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Graves' disease

Graves-Basedow disease is a form of thyroiditis, an autoimmune disorder that stimulates the thyroid gland, being the most common cause of hyperthyroidism (overactivity of the thyroid). Also known in the English-speaking world simply as Graves' disease, it occurs most frequently in women (8:1 compared to men) of middle age. Symptoms include fatigue, weight loss and rapid heart beat. Because similar antibodies to those stimulating the thyroid also affect the eye, eye symptoms are also commonly reported. Treatment is with medication that reduces the production of thyroid hormone (thyroxin), surgery thyroidectomy or with radioactive iodine if refractory. more...

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Christina Rossetti famously suffered from this disease in later life.

Signs and symptoms

Graves-Basedow disease is a disorder characterized by a triad of hyperthyroidism, goitre, and exophthalmos (bulging eyeballs).

Due to the many physiological actions of thyroid hormone, many symptoms and signs are linked to Graves' disease:

  • Cardiac: cardiac arrhythmias (especially atrial fibrillation), tachycardia (increased heart rate), collapsing pulse and widened pulse pressure (difference between systolic and diastolic BP) and congestive cardiac failure with peripheral edema, ascites, anasarca.
  • Endocrine: weight loss in the presence of increased appetite, intolerance to heat, elevated basal metabolic rate
  • Dermatological: profuse sweating, thyroid acropachy (clubbing) of the fingernails, onycholysis (fingernail destruction), palmar erythema, pretibial myxedema (3 to 5% of Graves' patients, not to be confused with the myxedema of hypothyroidism)
  • Neurological: tremor (especially noticeable on extending the arms), apprehension, weakness, headache, proximal myopathy (difficulty rising from a chair or squatting position) and hyperactive deep tendon reflexes
  • Gastrointestinal: diarrhea (common), vomiting (rare)
  • Ophthalmological: thyroid eye disease (TED) characteristic of Graves disease include lid retraction (Dalrymple sign) above the superior corneoscleral limbus, lid lag (von Graefe's sign), proptosis or forward displacement of the globes, periorbital swelling and chemosis.

Extremely manifested disease that can sometimes be life-threatening is called the thyroid storm.


On the basis of the signs and symptoms, thyroid hormone (thyroxine or T4, triiodothyronine or T3) and thyroid-stimulating hormone (TSH) are determined in the medical laboratory. Free T4 and Free T3 is markedly elevated, while TSH is suppressed due to negative feedback. An elevated protein-bound iodine level may be detected. A large goiter is sometimes seen on X-rays.

Thyroid-stimulating antibodies may be detected serologically.


Most features are due to the production of autoantibodies that bind to the TSH receptor, which is present on the follicular cells of the thyroid (the cells that produce thryoid hormone). These antibodies activate the cells in the same fashion as TSH itself, leading to an elevated production of thyroid hormone.

The infiltrative opthalmopathy (thyroid eye disease) that is frequently encountered has been explained by the expression of the TSH receptor on retroorbital tissue.

The exact cause of antibody production is not known. Viral infection may trigger antibodies against its epitopes, which cross-react with the human TSH receptor. There appears to be a genetic predisposition for Graves' disease, suggesting that some people are more prone than others to develop TSH receptor activating antibodies due to a genetic cause. HLA DR (especially DR3) appears to play a significant role.


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An update on thyroid eye disease
From American Family Physician, 6/1/05 by Anne D. Walling

The prevalence of Graves' disease in the United Kingdom is estimated at 1 to 2.7 percent of the population, and eye complications occur in one fourth to one half of cases. Changes in the eyes may develop before the onset of Graves' disease, and occasionally only one eye is involved. Although it rarely causes vision loss, thyroid eye disease can be painful and distressing with significant visual and cosmetic sequelae. Cawood and colleagues examined the clinical features of thyroid eye disease to clarify the pathophysiology of the condition and potential treatments.

Histologically, circulating sensitized orbital tissue-specific T lymphocytes and a local inflammatory cellular infiltrate are present in thyroid eye disease. The orbital fibroblasts appear key to the hypertrophy of adipose tissue and accumulation of glycosaminoglycans in the orbit. Despite recent research, the pathophysiology of Graves' disease remains unclear.

The clinical features of thyroid eye disease include ocular pain, photophobia, chemosis, diplopia, exophthalmos, and eye irritation ("gritty eyes"). Physical signs include proptosis, edema of the eyelid and conjunctiva, and diplopia (Table 1). The NO SPECS mnemonic often is used as a scoring system for severity of eye change (Table 2). Patients who develop blurred vision, reduced visual acuity or color perception, pupillary signs, or visual field defects may have optic neuropathy and must be referred to an ophthalmologist immediately. The clinical features of thyroid eye disease may persist after the phase of acute inflammation because of residual scarring of orbital tissues. Thyroid eye disease also may be accompanied by skin changes in the lower legs (pretibial myxedema), finger nails (acropachy), and at sites of previous skin trauma.

Smoking appears to be a major risk factor in developing eye symptoms in Graves' disease, because patients with eye involvement are four times more likely to be smokers than never-smokers. The risk also is associated with the number of cigarettes smoked per day. Other risk factors for thyroid eye disease are less well established. Older men may have a higher risk of more severe disease. Radioiodine therapy may cause a flare-up of eye disease.

Full ophthalmic assessment including computed tomography or magnetic resonance imaging can indicate the degree of involvement of the extraocular muscles and soft tissues. Orbital biopsy is required occasionally to establish the diagnosis.

In mild cases, only symptomatic care to protect the eyes from drying is required. Up to 35 percent of patients require high-dose steroids or orbital decompression therapy. The response rates to steroid therapy range from 33 to 66 percent. The dosage and regimen are individualized because no large randomized placebo-controlled trials have been conducted. Orbital radiotherapy also has been suggested for reducing progression of thyroid eye disease, but clinical trials have not demonstrated improvements, and adverse effects include cataracts, retinopathy, and risk of malignancy. Surgical decompression is indicated for severe cases during the acute phase and to improve function and appearance in later stages of the condition. Overall, outcomes of all treatments for thyroid eye disease are disappointing. More than one half of patients report persistent diplopia, about one third are dissatisfied with the cosmetic result, and more than one fourth have low visual acuity.

Potential future treatments include anticytokine therapy, particularly anti-tumor necrosis factor-alpha agents. Side effects limit use of these agents. Octreotide and colchicine have given disappointing results in recent clinical trials. [NOTE: Colchicine is no longer available in the United States.] The authors conclude that increased understanding of thyroid eye disease will likely lead to improvement of treatments in the future.

Cawood T, et al. Recent developments in thyroid eye disease. BMJ August 14, 2004;329:385-90.

COPYRIGHT 2005 American Academy of Family Physicians
COPYRIGHT 2005 Gale Group

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