 100.000/uL (p=0,014). Berdasarkan analisis multivariat, faktor yang memiliki pengaruh terhadap terjadinya PIV berat adalah usia gestasi < 32 minggu dan penggunaan alat bantu napas berupa ventilator dan high frequency oscillatory ventilation (HFOV). Derajat berat trombositopenia tidak memiliki korelasi dengan derajat berat PIV (koefisien korelasi 0,21). Simpulan: Trombositopenia tidak memiliki peranan pada terjadinya PIV berat. Derajat berat trombositopenia tidak memiliki korelasi dengan derajat berat PIV.

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ABSTRACTBackground: The prevalence of thrombocytopenia in neonates ranges from 22 to 35%, and the complication could be intraventricular hemorrhage (IVH). The previous research in Cipto Mangunkusumo Hospital (RSCM) Jakarta reported high incidence of IVH until gestational age < 35 weeks which is 43,47%. Intraventricular hemorrhage has caused a significant defect to neurologic development and mortality. In Indonesia, there were no research about the relationsghip between thrombocytopenia and IVH. Objective: To study the relation between thrombocytopenia and IVH in a baby with gestational age < 35 weeks and the correlation between the severity of thrombocytopenia and the severity of IVH. Methods: A cross sectional study was performed by medical records review in Neonatology Division of Child Health Department University of Indonesia RSCM. The subject of this study is neonates who were hospitalized from January 2012 until December 2014 with IVH diagnosis. Subjects were divided into mild moderate IVH (grade ≤ 2) and severe IVH (grade > 2). Thrombocyte count was recorded in the same day with the diagnosis of IVH. Pearson?s chi-squared, Fischer's tests, multivariate analysis, and correlation were used to analyzed the data. Results: Risk of severe IVH was 28,2% in neonates with thrombocyte count < 100,000/uL versus 10,4% in neonates without (p=0.014). From multivariate analysis, gestational age < 32 weeks and the use of respiratory support (ventilator and high frequency oscillatory ventilation) played a significant role in severe IVH. The severity of thrombocytopenia has no correlation with the severity of IVH (correlation coefficient = 0,21). Conclusion: Thrombocytopenia doesn?t have a role in severe IVH based on multivariate anlysis. The severity of thrombocytopenia has no correlation with the severity of IVH., Background: The prevalence of thrombocytopenia in neonates ranges from 22 to 35%, and the complication could be intraventricular hemorrhage (IVH). The previous research in Cipto Mangunkusumo Hospital (RSCM) Jakarta reported high incidence of IVH until gestational age < 35 weeks which is 43,47%. Intraventricular hemorrhage has caused a significant defect to neurologic development and mortality. In Indonesia, there were no research about the relationsghip between thrombocytopenia and IVH. Objective: To study the relation between thrombocytopenia and IVH in a baby with gestational age < 35 weeks and the correlation between the severity of thrombocytopenia and the severity of IVH. Methods: A cross sectional study was performed by medical records review in Neonatology Division of Child Health Department University of Indonesia RSCM. The subject of this study is neonates who were hospitalized from January 2012 until December 2014 with IVH diagnosis. Subjects were divided into mild moderate IVH (grade ≤ 2) and severe IVH (grade > 2). Thrombocyte count was recorded in the same day with the diagnosis of IVH. Pearson’s chi-squared, Fischer’s tests, multivariate analysis, and correlation were used to analyzed the data. Results: Risk of severe IVH was 28,2% in neonates with thrombocyte count < 100,000/uL versus 10,4% in neonates without (p=0.014). From multivariate analysis, gestational age < 32 weeks and the use of respiratory support (ventilator and high frequency oscillatory ventilation) played a significant role in severe IVH. The severity of thrombocytopenia has no correlation with the severity of IVH (correlation coefficient = 0,21). Conclusion: Thrombocytopenia doesn’t have a role in severe IVH based on multivariate anlysis. The severity of thrombocytopenia has no correlation with the severity of IVH.]"

"Latar Belakang: Risiko perdarahan tidak berkorelasi linear dengan jumlah trombosit pada kondisi trombositopenia. Terdapat perbedaan fungsi trombosit pada trombositopenia gangguan produksi dengan destruksi perifer. Pada trombositopenia, hasil fungsi agregasi trombosit dengan light transmission aggregometry tidak valid. Diperlukan pemeriksaan fungsi trombosit yang dapat dikerjakan pada kondisi trombositopenia.Tujuan: Mengkaji fungsi agregasi trombosit pada pasien trombositopeniaMetode: Studi potong lintang terhadap 60 pasien trombositopenia gangguan produksi dan destruksi perifer di Rumah Sakit Cipto Mangunkusumo selama Desember 2023 sampai April 2024. Dilakukan pemeriksaan jumlah trombosit, IPF, dan fungsi agregasi trombosit.Hasil: Terdapat perbedaan fungsi agregasi antara trombositopenia gangguan produksi dengan destruksi perifer (40% vs 77,7%). Didapatkan perbedaan nilai IPF antara trombositopenia gangguan produksi dengan destruksi perifer (5,65% vs 21%). Tidak didapatkan korelasi antara jumlah trombosit dengan fungsi agregasi trombosit pada trombositopenia gangguan produksi maupun destruksi perifer (r=0,214, p=0,231; r=0,364 p=0,062). Tidak didapatkan korelasi antara jumlah trombosit dengan fungsi agregasi trombosit pada trombositopenia gangguan produksi maupun destruksi perifer. Didapatkan titik potong IPF 10,25% untuk membedakan trombositopenia gangguan produksi dan destruksi perifer dengan sensitivitas 80,8% dan spesifisitas 68%.Kesimpulan: Fungsi agregasi trombosit pada trombositopenia destruksi perifer lebih baik daripada trombositopenia gangguan produksi. Fungsi agregasi trombosit tidak berkorelasi dengan jumlah trombosit maupun dengan IPF.

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Background: The risk of bleeding does not linearly correlate with platelet count in thrombocytopenia.There is difference between platelet function in central and peripheral thrombocytopenia. Platelet aggregation function assay performed by light transmission aggregometry is not valid in thrombocytopenia. Platelet aggregation assay that can be performed in thrombocytopenia is needed.

Objective: To assess platelet function in thrombocytopenia patients.

Methods: A cross-sectional study was conducted on 60 thrombocytopenic patients at Cipto Mangunkusumo Hospital from December 2023 to April 2024. Platelet count and immature platelet fraction (IPF) were done by automatic blood cell counter while platelet aggregation by Plateletworks ADP Kit

Results: There was a difference in platelet aggregation function between central thrombocytopenia and peripheral thrombocytopenia (40% vs 77.7%). A difference in IPF values was found between central thrombocytopenia and peripheral thrombocytopenia (5.65% vs. 21%). No correlation between platelet count and platelet aggregation function in thrombocytopenia (r=0.214, p=0.231 vs. r=0.364, p=0.062). No correlation was found between IPF and platelet aggregation function (r=-0.139, p=0.498 vs. r=-0.282, p=0.171). The cut-off value of IPF was 10.25% to distinguish central and peripheral thrombocytopenia.

Conclusion: Platelet aggregation function in peripheral thrombocytopenia was better than central thrombocytopenia. Platelet aggregation function did not correlate neither platelet count nor IPF."

"Trombositopenia merupakan manifestasi hematologis pada pasien lupus eritematosus sistemik (LES) yang berhubungan dengan prognosis buruk. Kadar C3, C4, dan anti-dsDNA berhubungan dengan aktivitas penyakit pada pasien LES. Peningkatan aktivitas penyakit berhubungan dengan penurunan kadar trombosit pada pasien LES melalui aktivasi komplemen dan interaksi autoantibodi dengan trombosit. Tujuan dari penelitian ini adalah mengetahui korelasi kadar serum C3, C4, dan anti-dsDNA terhadap hitung trombosit pada pasien LES dengan trombositopenia. Penelitian ini merupakan penelitian analitik observasional dengan menggunakan desain studi potong lintang. Penelitian ini merekrut subjek LES dengan hitung trombosit <150.000/µL. Kadar C3, C4, dan anti-dsDNA serta hitung trombosit diukur pada awal kunjungan pasien. Didapatkan 41 subjek LES dengan trombositopenia. Hitung trombosit memiliki korelasi yang bermakna terhadap kadar C3 (p=0.004; r=0.445) dan anti-dsDNA (p=0.001; r=-0.481). Namun, tidak ditemukan korelasi yang signifikan antara hitung trombosit dengan kadar C4 (p=0.052; r=0.306). Terdapat korelasi yang bermakna antara hitung trombosit dengan aktivitas penyakit dan kadar C3 serta anti-dsDNA pada subjek LES dengan trombositopenia. Namun, tidak terdapat korelasi yang bermakna antara hitung trombosit dengan kadar C4.

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Thrombocytopenia is a hematological manifestation in systemic lupus erythematosus (SLE) patients that is associated with a poor prognosis. C3, C4, and anti-dsDNA levels have been associated with disease activity in SLE patients. Increased disease activity is associated with decreased platelet levels in SLE patients through complement activation and autoantibody interactions with platelets. The aim of this study was to determine the correlation of serum levels of C3, C4, and anti-dsDNA with platelet counts in SLE patients with thrombocytopenia. This research is an observational analytical study using a cross-sectional study design. This study recruited subjects of SLE patients with platelet counts <150,000/µL. C3, C4, and anti-dsDNA levels and platelet counts were measured at the initial patient visit. This study recruit 41 samples of SLE patients with thrombocytopenia. Platelet count had a significant correlation with C3 levels (p=0.004; r=0.445) and anti-dsDNA (p=0.001; r=-0.481). However, no significant correlation was found between platelet count and C4 levels (p=0.052; r=0.306). There is  a significant correlation between platelet count and disease activity and C3 and anti-dsDNA levels in SLE patients with thrombocytopenia. However, there was no significant correlation between platelet count and C4 levels."

"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.

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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."

"Latar belakang. Transfusi trombosit ditujukan untuk mencegah dan mengatasi perdarahan pada pasien trombositopenia. Trombosit dapat mengalami aktivasi walaupun tidak terjadi perdarahan sehingga dapat menimbulkan suatu keadaan yang disebut hiperagregasi seperti pada trombosit dari seseorang dengan hiperlipidemia. AABB menganjurkan untuk membuang semua produk darah yang berasal dari donor dengan plasma yang lipemia. Penelitian ini bertujuan untuk mengetahui pengaruh status lipid donor trombosit aferesis terhadap fungsi trombosit dan kadar malondialdehid selama penyimpanan. Metodologi. Penelitian ini menggunakan desain deskriptif analitik pada 31 sediaan trombosit aferesis yang berasal dari donor trombosit aferesis yang memenuhi kriteria inklusi dan eksklusi. Sediaan trombosit aferesis dibagi menjadi dua grup, yaitu grup hiperlipidemia dan normolipidemia. Dilakukan pengujian terhadap kandungan trombosit, fungsi agregasi dan kadar MDA pada hari pertama, kedua dan keempat penyimpanan. Hasil. Terjadi peningkatan kandungan trombosit selama penyimpanan pada kedua grup, yang berhubungan dengan proses apoptosis. Pada hari keempat terjadi kenaikan kandungan trombosit yang lebih banyak pada grup hiperlipidemia. Pada hari kedua didapatkan perbedaan yang bermakna pada agregasi trombosit dengan agonis ADP 2 μM. Pada hari keempat didapatkan perbedaan kadar MDA yang bermakna. Didapatkan korelasi yang positif dan bermakna antara kolesterol total, LDL dan trigliserida terhadap kadar MDA. Tidak didapatkan korelasi yang bermakna antara kolesterol total, trigliserida dan kadar MDA terhadap agregasi trombosit. Simpulan. Status lipid donor meningkatkan terjadinya apoptosis trombosit aferesis, lebih sensitif terhadap agonis ADP dan peningkatan kadar MDA. Perlunya mengingatkan donor trombosit aferesis untuk diet rendah lemak sebelum proses aferesis dilaksanakan. Perlunya penelitian lebih lanjut untuk menentukan kadar lipid yang masih dapat ditoleransi.

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Background. Platelet transfusions is intended to prevent and resolve bleeding in patients with thrombocytopenia. Platelet activation may have occured although there were no bleeding that can lead to a condition called hyperaggregation as in someone with hyperlipidemia. AABB recommends to dispose of all products from donors with plasma lipemia. This study aimed to determine the effect of lipid status of the donor platelet apheresis to platelet function and levels of malondialdehyde with in storage.

Methodology. This study used descriptive analytic design in 31 platelet apheresis concentrates. Samples were divided into two groups, hyperlipidemia and normolipidemia. The assay for the content of platelets, aggregation functions and levels of MDA was tested on the first day, second and fourth of platelet storage.

Results. An increase in the content of platelets during storage in both groups, which are associated with the process of apoptosis. On the fourth day there was higher of contents platelets in hyperlipidemic grup than normolipidemic grup. There were significant difference in platelet aggregation with ADP 2 μM at second day and levels of MDA at fourth day. There were positive and significant correlations between total cholesterol, LDL and triglyceride to the levels of MDA. There were no significant correlation between total cholesterol, triglycerides and MDA levels to platelet aggregation.

Conclusion. Improved of the lipid status of the donor platelet apheresis will increase platelet apoptosis, more sensitive to agonist ADP and increase MDA levels. The need to remind donors platelet apheresis to a low fat dietary before apheresis process implemented. Need for further research to determine the lipid levels that can still be tolerated."

"Heparin-induced thrombocytopenia (HIT) adalah salah satu efek samping penggunaan heparin, yang dicurigai bila terdapat penurunan trombosit ≥50% pada hari ke-5 sampai ke-10 pascaheparinisasi dan dapat disertai komplikasi tromboemboli. Mekanisme HIT melibatkan pembentukan antibodi terhadap kompleks PF4-heparin (anti-PF4). Pemeriksaan diagnostik HIT terdiri dari uji fungsional dan immunoassay. Pemeriksaan immunoassay, yang mendeteksi anti- PF4 dengan metode ELISA memiliki sensitivitas tinggi dan paling sering digunakan untuk deteksi HIT. Angka kejadian HIT sangat bervariasi karena banyak faktor yang mempengaruhi. Tujuan penelitian ini adalah untuk mengetahui proporsi kejadian HIT dan proporsi pasien yang memiliki anti-PF4 pada pemberian terapi heparin di RSCM. Penelitian ini melibatkan 120 pasien rawat inap yang mendapat drip heparin atas indikasi profilaksis atau pengobatan, dengan dosis minimal 10.000 U/24 jam. Pasien yang memenuhi kriteria masukan dan tolakan dilakukan pencatatan data usia, jenis kelamin, diagnosis klinis, riwayat pemakaian heparin 3 bulan terakhir, dan dosis heparin yang dipakai. Pada hari ke-7 dan ke-10 pascaheparinisasi (H7 dan H10) dilakukan pengambilan darah untuk pemeriksaan hitung trombosit dan anti-PF4. Diagnosis HIT didasarkan atas penurunan hitung trombosit ≥50% pada H7 atau H10 yang disertai adanya antibodi anti-PF4. Hasil uji ketelitian within-run dan uji ketepatan pemeriksaan anti-PF4 mendapatkan CV 7,73% dan penyimpangan (d) 2,5-17,4%. Pada 19 dari 120 subjek (15,8%) ditemukan anti-PF4, tetapi kejadian HIT tidak ditemukan. Berdasarkan klasifikasi risiko terjadinya HIT menurut American College of Chest Physician (ACCP), terdapat 46/120 subjek (38,3%) berisiko rendah, 65/120 subjek (54,2%) berisiko tinggi, 8/120 subjek (6,7%) berisiko sangat tinggi, dan 1 orang tidak terklasifikasi. Uji statistik menunjukkan tidak ada hubungan antara temuan anti-PF4 dengan penurunan trombosit ≥50% (p=0,588). Hal ini diduga karena kurangnya jumlah subjek penelitian yang diperlukan. Antibodi anti-PF4 lebih sering ditemukan pada subjek perempuan dan dengan riwayat heparinisasi. Proporsi ditemukannya anti-PF4 berturut-turut lebih banyak pada pasien pascabedah vaskular dan ortopedi, trombosis arteri dan vena, kemudian pasien medis yang mendapat profilaksis heparin. Tidak ada perbedaan bermakna proporsi anti-PF4 positif pada subjek dengan atau tanpa riwayat heparinisasi (p=0,293), perbedaan dosis heparin (p=0,141), dan populasi risiko HIT rendah, tinggi, dan sangat tinggi (p=0,662). Empat dari 19 subjek yang memiliki anti-PF4 positif mengalami penurunan trombosit 20-46% pada H7 dan H10.

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Heparin-induced thrombocytopenia (HIT) is an adverse effect of heparin, that suspected when platelet count fall ≥50% in 5 to 10 days following heparin initiation and may be accompanied with thromboembolic complications. Mechanism of HIT is mediated by the formation of PF4-heparin complex antibody. There are 2 kind of diagnostic test for HIT, functional assay and immunoassay. Immunoassays, that detect anti-PF4 antibody using ELISA method, have high sensitivity and considered the most frequent assay for detecting HIT. The incidence of HIT varies due to many factors.

The aim of this research is to find the proportion of HIT events and also the proportion of anti-PF4-heparin antibody positive in patients with full-dose heparin in Cipto Mangunkusumo hospital. One hundred and twenty participants, who were our hospital in-patients given heparin infusion with minimal dose of 10.000U/24 h for profilactic or treatment indication, participated in this research. Patients met the inclusion and exclusion criteria were noted for age, gender, clinical diagnosis, heparin exposure in the last 3 months, and heparin dose. On day 7 and 10 after heparin initiation, blood sample were collected for platelet count and anti-PF4 antibody assay. Diagnosis of HIT was based on platelet count fall ≥50% on day 7 or 10 after heparin initiation accompanied with anti-PF4 antibody in the circulation.

Within run precision and accuracy tests for anti-PF4 assay showed a CV of 7,73% and deviations of -2,5 – 17%. Nineteen of 120 subjects (15,8%) had anti-PF4 antibodies, but HIT was not found. Based on the risk classification of HIT from American College of Chest Physician (ACCP), 46 subjects (38,3%) categorized as low risk to HIT, 65 (54,2%) high risk, 8 (6,7%) very high risk, and 1 as unclassified. Statistics showed there was no significant relationship between anti-PF4 antibodies in the circulation with platelet count fall of ≥50% (p=0,588). This was probably due to inadequate sample size for this study. Anti-PF4 antibodies were detected more frequent in females and subjects with past heparin exposure.

The proportion of positive anti-PF4 antibodies were highest in postoperative vascular or orthopedic surgery patients, followed by arterial or venous thrombosis patients, then medical patients using profilactic dose of heparin. There were no significant difference of positive anti-PF4 antibodies in subjects with vs without past heparin exposure (p=0,293), in subjects using 10.000U/24h vs >10.000U/24h heparin dose (p=0,141), and in subjects with low vs high vs very high risk of HIT (p=0,662). Four of 19 subjects having anti-PF4 antibodies had platelet count fall 20-46% on day 7 and day 10."