Kranial Radyonekroz ve Tedavisi

Yazarlar

Osman Ersegun Batçık

Özet

Kranial radyasyon nekrozu (RN), stereotaktik radyocerrahi (SRS) ve tüm beyin radyoterapisi gibi intrakranial tümör tedavilerinin ardından aylarca veya yıllarca sürebilen ciddi bir lokal geç doku reaksiyonudur. Uzun vadeli sağkalım oranlarının artmasıyla önemi büyüyen bu patoloji, vasküler endotel hasarı, kan-beyin bariyeri bozulması ve inflamatuar sitokinlerin salınımı gibi çok faktörlü mekanizmalarla tetiklenir. Akut, subakut ve kronik olmak üzere üç alt türde gelişen RN; doz-hacim etkileşimi, önceki radyasyon maruziyeti ve eş zamanlı kemoterapi kullanımı gibi faktörlerden doğrudan etkilenir. Tanı aşamasında, lezyonların tümör nüksünden ayırt edilmesi zorlu bir süreç olup, FDG PET, T1 SPECT, perfüzyon MR ve manyetik rezonans spektroskopi (MRS) gibi ileri görüntüleme yöntemlerinin entegrasyonunu gerektirir. Tedavi yaklaşımı ise semptomların varlığına göre şekillenir; küçük veya asemptomatik vakalarda yakın klinik takip yeterli olurken, semptomatik hastalarda ilk basamak olarak ödemi azaltan kortikosteroidler tercih edilir. Steroide dirençli olgularda VEGF hedefli bevacizumab kullanımı, hiperbarik oksijen tedavisi ya da lazer interstisyel termal tedavi (LITT) gibi yenilikçi modaliteler öne çıkmaktadır; kitle etkisinin giderilmesi gereken dirençli vakalarda ise cerrahi rezeksiyona başvurulmaktadır.

Cranial radiation necrosis (RN) is a severe, localized late tissue reaction that emerges months or years following intracranial tumor treatments such as stereotactic radiosurgery (SRS) and whole-brain radiation therapy. Increasingly significant due to prolonged patient survival rates, its complex pathophysiology is driven by initial vascular endothelial damage, blood-brain barrier disruption, and inflammatory cytokine cascades. Developing through acute, subacute, or chronic phases, RN risk is strictly modulated by predictive parameters including dose-volume interactions, previous radiation exposures, and concurrent chemotherapy usage. Diagnostic differentiation between necrosis and tumor recurrence remains highly challenging, necessitating advanced imaging modalities such as FDG PET, T1 SPECT, perfusion MRI, and magnetic resonance spectroscopy (MRS). Therapeutic management is strictly tailored based on clinical symptoms; small, asymptomatic lesions are managed through vigilant observation, whereas symptomatic presentations require immediate first-line oral corticosteroids to mitigate localized edema. For steroid-refractory instances, the anti-VEGF agent bevacizumab, hyperbaric oxygen therapy, or laser interstitial thermal therapy (LITT) offer viable treatment pathways, while surgical resection is reserved for intractable, symptomatic mass effects.

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315-324

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23 Ağustos 2022

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