Donald A. Meier

TREATMENT OF HYPERTHYROIDISM WITH RADIOACTIVE IODINE

Treatment of hyperthyroidism with RAI has been performed for more than a half century with efficacy and safety. For its optimal use, the physician must employ appropriate patient selection criteria and clinical judgment concerning pretreatment patient preparation. The dose of the 131I needed remains an area of uncertainty and debate; thus far, it has not been possible to resolve the trade-off between efficient definitive cure of hyperthyroidism and the high incidence of post-therapy hypothyroidism. Early side effects are uncommon and readily manageable. Other than the need for long-term monitoring and, in most cases, lifelong L-T4 treatment, late adverse consequences of this treatment remain only conjectural. The available follow-up studies support the current majority opinion of North American thyroid specialists that RAI treatment is an excellent choice for most hyperthyroid patients.

RADIOIODINE UPTAKE AND THYROID SCINTISCANNING

This article reviews the technical aspects and clinical applications of the radioactive iodine uptake test and thyroid scintiscanning. The choice of radionuclide for the tests is discussed. The main uses of the radioactive iodine uptake test are to identify the cause of hyperthyroidism and to aid in the selection of the I-131 dose in the treatment of hyperthyroidism. Factors other than thyroid diseases that alter uptake results are identified. Thyroid scintiscanning is used in the identification of normal and ectopic thyroid tissue, in the diagnosis of the cause of a patients hyperthyroidism, and as part of the evaluation of selected patients with thyroid nodules.

Are Silent Thyroiditis and Postpartum Silent Thyroiditis Forms of Chronic Thyroiditis or Different (New) Forms of Viral Thyroiditis

Subacute (granulomatous) thyroiditis has been regarded as a distinct clinical entity with characteristic histologic findings since the reports of Mygind and De Quervain which appeared near the turn of the century. The 1950 report of Crile and Rumsey1 is noteworthy because of the clear description of the variable clinical aspects of the disease, from the typical acute presentation to the less clinically overt form, which they designated chronic to indicate the ease with which the diagnosis may be missed. Many patients have hyperthyroidism with low 24-h radioactive iodine uptake (RAIU) which resolves spontaneously in several weeks. This is caused by a discharge of stored thyroid hormone occurring when the inflammatory process produces disruption of the thyroid follicles. As the disease resolves there is commonly a phase of hypothyroidism lasting for about 1 month. Within 3 to 6 months recovery is usually complete. Only a small proportion are left with goiter and even fewer have permanent hypothyrodism. In 10% of the patients the disease is unilateral initially.2 It may then spread over a few weeks to involve the rest of the gland.3,4

Is Thyroid Imaging an Overutilized Diagnostic Procedure

The technique for thyroid imaging has improved dramatically over the past 30 years so that modern images are remarkably clear and may provide striking pictures of abnormal thyroid structure. Also the patient radiation burden has been reduced by a factor of 100. However, advanced technology carries a correspondingly advanced price tag. As physicians are being held increasingly accountable for the rising cost of health care it becomes incumbent upon us to consider the cost effectiveness of thyroid imaging in relation to the indications for its use. This issue is particularly pertinent now because of improvement in the sensitivity and reliability of in vitro thyroid function testing. Also, needle biopsy is gaining favor as the procedure of choice for the diagnosis of the thyroid nodule.1

A large substernal goiter as a cause of a pulmonary perfusion defect

A pulmonary perfusion defect was caused by an extremely large anterior mediastinal mass subsequently proved by I-131 imaging to be an intrathoracic extension of a cervical goiter. Substernal goiter is not known to be reported previously as one of the causes of a perfusion defect in lung scanning.

Hypothyroidism and Thyroiditis

Case 1 presented to us in 1982, at age 67, after taking levothyroxine (T4) for 10 yr. Her thyroid was nontender, quite firm, and diffusely enlarged, with an estimated size of 50 g. Her antithyroid microsomal antibody titer was 1:1 600,000 and her antithyroglobulin antibody level was 50 radioimmunoassay (RIA) units*. On a T4 dose of 150 pg daily, her serum thyrotropin [thyroid stimulating hormone (TSH)] level was 3.5 mU/L (normal 0.5–5.2). The presumed diagnosis was chronic lymphocytic (Hashimoto’s) thyroiditis. T4 was continued. In 1987, because her thyroid size had not decreased, she had a fine-needle aspiration biopsy (FNAB), that produced only a few groups of oxyphilic follicular cells (Hurthle cells), consistent with Hashimoto’s thyroiditis, but insufficient for a definite diagnosis. Her goiter was stable until May 1995, when she reported 2 wk of severe anterior neck pain that radiated to her ears and jaw. Thyroid size was still about 50 g, the erythrocyte sedimentation rate (ESR) was 76 mm/h (normal up to 18) and the white blood cell count (WBC) was normal.

Thionamide Drug Therapy

Thionamide antithyroid drug therapy is one of the three standard treatments for hyperthyroidism caused by Graves’ disease, along with surgery and radioactive iodine (131I)(l–3). These treatments, all directed at the thyroid gland, are necessarily imperfect, because none stops production of stimulatory TSH receptor autoantibodies. It seems unlikely that therapy to interrupt the underlying process of thyroid autoimmunity will be available any time soon. Therefore, antithyroid drugs will continue to be needed. This chapter reviews their actions, use, side effects, and role in the management of the hyperthyroid patient.