Endocrine Lec: 4 Dr. Mohammed Alhamdany Graves’ ophthalmopathy

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Lec: 4 Dr.Mohammed Alhamdany

Graves’ ophthalmopathy

This condition is immunologically mediated but the autoantigen has not been identified.


There is cytokine-mediated proliferation of fibroblasts which secrete hydrophilic glycosaminoglycans. The resulting increase in interstitial fluid content, combined with a chronic inflammatory cell infiltrate, causes marked swelling and ultimately fibrosis of the extraocular muscles and a rise in retrobulbar pressure. The eye is displaced forwards (proptosis, exophthalmos) and in severe cases there is optic nerve compression.

Clinical feature:

It is helpful to distinguish patients with active inflammation from those in whom the inflammation has ‘burnt out’. The sign of active inflammation include:

1- periorbital oedema.

2- conjunctival inflammation.

3- changing orbital signs.

Eye disease is detectable in up to 50% of thyrotoxic patients at presentation, but active ocular inflammation may occur before or after thyrotoxic episodes. It is more common in cigarette smokers and is exacerbated by poor control of thyroid function, especially hypothyroidism.

The symptoms include:

1- There may be excessive lacrimation made worse by wind and bright light.

2- A ‘gritty’ sensation in the eye.

3- Pain due to conjunctivitis or corneal ulceration.

4- There may be reduction of visual acuity and/or visual fields as a consequence of corneal edema or optic nerve compression. Other signs of optic nerve compression include reduced colour vision and a relative afferent pupillary defect, if the extraocular muscles are involved diplopia results.


1- The majority of patients require no treatment.

2- Smoking cessation.

3- Methylcellulose eye drops and gel reduce gritty discomfort of dry eyes.

4- Tinted glasses reduce the excessive lacrimation triggered by sun or wind.

5- In patients with mild Graves’ ophthalmopathy, oral selenium (100 μg twice daily for 6 months) improves quality of life, reduces ocular involvement and slows progression of disease; the benefits persisted 6 months following cessation of therapy.

6- More severe inflammatory episodes are treated with glucocorticoids (e.g. daily oral prednisolone or pulsed IV methylprednisolone).

7- Sometimes orbital radiotherapy.

8- Immunosuppressant therapies, such as ciclosporin, in combination with glucocorticoids.

9- Loss of visual acuity is an indication for urgent surgical decompression of the orbit. In ‘burnt-out’ disease, surgery to the eyelids and/or ocular muscles may improve conjunctival exposure, cosmetic appearance and diplopia.

Pretibial myxoedema

This infiltrative dermopathy occurs in fewer than 10% of patients with Graves’ disease and has similar pathological features as occur in the orbit. It takes the form of raised pink-coloured or purplish plaques on the anterior aspect of the leg, and may be itchy and the skin may have a ‘peau d’orange’ appearance, rarely the face and arms are affected. Treatment is rarely required, but in severe cases topical glucocorticoids may be helpful.

Hashimoto’s thyroiditis


Hashimoto’s thyroiditis is characterized by destructive lymphoid infiltration of the thyroid, ultimately leading to a varying degree of fibrosis and thyroid enlargement. There is an increased risk of thyroid lymphoma, although this is rare.

Pathologically the disease of two types; the first called ‘Hashimoto’s thyroiditis’ for patients with positive antithyroid peroxidase autoantibodies and a firm goitre who may or may not be hypothyroid, and the second called ‘spontaneous atrophic hypothyroidism’ for hypothyroid patients without a goitre in whom TSH receptor-blocking antibodies may be more important than antiperoxidase antibodies.

Hashimoto’s thyroiditis increases in incidence with age and affects approximately 3.5 per 1000 women.

Clinical feature and investigation: Many present with a small or moderately sized diffuse goiter, which is characteristically firm or rubbery in consistency. Around 25% of patients are hypothyroid at presentation. In the remainder, serum T4 is normal and TSH normal or raised, but these patients are at risk of developing overt hypothyroidism in future years.

Antithyroid peroxidase antibodies are present in the serum in more than 90% of patients with Hashimoto’s thyroiditis. In those under the age of 20 years, antinuclear factor (ANF) may also be positive.

Treatment: Levothyroxine therapy is indicated as treatment for hypothyroidism, and also to shrink an associated goiter.

Transient thyroiditis

Subacute (de Quervain’s) thyroiditis

In its classical painful form, subacute thyroiditis is a transient inflammation of the thyroid gland occurring after infection with Coxsackie, mumps or adenoviruses, and rarely caused by drug like interferon-α and lithium.

Clinical feature: There is pain in the region of the thyroid that may radiate to the angle of the jaw and the ears, and is made worse by swallowing, coughing and movement of the neck. The thyroid is usually palpably enlarged and tender. Systemic upset is common. Affected patients are usually females aged 20–40 years.

Investigation: inflammation in the thyroid gland occurs and is associated with release of colloid and stored thyroid hormones, but also with damage to follicular cells and impaired synthesis of new thyroid hormones. As a result, T4 and T3 levels are raised for 4–6 weeks until the pre-formed colloid is depleted. Thereafter, there is usually a period of hypothyroidism of variable severity before the follicular cells recover and normal thyroid function is restored within 4–6 months. Low-titer thyroid autoantibodies appear transiently in the serum, and the erythrocyte sedimentation rate (ESR) is usually raised. High-titre autoantibodies suggest an underlying autoimmune pathology and greater risk of recurrence and ultimate progression to hypothyroidism.

Treatment: The pain and systemic upset usually respond to simple measures such as non-steroidal anti-inflammatory drugs (NSAIDs). Occasionally, however, it may be necessary to prescribe prednisolone 40 mg daily for 3–4 weeks. The thyrotoxicosis is mild and treatment with a β-blocker is usually adequate. Antithyroid drugs are of no benefit because thyroid hormone synthesis is impaired rather than enhanced. levothyroxine can be prescribed temporarily in the hypothyroid phase.
Post-partum thyroiditis

Pathophysiology: The maternal immune response, which is modified during pregnancy to allow survival of the fetus, is enhanced after delivery and may unmask previously unrecognized subclinical autoimmune thyroid disease. Surveys have shown that transient biochemical disturbances of thyroid function occur in 5–10% of women within 6 months of delivery. Those affected are likely to have anti-thyroid peroxidase antibodies in the serum in early pregnancy.

Clinical feature and investigation: Symptoms of thyroid dysfunction are rare. However, symptomatic thyrotoxicosis presenting for the first time within 12 months of childbirth is likely to be due to post-partum thyroiditis and the diagnosis is confirmed by a negligible radio-isotope uptake. The thyroid function test show feature of primary hyperthyroidism at beginning than show feature of primary hypothyroidism, than retune back to the normal.

Treatment: same as painless subacute thyroiditis.


Postpartum thyroiditis tends to recur after subsequent pregnancies, and eventually patients progress over a period of years to permanent hypothyroidism.

Simple and multinodular goitre

These terms describe diffuse or multinodular enlargement of the thyroidThese terms describe diffuse or multinodular enlargement of the thyroid.

Simple diffuse goiter

This form of goitre usually presents between the ages of 15 and 25 years, often during pregnancy, there is a tight sensation in the neck, particularly when swallowing. The goitre is soft and symmetrical, and the thyroid enlarged to two or three times normal. There is no tenderness, lymphadenopathy or overlying bruit. All thyroid investigations are normal and need no treatment.


The goitre usually regresses. In some, however, the unknown stimulus to thyroid enlargement persists and, as a result of recurrent episodes of hyperplasia and involution during the following 10–20 years, the gland becomes multinodular with areas of autonomous function.

Multinodular goitre

Natural history:

Clinical features and investigations

Multinodular goitre is usually diagnosed in patients presenting with thyrotoxicosis, a large goitre with or without tracheal compression, or sudden painful swelling caused by haemorrhage into a nodule or cyst. The goitre is nodular or lobulated on palpation and may extend retrosternally. Very large goitres may cause mediastinal compression with stridor, dysphagia and obstruction of the superior vena cava. Hoarseness due to recurrent laryngeal nerve palsy can occur, but is far more suggestive of thyroid carcinoma.

The diagnosis can be confirmed by ultrasonography and/or thyroid scintigraphy. In patients with large goiters, a flow-volume loop is a good screening test for significant tracheal compression, and confirm by a CT or MRI of the thoracic inlet. Nodules should be evaluated for the possibility of thyroid neoplasia.


If the goitre is small: no treatment is necessary but annual thyroid function testing should be arranged, as the natural history is progression to a toxic multinodular goitre.

For euthyroid patients: Thyroid surgery is indicated for large goiters which cause mediastinal compression or which are cosmetically unattractive. 131I can result in a significant reduction in thyroid size and may be of value in elderly patients. Levothyroxine therapy is of no benefit in shrinking multinodular goitres in iodine-sufficient countries and may simply aggravate any associated thyrotoxicosis.

For thyrotoxicosis patients: treatment is usually with 131I, In thyrotoxic patients with a large goitre, thyroid surgery may be indicated. Long-term treatment with antithyroid drugs is not usually employed, as relapse is invariable after drug withdrawal.

For Asymptomatic patients with subclinical thyrotoxicosis: are increasingly being treated with 131I on the grounds that a suppressed TSH is a risk factor for atrial fibrillation and, particularly in post-menopausal women, osteoporosis.

With best regard

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