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HBeAg Pozitif Kronik Hepatit B’li Bir Hastada Peginterferon α-2A ile İlişkili Tiroidit

Thyroiditis Associated With Peginterferon α-2A in a Patient with HBeAg Positive Chronic Hepatitis B

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DOI: 
http://dx.doi.org/10.5505/abantmedj.2012.65375

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Abstract (2. Language): 
Interferons are used to treat chronic viral hepatitis, due to antiviral activity, are substances of protein structure. IF can lead to disorders of thyroid function during their use for treatment. PEG-IFN α-2a 120 mcg sc / week to thirty-threeyear- old male patient was started with the diagnosis of HBeAg (+) chronic hepatitis B. In the beginning of treatment, thyroid stimulating hormone (TSH), free T3 (FT3), free T4 (FT4) levels were normal and antinuclear antibody (ANA) was negative. In the sixth month of treatment the patient's; TSH was 60.52 (↑), FT3 was 4.06 (N), FT4 was 4.48 (↓), thyroglobulin (TG) was 1.6 ng / ml (N), anti-thyroglobulin antibody (ATA) was 631 IU / ml (↑), anti-microsomal antibody (AMA) was 1000IU/ml (↑). Thyroid ultrasonography revealed bilateral hypoechoic fibrous septa (pseudolobulation) and increased blood flow (Hashimoto's thyroiditis? ) in the thyroid parenchyma. In Thyroid scintigraphy; nonhomogeneous hyperplastic thyroid gland and hyperactive nodule in left lobe were seen. The result of thyroid biopsy were evaluated as benign cytology. Hashimoto's thyroiditis associated with interferon was thought. Later, IFN therapy was discontinued and lamivudine was started. Due to iatrogenic hyperthyroidism for the patient, levotiron 1x1 was started. In third months of levotiron therapy, TSH was 0.190, T3 was 5.6, T4 was 21: 24. Levotiron treatment was stopped. In 6 months after discontinuation of interferon therapy TSH was 0742, FT3 was 5: 33, FT4 was 14: 53. There was no thyroid disfunction in follow-up of the patient.
Abstract (Original Language): 
İnterferon (IFN) lar antiviral etkinliğinden dolayı kronik viral hepatit tedavisinde kullanılan protein yapıdaki maddelerdir. Tedavi amacıyla kullanımları sırasında tiroid fonksiyon bozukluklarına sebep olabilmektedirler. Otuz üç yaşında erkek hastaya HBeAg (+) kronik hepatit B tanısıyla PEG- IFN α-2a 120 mcg s.c./hafta tedavisi başlanıldı. Tedavi başlangıcında tiroid stimülan hormon (TSH), serbest T3 (ST3), serbest T4 (ST4) düzeyleri normal, antinükleer antikor (ANA) negatif idi. Tedavinin altıncı ayında hastanın; TSH 60.52 (↑), FT3 4.06 (N), FT4 4.48 (↓), Tiroglobulin (TG) 1.6 ng/ml (N), antitiroglobulin antikor (ATA) 631 IU/ml (↑), anti-mikrozomal antikor (AMA) 1000IU/ml (↑) olarak tespit edildi. Tiroid ultrasonografisinde; bilateral hipoekoik olan tiroid parenkimi içerisinde fibröz septalar (psödolobülasyon) ve artmış kanlanma (Hashimato tiroiditi ?) görüldü. Tiroid sintigrafisinde; non-homojen hiperplazik tiroid glandı ve sol lobta hiperaktif nodül tespit edildi. Tiroid biyopsisi; benin sitoloji olarak değerlendirildi. Hastada interferona bağlı hashimato tiroiditi düşünülerek IFN tedavisi kesildi ve lamivudin tedavisine geçildi. Hastaya iyatrojenik hipertiroidi nedeniyle levotiron 1x1 tedavisi başlanıldı. Levotiron tedavisinin 3. ayında TSH 0.190, ST3 5.6, ST4 21.24 olarak saptandı ve levotiron kesildi. İnterferon tedavisi kesildikten 6 ay sonra yapılan tetkiklerinde TSH 0.742, ST3 5.33, ST4 14.53 idi. Daha sonraki takiplerinde tiroid fonksiyonlarında bozukluk tespit edilmedi.
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