What is Thyroid Eye Disease?
Thyroid Eye Disease (TED) – otherwise known as Graves Orbitopathy (GO) – is the most common orbital disease in the UK, affecting 1 in 20 people. Thyroid Eye Disease is generally associated with thyroid immune disorders, such as Graves’ Disease or Hashimoto’s Thyroiditis, and affects more women than men – usually between their second and sixth decades.
Most patients with eye disease have a current or past history of abnormal systemic thyroid hormone levels, while some may go on to develop abnormal levels, and a small number of patients may be euthyroid. While 25 to 50% of patients with immune thyroid disease develop orbital involvement, commonly within 12-18 months of their hormonal disorder, 5 to 10% of these may develop more severe consequences – such as increased inflammation and congestion, impaired motility, or compressive optic neuropathy. Other contributing factors include smoking and a family history of thyroid disorders.
What causes Thyroid Eye Disease?
The cells of the thyroid gland (epithelial cells) are covered in surface receptors, which bind to the thyroid stimulating hormone (TSH, thyrotropin) – a hormone which is secreted by the pituitary gland to control the release of thyroid hormones. In both Graves’ Disease and Hashimoto’s Thyroiditis, thyrotropin-receptor antibodies (TSH-R Antibodies, TRAb) are also present, and these can bind to the receptors: initiating and perpetuating the disease. These circulating antibodies are thought to be mediators in orbit disease, with their likely target being the orbital fibroblasts, which are found in the extra-ocular muscles and in the orbital fat. This is why orbital fibroblasts from patients with Thyroid Eye Disease have increased numbers of TSH receptors, which are thought to bind to circulating autoantibodies (TRAb): thereby stimulating fat cell formation and the deposition of hyaluronic acid within orbital muscle and fat – the histologic hallmark of Thyroid Eye Disease (see figure 1).
How do you treat Thyroid Eye Disease?
Thyroid Eye Disease symptoms are graded into activity (on a scale of 0 to 10, based on inflammatory signs) and severity (mild, moderate, severe and sight-threatening). While mild, non-inflammatory disease is generally treated with lubricant drops and oral selenium (200 mcg/day for 6 months), mild inflammatory disease may also require additional non-steroidal anti-inflammatory drugs (NSAIDS) or steroids. Double vision is managed with stick on Fresnel prisms, which can be placed on spectacle lenses to help realign the eyes. Immunosuppressive treatment with steroids, radiotherapy and surgery in the “active” phase is reserved for moderate and severe, sight-threatening eye disease with an increasing inflammatory index.
Pulsed Intravenous methylprednisolone has been found to be 85% effective, and oral prednisolone to be 60% effective in reducing inflammatory signs of Thyroid Eye Disease. Other immunosuppressive drugs like Azathioprine, Cyclosporine and Rituximab are also used in some cases. Urgent Orbital decompression is an treatment option for sight-threatening dysthyroid optic neuropathy, whilst lid surgery is reserved for corneal exposure threatening the sight.
Radiotherapy has been found to be useful in active progressive disease, while rehabilitative or restorative surgery is offered once the disease is stable and quiescent in the post-inflammatory phase. This includes orbital decompression for bulging eyes, squint surgery to help correct double vision, lid-lowering surgery for staring eyes, and blepharoplasty surgery for eye bags.
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Patient Questions
Commonly Asked Questions about Thyroid Eye Disease (TED)
What are the symptoms of Thyroid Eye Disease?
Thyroid Eye Disease is commonly indicated by sore, red and watery eyes with swollen eyelids; however, various symptoms are also frequently seen. 90% of Thyroid Eye Disease sufferers experience lid retraction (where the eyes appear to “stare”); 60% experience bulging eyes (known as Proptosis or Exophthalmos), and 40% suffer from double vision.
Thyroid Eye Disease typically has an “active” (in other words, progressive) inflammatory phase, which can last between 6 to 18 months, followed by an “inactive” (stable) post-inflammatory phase. Rundle first described this pattern of the disease, and the plot of orbital disease severity against time has been called Rundle’s curve (see fig 2).
The steepness of the graph in the active phase reflects the speed of progression, with a steeper slope often leading to more serious side effects, which need to be actively managed. This is usually through the use of steroids, radiotherapy, or other immunosuppressive agents – in order to limit the destructive consequences of the active phase. Rarely the disease can reactivate: if it does, it is usually associated with a major life stress.
Fig 1 : Enlargement of the fat & extra ocular muscles of the eye socket in GO
Fig 2. Rundles Curve
How can I manage the active stage of Thyroid Eye Disease?
In the active stage, Dr Sabrina recommends making some positive lifestyle changes, in order to help you improve Thyroid Eye Disease. Adopting an anti-stress or mindfulness practice, such as yoga, Pilates, counselling, can help to improve your experience of Thyroid Eye Disease, while frequent monitoring of your thyroid status (every 4 to 6 weeks) is recommended.
Smoking is known to adversely affect the course of Graves Orbitopathy (GO) and your response to treatment – therefore smokers are advised to quit (and if necessary, seek professional help to do so). Finally, you should aim to achieve and maintain euthyroid status – and this needs to be overseen by an endocrinologist, using medications or radioactive iodine or thyroidectomy. (Note : Radioactive iodine is contraindicated in young children, women, pregnancy & severe eye disease).
Stability of eyelid height after graded anterior-approach lid lowering for dysthyroid upper lid retraction.
Thyroid orbitopathy possibly predisposes to late-onset of periocular lymphoma.
About Dr Sabrina Shah-Desai MS, FRCS
Dr Sabrina Shah-Desai is a distinguished oculoplastic surgeon and one of London’s leading eye specialists. She has over two decades of surgical experience and is renowned for her ability to create a natural look.
Dr Sabrina has a deep anatomical knowledge of the periorbital area and an appreciation for the differences in treating both men and women. When raising the brows and eyelids in a male Upper-Lid Blepharoplasty, it is important to preserve the T-shaped brow – in order not to feminise their appearance.
Publications
Stability of eyelid height after graded anterior-approach lid lowering for dysthyroid upper lid retraction.
Shortt AJ, Bhogal M, Rose GE, Shah-Desai S.
Orbit. 2011 Dec;30(6):280-8. doi: 10.3109/01676830.2011.604897.
PMID: 22132845
Thyroid orbitopathy possibly predisposes to late-onset of periocular lymphoma.
Nutting CM, Shah-Desai S, Rose GE, Norton AP, Plowman PN.
Eye (Lond). 2006 Jun;20(6):645-8. Epub 2005 Aug 26.
PMID: 16123786
