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"ABSTRAKLatar belakang: Karbamazepin KBZ merupakan obat terpilih untuk epilepsi fokaldan dapat digunakan juga untuk pengobatan nyeri neuropatik dan gangguan bipolar,namun dapat menyebabkan reaksi obat yang berat berupa sindrom Stevens-Johnson SSJ /nekrolisis epidermal toksik NET . Saat ini banyak penelitian yangmembuktikan terdapat hubungan antara HLA-B 1502 dengan SSJ/NET yangdisebabkan oleh KBZ pada orang Asia.Tujuan: Meneliti apakah HLA-B 1502 dapat dijadikan marker terjadinya SSJ/NETyang disebabkan oleh KBZ di Indonesia.Metode: Subjek penelitian direkrut dari poliklinik saraf RSUPN CiptoMangunkusumo Jakarta, RS Hasan Sadikin Bandung 2 kasus dan RSUP Prof RDKandou Manado 2 kasus pada Mei 2015 sampai dengan Desember 2016. Subjekdengan riwayat SSJ/NET yang disebabkan KBZ dan toleran KBZ dilakukanpemeriksaan typing HLA-B dengan metode sequence specific oligonucleotidesprobes, dibaca dengan Luminex 200 dan dianalisis dengan perangkat lunak HLAfushion4.0. Dipilih beberapa subjek SSJ/NET dengan HLA-B 1502 positif dannegatif dan toleran dengan HLA-B 1502 positif dan negatif. Subjek yang dipilih inidilakukan kultur PBMC dengan perlakuan penambahan KBZ dan tanpa perlakuanselama 24 dan 48 jam, kemudian diukur kadar granulisin, granzim B dan perforindalam medium kultur dengan metode ELISA, untuk melihat peranan HLA-B 1502dalam terjadinya SJS/NET.Hasil: Total subjek 67 orang, 14 kasus dan 53 toleran. Pada semua subjek dilakukantyping HLA-B, sedangkan kultur dan pemeriksaan kadar granulisin, granzim B danperforin dilakukan pada 17 subjek 6 SSJ/NET dengan HLA-B 1502 positif dan 3negatif; 5 toleran HLA-B 1502 positif dan 3 negatif HLA-B 1502 positifditemukan pada 8 kasus 57,14 dan 14 toleran 26,42 , dengan rasio prevalensi2,73 dan p= 0,0353. Terdapat kecenderungan lonjakan kadar granulisin padakelompok subjek dengan SSJ/NET dibandingkan kelompok toleran KBZ.Kesimpulan: HLA-B 1502 dapat digunakan sebagai marker pada SSJ/NET karenaKBZ.Kata Kunci: HLA-B 1502, KBZ, SJS/NET, Indonesia

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ABSTRACTBackground Carbamazepine CBZ is a drug of choice for focal epilepsy and canbe used for neuropatic pain and bipolar disorder, but it can also causes severe drugreaction in the form of Stevens Johnson Syndrome SJS toxic epidermal necrolysis TEN . Currently, there are many studies that prove the relationship between HLAB 1502and SJS TEN caused by CBZ in Asian ancestry.Objective To study whether HLA B 1502 can be used as marker for SJS TENcaused by CBZ in Indonesia.Method Subjects were recruited from neurology clinic RSUPN CiptoMangunkusumo, RS Hasan Sadikin Bandung two cases , and RSUP Prof. RDKandou Manado two cases , from May 2015 to December 2016. Subjectswith SJS TEN history caused by CBZ and CBZ tolerant went through HLA Btyping examination with sequence specific oligonucleotides probes method, readwith Luminex 200 and analyzed with HLA fusion 4.0 software. Some subjectswith SJS TEN with HLA B 1502 positive and negative, and tolerant subjects withHLA B 1502 positive and negative, were chosen. These subjects went throughPBMC culture with and without CBZ addition for 24 and 48 hours, then granulysin,granzyme B and perforin concentration in culture medium were measured usingELISA method to see the role of HLA B 1502 in SJS TEN occurrence.Result Total number of subjects were 67 with, 14 CBZ induced SJS NET cases and53 CBZ tolerants. All subjects went through HLA typing, while culture andgranulysin, granzyme B and perforin examination were conducted in 17 subjects 6with SJS TEN with HLA B 1502 positive and 3 negative 5 tolerant HLA B 1502positive and 3 negative . HLA B 1502 positive were found in 8 cases 57,14 and14 tolerant 26,42 , with prevalence ratio 2,73 p 0,035. There is a tendencyincreased of granulysin level in CBZ induced SSJ NET cases.Conclusion HLA B 1502 can be used as marker in SJS TEN induced by CBZ. "

"[ABSTRAK Latar belakang: Obat antiepilepsi (OAE), seperti asam valproat (valproic acid,VPA) dan karbamazepin (carbamazepin, CBZ) sering digunakan dalam jangka waktupanjang. Obat-obatan tersebut dapat mengganggu fungsi tubulus ginjal. N-acetylbeta-D-glucosaminidase(NAG) urin merupakan enzim yang dapat dipakai sebagaimarka fungsi tubulus sehingga diharapkan dapat mendeteksi jejas tubulus. Penelitianmengenai efek nefrotoksik VPA dan CBZ terhadap tubulus menggunakan penandaNAG urin ini belum pernah dilakukan di Indonesia.Tujuan: Mengukur indeks NAG (iNAG) urin pada anak epilepsi yang mendapatVPA dan atau CBZ jangka panjang untuk mendeteksi efek nefrotoksik kedua OAEtersebut pada tubulus ginjal.Metodologi: Penelitian ini menggunakan studi potong lintang yang dilakukan padaJanuari-Maret 2015. Subjek penelitian ini adalah 36 anak epilepsi dengan monoterapiVPA, 14 dengan monoterapi CBZ, 14 dengan kombinasi VPA dan CBZ, rentang usia3-16 tahun. Pada seluruh subjek dilakukan pemeriksaan kadar kreatinin urin dankadar NAG urin. Sebagai nilai acuan kadar NAG urin, dipilih 30 anak sehat denganusia yang disesuaikan dengan subjek penelitian. Untuk menghilangkan variabilitasharian, maka NAG urin dibagi dengan kreatinin urin, menjadi iNAG (satuan U/gkreatinin). Indeks NAG dikategorikan meningkat bila nilainya lebih dari rerata NAG+ 2 SD kelompok anak sehat.Hasil: Rerata iNAG urin pada kelompok anak sehat, monoterapi VPA, monoterapiCBZ dan kombinasi VPA dan CBZ berturut-turut adalah 3,01; 5,9; 4,07; 6,9. Tiapkelompok kasus memiliki rerata iNAG urin lebih tinggi dibandingkan anak sehat.Proporsi kenaikan iNAG urin ditemukan pada 11/ 36 anak dengan monoterapi VPA,2/14 pada kelompok monoterapi CBZ, dan 9/14 pada terapi kombinasi VPA danCBZ.Simpulan: Pemberian VPA jangka panjang dapat menyebabkan jejas pada tubulus ginjal dengan parameter kenaikan iNAG urin, dan jejas tubulus ini meningkat dengan pemakaian VPA dan CBZ secara kombinasi.ABSTRACT Background: Antiepileptic drugs such as valproic acid (VPA) and carbamazepine

(CBZ) are often used in the long term manner. These drugs may disrupt the function

of the kidney tubules. Urinary N-acetyl-beta-D-glucosaminidase (NAG) is an enzyme

that can be utilised as marker of tubular function and is therefore expected to be

useful in detecting kidney tubular injuries. There have been no studies conducted in

Indonesia on the nephrotoxic effect of VPA and CBZ to tubules using urinary NAG

as marker.

Objectives: To measure urinary NAG index (iNAG) in epileptic children with longterm

use of VPA and CBZ in order to detect their nephrotoxic effects on kidney

tubules.

Methods: This is a cross-sectional study performed on January to March 2015. The

subject includes 36 patients on VPA monotherapy, 14 patients on CBZ monotherapy,

and 14 patients on VPA-CBZ combination therapy with age ranging from 3 to 16

years old. Urine creatinine concentration and urinary NAG values of all the patients

are measured. Thirty age-adjusted healthy children are included in the study for NAG

value reference. To eliminate NAG diurnal variability, iNAG is calculated by

dividing urinary NAG value and urine creatinine concentration. Urinary iNAG values

that fall above the +2 standard deviations from the mean of healthy children are

considered elevated.

Results: Urinary iNAG values of the healthy children, VPA monotherapy, CBZ

monotherapy, and VPA-CBZ comination therapy groups are 3.01; 5.9; 4.07; 6.9 U/g

respectively. Each case group has higher urinary iNAG mean value than the control

group. Urinary iNAG urine increased proportion is found in 11/36 children on VPA

monotherapy, 2/14 children on CBZ monotherapy, and 9/14 children on VPA-CBZ

combination therapy.

Conclusions: Long-term VPA use may cause renal tubular injuries with increased urinary iNAG value as parameter. Tubular injury is increased with the use of VPA and CBZ in combination. ;Background: Antiepileptic drugs such as valproic acid (VPA) and carbamazepine

(CBZ) are often used in the long term manner. These drugs may disrupt the function

of the kidney tubules. Urinary N-acetyl-beta-D-glucosaminidase (NAG) is an enzyme

that can be utilised as marker of tubular function and is therefore expected to be

useful in detecting kidney tubular injuries. There have been no studies conducted in

Indonesia on the nephrotoxic effect of VPA and CBZ to tubules using urinary NAG

as marker.

Objectives: To measure urinary NAG index (iNAG) in epileptic children with longterm

use of VPA and CBZ in order to detect their nephrotoxic effects on kidney

tubules.

Methods: This is a cross-sectional study performed on January to March 2015. The

subject includes 36 patients on VPA monotherapy, 14 patients on CBZ monotherapy,

and 14 patients on VPA-CBZ combination therapy with age ranging from 3 to 16

years old. Urine creatinine concentration and urinary NAG values of all the patients

are measured. Thirty age-adjusted healthy children are included in the study for NAG

value reference. To eliminate NAG diurnal variability, iNAG is calculated by

dividing urinary NAG value and urine creatinine concentration. Urinary iNAG values

that fall above the +2 standard deviations from the mean of healthy children are

considered elevated.

Results: Urinary iNAG values of the healthy children, VPA monotherapy, CBZ

monotherapy, and VPA-CBZ comination therapy groups are 3.01; 5.9; 4.07; 6.9 U/g

respectively. Each case group has higher urinary iNAG mean value than the control

group. Urinary iNAG urine increased proportion is found in 11/36 children on VPA

monotherapy, 2/14 children on CBZ monotherapy, and 9/14 children on VPA-CBZ

combination therapy.

Conclusions: Long-term VPA use may cause renal tubular injuries with increased urinary iNAG value as parameter. Tubular injury is increased with the use of VPA and CBZ in combination. , Background: Antiepileptic drugs such as valproic acid (VPA) and carbamazepine

(CBZ) are often used in the long term manner. These drugs may disrupt the function

of the kidney tubules. Urinary N-acetyl-beta-D-glucosaminidase (NAG) is an enzyme

that can be utilised as marker of tubular function and is therefore expected to be

useful in detecting kidney tubular injuries. There have been no studies conducted in

Indonesia on the nephrotoxic effect of VPA and CBZ to tubules using urinary NAG

as marker.

Objectives: To measure urinary NAG index (iNAG) in epileptic children with longterm

use of VPA and CBZ in order to detect their nephrotoxic effects on kidney

tubules.

Methods: This is a cross-sectional study performed on January to March 2015. The

subject includes 36 patients on VPA monotherapy, 14 patients on CBZ monotherapy,

and 14 patients on VPA-CBZ combination therapy with age ranging from 3 to 16

years old. Urine creatinine concentration and urinary NAG values of all the patients

are measured. Thirty age-adjusted healthy children are included in the study for NAG

value reference. To eliminate NAG diurnal variability, iNAG is calculated by

dividing urinary NAG value and urine creatinine concentration. Urinary iNAG values

that fall above the +2 standard deviations from the mean of healthy children are

considered elevated.

Results: Urinary iNAG values of the healthy children, VPA monotherapy, CBZ

monotherapy, and VPA-CBZ comination therapy groups are 3.01; 5.9; 4.07; 6.9 U/g

respectively. Each case group has higher urinary iNAG mean value than the control

group. Urinary iNAG urine increased proportion is found in 11/36 children on VPA

monotherapy, 2/14 children on CBZ monotherapy, and 9/14 children on VPA-CBZ

combination therapy.

Conclusions: Long-term VPA use may cause renal tubular injuries with increased urinary iNAG value as parameter. Tubular injury is increased with the use of VPA and CBZ in combination. ]"