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"Selama kehamilan terjadi perubahan hormonal dan metabolik yang kompleks pada wanita hamil, yang dapat memperlihatkan gambaran klinik klasik mirip hipertiroid, sehingga diagnosis hipertiroid pada masa kehamilan menjadi lebih sulit. Perubahan hasil tes fungsi tiroid pada masa kehamilan lebih mempersulit lagi diagnosis tersebut, sehingga perlu dicari parameter yang relatif tidak dipengaruhi kehamilan. Diharapkan pemeriksaan kadar TSH dapat menggantikan parameter yang dipakai sekarang.Tujuan penelitian ini adalah mengetahui adakah perbedaan kadar TSH antara wanita hamil dengan wanita tidak hamil dan antara wanita hamil trimester II dengan trimester III. Selain itu untuk mendapatkan nilai rujukan kadar TSH pada wanita hamil.Dari bulan April sampai September 1990 di UPF Bagian Patologi Klinik FKUI- RSCM telah dilakukan pemeriksaan kadar TSH-IRMA terhadap 30 orang wanita usia subur dan 60 orang wanita hamil trimester II, pemeriksaan diulang kembali pada kehamilan trimester III.Kadar TSH-IRMA pada 30 orang wanita usia subur berkisar antara 0,4 - 3,1 mIU/l dengan nilai rata- rata 1,2 mIU/l. Kadar TSH-IRMA 60 orang wanita hamil trimester II berkisar antara 0,2 - 3,1 mIU/1 dengan nilai rata- rata 1,26 mIU/l. Nilai rujukan kadar TSH-IRMA wanita hamil trimester II adalah 0,29-3,73 mIU/1. Dan kadar TSH-IRMA pada 52 orang wanita hamil trimester III berkisar antara 0,2 - 3,3 mIU/1 dengan nilai rata- rata 1,17 mIU/l. Nilai rujukan kadar TSH-IRMA wanita hamil trimester III adalah 0,26-3,59mIU/1.Hasil uji distribusi dari ke 3 kelompok data dengan tes Anderson Darling didapat distribusi log Gaussian.Uji student's t test untuk membandingkan antara wanita usia subur sebagai kontrol dengan wanita hamil trimester II didapat kadar TSH-IRMA ke 2 kelompok tidak berbeda bermakna ( p=O,6955 ). Juga antara kontrol dengan trimester III dan antara trimester II dengan trimester III dengan p=0,7333 dan p=0,297.Uji korelasi antara trimester II dan trimester III dengan Pearson's r product moment correlation didapat adanya korelasi antara ke 2 kelompok dengan r=0,5783 dan persamaan garis regresi y = 0,6251x± O,38O3.Kesimpulan penelitian ini adalah kadar TSH wanita usia subur yang tidak hamil tidak berbeda dengan kadar TSH wanita hamil trimester II dan trimester III. Juga tidak terdapat perbedaan antara kadar TSH wanita hamil trimester II dengan trimester III.Disarankan untuk melakukan penelitian serupa dengan subjek yang lebih banyak termasuk wanita hamil trimester I untuk mendapatkan nilai rujukan yang lebih memenuhi syarat.Juga disarankan melakukan penelitian kadar TSH pada wanita hamil yang menderita hipo/ hipertiroid.

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During pregnancy, there are hormonal and metabolic changes, which can mimic the classical picture of hyperthyroid, so diagnosis of hyperthyroid during pregnancy is difficult. The changes of thyroid function test results make the diagnosis even more difficult. It is necessary to find a parameter which is relatively not influence by pregnancy.

The aims of this study are to evaluate the differences of TSH level between pregnant women with non pregnant women and between pregnant women trimester II with trimester III. Beside these, to get the reference range of TSH level in pregnant women.

From April to September 1990 in Department of Clinical Pathology, Dr Cipto Mangunkusumo Hospital/ University of Indonesia, 30 women in child bearing period and 60 pregnant women trimester II had been evaluated their TSH-IRMA level, this test had been repeated in pregnancy trimester III.

TSH-IRMA level in 30 women was between 0,4-3,1 mIU/1 (mean : 1,2 mIU/1). In 60 pregnant women trimester II TSH level was between 0,2 - 3,1 mIU/l (mean 1,28 mIU/1). The reference range was between 0,29 - 3,73 mIU/1. In 52 women trimester III TSH-IRMA level was between 0,2 - 3,3 mIU/1 (mean : 1,17 mIU/1). The reference range was between 0,28 - 3,59 mIU/l.

The data of these 3 groups with Anderson Darling's test were found to be log Gaussian distribution.

TSH-IRHA level of pregnant women trimester II and trimester Ill were not significantly different from control. (p = 0,6955 and p = 0,7333). Also between trimester II and trimester III with p = 0, 297.

There is a correlation between trimester II and trimester III' with r = 0,5783 and regression line Y = 0,6251X ± 0,3803.

In conclusions, TSH level in non pregnant woman, did not differ to pregnant women trimester II and trimester III. There was no difference between TSH level trimester II; and trimester III.

We suggest to make the same evaluation with more subject included pregnant women in trimester I for getting more acceptable reference range.

Also we suggest to evaluate TSH level in pregnant women who suffer hypo/ hyperthyroidism."

"Leukemia merupakan keganasan utama pada anak dan merupakan penyebab utama kematian karena kanker pada anak. Penelitian yang dilakukan di RSUPNCM melaporkan leukemia merupakan jenis keganasan paling sering yaitu 30-40% dari seluruh keganasan pada anak. Pemeriksaan sitologi cairan otak merupakan baku emas dalam menegakkan diagnosis leukemia meningeal, akan tetapi sensitivitasnya hanya 71%. Oleh sebab itu dicari metode yang lebih baik untuk menilai keterlibatan SSP pada leukemia akut yang tidak mahal dan memiliki sensitivitas baik. Sel blas dijumpai pada 8 (9,6%) dari 83 cairan otak yang berasal dari 58 pasien anak dengan L. CV pemeriksaan protein dengan pyrogallol red berkisar antara 2,5% sampai 7,5%. Difference (%) pemeriksaan protein dengan pyrogallol red adalah (-17,6 - 5,01%). Pemeriksaan protein dengan pyrogallol red dan asam sulfosalisilat 3% memberikan korelasi positif derajat sedang dengan r=0,52. Nilai median protein menggunakan pyrogallol red pada cairan otak dengan sel blas positif dan negatif adalah 23 mg/dL dan 15 mg/dL. Nilai rerata kadar beta 2 mikroglobulin cairan otak dengan sel blas positif dan negatif adalah 1,13 mg/L dan 0,95 mg/L. Jumlah leukosit cairan otak dengan sel blas positif dan negatif adalah 20 dan 10/μL. Pemeriksaan protein dengan pyrogallol red dan asam sulfosalisilat 3% memberikan korelasi positif derajat sedang. Ketelitian dan ketepatan pemeriksaan protein dengan metode ikat zat warna menggunakan reagen pyrogallol red cukup baik. Ketelitian pemeriksaan protein dengan metode turbidimetri dengan asam sulfosalisilat 3% cukup baik, sedangkan ketepatannya kurang baik. Kadar protein, kadar β2 mikroglobulin, dan jumlah leukosit pada cairan otak dengan sel blas mempunyai median atau rerata lebih tinggi dibanding cairan otak tanpa sel blas.

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Leukemia is the major cause of children malignancy and most common cause of death in children cancer. Studies conducted in Ciptomangunkusumo Hospital reported it as the most frequent malignancy in children, contributing 30-40% of all malignancies. Cytology of cerebrospinal fluid (CSF) is the gold standard for meningeal leukemia diagnosis, but its sensitivity was only 71%. Therefore, it is necessary to find a more sensitive and cheaper method to evaluate central nervous system involvement in acute leukemia.

Blasts were found in 8 of 83 CSF from 58 children with acute lymphoblastic leukemia. Protein examination with pyrogallol red had a CV of 2,5-7,5%. Difference (d) was -(17,6)-5,01% for pyrogallol red. Protein examination with 3% sulfosalicylic acid and pyrogallol red showed a positive moderate correlation (r = 0,52). Protein levels determined with pyrogallol red had a median of 23 mg/dL and 15 mg/dL. Mean β2 microglobulin levels in blast positive CSF and blast negative CSF were 1,13 mg/L and 0,95 mg/L respectively. Leukocyte count was 20 cells/μL for blast positive CSF and 10 cells/μL for blast negative CSF.

Protein tests using 3% sulfosalicylic acid and pyrogallol red had a moderate positive correlation. The one using pyrogallol red had good precision and accuracy. Precision of protein test using 3% sulfosalicylic acid was good, but the accuracy was not as good as pyrogallol red. Protein, β2 microglobulin level, and leukocyte count on blast positive CSF had a higher median or mean than blast negative CSF."

"Diabetes melitus (DM) merupakan ancaman serius bagi pembangunan kesehatan dan pertumbuhan ekonomi nasional serta merupakan penyebab penting timbulnya kecacatan dan kematian. Dari semua kasus DM, DM tipe 2 mencakup lebih dari 90% dari semua pasien diabetes. Nefropati diabetik dan retinopati diabetik merupakan komplikasi mikroangiopati pada DM tipe 2 yang paling ditakuti dan keduanya sering ditemukan bersamaan. Perkembangan lanjut dari keduanya menyebabkan gagal ginjal tahap akhir dan kebutaan. Tujuan dari penelitian ini adalah untuk mengetahui kadar albumin urin dalam membedakan retinopati diabetik dan non retinopati diabetik. Penelitian potong lintang ini terdiri dari 100 subyek yang terbagi atas kelompok retinopati diabetik 50 orang dan non retinopati diabetik 50 orang dari populasi DM tipe 2. Penderita didiagnosis DM tipe 2 oleh dokter Divisi Metabolik Endokrin Departemen Ilmu Penyakit Dalam Rumah Sakit Ciptomangunkusumo. Untuk retinopati diabetik dan non retinopati diabetik, diagnosis dilakukan dengan foto fundus pada pupil yang didilatasi oleh dokter Divisi Retina Departemen Ilmu Penyakit Mata Rumah Sakit Ciptomangunkusumo. Pada kedua kelompok dicatat data karakteristik subyek dan dilakukan pemeriksaan kadar albumin urin. Kadar albumin urin pada kelompok retinopati diabetik lebih tinggi secara bermakna dibandingkan pada kelompok non retinopati diabetik (303,41±11,14 mg/g kreatinin vs 28,14±4,90 mg/g kreatinin, p <0,001). Nilai cut-off kadar albumin urin untuk membedakan retinopati diabetik dan non retinopati diabetik adalah 118 mg/g kreatinin dengan sensitivitas 72%, spesifisitas 78%, nilai duga positif 77%, nilai duga negatif 74%, rasio kemungkinan positif 3,27 dan rasio kemungkinan negatif 0,36. Kami menyimpulkan pemeriksaan kadar albumin urin dapat dipakai untuk membedakan retinopati diabetik dan non retinopati diabetik.

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Diabetes mellitus (DM) is a worldwide public health concern as they impose enormous medical, economic and social costs on both patient and the health care system. Together they contribute to serious morbidity and mortality. Type 2 DM affects more than 90% of all DM cases. Diabetic nephropathy and diabetic retinopathy are the two most dreaded complications of diabetes and frequently found together. Progression of both is the leading cause of end-stage renal disease and blindness. The aim of this study is to investigate albumin urine level in distinguishing diabetic retinopathy and non-diabetic retinopathy.

This cross-sectional study consisted of 100 respondents, in which 50 of them were categorized as diabetic retinopathy and 50 as non-diabetic retinopathy. The patients were diagnosed with type 2 DM by a doctor from Endocrinology Metabolic Division of Internal Medicine Department at Ciptomangunkusumo Hospital. Meanwhile diabetic retinopathy and non-diabetic retinopathy were diagnosed by ophthalmologist from Retina Division of Eye Medicine Department at Ciptomangunkusumo Hospital. Baseline characteristics of both groups were recorded and the albumin urine level was measured.

The albumin urine level in diabetic retinopathy group was significantly higher than that in the non-diabetic retinopathy group (303,41±11,14 mg/g kreatinin vs 28,14±4,90 mg/g kreatinin, p <0,001). The albumin urine level cut-off value used to distinguish diabetic retinopathy and non-diabetic retinopathy was 118 mg/g creatinine with sensitivity of 72%, specificity of 78%, positive predictive value of 77%, , negative predictive value of 74%, positive likelihood ratio of 3,27, and negative likelihood ratio of 0,36.

We conclude that albumin urine level test can be utilized to distinguish diabetic retinopathy from non-diabetic retinopathy."

"Masalah resistensi antimikroba yang berkembang menyebabkan munculnya kuman panresisten, yang resisten terhadap semua antimikroba yang tersedia. Munculnya bakteri panresisten ini menggambarkan suatu titik akhir yang mengkhawatirkan karena tidak tersedia pilihan terapi antibiotik yang rasional. Peningkatan kejadian resistensi antibiotik disertai penurunan produksi antibiotik baru sehingga diperlukan evaluasi dari kombinasi antibiotik yang sudah ada. Fosfomisin adalah antibiotik lama yang tidak memiliki resistensi silang dengan golongan antibiotik lain sehingga berpotensi menimbulkan interaksi yang sinergis terhadap bakteri resisten. Penelitian ini bertujuan untuk mengetahui interaksi antibakteri in vitro kombinasi fosfomisin dan beberapa antibiotik lain, yaitu doripenem, moksifloksasin, kolistin dan amikasin terhadap kuman batang Gram negatif panresisten. Pada penelitian ini dilakukan uji kombinasi antibiotik menggunakan metode Etest terhadap 15 isolat kuman panresisten, yang terdiri dari Acinetobater baumanii (n=8), Pseudomonas aeruginosa (n=5) dan Klebsiella pneumoniae (n=2). Interaksi yang terjadi dinilai berdasarkan indeks Fractional Inhibitory Concentration (FIC), yaitu sinergi bila indeks FIC ≤ 0,5, indiferen bila indeks FIC 0,5 sampai 4, dan antagonis bila indeks FIC > 4. Isolat kuman berasal dari berbagai jenis spesimen yang diperiksakan di laboratorium otomasi RSUPNCM. Interaksi antibakteri in vitro yang terjadi terhadap isolat kuman A. baumanii, P. aeruginosa, dan K. pneumoniae panresisten, baik dengan kombinasi fosfomisin dan amikasin, fosfomisin dan doripenem, fosfomisin dan moksifloksasin, serta fosfomisin dan kolistin pada semua isolat bersifat indiferen (100%). Tidak ditemukan interaksi yang bersifat sinergi atau antagonis.

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The evolving problem of antimicrobial resistance in Pseudomonas aeruginosa, Acinetobacter baumannii and Klebsiella pneumoniae has led to the emergence of clinical isolates to pandrug-resistant (PDR) isolates, i.e. resistant to all available antibiotics.The emergence of pandrug-resistant (PDR) bacteria represents a worrying endpoint in the development of antimicrobial resistance. The increased incidence of antibiotic resistance accompanied by decreased production of new antibiotics required the evaluation of combinations of existing antibiotics.

The aim of this study to evaluate the in vitro antibacterial interaction of combination fosfomycin with doripenem, amikacin, colistin and moxifloxacin against PDR Gram negative bacteria. We evaluated antibiotic combinatinons against 15 panresistant clinical isolates, which consisted of Acinetobater baumanii (n=8), Pseudomonas aeruginosa (n=5) dan Klebsiella pneumoniae (n=2). The in vitro antibacterial interactions were evaluated by determination of fractional inhibitory concentration (FIC) index. Synergy was defined as FIC index ≤ 0,5, indiferen as FIC index 0,5 to 4, and antagonism as FIC index > 4. The isolates were collected at RSUPNCM hospital from various clinical specimens.

The in vitro antibacterial interaction against A. baumannii, P. aeruginosa, and K. pneumoniae panresistant isolates, either with the combination of fosfomycin and amikacin, fosfomycin and doripenem, fosfomycin and moxifloxacin, as well as fosfomycin and colistin showed indifferent to all isolates (100%). No interaction was found synergistic or antagonistic."

"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."

"Sepsis merupakan tantangan besar di dunia kedokteran. Terdapat banyak penelitian yang mencari penanda sepsis yang handal dan soluble Cluster of Differentiation-14 subtype (sCD14-ST) mulai banyak diteliti sebagai penanda sepsis. Kadar sCD14-ST meningkat secara bermakna di dalam sirkulasi pada fase awal inflamasi dan sepsis. Saat ini belum terdapat data mengenai apakah sCD14- ST dapat digunakan sebagai penanda prognostik sepsis. Tujuan penelitian ini dilakukan untuk mengetahui apakah sCD14-ST dapat digunakan sebagai penanda prognostik pada pasien sepsis yang datang di instalasi gawat darurat. Desain penelitian potong lintang, terdiri dari 65 pasien sepsis dibagi bedasarkan mortalitas 28 hari, yaitu 37 pasien hidup dan 28 pasien meninggal. Diagnosis sepsis berdasarkan modifikasi definisi sepsis oleh International Sepsis Definitions Conference 2001. Kadar sCD14-ST didapatkan menggunakan pemeriksaan dengan prinsip noncompetitive chemiluminescent enzyme immunoassay pada alat Pathfast. Pada kedua kelompok tersebut dicatat data karakteristik subyek dan dilakukan pemeriksaan sCD14-ST. Median kadar sCD14-ST pada pasien hidup adalah 618,00 pg/mL dengan rentang 349,50 - 1628 pg/mL dan median kadar sCD14-ST pada pasien yang meninggal adalah 1287,00 pg/mL dengan rentang 720,75 - 2738,00 pg/mL. Terdapat perbedaan bermakna kadar sCD14-ST pada kedua kelompok dengan nilai p 0,005. Ditentukan nilai cut-off sCD14-ST 677,00 pg/mL untuk menentukan prognosis pasien sepsis, dengan AUC 0,706 (IK 95% 0,582 - 0,831), sensitivitas 82,1%, dan spesifisitas 54,1%. Kurva Kapplan Meier berdasarkan nilai cut-off 677,00 pg/mL menunjukkan gambar yang memenuhi asumsi proporsional hazard dengan rasio hazard 3,794 (IK 95% 1,437 - 10,013), p 0,007. Kami menyimpulkan kadar sCD14-ST pasien sepsis dapat digunakan untuk memprediksi pasien yang meninggal dilihat dari mortalitas 28 hari, dengan nilai AUC sedang. Cut-off kadar sCD14-ST 677,00 pg/mL dapat digunakan sebagai cut-off dalam tatalaksana pasien sepsis.

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Sepsis is a major challenge in the medicine world. Many studies try to find

reliable sepsis marker and scientists start to explore soluble Cluster of Differentiation-14 subtype (sCD14-ST) as sepsis marker. Concentration of sCD14-ST significantly increases in circulation on early phase of inflammation and sepsis. Nowadays there is no data whether sCD14-ST can be used as prognostic marker of sepsis.

The objective of this study is to investigate the prognostic value of sCD14-ST in sepsis patients presenting at the emergency department. This was a cross-sectional study, from 65 sepsis patient grouped based on 28-day mortality, 37 patients are survivors and 28 patients are nonsurvivors. Sepsis diagnosis is made based on modified sepsis definition from International Sepsis Definitions Conference 2001. The concentration sCD14-ST was analysed using Pathfast analyzer with noncompetitive chemiluminescent enzyme immunoassay test method. Baseline characteristics of subjects were recorded and sCD14-ST concentration were measured in study subjects.

Median of sCD14-ST in the survivors group is 618,00 pg.mL with range of 349,50 - 1628,00 pg/mL and the median in the nonsurvivors group is 1287,00 pg/mL with range of 720,75 - 2738,00 pg/mL. The difference between the two groups is significant with p 0,005. sCD14-ST cut-off of 677,00 pg/mL is found with AUC 0,706 (CI 95% 0,582 - 0,831), sensitivity 82,1%, and specificity 54,1%. Kapplan Meier curve based on 677,00 pg/mL cut-off demonstrates that hazard proportion is fulfilled with hazard ratio 3,794 (CI 95% 1,437 - 10,013), p 0,007.

It is concluded that sCD14-ST concentration in sepsis patients can be used to predict nonsurvivors based on 28-day mortality, with moderate AUC. Cut-off sCD14-ST of 677,00 pg/mL can be used as cut-off for sepsis patient management."

"[ABSTRAKHuman Papilloma Virus (HPV) merupakan penyebab infeksi menular seksual yang paling sering di dunia. HPV genital berdasarkan potensi onkogeniknya terdiri dari low risk HPV (lr-HPV) dan high risk HPV (hr-HPV). Kondiloma akuminata merupakan penyakit menular seksual yang disebabkan oleh HPV dan memiliki angka morbiditas paling tinggi di seluruh dunia termasuk di RS Cipto Mangunkusumo. Sebagian besar kondiloma akuminata disebabkan oleh lr- HPV, tetapi dewasa ini diketahui terdapat proporsi infeksi hr-HPV yang cukup besar pada kondiloma akuminata. Infeksi hr-HPV pada kondiloma akuminata merupakan salah satu faktor risiko terjadinya keganasan anogenital. Penelitian ini bertujuan untuk mendapatkan proporsi hr- HPV serta HPV 16 dan 18 pada lesi kondiloma akuminata atipikal regio anogenital di RS dr. Cipto Mangunkusumo dengan metoda Real Time Polymerase Chain Reaction (PCR). Dilakukan pemeriksaan PCR terhadap 21 lesi kondiloma akuminata atipikal dari 20 subyek penelitian. Hasil pemeriksaan mendapatkan proporsi hr-HPV sebesar 42,9% (9 dari 21 lesi) serta proporsi HPV 16 dan 18 sebesar 23,8% (5 dari 21 lesi).

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ABSTRACTHuman papillomavirus (HPV) is the most common cause of sexually transmitted disease in the world. In accordance to its oncogenic property, genital HPV is known to be low risk HPV (lr-HPV) and high risk HPV (hr-HPV). Condyloma acuminata is a sexually transmitted disease caused by HPV and has a high morbidity worldwide including in Cipto Mangunkusumo National Hospital. Most of condyloma acuminata caused by lr-HPV, although recently findings revealed a high proportion of hr-HPV in condyloma acuminata. Infection of hr-HPV in condyloma acuminata is one of risk factor for anogenital malignancy. This study aimed to obtain the proportion of hr-HPV in atypical lesion of condyloma acuminata in anogenital region at Cipto Mangunkusumo National Hospital with Real Time Polymerase Chain Reaction (PCR). Real Time PCR was conducted on 21 atypical lesion from 20 subject. The proportion of hr-HPV from those lesions was 42,9% and HPV 16/18 was 23,8%. ;Human papillomavirus (HPV) is the most common cause of sexually transmitted disease in the world. In accordance to its oncogenic property, genital HPV is known to be low risk HPV (lr-HPV) and high risk HPV (hr-HPV). Condyloma acuminata is a sexually transmitted disease caused by HPV and has a high morbidity worldwide including in Cipto Mangunkusumo National Hospital. Most of condyloma acuminata caused by lr-HPV, although recently findings revealed a high proportion of hr-HPV in condyloma acuminata. Infection of hr-HPV in condyloma acuminata is one of risk factor for anogenital malignancy. This study aimed to obtain the proportion of hr-HPV in atypical lesion of condyloma acuminata in anogenital region at Cipto Mangunkusumo National Hospital with Real Time Polymerase Chain Reaction (PCR). Real Time PCR was conducted on 21 atypical lesion from 20 subject. The proportion of hr-HPV from those lesions was 42,9% and HPV 16/18 was 23,8%. , Human papillomavirus (HPV) is the most common cause of sexually transmitted disease in the world. In accordance to its oncogenic property, genital HPV is known to be low risk HPV (lr-HPV) and high risk HPV (hr-HPV). Condyloma acuminata is a sexually transmitted disease caused by HPV and has a high morbidity worldwide including in Cipto Mangunkusumo National Hospital. Most of condyloma acuminata caused by lr-HPV, although recently findings revealed a high proportion of hr-HPV in condyloma acuminata. Infection of hr-HPV in condyloma acuminata is one of risk factor for anogenital malignancy. This study aimed to obtain the proportion of hr-HPV in atypical lesion of condyloma acuminata in anogenital region at Cipto Mangunkusumo National Hospital with Real Time Polymerase Chain Reaction (PCR). Real Time PCR was conducted on 21 atypical lesion from 20 subject. The proportion of hr-HPV from those lesions was 42,9% and HPV 16/18 was 23,8%. ]"

"ABSTRAK Soluble CD14-ST presepsin merupakan penanda sepsis baru untuk diagnosis dan prognosis sepsis neonatorum. Kadar presepsin meningkat pada keadaan sepsis disebabkan oleh aktivitas protease di fagolisosom. Penelitian ini bertujuan untuk mengetahui manfaat pemeriksaan serial kadar presepsin sebagai penanda pemantauan respons terapi dan prognosis pada pasien SNAL secara bedside dengan menggunakan sampel darah kapiler. Desain penelitian kohort prospektif. Subjek penelitian terdiri dari 20 neonatus sehat dan 42 pasien SNAL. Pemeriksaan kadar presepsin dengan alat Pathfast pada hari ke-1, ke-3, dan ke-6 setelah diterapi. Kadar presepsin pada pasien SNAL 1104 pg/mL (608 ? 6225 pg/mL) lebih tinggi dibandingkan pada neonatus sehat 448 pg/mL (191 ? 513 pg/mL), nilai p 0,000. Pada pasien SNAL kelompok respons terapi kadar presepsin lebih rendah dibandingkan dengan kelompok non respons pada hari ke-3 dan ke-6 (p<0,05). Pada pasien SNAL kelompok non survivor kadar presepsin lebih tinggi dibandingkan dengan kelompok survivor hari ke-6 (p<0,05). Kadar presepsin berkorelasi positif dengan kadar CRP (r=0,488) dan jumlah leukosit (r=0,321). Nilai cut-off kadar presepsin hari ke-6 untuk penentuan prognosis 1365 pg/mL mempunyai AUC 0,789 (IK 95% 0,652 ? 0.926), sensitivitas 90.9%, dan spesifisitas 67,7%. Pemeriksaan presepsin hari ke-3 atau ke-6 secara bedside dengan darah kapiler bermanfaat untuk pemantauan terapi dan prognostik pasien SNAL.ABSTRACT Soluble CD14-ST presepsin as a new septic marker for diagnostic and prognostic of neonatal sepsis. Concentration of presepsin significantly increases in bacterial sepsis induced by phagolysosome protease activity. The objective of this study is to investigate the prognostic and monitoring value of presepsin in late onset neonatal sepsis (LOS) with serial capillary whole blood assay. This was prosphective cohort, from 20 healthy neonates and 42 LOS patient. The concentration of presepsin was analysed using Pathfast analyzer at 1st, 3rd & 6th day after therapy. Median of presepsin in LOS patient is 1104 pg/mL (608 ? 6225 pg/mL) significantly higher than healty neonates 448 pg/mL (191 ? 513 pg/mL), p value 0.000. Median of presepsin at 3rd & 6th day after therapy in LOS with therapeutic respons is significantly lower than LOS with no respons (p<0.05). Median of presepsin at 6th day after therapy in nonsurvivor is significantly higher than in survivor (p<0.05). There are positive correlation between presepsin and CRP (r=0.488) or leucocyte count (r=0.321). Cut-off presepsin at 6th day after therapy 1365 pg/mL is found with AUC 0.789 (CI 95% 0.652 ? 0.926), sensitivity 90.9%, dan spesificity 67.7%. Presepsin assay at 3rd or 6th day after therapy with capillary whole blood can be used to predict the prognostic and therapeutic respons in LOS patient.;Soluble CD14-ST presepsin as a new septic marker for diagnostic and prognostic of neonatal sepsis. Concentration of presepsin significantly increases in bacterial sepsis induced by phagolysosome protease activity. The objective of this study is to investigate the prognostic and monitoring value of presepsin in late onset neonatal sepsis (LOS) with serial capillary whole blood assay. This was prosphective cohort, from 20 healthy neonates and 42 LOS patient. The concentration of presepsin was analysed using Pathfast analyzer at 1st, 3rd & 6th day after therapy. Median of presepsin in LOS patient is 1104 pg/mL (608 ? 6225 pg/mL) significantly higher than healty neonates 448 pg/mL (191 ? 513 pg/mL), p value 0.000. Median of presepsin at 3rd & 6th day after therapy in LOS with therapeutic respons is significantly lower than LOS with no respons (p<0.05). Median of presepsin at 6th day after therapy in nonsurvivor is significantly higher than in survivor (p<0.05). There are positive correlation between presepsin and CRP (r=0.488) or leucocyte count (r=0.321). Cut-off presepsin at 6th day after therapy 1365 pg/mL is found with AUC 0.789 (CI 95% 0.652 ? 0.926), sensitivity 90.9%, dan spesificity 67.7%. Presepsin assay at 3rd or 6th day after therapy with capillary whole blood can be used to predict the prognostic and therapeutic respons in LOS patient.;Soluble CD14-ST presepsin as a new septic marker for diagnostic and prognostic of neonatal sepsis. Concentration of presepsin significantly increases in bacterial sepsis induced by phagolysosome protease activity. The objective of this study is to investigate the prognostic and monitoring value of presepsin in late onset neonatal sepsis (LOS) with serial capillary whole blood assay. This was prosphective cohort, from 20 healthy neonates and 42 LOS patient. The concentration of presepsin was analysed using Pathfast analyzer at 1st, 3rd & 6th day after therapy. Median of presepsin in LOS patient is 1104 pg/mL (608 ? 6225 pg/mL) significantly higher than healty neonates 448 pg/mL (191 ? 513 pg/mL), p value 0.000. Median of presepsin at 3rd & 6th day after therapy in LOS with therapeutic respons is significantly lower than LOS with no respons (p<0.05). Median of presepsin at 6th day after therapy in nonsurvivor is significantly higher than in survivor (p<0.05). There are positive correlation between presepsin and CRP (r=0.488) or leucocyte count (r=0.321). Cut-off presepsin at 6th day after therapy 1365 pg/mL is found with AUC 0.789 (CI 95% 0.652 ? 0.926), sensitivity 90.9%, dan spesificity 67.7%. Presepsin assay at 3rd or 6th day after therapy with capillary whole blood can be used to predict the prognostic and therapeutic respons in LOS patient.;Soluble CD14-ST presepsin as a new septic marker for diagnostic and prognostic of neonatal sepsis. Concentration of presepsin significantly increases in bacterial sepsis induced by phagolysosome protease activity. The objective of this study is to investigate the prognostic and monitoring value of presepsin in late onset neonatal sepsis (LOS) with serial capillary whole blood assay. This was prosphective cohort, from 20 healthy neonates and 42 LOS patient. The concentration of presepsin was analysed using Pathfast analyzer at 1st, 3rd & 6th day after therapy. Median of presepsin in LOS patient is 1104 pg/mL (608 ? 6225 pg/mL) significantly higher than healty neonates 448 pg/mL (191 ? 513 pg/mL), p value 0.000. Median of presepsin at 3rd & 6th day after therapy in LOS with therapeutic respons is significantly lower than LOS with no respons (p<0.05). Median of presepsin at 6th day after therapy in nonsurvivor is significantly higher than in survivor (p<0.05). There are positive correlation between presepsin and CRP (r=0.488) or leucocyte count (r=0.321). Cut-off presepsin at 6th day after therapy 1365 pg/mL is found with AUC 0.789 (CI 95% 0.652 ? 0.926), sensitivity 90.9%, dan spesificity 67.7%. Presepsin assay at 3rd or 6th day after therapy with capillary whole blood can be used to predict the prognostic and therapeutic respons in LOS patient."

"ABSTRAK Hipertensi merupakan kelainan yang umum dijumpai pada kehamilan.Sekitar 70% wanita hamil mengalami gestational hypertension dan preeklampsia.Disfungsi endotel pada preeklampsia menyebabkan permukaan endotel yangnontrombogenik menjadi trombogenik sehingga dapat terjadi aktivasi koagulasi.Preeklampsia meningkatkan keadaan hiperkoagulabel yang sudah ada padakehamilan normal. Gestational hypertension pada wanita hamil adalah hipertensiyang tidak memenuhi kriteria preeklampsia. Hampir setengah dari pasien dengangestational hypertension akan berkembang menjadi preeklampsia. Fibrinmonomer merupakan petanda aktivasi koagulasi yang digunakan pada keadaan pretrombotik oleh karena terbentuk terlebih dahulu pada keadaan hiperkoagulabel daripada D-dimer yang terbentuk setelah fibrinolisis. Tujuan penelitian adalahmendapatkan gambaran fibrin monomer pada gestational hypertension danpreeklampsia. Penelitian ini adalah penelitian potong lintang pada 30 wanitahamil gestational hypertension dan 30 wanita hamil preeklampsia yang dilakukanpada Oktober sampai November 2015. Pemeriksaan FM menggunakan reagenSTA-Liatest memakai koagulometer STA Compact Analyzer. Kadar fibrinmonomer pada gestational hypertension didapatkan mean 4,61 µg/mL denganstandar deviasi 0,86 µg/mL. Kadar fibrin monomer pada preeklampsia didapatkanmedian 10,5 µg/mL dengan mean 11.99 µg/mL dan rentang 6,12 ? 23,26 µg/mL.Didapatkan perbedaan bermakna kadar fibrin monomer pada gestationalhypertension dan preeklampsia dengan nilai p<0,001.ABSTRACT Hypertension is a common disorder in pregnancy. Approximately 70% ofpregnant women is gestational hypertension and preeclampsia. Endothelialdysfunction in preeclampsia causes the endothelial surface of the nonthrombogenicbe thrombogenic so it can activated coagulation. Preeclampsiaincrease hypercoagulability state in normal pregnancy. Gestational hypertension isa hypertension in pregnancy who do not meet the criteria of preeclampsia. Nearlyhalf of patients with gestational hypertension develop into preeclampsia. Fibrinmonomers are used for coagulation activation marker on the prethrombotic statetherefore formed before on hypercoagulability state hiperkoagulabel than D-dimerformed after fibrinolysis. The objective of this study is to gain description offibrin monomer levels and it was a cross-sectional study 30 pregnant women withgestational hypertension and 30 pregnant women with preeclampsia. The studywas conducted in October and November 2015. Examination of fibrin monomerusing the reagent STA-Liatest and analyzer STA Compact. Mean of fibrinmonomer in gestational hypertension was 4.61 µg/mL with standard deviationwas 0.86 µg/mL. Median of fibrin monomer in preeclampsia was 10.5 µg / mLwith range was 6.12 to 23.26 µg/mL. Fibrin monomer levels found significantdifferences in gestational hypertension and preeclampsia with p <0.001.;Hypertension is a common disorder in pregnancy. Approximately 70% ofpregnant women is gestational hypertension and preeclampsia. Endothelialdysfunction in preeclampsia causes the endothelial surface of the nonthrombogenicbe thrombogenic so it can activated coagulation. Preeclampsiaincrease hypercoagulability state in normal pregnancy. Gestational hypertension isa hypertension in pregnancy who do not meet the criteria of preeclampsia. Nearlyhalf of patients with gestational hypertension develop into preeclampsia. Fibrinmonomers are used for coagulation activation marker on the prethrombotic statetherefore formed before on hypercoagulability state hiperkoagulabel than D-dimerformed after fibrinolysis. The objective of this study is to gain description offibrin monomer levels and it was a cross-sectional study 30 pregnant women withgestational hypertension and 30 pregnant women with preeclampsia. The studywas conducted in October and November 2015. Examination of fibrin monomerusing the reagent STA-Liatest and analyzer STA Compact. Mean of fibrinmonomer in gestational hypertension was 4.61 µg/mL with standard deviationwas 0.86 µg/mL. Median of fibrin monomer in preeclampsia was 10.5 µg / mLwith range was 6.12 to 23.26 µg/mL. Fibrin monomer levels found significantdifferences in gestational hypertension and preeclampsia with p <0.001.;Hypertension is a common disorder in pregnancy. Approximately 70% ofpregnant women is gestational hypertension and preeclampsia. Endothelialdysfunction in preeclampsia causes the endothelial surface of the nonthrombogenicbe thrombogenic so it can activated coagulation. Preeclampsiaincrease hypercoagulability state in normal pregnancy. Gestational hypertension isa hypertension in pregnancy who do not meet the criteria of preeclampsia. Nearlyhalf of patients with gestational hypertension develop into preeclampsia. Fibrinmonomers are used for coagulation activation marker on the prethrombotic statetherefore formed before on hypercoagulability state hiperkoagulabel than D-dimerformed after fibrinolysis. The objective of this study is to gain description offibrin monomer levels and it was a cross-sectional study 30 pregnant women withgestational hypertension and 30 pregnant women with preeclampsia. The studywas conducted in October and November 2015. Examination of fibrin monomerusing the reagent STA-Liatest and analyzer STA Compact. Mean of fibrinmonomer in gestational hypertension was 4.61 µg/mL with standard deviationwas 0.86 µg/mL. Median of fibrin monomer in preeclampsia was 10.5 µg / mLwith range was 6.12 to 23.26 µg/mL. Fibrin monomer levels found significantdifferences in gestational hypertension and preeclampsia with p <0.001.;Hypertension is a common disorder in pregnancy. Approximately 70% ofpregnant women is gestational hypertension and preeclampsia. Endothelialdysfunction in preeclampsia causes the endothelial surface of the nonthrombogenicbe thrombogenic so it can activated coagulation. Preeclampsiaincrease hypercoagulability state in normal pregnancy. Gestational hypertension isa hypertension in pregnancy who do not meet the criteria of preeclampsia. Nearlyhalf of patients with gestational hypertension develop into preeclampsia. Fibrinmonomers are used for coagulation activation marker on the prethrombotic statetherefore formed before on hypercoagulability state hiperkoagulabel than D-dimerformed after fibrinolysis. The objective of this study is to gain description offibrin monomer levels and it was a cross-sectional study 30 pregnant women withgestational hypertension and 30 pregnant women with preeclampsia. The studywas conducted in October and November 2015. Examination of fibrin monomerusing the reagent STA-Liatest and analyzer STA Compact. Mean of fibrinmonomer in gestational hypertension was 4.61 µg/mL with standard deviationwas 0.86 µg/mL. Median of fibrin monomer in preeclampsia was 10.5 µg / mLwith range was 6.12 to 23.26 µg/mL. Fibrin monomer levels found significantdifferences in gestational hypertension and preeclampsia with p <0.001.;Hypertension is a common disorder in pregnancy. Approximately 70% ofpregnant women is gestational hypertension and preeclampsia. Endothelialdysfunction in preeclampsia causes the endothelial surface of the nonthrombogenicbe thrombogenic so it can activated coagulation. Preeclampsiaincrease hypercoagulability state in normal pregnancy. Gestational hypertension isa hypertension in pregnancy who do not meet the criteria of preeclampsia. Nearlyhalf of patients with gestational hypertension develop into preeclampsia. Fibrinmonomers are used for coagulation activation marker on the prethrombotic statetherefore formed before on hypercoagulability state hiperkoagulabel than D-dimerformed after fibrinolysis. The objective of this study is to gain description offibrin monomer levels and it was a cross-sectional study 30 pregnant women withgestational hypertension and 30 pregnant women with preeclampsia. The studywas conducted in October and November 2015. Examination of fibrin monomerusing the reagent STA-Liatest and analyzer STA Compact. Mean of fibrinmonomer in gestational hypertension was 4.61 µg/mL with standard deviationwas 0.86 µg/mL. Median of fibrin monomer in preeclampsia was 10.5 µg / mLwith range was 6.12 to 23.26 µg/mL. Fibrin monomer levels found significantdifferences in gestational hypertension and preeclampsia with p <0.001."

"ABSTRAK Diagnosis infark miokard akut ditegakkan apabila memenuhi 2 dari 3 kriteria, yaitu klinis, perubahan EKG, dan peningkatan kadar penanda biokimia jantung. Troponin merupakan penanda biokimia jantung yang spesifik untuk infark miokard, akan tetapi memiliki keterbatasan yaitu kurang sensitif apabila dilakukan pada fase awal karena troponin akan meningkat dalam darah setelah 4 -10 jam setelah infark miokard. Copeptin merupakan penanda stres endogen, yang dapat meningkat pada awal onset infark miokard akut, namun kurang spesifik. Penelitian tentang copeptin-us sebagai penanda biokimia jantung masih sedikit dan di Indonesia penelitian tentang copeptin-us sebagai penanda biokimia jantung belum pernah dilakukan.Penelitian ini mengikutsertakan 91 pasien tersangka sindrom koroner akut yang terbagi atas 15 (16,5%) NSTEMI, 43 (47,3%) UA, dan 33 (36,3%) non SKA. Diagnosis ditegakkan oleh dokter di IGD RS Jantung dan Pembuluh Darah Harapan Kita. Karakteristik pasien yang memenuhi kriteria inklusi dan eksklusi dicatat dan kemudian dilakukan pemeriksaan copeptin-us.Nilai rerata copeptin-us pada NSTEMI adalah 151,80 ± 130,03 pmol/L, median copeptin-us pada UA adalah 7,12(1,145 ? 62,23) pmol/L, dan rerata copeptin-us pada non SKA adalah 7,36 ± 4,17 pmol/L. Nilai cut off copeptin-us untuk membedakan NSTEMI dengan UA/non SKA adalah 13,97 pmol/L. Area under curve (AUC) kombinasi hs-cTnT saat masuk rumah sakit dengan copeptin-us adalah 0,941 (0,882 ? 1,00), hs-cTnT saat masuk rumah sakit 0,885 (0,790 ? 0,98), dan AUC hs-cTnT 3 jam kemudian adalah 0,925 (0,824 ? 1,00). Nilai median hs-cTnT saat masuk RS pada NSTEMI adalah 114(29-1102) pg/mL, pada UA adalah 16 (3-3352) pg/mL, dan pada non SKA adalah 6(3-366) pg/mL. Nilai median hs-cTnT 3 jam pada NSTEMI adalah 488 (81-18437) pg/mL, pada UA 14(3-2224) pg/mL, dan pada non SKA adalah 3(3-679) pg/mL. Kombinasi copeptin-us ≥ 13,97 pmol/L dan hs-cTnT ≥ 14 pg/mL dan untuk membedakan NSTEMI dengan UA/non SKA memberikan sensitivitas 100%, spesifisitas 90,78%, NPP 68,18%, dan NPN 100%.Uji diagnostik kombinasi copeptin-us dan hs-cTnT saat masuk RS lebih baik dibandingkan hs-cTnT saat masuk RS saja dan dapat digunakan untuk rule out NSTEMI.ABSTRACT Diagnosis of acute myocardial infarction is made when two of the followed criterias are met; clinical, ECG changes, and increased levels of cardiac biochemical markers. Troponin is a specific cardiac biochemical marker for myocardial infarction but has limitation. It is less sensitive when measured in the early phase, because troponin will increase in blood after 4 -10 hours post myocardial infarction. Copeptin is an endogenous stress marker, it level increases in the early onset of acute myocardial infarction but study on copeptin-us as cardiac biochemical marker are limited and in Indonesia there is no study on copeptin-us has been done.In this study 91 consecutive patients fulfilled the inclusion and exclusion criteria, consist of 15 (16,5%) NSTEMI, 43 (47,3%) unstable angina, and 33 (36,3%) non acute coronary syndrome. Diagnosis was made by the emergency physician at Harapan Kita cardiovascular centre. Characteristics of these subject were recorded and then the copeptin-us levels were measured.The mean value of copeptin-us in NSTEMI is 151,80 ± 130,03 pmol/L, median copeptin-us in UA is 7,12(1,145 ? 62,23) pmol/L, and the mean copeptin-us in non ACS is 7,36 ± 4,17 pmol/L. Cut off value of copeptin-us to distinguish NSTEMI from UA/non ACS is 13,97 pmol/L. Area under curve of the combination hs-cTnT on admission and copeptin-us is 0,941 (0,882 ? 1,00), hs-cTnT on admission is 0,885 (0,790 ? 0,98), and hs-cTnT 3 hours laters is 0,925 (0,824 ? 1,00). Median value hs-cTnT on admission in NSTEMI is 114(29-1102) pg/mL, in UA is 16 (3-3352) pg/mL, and in non ACS is 6(3-366) pg/mL. Median hs-cTnT 3 hours in NSTEMI is 488(81-18437) pg/mL, in UA is 14(3-2224) pg/mL, and in non ACS is 3(3-679) pg/mL. Combination of copeptin-us ≥ 13,97 pmol/L and hs-cTnT ≥14 pg/mL to distinguish NSTEMI from UA/non ACS has sensitivity 100%, specificity 90,78%, PPV 68,18%, and NPV 100%.The diagnostic value of combination on copeptin-us and hs-cTnT is better than only hs-cTnT on admission so that it can be used to rule out NSTEMI.;Diagnosis of acute myocardial infarction is made when two of the followed criterias are met; clinical, ECG changes, and increased levels of cardiac biochemical markers. Troponin is a specific cardiac biochemical marker for myocardial infarction but has limitation. It is less sensitive when measured in the early phase, because troponin will increase in blood after 4 -10 hours post myocardial infarction. Copeptin is an endogenous stress marker, it level increases in the early onset of acute myocardial infarction but study on copeptin-us as cardiac biochemical marker are limited and in Indonesia there is no study on copeptin-us has been done.In this study 91 consecutive patients fulfilled the inclusion and exclusion criteria, consist of 15 (16,5%) NSTEMI, 43 (47,3%) unstable angina, and 33 (36,3%) non acute coronary syndrome. Diagnosis was made by the emergency physician at Harapan Kita cardiovascular centre. Characteristics of these subject were recorded and then the copeptin-us levels were measured.The mean value of copeptin-us in NSTEMI is 151,80 ± 130,03 pmol/L, median copeptin-us in UA is 7,12(1,145 ? 62,23) pmol/L, and the mean copeptin-us in non ACS is 7,36 ± 4,17 pmol/L. Cut off value of copeptin-us to distinguish NSTEMI from UA/non ACS is 13,97 pmol/L. Area under curve of the combination hs-cTnT on admission and copeptin-us is 0,941 (0,882 ? 1,00), hs-cTnT on admission is 0,885 (0,790 ? 0,98), and hs-cTnT 3 hours laters is 0,925 (0,824 ? 1,00). Median value hs-cTnT on admission in NSTEMI is 114(29-1102) pg/mL, in UA is 16 (3-3352) pg/mL, and in non ACS is 6(3-366) pg/mL. Median hs-cTnT 3 hours in NSTEMI is 488(81-18437) pg/mL, in UA is 14(3-2224) pg/mL, and in non ACS is 3(3-679) pg/mL. Combination of copeptin-us ≥ 13,97 pmol/L and hs-cTnT ≥14 pg/mL to distinguish NSTEMI from UA/non ACS has sensitivity 100%, specificity 90,78%, PPV 68,18%, and NPV 100%.The diagnostic value of combination on copeptin-us and hs-cTnT is better than only hs-cTnT on admission so that it can be used to rule out NSTEMI.;Diagnosis of acute myocardial infarction is made when two of the followed criterias are met; clinical, ECG changes, and increased levels of cardiac biochemical markers. Troponin is a specific cardiac biochemical marker for myocardial infarction but has limitation. It is less sensitive when measured in the early phase, because troponin will increase in blood after 4 -10 hours post myocardial infarction. Copeptin is an endogenous stress marker, it level increases in the early onset of acute myocardial infarction but study on copeptin-us as cardiac biochemical marker are limited and in Indonesia there is no study on copeptin-us has been done.In this study 91 consecutive patients fulfilled the inclusion and exclusion criteria, consist of 15 (16,5%) NSTEMI, 43 (47,3%) unstable angina, and 33 (36,3%) non acute coronary syndrome. Diagnosis was made by the emergency physician at Harapan Kita cardiovascular centre. Characteristics of these subject were recorded and then the copeptin-us levels were measured.The mean value of copeptin-us in NSTEMI is 151,80 ± 130,03 pmol/L, median copeptin-us in UA is 7,12(1,145 ? 62,23) pmol/L, and the mean copeptin-us in non ACS is 7,36 ± 4,17 pmol/L. Cut off value of copeptin-us to distinguish NSTEMI from UA/non ACS is 13,97 pmol/L. Area under curve of the combination hs-cTnT on admission and copeptin-us is 0,941 (0,882 ? 1,00), hs-cTnT on admission is 0,885 (0,790 ? 0,98), and hs-cTnT 3 hours laters is 0,925 (0,824 ? 1,00). Median value hs-cTnT on admission in NSTEMI is 114(29-1102) pg/mL, in UA is 16 (3-3352) pg/mL, and in non ACS is 6(3-366) pg/mL. Median hs-cTnT 3 hours in NSTEMI is 488(81-18437) pg/mL, in UA is 14(3-2224) pg/mL, and in non ACS is 3(3-679) pg/mL. Combination of copeptin-us ≥ 13,97 pmol/L and hs-cTnT ≥14 pg/mL to distinguish NSTEMI from UA/non ACS has sensitivity 100%, specificity 90,78%, PPV 68,18%, and NPV 100%.The diagnostic value of combination on copeptin-us and hs-cTnT is better than only hs-cTnT on admission so that it can be used to rule out NSTEMI."