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Thyroid Cancer
131 I therapy of differentiated thyroid carcinoma. Based on its concentration by thyroid cancer cells 131I is used for therapy in patients with papillary and follicular thyroid carcinoma for both ablation of thyroid remnants and treatment of metastases. For ablation 131I is usually given in a dosage of 1.85-3.7 GBq (50-100 mCi) 4 to 6 weeks after total or near-total thyroidectomy. For pre-ablation diagnostic 131I scintigraphy low tracer dosages are recommended in order to avoid thyroid tissue stunning (1). During post-surgery period any thyroid hormone treatment is withheld. Ablation of residual normal thyroid tissue may enable subsequent scintigraphic detection and possibly radionuclide treatment of local or distant metastases, which may not sufficiently concentrate 131I in the presence of thyroid remnants. For treatment of metastases 131I is often administered, following TSH stimulation obtained after thyroid hormone withdrawal, in a dosage of 7.4 GBq (200 mCi), which usually may deliver appropriate radiation doses per gram thyroid cancer tissue. Lower dosage is recommended (80-120 mCi) if diffuse lung metastases are present in order to prevent lung fibrosis (2). The efficacy of 131I therapy (Fig. 1) has principally been documented in terms of survival. Patients treated with surgery and 131I appear to have a significantly longer survival than patients treated with surgery alone (3). A better prognosis has been found for patients with 131I-avid metastases (4) and therapy is less effective in bone metastases (5). In the treatment of bone metastases 131I therapy has been combined with surgery, radiotherapy and more recently with embolization (6). Also the combination with surgery is advocated for the treatment of neck recurrences (1).
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Figure 1. 131I-therapy of liver metastases in a patient with follicular thyroid carcinoma. Initial scintigraphy (A) and CT (B) showing extensive liver metastases with intense 131I uptake. After a cumulative dose of 500 mCi 131I a significant reduction is observed (C, D).
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Therapy possibilities in 131I-non-avid thyroid carcinoma. Medullary thyroid cancer, Hürthle cell carcinoma, poorly differentiated papillary carcinoma and undifferentiated thyroid carcinoma do not concentrate radioiodine. Also differentiated thyroid carcinoma may loss the ability to concentrate radioiodine during the course of tumor progression. 131I-MIBG has been used for medullary thyroid cancer with objective response in 38% and palliative effect in 50% of the cases. Nevertheless MIBG is concentrated in only 40% of the cases (7). Recently, radioimmunotherapy (single dosis varying from 40 to 100 mCi) with a bispecific antibody (anti-CEA anti-DTPA F6-734) and 131I-labeled bivalent hapten was used in a phase I escalation study. The experimental demonstration of high tissue concentrations of 111In-DTPAOC in Hürthle cell carcinoma (Fig. 2), papillary thyroid carcinoma and medullary thyroid carcinoma (which containing somastotatin receptors subtype sst2, reached the highest octreotide concentration) led to the therapeutic application of radiolabeled octreotide in these malignancies (8). In 12 patients with medullary thyroid carcinoma and in 8 with non-131I-concentrating differentiated thyroid carcinoma cumulative dosages of 6-7.4 GBq 90Y-DOTATOC resulted in anti-tumor effect in 35% of the cases (42% for medullary thyroid carcinoma) (9). Another approach to treat non-131I-concentrating thyroid cancer is based on the improvement of the uptake of radioiodine in tumor tissue by redifferentiation related to administration of retinoids during two months previously to the use of 131I (10).
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Figure 2. Total body anterior images with 131I (A) and 111In-octreotide (B) of a patient with multiple metastases of a Hürthle cell carcinoma of the thyroid. Note that metastases do not concentrate radioiodine. By contrast uptake of 111In-octreotide in tumor sites is intense
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