Tiroid Oftalmopati
Özet
Tiroid Oftalmopati (TO), tiroid disfonksiyonunun eşlik ettiği, üst kapak retraksiyonu, propitozis, restriktif şaşılık ve görmeyi tehdit eden optik nöropati gibi klinik bulgularla seyreden otoimmün bir yörünge hastalığıdır. Patogenezinde orbital fibroblastların glikozaminoglikan üretimi ve yağ dokusu hiperplazisi rol oynar; sigara kullanımı ise hastalığın seyrini ve tedavi başarısını olumsuz etkileyen majör bir çevresel risk faktörüdür. Hastalık inflamasyonun baskın olduğu aktif faz ve fibrozisin geliştiği inaktif faz olmak üzere iki aşamada ilerler. Klinik değerlendirmede Klinik Aktivite Skorlaması (CAS) ile EUGOGO veya VISA sınıflamaları kullanılarak hastalığın aktivitesi ve ciddiyeti belirlenir. Tedavi yaklaşımı hastalığın evresine göre planlanır; hafif olgularda topikal lubrikanlar ve selenyum takviyesi yeterliyken, orta-ciddi aktif olgularda birinci basamak olarak intravenöz kortikosteroidler (metilprednizolon) ve mikofenolat sodyum kombinasyonu tercih edilir. Dirençli vakalarda orbital radyoterapi, siklosporin, teprotumumab veya tocilizumab gibi biyolojik ajanlar ikinci seçenek olarak devreye girer. Görmeyi tehdit eden distroid optik nöropati varlığında ise acil yüksek doz IV steroid tedavisi uygulanır, yanıt alınamazsa acil cerrahi dekompresyon planlanır. En az altı ay boyunca inaktif dönemde kalan orta-ciddi olgularda ise sırasıyla orbita dekompresyonu, şaşılık ve kapak cerrahisinden oluşan aşamalı rehabilitasyon cerrahisi uygulanarak hastaların görsel fonksiyonları ve yaşam kaliteleri optimize edilir.
Thyroid Ophthalmopathy (TO) is an autoimmune orbital disease associated with thyroid dysfunction, characterized by clinical manifestations such as upper eyelid retraction, proptosis, restrictive strabismus, and sight-threatening optic neuropathy. Its pathogenesis involves glycosaminoglycan production by orbital fibroblasts and adipose tissue hyperplasia, with smoking identified as a major environmental risk factor that adversely affects disease progression and treatment outcomes. The disease progresses through two distinct phases: an active inflammatory phase and a subsequent inactive fibrotic phase. Clinical assessment utilizes the Clinical Activity Score (CAS) alongside EUGOGO or VISA classifications to establish disease activity and severity. Treatment strategies are tailored to the disease stage; mild cases are managed with topical lubricants and selenium supplementation, whereas moderate-to-severe active cases rely on a combination of intravenous corticosteroids (methylprednisolone) and mycophenolate sodium as the first-line therapy. In refractory instances, orbital radiotherapy or biological agents such as cyclosporine, teprotumumab, and tocilizumab serve as second-line options. Sight-threatening dysthyroid optic neuropathy necessitates immediate high-dose IV steroid therapy, failing which prompt surgical decompression is required. For moderate-to-severe cases remaining inactive for at least six months, a sequential rehabilitative surgery involving orbital decompression, strabismus surgery, and eyelid surgery is performed to improve visual functions and quality of life.
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