Thyroid neoplasms may be benign (adenomas) or malignant (carcinomas). Carcinomas of the follicular epithelium include papillary, follicular, and anaplastic thyroid cancer. Thyroid cancer incidence is ∼14/100,000 per year and increases with age. Papillary thyroid cancer is the most common type of thyroid cancer (70-90%). It tends to be multifocal and to invade locally. Follicular thyroid cancer is difficult to diagnose via FNA because the distinction between benign and malignant follicular neoplasms rests largely on evidence of invasion into vessels, nerves, or adjacent structures. It tends to spread hematogenously, leading to bone, lung, and CNS metastases. Anaplastic carcinoma is rare, highly malignant, and rapidly fatal. Thyroid lymphoma may arise in the background of Hashimoto's thyroiditis and occurs in the setting of a rapidly expanding thyroid mass. Medullary thyroid carcinoma arises from parafollicular (C) cells producing calcitonin and may occur sporadically or as a familial disorder, sometimes in association with multiple endocrine neoplasia type 2.
Features suggesting carcinoma include recent or rapid growth of a nodule or mass, history of neck irradiation, lymph node involvement, hoarseness, and fixation to surrounding tissues. Glandular enlargement may result in compression and displacement of the trachea or esophagus and obstructive symptoms. Age <20 or >45, male sex, and larger nodule size are associated with a worse prognosis.
An approach to the evaluation of a solitary nodule is outlined in Fig. 173-4. Approach to the Pt with a Thyroid Nodule.
| TREATMENT | ||
Thyroid NeoplasmsBenign nodules should be monitored via serial examination. TSH suppression with levothyroxine does not usually reduce nodule size in iodine-sufficient populations. If suppression therapy is used, TSH levels should be reduced to just below the normal range and suppressive therapy should not exceed 6-12 months if unsuccessful. Follicular adenomas cannot be distinguished from follicular carcinomas on the basis of cytologic analysis of FNA specimens. The extent of surgical resection (lobectomy vs. near-total thyroidectomy) should be discussed prior to surgery. Near-total thyroidectomy is required for papillary and follicular carcinoma and should be performed by a surgeon who is highly experienced in the procedure. If risk factors and pathologic features indicate the need for radioiodine treatment, the pt should be treated for several weeks postoperatively with liothyronine (T3, 25 µg two to three times a day), followed by withdrawal for an additional 2 weeks, in preparation for postsurgical radioablation of remnant tissue. A therapeutic dose of 131 I is administered when the TSH level is >25 IU/L. Alternatively, recombinant TSH (0.9 mg) is administered as two daily consecutive injections followed by 131 I 24 h after the second injection. This appears to be equally effective as thyroid hormone withdrawal for radioablation therapy. For pts either at intermediate or high risk of recurrence, TSH levels should be kept to 0.1-0.5 mIU/L and <0.1 mIU/L, respectively, if there are no strong contraindications to mild thyrotoxicosis. TSH should be <0.1 mIU/L for those with known metastatic disease. Follow-up scans and serum thyroglobulin levels (acting as a tumor marker in an athyreotic pt) should be performed at regular intervals after either thyroid hormone withdrawal or administration of recombinant human TSH. Kinase inhibitors are being explored as a means to target pathways known to be active in thyroid cancer, including the RAS, BRAF, RET, EGFR, VEGFR, and angiogenesis pathways. The management of medullary thyroid carcinoma is surgical, as these tumors do not take up radioiodine. Testing for RET mutations should be performed to assess for the presence of MEN 2, and the family should be screened if testing is positive. Following surgery, serum calcitonin provides a marker of residual or recurrent disease. |