STATUS SENG (Zn) DAN IMUNITAS SELULER : FOKUS PADA FUNGSI FAGOSITOSIS PMN, PADA PASIEN DIABETES MELITUS TIPE 2 DENGAN REGULASI GLUKOSA DARAII BAIK DAN BURUK ZINC STATUS AND CELLULAR IMMUNITY IN TYPE 2 DIABETES MELLITUS WITH GOOD AND POORLY CONTROLLED

Abstract

Background. Infection is an important factor in diabetic ketoacidosis patients, leading to death. Good immune response is needed to handle infection. Host immune response in diabetics, both the cellular and the humoral component are notoriously consider to be impaired. Studies on this area are scanty and found controversial results. Zinc deficiency occurs in type 2 diabetics, which may play role in abnormal immune response, especially cellular immunity leading to increase infection. Objective. This study will identify Zn status and cellular immunity in type 2 diabetics with good and poorly controlled. Patients and methodes. This study was conducted cross sectionally in forty six subjects diagnosed type 2 diabetic attending outpatients clinic at Dr. Kariadi hospital in Semarang who were recruited into this study between March and June 2003.. Grouping for good and poorly controlled diabetics were based on their A 1C level. Determination concentration of minerals was performed by Flame Atomic Absorption Spect•ophotometry (FAAS). Determination cellular immune response was performed by T rossete-lymphocyte assay and oxydative killing by determining NO PMN concentration (using Griess methode) dan PMN fagocyte function (percentage and index of NBT reduction by PMN). The t tes was used for differences in mean between two groups. Results. Grouping based on A 1C level: 16 (50%) were good controlled and 16 (50%) were poorly controlled. The remaining were excluded Zinc serum level in type 2 diabetic both group were not different (80.33 ± 27.87 vs 78.22 ± 21.14 ittg/dL; p =. 0.811). For cellular immunity: T-lymphocyte count in type 2 diabetic both group were not different (59.69 ± 7.25 vs 60.31 ± 10.05 %; p = 0.841) and type 2 diabetic with good controlled had better oxydative killing compared to poorly controlled: Good controlled diabetic had upper NO PMN concentration than poorly controlled (13.88 ± 9.27 vs 7.84 ± 3.57 uM; p = 0.025), good controlled had upper percentage of NBT reduction by PMN than poorly controlled ( 80.75 ± 13.97 vs 62.88 + 10.48%; p = 0.001) and good controlled also had upper reduction index of NBT by PMN than poorly controlled (43.62 ± 7.39 vs 28.31 ± 9.04; p = 0.001) Conclusion. There were no difference on Zn serum level and T-lymfocyte count between good and poorly controlled type 2 diabetic patients. Good controlled type 2 diabetic had better oxydative killing (NO PMN concentration, percentage and index of reduction NBT by PMN) than poorly controlled. Latar belakang: Infeksi pada diabetes menjadi faktor pencetus yang penting pada kematian akibat ketoasidosis diabetik. Untuk mengatasi infeksi diperlukan respon imun tubuh yang baik. Pada diabetes diduga ada penurunan fungsi respon imun baik seluler maupun humoral Penelitian-penelitian mengenai respon imun pada diabetes menunjukkan hasil yang kontroversi. Pasien diabetes tipe 2 dapat mengalami perubahan mikronutrien, di antaranya kadar Zn yang rendah, yang mungkin ikut berperan menyebabkan terganggunya sistem imunitas terutama imunitas seluler. Tujuan penelitian: Untuk mengetahui status Zn dan imunitas seluler pasien diabetes tipe 2 dengan regulasi glukosa darah baik dan buruk. Pasien dan metode:Penelitian dilakukan secara cross sectional pada empat puluh enam pasien diabetes tipe 2 yang kontrol di poliklinik Endokrinologi dan Metabolik RS Dr. Kariadi Semarang antara bulan Maret sampai Juni 2003, kemudian diperiksa kadar A1C dan dikelompokkan dalam regulasi glukosa baik dan buruk. Selanjutnya dilakukan pemeriksaan kadar Zn serum dengan metode Flame Atomic Absorption Spectrophotometry (FAAS) dan imunitas seluler. Parameter imunitas seluler yang diperiksa adalah jumlah limfosit T dengan metode rossette, dan oxydative killing dengan mengukur kadar NO PMN dengan metode Griess serta persentase dan indeks reduksi NBT PMN. Analisis statistik deskriptif untuk menentukan rerata dan sebaran, dan analisis analitik dengan uji t independent untuk menentukan ada tidaknya perbedaan pada kelompok regulasi baik dan buruk. Hasil: Berdasarkan A1C dikelompokkan 16 pasien regulasi baik dan 16 pasien regulasi buruk. Empat belas pasien dengan regulasi sedang dikeluarkan dari peneltian. Kadar Zn serum kelompok regulasi baik tidak berbeda bermalcna dibandingkan regulasi buruk (80.33 + 27.87 vs 78.22 + 21.14 gg/dL; p=0.811). Parameter imunitas seluler: jumlah limfosit T kelompok regulasi baik dan buruk tidak berbeda bermakna (59.69 + 7.25 vs 60.31 + 10.05 %; p=0.841), kadar NO PMN kelompok regulasi baik lebih tinggi dibandingkan regulasi buruk (13.88 + 9.27 vs 7.84 + 3.57 gM; p=0.025), persentase sel PMN mereduksi NBT kelompok regulasi baik lebih tinggi dibandingkan regulasi buruk (80.75 + 13.97 vs 62.88 + 10,48 %; p= 0.0001), indeks reduksi NBT PMN kelompok regulasi baik lebih tinggi dibandingkan regulasi buruk (43.62 + 7.39 vs 28.31 + 9.04; p = 0.0001) Kesimpulan: Kadar Zn serum pasien diabetes tipe 2 regulasi glukosa darah baik dan buruk tidak berbeda. Jumlah limfosit T pasien diabetes tipe 2 regulasi glukosa baik dan buruk tidak berbeda. Oxydative killing ( NO PMN dan NBT PMN) pasien diabetes tipe 2 regulasi glukosa darah baik lebih baik dibandingkan regulasi glukosa darah buruk.