Orbital Tissue Inflammation in Thyroid Eye Disease: An Immune-Based Process

Orbital Tissue Inflammation in Thyroid Eye Disease: An Immune-Based Process

Thyroid Eye Disease (TED), also known as Graves' orbitopathy, is an autoimmune disorder that affects the orbital tissues surrounding the eyes. Approximately 25-50% of people with Graves' disease develop TED, a condition characterised by inflammation and tissue changes.

TED presents with several distinctive symptoms, including proptosis (bulging eyes), eyelid retraction or swelling, dry eyes and excessive tearing, diplopia (double vision), eye pain and sensitivity to light, and conjunctival injection (redness and inflammation of the conjunctiva).

The disease progresses through several stages. The inflammatory phase, which lasts 6-18 months, is characterised by proptosis, eyelid retraction, and inflammation. This is followed by the static phase, where there is a decrease in inflammation with minimal improvement, and the quiescent phase, where there is gradual improvement in motility and retraction of muscles.

The primary risk factor for TED is an autoimmune response, often linked to Graves' disease. Other contributing factors include autoantibodies directed against the thyroid-stimulating hormone receptor (TSHR) and insulin-like growth factor I receptor (IGF-1R), a genetic predisposition, and smoking.

During the active phase of TED, the immune system sends out "rogue signals" (autoantibodies) that jam the TSHR on both the thyroid gland and the eye socket's "construction workers" (fibroblasts), causing them to build too much, leading to the expansion of the eye socket. This expansion can result in permanent proptosis, diplopia, and potentially optic neuropathy.

Physicians treat the active phase with immunosuppression, using steroids or biologics. To address the issues arising from the expansion of the eye socket, surgeons perform interventions like orbital decompression or strabismus surgery.

Researchers are developing new targeted therapies, such as Teprotumumab, an IGF-1R inhibitor, which blocks both IGF-1R and TSHR signalling, reducing inflammation and eye bulging. They are also experimenting with anti-IL-6 drugs like Tocilizumab, which target inflammation, and JAK inhibitors, which block inflammatory pathways.

TED imposes a significant physical and psychosocial burden, necessitating early treatment to prevent long-term vision impairment and quality-of-life issues. The cosmetic changes associated with TED, such as proptosis and lid retraction, negatively affect patients' mental health and social interactions. Severe TED significantly impacts both vision and quality of life, and compressive optic neuropathy can cause irreversible vision loss.

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