Radyoterapinin Endokrinolojik Komplikasyonları

Yazarlar

Saliha Ahmetoğlu

Özet

Radyasyon tedavisi, bezlerde hormon disfonksiyonu ve neoplazm gelişimi için ana risk faktörüdür ve endokrin komplikasyonlar akut veya kronik geç etkiler olarak ortaya çıkabilir. Çocukluk çağı kanserinden kurtulanların %50'sini etkileyen bu hasarların patofizyolojisi çok faktörlü olup; doğrudan hücresel hasar, vasküler dejenerasyon ve DNA hasarı ile ilişkilidir. Kraniyal ışınlama sonrasında hipofiz-hipotalamus ekseni sıklıkla etkilenir; somatotropik hücrelerin hassasiyeti nedeniyle en yaygın sekel büyüme hormonu eksikliğidir. Ayrıca hastalarda santral hipogonadizm, ACTH ve TSH eksiklikleri ile hiperprolaktinemi gelişebilir. Tiroid bezinin doğrudan ışınlanması primer hipotiroidizme yol açarken, doz-hacim kısıtlamaları (V40 ≤ %85) bu riski azaltabilir; ayrıca maruziyetten yıllar sonra tiroid nodülü ve diferansiye tiroid kanseri riski belirgin şekilde artar. Boyun ışınlaması alanlarda primer hiperparatiroidizm ve hipoparatiroidizm gelişebilir. Kraniyal ve abdominal radyasyon veya total vücut ışınlaması; adrenal yetmezliğe, üreme fonksiyon bozukluklarına (erkeklerde spermatogenez bozukluğu, kadınlarda primer ovaryen yetmezlik ve uterus hasarı), kemik mineral dansitesinde azalma ile kırık riskine ve metabolik sendrom ile obezite gibi kardiyovasküler risk faktörlerine neden olur. Bu sekellerin erken teşhisi ve yaşam boyu takibi için düzenli kılavuz taramaları kritik önem taşır.

Radiation therapy is the primary risk factor for hormone dysfunction and neoplasm development in irradiated glands, with endocrine complications manifesting as acute or chronic late effects. Affecting 50% of childhood cancer survivors, the pathophysiology of this damage is multifactorial, involving direct cellular injury, vascular degeneration, and DNA damage. Cranial radiotherapy frequently impairs the pituitary-hypothalamic axis, where growth hormone deficiency is the most common sequel due to high somatotropic vulnerability. Additionally, patients may develop central hypogonadism, ACTH and TSH deficiencies, and hyperprolactinemia. Direct thyroid irradiation causes primary hypothyroidism, which can be mitigated by dose-volume constraints (V40 ≤ 85%), and significantly increases the risk of thyroid nodules and differentiated thyroid cancers decades later. Patients receiving neck irradiation are at risk for primary hyperparathyroidism and hypoparathyroidism. Cranial, abdominal, or total body irradiation also leads to adrenal insufficiency, reproductive dysfunction (impaired spermatogenesis in men, primary ovarian failure and uterine damage in women), reduced bone mineral density with increased fracture risks, and cardiovascular risk factors such as obesity and metabolic syndrome. Regular guideline-based surveillance is critical for early detection and lifelong management of these sequelae.

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23 Ağustos 2022

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