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USMLE - Hyperthyroidism Associated with a Low Iodine Uptake - Subacute de Quervain's Thyroiditis | Step 1, Step 2 CK and Step 3
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USMLE – Hyperthyroidism Associated with a Low Iodine Uptake – Subacute de Quervain’s Thyroiditis

In patients with hyperthyroidism, the thyroid uptake of 131-I is usually high but a low or negligible uptake of iodine occurs in some rarer causes. If the radioactive iodine uptake test is not routinely performed in patients with thyrotoxicosis who do not have obvious Graves’ disease or nodular goiter, the correct diagnosis may not be made and inappropriate treatment may be given.

Subacute (de Quervain’s) thyroiditis
Subacute thyroiditis is a virus-induced (Coxsackie, mumps or adenovirus) inflammation of the thyroid gland which results in release of colloid and its constituents into the circulation.

This form of hyperthyroidism is characterized by pain in the region of the thyroid gland which may radiate to the angle of 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.

Thyroid hormone levels are raised for 4-6 weeks until the preformed colloid is depleted. The iodine uptake is low because the damaged follicular cells are unable to trap iodine and because endogenous TSH secretion is suppressed. Low-titer thyroid autoantibodies appear transiently in the serum, and the ESR is usually raised. The hyperthyroidism is followed by a period of hypothyroidism which is usually asymptomatic and finally by full recovery of thyroid function within 4-6 months. The pain and systemic upset usually respond to simple measures such as aspirin or other non-steroidal anti-inflammatory drugs. Occasionally, however, it may be necessary to prescribe prednisolone 40 mg daily for 3-4 weeks. The hyperthyroidism is mild and treatment with propranolol 160 mg daily is usually adequate. Antithyroid drugs are of no benefit.

Post-partum thyroiditis
The maternal immune response which is modified during pregnancy to allow survival of the fetal homograft is enhanced after delivery and may unmask previously unrecognized subclinical autoimmune thyroid disease. Surveys have shown that transient biochemical disturbances of thyroid function, i.e. hyperthyroidism, hypothyroidism and hyperthyroidism followed by hypothyroidism, lasting a few weeks occur in 5-10% of women within 6 months of delivery. Those affected are likely to possess antithyroid peroxidase (microsomal) antibodies in the serum in early pregnancy. Thyroid biopsy shows a lymphocytic thyroiditis. Symptoms of thyroid dysfunction are rare and there is no association between postnatal depression and abnormal thyroid function tests. However, symptomatic hyperthyroidism presenting for the first time within 6 months of childbirth is unlikely to be due to Graves’ disease, and the diagnosis of post-partum thyroiditis can be confirmed by a negligible radio-iodine uptake.

If treatment of the hyperthyroid phase is necessary, a beta-adrenoceptor antagonist should be prescribed and not an antithyroid drug. Post-partum thyroiditis tends to recur after subsequent pregnancies and eventually patients progress over a period of years to permanent hypothyroidism.

A similar painless form of thyroiditis, unrelated to pregnancy, has been increasingly recognized in North America and Japan and accounts in these countries for up to 20% of all cases of hyperthyroidism.

Iodine-induced hyperthyroidism
The administration of iodine, either in prophylactic iodinization programs in iodine-deficient parts of the world or as a radiographic contrast medium, may result in the development of hyperthyroidism which is usually mild and self-limiting. Affected individuals are thought to have underlying thyroid autonomy, such as nodular goiter or Graves’ disease in remission. This form of hyperthyroidism is now most often seen as a result of treatment with the anti-arrhythmic agent, amiodarone, which contains significant amounts of iodine. In some patients amiodarone causes a thyroiditis-like picture and mild transient hyperthyroidism, but in those with thyroid autonomy severe thyrotoxicosis may be precipitated and may even present for the first time up to 6 months after the drug has been stopped due to its slow release from adipose tissue. Treatment is with an antithyroid drug for as long as amiodarone is prescribed.

Assessment of thyroid function may be difficult in patients taking amiodarone, as the drug inhibits the peripheral conversion of T4 to T3. As a result, in euthyroid individuals it is not uncommon to record markedly elevated serum T4 concentrations and even suppressed serum TSH, but serum T3 is usually in the lower part of the normal range. In those developing hyperthyroidism, serum T3 is clearly elevated but, if the value is equivocal, the decision to treat will depend upon the presence of other features of thyroid disease, such as goiter and ophthalmopathy.

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