Abstract
Thyroid cancer, though uncommon as a clinical entity and as a cause of death, has attracted the attention of clinicians for many years. The reasons for this attention, which is out of proportion to the incidence of the disease, lie in the unique biological behaviour of the variants of the disease. The death rate from thyroid cancer for patients with clinical papillary cancer of the thyroid is probably less than 10per cent (Cady et al, 1976), survival must be measured over decades, and patients with lung metastases have been known to survive for many years with no therapy. Giant and Spindle cell cancer of the thyroid, on the other hand, is one of the most malignant soft tissue tumours known to man; it is almost uniformly fatal, and survival with this disease is measured in months (Rawson and Leeper, 1968). Another unique feature of thyroid cancer as compared to most cancers is that the radioactive form of a precursor (Ill I) used by the normal gland to produce thyroid hormone can be used to treat most of the differentiated forms of thyroid cancer. Lieberman, Foote and Schottenfeld (1972) have classified thyroid cancer as shown in Table 1. This classification is based on the Memorial Hospital series and has relevance to prognosis and therapy. When sex, age, and extent of disease adjustments are made in a particular patient Cady et al (1979) have shown that a fairly accurate prognosis can be made. The histological nature of a particular tumour when modified by the above prognostic features can also be used to guide the type and extent of therapy. The following discussion will focus on the treatment of metastatic thyroid cancer with III I and chemotherapy. Surgery has been covered elsewhere by Thompson, Nishiyama and Harness (1978), and external beam radiation should probably be used only for anaplastic tumours or palliation when other modalities of treatment have failed or in conjunction with chemotherapy. One area which will not be covered in great depth but which is important is the place of thyroid hormone suppression in the management of differentiated thyroid carcinoma. Thyroid hormone replacement blocks thyrotropin (TSH) secretion by the pituitary and thus decreases a presumed growth stimulus to malignant cells. Cady et al (1976) reported that there was
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