ABSTRAK
Latar belakang. Penggunaan antikonvulsan jangka panjang, terutama golonganpenginduksi enzim, berkaitan dengan penurunan kadar 25-hidroksivitamin D(25[OH]D) dan peningkatan prevalens defisiensi vitamin D. Namun demikian,hasil yang tidak konsisten ditunjukkan pada penggunaan antikonvulsan nonpenginduksienzim seperti asam valproat. Sampai saat ini belum ada penelitian diIndonesia yang melihat hubungan penggunaan antikonvulsan jangka panjangdengan kadar 25(OH)D.Tujuan. Penelitian ini bertujuan untuk mengetahui kadar 25(OH)D dan prevalensdefisiensi/insufisiensi vitamin D pada anak epilepsi yang menggunakanantikonvulsan jangka panjang serta faktor-faktor yang memengaruhinya.Metode. Penelitian potong lintang di dua poliklinik neurologi anak di Jakartapada bulan Maret hingga Juni 2013 pada anak epilepsi usia 6 – 11 tahun yangmenggunakan asam valproat, karbamazepin, fenobarbital, fenitoin, atauokskarbazepin, baik tunggal maupun kombinasi, selama 1 tahun atau lebih.Penelitian menggunakan kontrol matching usia dan jenis kelamin. Pemeriksaankadar 25(OH)D menggunakan metode enzyme immunoassay.Hasil. Terdapat 31 subjek epilepsi dan 31 kontrol dengan rerata usia 9,1 (SD 1,8)tahun. Sebagian besar subjek menggunakan asam valproat (25/31) dan diberikanmonoterapi (21/31). Rerata lama pemakaian antikonvulsan adalah 41,9 (SD 20)bulan. Rerata kadar 25(OH)D subjek epilepsi adalah 41,1 (SD 16) ng/mL, lebihrendah dibanding kontrol dengan selisih 9,7 ng/mL (IK95% 1,6 sampai 17,9).Tidak ditemukan defisiensi vitamin D pada kedua kelompok. Prevalensinsufisiensi vitamin D pada subjek epilepsi lebih besar dibanding kontrol (12/31vs 4/31; p=0,020). Berdasarkan analisis multivariat, tidak ada faktor yangmemengaruhi penurunan kadar 25(OH)D pada anak epilepsi yang menggunakanantikonvulsan jangka panjang.Simpulan. Kadar vitamin D pada anak epilepsi yang menggunakan antikonvulsanjangka panjang lebih rendah dibanding dengan kontrol namun tidak sampaimenyebabkan defisiensi vitamin D.
ABSTRACT
Background. Long-term anticonvulsants therapy, especially the enzyme inducer,are associated with low level of 25-hidroxyvitamin D (25[OH]D) and highprevalence of vitamin D deficiency. However, studies had showed inconsistentresults on long-term usage of non-enzyme inducer anticonvulsant such as valproicacid. Until now, there is no study ever conducted in Indonesia to evaluate theassociation between long-term usage of anticonvulsant with 25(OH)D level.Objectives. To investigate 25(OH)D level and the prevalence of vitamin Ddeficiency/insufficiency in epileptic children who are using long-termanticonvulsant and to describe the associated factors.Method. This was a cross-sectional study conducted at two pediatric outpatientneurology clinics in Jakarta, between March to June 2013. Subjects were epilepticchildren, aged 6 – 11 years old who had been using valproic acid, carbamazepine,phenobarbital, phenytoin, or oxcarbazepine, as single or combination therapy, for1 year or more. We performed a matched control for age and sex. The 25(OH)Dlevel was measured with enzyme immunoassay method.Results. There were 31 epileptic children and 31 controls. The mean age was 9,1(SD 1.8) years old. Most of the subjects were treated with valproic acid (25/31)and administered as monotherapy (21/31). The mean duration of anticonvulsantconsumption was 41.9 (SD 20) months. The mean 25(OH)D level of epilepticchildren was 41.1 (SD 16) ng/mL, lower than control with difference 9.7 ng/mL(95% CI 1.6 to 17.9). There was no vitamin D deficiency found in this study. Theprevalence of vitamin D insufficiency in epileptic children was higher than control(12/31 vs 4/31; p=0,020). Based on the multivariate analysis, no identified riskfactors were associated with low level of 25(OH)D in epileptic children with longtermanticonvulsant therapy.Conclusion. Vitamin D level in epileptic children with long-term anticonvulsanttherapy is lower than control but none have vitamin D deficiency. |
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