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Can Thyroid Affect Your Eyes

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Can Thyroid Affect Your Eyes – Thyroid-associated ophthalmopathy (TAO), also known as thyroid eye disease or Graves’ ophthalmopathy, is the most common autoimmune inflammatory disease of the orbit and periorbital tissue, affecting approximately three million Americans.

This prevalence is similar to that of glaucoma in the United States. Historically, TAO has been limited to patients with the clinical triad of Graves’ disease and orbital features, hyperthyroidism and pretibial myxema.

Can Thyroid Affect Your Eyes

Research now shows that only 80% of patients with TAO have Graves’ (hyperthyroidism); the remaining 20% ​​are hypothyroid (10%) and euthyroid (5-10%) patients.

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Since TAO can precede, overlap, or follow the diagnosis of thyroid dysfunction, optometrists must be able to make an early diagnosis, because TAO can threaten vision, affect the patient’s appearance, and cause a decrease in quality of life.

Three broad categories summarize the pathogenesis of TAO: (1) periorbital soft tissue inflammation; (2) activation of a subpopulation of orbital fibroblasts capable of undergoing adipocyte differentiation leading to adipose tissue hyperplasia; and (3) overproduction of glycosaminoglycans by orbital fibroblasts.

Orbital fibroblasts produce collagen and glycosaminoglycans in the extracellular matrix and generate a strong polyanionic charge that causes a very high osmotic pressure, leading to extraocular muscle swelling and possible optic nerve compression.

TAO occurs in two distinct phases: an active inflammatory phase and an inactive or stable phase. Usually, the stronger and more aggressive the active phase, the greater the likelihood of more severe consequences.

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The period of active inflammation usually lasts six to 24 months and is followed by a stable, chronic fibrotic period.

In the early active phase, immunomodulators and radiotherapy can limit the progression of TAO. If the disease is inactive, surgery can help improve cosmesis, comfort, and function.

Figure 2. Above, limited movement of the left eye in temporal view. Inferiorly, a coronal CT scan of the orbit shows increased thickness of the left middle rectum and both lower rectums.

The clinical features of TAO are broad, with most patients experiencing eyelid retraction, proptosis, and other eye contact symptoms such as epiphoria, photophobia, pain, spasms, diplopia, and decreased vision.

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When inflammation extends to the extraocular muscles, patients may experience conjunctival erythema, chemosis, limited extraocular myopathy, hypotropia, diplopia, and compressive optic neuropathy (Figure 1).

You can diagnose TAO based on eye signs and symptoms. Appearance changes and exposure symptoms are the most common early findings of TAO.

Other symptoms are vague and often due to normal aging, especially in middle-aged women with eyelid swelling worse in the morning.

This may be due to increased sympathetic tone, overwork of the levator and superior rectus muscles to compensate for narrowing of the inferior rectus, or inflammation and scarring of the levator complex (Figure 2).

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Another common sign is proptosis (62%) due to enlargement of orbital fat, muscle, or both (Figure 3). Proptosis can be measured with an exophthalmometer. Values ​​greater than 18–20 mm in Caucasians, 16–18 mm in Asians, and 20–22 mm in African Americans indicate proptosis. Asymmetry of 2 mm or greater also indicates proptosis.

If the doctor does not have an exophthalmometer, an orbital CT scan can also assess the amount of proptosis.

Proptosis and eyelid retraction can lead to increased corneal exposure and ocular surface disease, a common reason patients see an ophthalmologist. If the condition is aggressive, proptosis and lid retraction can cause lagophthalmos, contact keratopathy, microbial keratitis, and perforation. Patients at risk of perforation usually have significant lagophthalmos and the absence of Bell’s phenomenon due to fibrosis of the inferior rectus muscle.

Vision-threatening but potentially reversible dysthyroid optic neuropathy should be suspected with color saturation, afferent pupillary defects, or decreased vision.

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Some believe that patients with tight eyelids have limited anterior movement of the globe, putting them at greater risk for optic nerve compression.

Figure 3. Upper eyelid retraction and proptosis in a patient with active phase orbital occlusion (conjunctival injection).

Other signs include temporal aggravation, conjunctival injection and chemosis, Von Graefe’s sign (lid delay during downward gaze), and Dalrymple’s sign (widening of the palpebral fissure). Clinical signs are usually bilateral and symmetrical, but may be asymmetrical or unilateral. In these cases, asking for symptoms of thyroid dysfunction (eg, hair loss, heat or cold intolerance, weight changes, skin changes, memory problems and mood changes) can lead to a diagnosis (Table 1).

If unilateral presence is suspected and the patient reports few or no systemic symptoms, consider orbital imaging and serum thyroid testing. If you find normal or mildly abnormal thyroid function, consider alternative etiologies (Figure 4).

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Non-specific orbital inflammation may present with TAO symptoms such as proptosis, extraocular muscle block, red eyes and chemosis. Nonspecific orbital inflammation is usually acute and painful, but if the clinical picture is unclear, orbital imaging can help distinguish between these different disease processes.

For example, a TAO CT scan shows a pathognomonic pattern of extraocular muscle enlargement while sparing the muscle tendon. Orbital pseudotumors, however, show enlargement of both extraocular muscles and tendons.

Figure 4. This patient has unilateral proptosis. TAO recommended exam results; but additional testing, including this MRI, revealed an inferolateral postseptal orbital mass (here hyperintense) involving the inferior and lateral rectus muscles. These features are highly suggestive of orbital cavernous malformation (hemangioma).

Several clinical scoring systems exist to assess the severity of TAO, including the NO SPECS and VISA mnemonics. These systems can help you evaluate and treat patients with TAO, but no system currently serves as the gold standard.

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Most physicians know the classic NO SPECS classification: no physical signs or symptoms, only signs, soft tissue involvement, proptosis, extraocular muscle involvement, corneal involvement, and vision loss (from optic nerve compression).

Although helpful, it does not assess clinical activity or provide sufficient information to document disease between visits to guide management.

The VISA classification—vision, inflammation, strabismus, and appearance—was developed to allow assessment of both clinical severity and activity based on subjective and objective input (Figure 5).

The system helps guide appropriate management in a logical sequence, targeting the most important aspects of the disease that affect the patient. For example, visual disturbances caused by the optic nerve are prioritized. VISA is also useful in assessing changes in TAO and grade and can guide therapy.

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The European Grave Orbitopathy Working Group (EUGOGO) defines mild disease as minimal eyelid swelling, eyelid retraction, or proptosis with little or no extraocular muscle dysfunction. Moderate to severe TAO consists of some active disease with or without ocular motor dysfunction characterized by diplopia and inflammation that interferes with function. It may also include significant proptosis. Severe disease refers to vision-threatening conditions such as dysthyroid optic neuropathy and corneal ulcers.

When diagnosing TAO, it is important to assess the severity of orbital changes, but this only gives a picture of the situation. Equally important is the temporal assessment of the course of the disease and its location on the Rundle curve.

The key to determining whether a patient with TAO is vision threatening is to assess whether the patient is in an active inflammatory phase or a stable latent chronic fibrotic phase.

Active. Most patients who develop vision loss due to corneal exposure or compressive optic neuropathy due to TAO do so during the active inflammatory phase. You can use the Clinical Activity Score (CAS) to identify active disease (Table 2).

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This phase is typically characterized by periorbital erythema and edema, conjunctival injection, chemosis, orbital inflammation and congestion, eyelid retraction, proptosis, and diplopia. The active phase is usually a self-limiting disease process that lasts for one year in non-smokers and two to three years in smokers.

When using CAS, remember that severe disease complications such as dysthyroid optic neuropathy are still possible with a low CAS score, and patients with a high CAS score may experience long-term congestive changes that do not respond to any immunotherapy, requiring mechanical surgical decompression.

Latent. After the plateau of the active phase, the patient enters a phase of quiet fatigue. This latent chronic fibrotic phase has similar clinical findings to the active inflammatory phase (ie, eyelid retraction, proptosis, and diplopia), but lacks many of the signs of inflammation seen in the active phase (ie, conjunctival injection and chemosis) (Figure) . 6).

These patients require frequent monitoring, as inflammation may occur in 5-10% of patients during their lifetime.

Thyroid Eye Disease Symptoms And Ways To Have It Treated

With no known disease biomarkers, thyroid dysfunction is now detected by serum tests. However, a recent study examining the tears of patients with TAO identified three new potential biomarkers, suggesting that tears may be a source for early diagnosis of TAO and potentially also the amount of inflammation present.

As for treatment options, researchers have recently linked a newly discovered signaling pathway involving the activation of immunoglobulins to the insulin-like growth factor receptor I (IGF-I) (IGF-IR) in Graves’ disease patients.

Studies show that inhibitory antibodies targeting IGF-IR can attenuate the effects of IGF-I, thyrotropin, thyroid-stimulating immunoglobulin and immunoglobulin associated with Graves’ disease.

This compound is a fully human IGF-IR inhibitory monoclonal antibody that can block IGF-I signaling and reduce the body’s sensitivity to thyrotropin, thereby

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