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In TED optic neuropathy, the optic nerve becomes compressed by the enlarged muscles at the narrow orbital apex where the nerve exits the orbit to enter the brain cavity. The patient symptoms may include central visual blurring, loss of peripheral vision or colour desaturation.
Objective measures of optic neuropathy include a loss in central visual acuity and colour vision, an afferent pupil defect, and infrequently congestion or pallor of the optic nerve. Ancillary testing includes coronal CT or MR Scans to confirm crowding of the orbital apex, standardized visual fields, and rarely VEP or optic nerve head photos. Because the disease is usually in the active or progressive phase when optic neuropathy develops, some clinicians may arrange additional radiotherapy subsequent to the decompression to prevent further enlargement of the muscles and recurrence of neuropathy. Success of therapy for TED optic neuropathy from both a clinical or research standpoint is based on specific improved measurements for central vision, colour vision and visual fields.
Symptoms of ocular and periocular soft tissue inflammation include orbital aching at rest or with movement, and eyelid or conjunctival swelling and redness. The Clinical Activity Score (CAS) described and validated by Mourits and the Amsterdam Orbitopathy group assigns one point for each of the following: orbital pain at rest, orbital pain with movement, chemosis, caruncular edema, eyelid edema, conjunctival injection and eyelid injection. The VISA Inflammatory Score modifies the CAS slightly by widening the grade for chemosis and lid edema from 0-2.
Lid edema is graded as 1 if it is present but not causing overhanging of the tissues, and as 2 if it causes a roll in the lid skin including festoons in the lower lid. The pain score is based on the patient’s report of deep orbit discomfort rather than ocular surface irritation (0 = no pain, 1 = pain with movement, 2 = pain at rest). Treatment of active inflammation in TED depends on its inflammatory score and evidence of progression. In general, if the inflammatory grade is 5 or more, or if there is subjective or objective evidence of progression in the inflammation, more aggressive therapy should be considered, including oral or intravenous corticosteroids, radiotherapy, and in refractory cases, immunosuppressive agents.
Combination therapy is receiving increasing attention in severe, progressive cases [26, 27] and interest is also turning to new immunomodulatory agents, such as anti-tumor necrosis factor agents (etanercept, infliximab) or B-lymphocyte directed therapy (rituximab). The symptoms for strabismus include a progression from no diplopia (double vision), diplopia with horizontal or vertical gaze, intermittent diplopia in straight gaze, and constant diplopia in straight gaze.
Strabismus can be measured objectively by prism cover testing in different gaze directions. Ancillary testing includes using the Goldmann perimeter to quantify ocular ductions in four directions.  The patient keeps both eyes open and follows the V4e light target, tapping a coin when the image becomes double. Figure 4b: Once the inflammation controlled and the strabismus measurements are stable, prisms may be offered or alignment surgery with adjustable sutures can be performed.
Symptoms in this category include appearance concerns such as bulging of the eyes, eyelid retraction and fat pockets, as well as exposure complaints of foreign body sensation, glare, dryness or secondary tearing. Objective measures of appearance change include eyelid retraction (measured in millimeters), proptosis (measured with the Hertel exophthalmometer), and documentation of redundant skin and fat prolapse.  Measures of exposure include corneal staining or ulceration. Rarely a tarsorrhaphy (temporarily suturing the upper and lower lids) or emergency orbital decompression may be required for severe exposure or corneal ulceration. Once the inflammatory phase has settled, management for proptosis might include orbital decompression and for eyelid retraction may include upper lid lowering from an anterior or posterior approach or lower lid elevation.31  These surgical measures often relieve many of the exposure complaints. ITEDS is a non-profit society dedicated to educating the public and physicians about thyroid eye disease as well as conducting research to understand the disease and lead to prevention and cures.
Hyperthyroidism is a set of disorders that involve excess synthesis and secretion of thyroid hormones by the thyroid gland, which leads to the hypermetabolic condition of thyrotoxicosis. Bilateral erythematous infiltrative plaques on lower extremities in 42-year-old man with Graves disease are consistent with pretibial myxedema. If the etiology of thyrotoxicosis is not clear after physical examination and other laboratory tests, it can be confirmed by scintigraphy: the degree and pattern of isotope uptake indicates the type of thyroid disorder. Treatment of hyperthyroidism includes symptom relief, as well as therapy with antithyroid medications, radioactive iodine-131 (131I), or thyroidectomy. Guidelines for the management of hyperthyroidism and other causes of thyrotoxicosis have been developed by the American Thyroid Association and the American Association of Clinical Endocrinologists.[2] These guidelines include 100 evidence-based recommendations concerning the care of these patients. Hyperthyroidism is a set of disorders that involve excess synthesis and secretion of thyroid hormones by the thyroid gland. Thus, although many clinicians (endocrinologists excluded) use the terms hyperthyroidism and thyrotoxicosis interchangeably, the 2 words have distinct meanings.
The most common forms of hyperthyroidism include diffuse toxic goiter (Graves disease), toxic multinodular goiter (Plummer disease), and toxic adenoma (see Etiology).
The most reliable screening measure of thyroid function in the healthy ambulatory adult population is the TSH level.
Treatment of hyperthyroidism includes symptom relief, as well as therapy with antithyroid medications, radioactive iodine, or thyroidectomy. Normally, the secretion of thyroid hormone is controlled by a complex feedback mechanism involving the interaction of stimulatory and inhibitory factors (see the image below). Binding of TSH to receptors on the thyroid gland leads to the release of thyroid hormonesa€”primarily T4 and to a lesser extent T3.
Any process that causes an increase in the peripheral circulation of unbound thyroid hormone can cause thyrotoxicosis. In Graves disease, circulating autoantibodies against the thyrotropin receptor provide continuous stimulation of the thyroid gland. The underlying pathophysiology of Graves ophthalmopathy (also called thyroid-associated orbitopathy) is not completely characterized. These immune processes lead to an active phase of inflammation, with lymphocyte infiltration of the orbital tissue and release of cytokines that stimulate orbital fibroblasts to multiply and produce mucopolysaccharides (glycosaminoglycans), which absorb water. Cigarette smoking and a high TSH receptor autoantibody level are significant risk factors for ophthalmopathy. Several genetic syndromes have been associated with hyperthyroidism, especially autoimmune thyroid disease.
A number of disorders of thyroid function have been found to be caused by mutations in the TSHR gene, which encodes the TSH receptor protein. Type II autoimmune polyendocrine syndrome is associated with hyperthyroidism and hypothyroidism, as well as type 1 diabetes mellitus and adrenal insufficiency.
Autoimmune thyroid disease has a higher prevalence in patients with human leukocyte antigen (HLA)-DRw3 and HLA-B89. With the availability of genome-wide association studies, more than a dozen genes and gene regions have been found to be associated with an increased risk for development of thyrotoxicosis, particularly Graves disease.[5, 6, 7, 8, 9, 10] Unsurprisingly, these studies have shown associations between these same genes and the development of other endocrine autoimmune disorders, such as type 1 diabetes mellitus. The loci for which specific function can be deduced appear to involve genes related to HLA, non-HLA immune function, and thyroid function.[9] However, the odds ratios that have been determined generally indicate only a mildly increased risk for Graves disease. Most of the genome-wide association studies have focused on diffuse toxic goiter (ie, Graves disease).
The most important autoantibody is TSI, which is directed toward epitopes of the TSH receptor and acts as a TSH-receptor agonist. Iodine 123 (123I) nuclear scintigraphy: 123I scans of normal thyroid gland (A) and common hyperthyroid conditions with elevated radioiodine uptake, including Graves disease (B), toxic multinodular goiter (C), and toxic adenoma (D). The next most common cause of thyrotoxicosis is subacute thyroiditis (approximately 15-20% of cases), a destructive release of preformed thyroid hormone. Absence of iodine 123 (123I) radioactive iodine uptake in patient with thyrotoxicosis and subacute painless or lymphocytic thyroiditis. Three multinuclear giant cell granulomas observed in fine-needle aspiration biopsy of thyroid from patient with thyrotoxicosis from subacute painful or granulomatous thyroiditis. Toxic multinodular goiter (Plummer disease) accounts for 15-20% of thyrotoxicosis cases (see the image below).
Symptoms of thyrotoxicosis are mild, often because only a slight elevation of thyroid hormone levels is present, and the signs and symptoms of thyrotoxicosis often are blunted (apathetic hyperthyroidism) in older patients. Iodide-induced thyrotoxicosis (Jod-Basedow syndrome) occurs in patients with excessive iodine intake (eg, from an iodinated radiocontrast study). Iodide-induced thyrotoxicosis appears to result from loss of the normal adaptation of the thyroid to iodide excess. Patients with a molar hydatidiform pregnancy or choriocarcinoma have extremely high levels of beta human chorionic gonadotropin (I?-hCG), which can weakly activate the TSH receptor.
Graves disease is the most common form of hyperthyroidism in the United States, causing approximately 60-80% of cases of thyrotoxicosis.


Toxic multinodular goiter (15-20% of thyrotoxicosis) occurs more frequently in regions of iodine deficiency. Autoimmune thyroid disease occurs with the same frequency in Caucasians, Hispanics, and Asians but at lower rates in African Americans. Hyperthyroidism from toxic multinodular goiter and toxic adenoma is permanent and usually occurs in adults.
Patients with Graves disease may become hypothyroid in the natural course of their disease, regardless of whether treatment involves radioactive iodine or surgery. Thyroid hormone excess causes left ventricular thickening, which is associated with an increased risk of heart failure and cardiac-related death. A study by Zhyzhneuskaya et al of patients with subclinical hyperthyroidism due to Graves disease suggested that approximately one third will progress to overt hyperthyroidism, about one third will develop normalized thyroid function, and just under one third will remain in a state of subclinical hyperthyroidism.
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Burches-Feliciano MJ, Argente-Pla M, Garcia-Malpartida K, Rubio-Almanza M, Merino-Torres JF. Severe proptosis, periorbital edema, and eyelid retraction from thyroid-related orbitopathy.
Gross photo of subtotal thyroidectomy for diffuse toxic goiter (Graves Disease) showing homogenous enlargement without nodules. Low-power photomicrograph showing diffuse papillary hyperplasia (hallmark histologic feature of Graves disease). High-power photomicrograph showing papillary hyperplasia of follicular cells with increased nuclear size and small nucleoli. Medscape's clinical reference is the most authoritative and accessible point-of-care medical reference for physicians and healthcare professionals, available online and via all major mobile devices. The clinical information represents the expertise and practical knowledge of top physicians and pharmacists from leading academic medical centers in the United States and worldwide. More than 6000 evidence-based and physician-reviewed disease and condition articles are organized to rapidly and comprehensively answer clinical questions and to provide in-depth information in support of diagnosis, treatment, and other clinical decision-making. More than 1000 clinical procedure articles provide clear, step-by-step instructions and include instructional videos and images to allow clinicians to master the newest techniques or to improve their skills in procedures they have performed previously. More than 100 anatomy articles feature clinical images and diagrams of the human body's major systems and organs. More than 7100 monographs are provided for prescription and over-the-counter drugs, as well as for corresponding brand-name drugs, herbals, and supplements.
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All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This interferes with flow of information through the optic nerve connecting the eyes to the brain. As a summary grade, VISA lists optic neuropathy as present or absent since most clinicians would attempt some treatment for this condition if present.
The common treatment for TED optic neuropathy initially is high dose corticosteroids either by intravenous route (1 gram Methyl-prednisolone over 30 minutes on alternate days for 3 treatments) or oral route (100 mg prednisone daily on a tapering dose) with an expectation that vision should improve within days of therapy.
Radiotherapy is administered using a lateral port focused behind the globe to minimize the risk of retinal or lens exposure; it is divided into 10 fractions of 200 rads over two weeks [23] and is contraindicated in diabetics because of the risk of inciting or aggravating retinopathy. The worst scores from any of the four eyelids are recorded in the inflammatory score table on the far right section of the table. The additional grading scores for chemosis and lid edema allow for documentation of more subtle changes in inflammatory features between visits.
If the score is less than 4 out of 10, and there is no deterioration based on history or sequential clinical examination, conservative management is offered with reassurance, cool compresses, nocturnal head elevation, and non-steroidal anti-inflammatories.
The most common forms of hyperthyroidism include diffuse toxic goiter (Graves disease), toxic multinodular goiter (Plummer disease), and toxic adenoma. Myxedematous changes of skin usually occur in pretibial areas and resemble orange peel in color and texture. The resulting elevation in levels of free thyroxine (FT4), free triiodothyronine (FT3), or both leads to the hypermetabolic condition of thyrotoxicosis. For example, both exogenous thyroid hormone intake and subacute thyroiditis can cause thyrotoxicosis, but neither constitutes hyperthyroidism, because the conditions are not associated with new hormone production.
Together with subacute thyroiditis, these conditions constitute 85-90% of all causes of thyrotoxicosis.
However, antithyroid medications are not effective in thyrotoxicosis from subacute thyroiditis, because these cases result from release of preformed thyroid hormone. Thyrotropin-releasing hormone (TRH) from the hypothalamus stimulates the pituitary to release TSH.
Schematic representation of negative feedback system that regulates thyroid hormone levels. In turn, elevated levels of these hormones act on the hypothalamus to decrease TRH secretion and thus the synthesis of TSH. Dietary inorganic iodide is transported into the gland by an iodide transporter, converted to iodine, and bound to thyroglobulin by the enzyme thyroid peroxidase through a process called organification. More than 99.9% of T4 and T3 in the peripheral circulation is bound to plasma proteins and is inactive.
Disturbances of the normal homeostatic mechanism can occur at the level of the pituitary gland, the thyroid gland, or in the periphery. These antibodies cause release of thyroid hormones and thyroglobulin, and they also stimulate iodine uptake, protein synthesis, and thyroid gland growth. It most likely involves an antibody reaction against the TSH receptor that results in activation of T cells against tissues in the retro-orbital space that share antigenic epitopes with thyroid follicular cells.
In consequence, the extraocular muscles thicken and the adipose and connective tissue of the retro-orbit increase in volume. In addition, patients who smoke appear to be more likely to experience worsening of their ophthalmopathy if treated with radioactive iodine, as do patients who have high pretreatment T3 levels and posttherapy hypothyroidism. Autoimmune thyroid disease, including Hashimoto hypothyroidism and Graves disease, often occurs in multiple members of a family. Graves disease is felt to be an HLA-related, organ-specific defect in suppressor T-cell function.
One study, however, found an association between development of toxic multinodular goiter (Plummer disease) and a single-nucleotide polymorphism (SNP) in the TSHR gene.[11] . Clearly, patients in borderline iodine-deficient areas of the world develop nodular goiter, often with areas of thyroid autonomy.
Graves disease is an organ-specific autoimmune disorder characterized by a variety of circulating antibodies, including common autoimmune antibodies, as well as anti-TPO and anti-TG antibodies. Like TSH, TSI binds to the TSH receptor on the thyroid follicular cells to activate thyroid hormone synthesis and release and thyroid gland growth (hypertrophy).
Generalized hypervascularity is visible throughout gland (note red areas), which often can be heard as hum or bruit with stethoscope. Clinical findings specific to Graves disease include thyroid ophthalmopathy (periorbital edema, chemosis [conjunctival edema], injection, or proptosis) and, rarely, dermopathy over the lower extremities. A typical nuclear scintigraphy scan shows no radioactive iodine uptake (RAIU) in the thyrotoxic phase of the disease (see the images below). It occurs more commonly in elderly individuals, especially those with a long-standing goiter.


However, very high thyroid hormone levels may occur in this condition after high iodine intake (eg, with iodinated radiocontrast or amiodarone exposure). The antiarrhythmic drug amiodarone, which is rich in iodine and bears some structural similarity to T4, may cause thyrotoxicosis (see Thyroid Dysfunction Induced by Amiodarone Therapy). It is treated with cessation of the excess iodine intake and with administration of antithyroid medication. At very high levels of I?-hCG, activation of the TSH receptors is sufficient to cause thyrotoxicosis.
These lesions maintain the ability to make thyroid hormone, and in patients with bulky tumors, production may be high enough to cause thyrotoxicosis. Most persons in the United States receive sufficient iodine, and the incidence of toxic multinodular goiter in the US population is lower than that in areas of the world with iodine deficiency. Compared with regions of the world with less iodine intake, the United States has more cases of Graves disease and fewer cases of toxic multinodular goiters.
Toxic multinodular goiters occur in patients who usually have a long history of nontoxic goiter and who therefore typically present when they are older than age 50 years. After normalization of thyroid function with antithyroid medications, radioactive iodine ablation usually is recommended as the definitive therapy.
Those who become hypothyroid after radioactive iodine therapy are easily maintained on thyroid hormone replacement therapy, with T4 taken once daily. Bone loss, measured by bone mineral densitometry, can be seen in severe hyperthyroidism at all ages and in both sexes. Hyperthyroidism and other causes of thyrotoxicosis: management guidelines of the American Thyroid Association and American Association of Clinical Endocrinologists.
Activating Gsalpha mutations: analysis of 113 patients with signs of McCune-Albright syndrome--a European Collaborative Study. Autoimmune adrenal insufficiency and autoimmune polyendocrine syndromes: autoantibodies, autoantigens, and their applicability in diagnosis and disease prediction. Association of Fc receptor-like 5 (FCRL5) with Graves' disease is secondary to the effect of FCRL3.
Follow-up of potential novel Graves' disease susceptibility loci, identified in the UK WTCCC genome-wide nonsynonymous SNP study.
Recent advances in the association studies of autoimmune thyroid disease and the functional characterization of AITD-related transcription factor ZFAT. Polymorphisms in the ADRB2 gene and Graves disease: a case-control study and a meta-analysis of available evidence. Germline polymorphism of codon 727 of human thyroid-stimulating hormone receptor is associated with toxic multinodular goiter. Serum TSH, T(4), and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III). Management of thyroid dysfunction during pregnancy and postpartum: an Endocrine Society clinical practice guideline. Radioiodine therapy versus antithyroid drugs in Graves' disease: a meta-analysis of randomized controlled trials. Radiation safety in the treatment of patients with thyroid diseases by radioiodine A?A?A?i: practice recommendations of the american thyroid association. Randomized controlled trial on single dose steroid before thyroidectomy for benign disease to improve postoperative nausea, pain, and vocal function. This patient also had optic nerve dysfunction and chemosis (conjunctival edema) from thyroid-related orbitopathy.
RAIU or scanning should not be performed in a woman who is pregnant (with the exception of a molar pregnancy) or breastfeeding. Topics are richly illustrated with more than 40,000 clinical photos, videos, diagrams, and radiographic images. The articles assist in the understanding of the anatomy involved in treating specific conditions and performing procedures.
Check mild interactions to serious contraindications for up to 30 drugs, herbals, and supplements at a time.
Plus, more than 600 drug monographs in our drug reference include integrated dosing calculators. The severity of the neuropathy is reflected in the individual measurements of central and colour vision. In most cases, this treatment will cause incomplete or only temporary visual improvement so that surgical decompression of the medial wall is required (through a Lynch, transcaruncular or endoscopic transethmoidal approach) or through a lateral approach (thinning the outer boney wall of the orbit near the apex) in order to relieve pressure more permanently on the optic nerve at the crowded orbital apex.
An additional point is assigned for diurnal variation of symptoms, to reflect the variability in congestion typically seen during the active phase. Autoantibody testing, and nuclear thyroid scintigraphy in some cases, can provide useful etiologic information. This results in the formation of monoiodotyrosine (MIT) and diiodotyrosine (DIT), which are coupled to form T3 and T4; these are then stored with thyroglobulin in the thyroida€™s follicular lumen.
Regardless of etiology, the result is an increase in transcription in cellular proteins, causing an increase in the basal metabolic rate. This gene encodes the stimulatory G-protein alpha subunit, which is a key component of many signal transduction pathways. Similarly, subacute painful or granulomatous thyroiditis occurs more frequently in patients with HLA-Bw35. When members of this population move to areas of sufficient iodine intake, thyrotoxicosis occurs. This results in the characteristic picture of Graves thyrotoxicosis, with a diffusely enlarged thyroid, very high radioactive iodine uptake, and excessive thyroid hormone levels compared with a healthy thyroid (see the images below). This autoimmune condition may be associated with other autoimmune diseases, such as pernicious anemia, myasthenia gravis, vitiligo, adrenal insufficiency, celiac disease, and type 1 diabetes mellitus. Absence of thyroid uptake, low T3-to-T4 ratio, and low ESR confirm diagnosis of subacute painless thyroiditis. Thyroid hormone excess develops very slowly over time and often is only mildly elevated at the time of diagnosis.
The excess secretion of thyroid hormone occurs from a benign monoclonal tumor that usually is larger than 2.5 cm in diameter. Iodide-induced thyrotoxicosis also occurs in patients with areas of thyroid autonomy, such as a multinodular goiter or autonomous nodule. Usually, after depletion of the excess iodine, thyroid functions return to preexposure levels. Patients with toxic adenomas present at a younger age than do patients with toxic multinodular goiter.
In mild subclinical disease, however, bone loss has been convincingly shown only in postmenopausal women. Customize your Medscape account with the health plans you accept, so that the information you need is saved and ready every time you look up a drug on our site or in the Medscape app. Free T3 acts by binding to nuclear receptors (DNA-binding proteins in cell nuclei), regulating the transcription of various cellular proteins. In many ways, signs and symptoms of hyperthyroidism resemble a state of catecholamine excess, and adrenergic blockade can improve these symptoms. Like other immune diseases, these thyroid conditions occur more frequently in women than in men. Evidence exists that iodine can act as an immune stimulator, precipitating autoimmune thyroid disease and acting as a substrate for additional thyroid hormone synthesis.
Toxic multinodular goiters and toxic adenomas probably will continue to grow slowly in size during antithyroid pharmacotherapy.
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RAIU usually is normal, and the radioactive iodine scan shows only the hot nodule, with the remainder of the normal thyroid gland suppressed because the TSH level is low.



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