Hubungan antara Kadar Hepcidin dengan Kadar SGOT dan SGPT pada Pasien Talasemia Beta Mayor di RS Universitas Airlangga

Talasemia beta mayor merupakan kelainan genetik yang ditandai dengan gangguan sintesis rantai beta globin sehingga pasien memerlukan transfusi darah rutin sepanjang hidupnya. Pasien talasemia beta mayor memerlukan transfusi darah rutin untuk mempertahankan kadar hemoglobin, namun terapi ini dapat menyebabkan kelebihan besi yang meningkatkan risiko kerusakan organ, terutama hepar. Hepcidin merupakan hormon utama yang mengatur homeostasis besi dalam tubuh, sedangkan Serum Glutamic Oxaloacetic Transaminase (SGOT) dan Serum Glutamic Pyruvic Transaminase (SGPT) merupakan biomarker yang umum digunakan untuk mendeteksi dini cedera hepatoseluler. Tingginya risiko gangguan hepar pada pasien talasemia beta mayor dan masih terbatasnya penelitian mengenai hubungan hepcidin dengan biomarker fungsi hepar. Penelitian ini menggunakan desain analitik observasional dengan pendekatan cross-sectional dengan sampel sebanyak 36 pasien. Perhitungan kadar menggunakan metode ELISA dan kinetik. Hasil analisis menunjukkan rerata hepcidin 4,468 ± 0.128 ng/mL, rerata SGOT 41,83 ± 23,07 U/L, dan rerata SGPT 38,17 ± 22,8 U/L. Terdapat korelasi negatif yang lemah antara kadar hepcidin serum dengan kadar SGOT maupun SGPT. Tidak ditemukan hubungan yang bermakna antara kadar hepcidin serum dengan kadar SGOT (r = -0,066; p = 0,701) maupun SGPT (r = -0,80; p = 0,644). Temuan ini menunjukkan bahwa kadar hepcidin serum berhubungan secara tidak signifikan dengan peningkatan enzim hepar pada populasi pasien talasemia beta mayor. Hubungan yang negatif menunjukkan bahwa penurunan kadar hepcidin berbanding terbalik dengan peningkatan SGOT dan SGPT.

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Beta thalassemia major is a genetic disorder characterized by impaired synthesis of the beta globin chain, requiring patients to undergo regular blood transfusions throughout their lives. Patients with beta thalassemia major need regular blood transfusions to maintain hemoglobin levels, but this therapy can lead to iron overload, increasing the risk of organ damage, particularly the liver. Hepcidin is the main hormone that regulates iron homeostasis in the body, while Serum Glutamic Oxaloacetic Transaminase (SGOT) and Serum Glutamic Pyruvic Transaminase (SGPT) are commonly used biomarkers to detect early hepatocellular injury. The high risk of liver dysfunction in patients with major beta thalassemia and the limited research on the relationship between hepcidin and liver function biomarkers. This study used an observational analytical design with a cross-sectional approach with a sample of 36 patients. The concentration was measured using the ELISA and kinetic methods. The analysis results show an average hepcidin level of 4.468 ± 0.128 ng/mL, an average SGOT level of 41.83 ± 23.07 U/L, and an average SGPT level of 38.17 ± 22.8 U/L. There is a weak negative correlation between serum hepcidin levels and SGOT or SGPT levels. No significant relationship was found between serum hepcidin levels and SGOT levels (r = -0.066; p = 0.701) or SGPT levels (r = -0.80; p = 0.644). These findings indicate that serum hepcidin levels are not significantly related to the increase in liver enzymes in the population of patients with major beta thalassemia. The negative relationship suggests that a decrease in hepcidin levels is inversely related to an increase in SGOT and SGPT.