No abstract

Over a period of 20 years 84 papillary and 82 follicular carcinomas operated on by one surgeon and examined by one pathologist were documented prospectively, treated selectively, and followed for 1 to 20 years (median 7 years). Tumors with a low risk of recurrence or incurable disease-i.e., papillary carcinoma pT1-3 N0 M0 (n = 56) and minimally invasive follicular carcinoma (n = 37)-were treated by a limited-radicality hemithyroidectomy or total thyroidectomy without radioiodine in 79 of the 93 cases (85%). No unfavorable course was observed, and only one curable recurrence (1.3%) developed contralaterally after hemithyroidectomy for papillary cancer. Of the remaining 73 patients, including 100% of those with nodal involvement, 65 (89%) underwent total thyroidectomy with radioiodine. Total thyroidectomy was achieved in 34% of the cases by completion thyroidectomy, based on definitive histologic examination. No instance of a serious, potentially incurable recurrence and no tumor-related death was observed in patients with a papillary TNM stage I+II or with a minimally invasive follicular carcinoma. Five of the patients (6%) with papillary carcinoma, all with TNM stage III or IV, and seven of the patients (8.5%) with follicular carcinoma, all grossly invasive and pT3 or pT4, had tumor-related deaths following total thyroidectomy in all and with remnant ablation in 10 cases. A potentially curable node recurrence occurred in two patients 1 and 10 years, respectively, after primary treatment. Permanent hypoparathyroidism (n = 4) (2.4%) and permanent recurrent laryngeal nerve palsy (n = 2) (1.2%) were observed only in patients with a grossly invasive follicular carcinoma and concomitant benign recurrent goiter. We conclude that (1) hemithyroidectomy or total thyroidectomy without radioiodine is adequate for papillary carcinoma pT1-3 N0 and minimally invasive follicular carcinoma; (2) there were no nodal recurrences in tumors recognized as node-negative; and (3) extracapsular excision of one or both lobes can be carried out technically with low morbidity. The study confirms the prognostic value of age-related TNM classification for papillary carcinoma; classification of follicular thyroid carcinoma as minimally invasive or grossly invasive proved to be useful.

The thyrotropin (TSH) response to thyrotropin-releasing hormone(TRH) (200 mug iv) was determined in 80 surgical patients with nontoxic multinodular goiter. The TSH reserve was normal in multinodular goiter. The TSH reserve was normal in 55 and elavated in 8 patients. No TSH response to TRH (deltaTSH less than or equal to 1 muU/ml) was detectable in 17 patients (21%). Individual and mean serum T4, FT4I and serum T3 values did not differ from normal in 13 of the TRH unresponsive patients; in 4 patients FT4I or serum T3 was marginally elevated. No statistical differences were noted for I131-uptake, PBI131 and conversion rate between controls and TRH unresponsive patients. All patients who failed to respond to TRH were euthyroid on clinical evaluation. Goiters were large multinodular and long-standing in most instances. In 12 tested subjects TRH responsiveness recovered following partial thyroidectomy. In 3 of 7 TRH unresponsive euthyroid patients tested 9-12 days post surgery a transient lack of TSH to respond to TRH was observed. Recovery of TRH responsiveness was accompanied by a significant (P IS LESS THAN 0, 02) decrease in serum T4and FT4I in the euthyroid range, whereas no change in serum T3 occurred. It is suggested that TRH unresponsiveness represents a state of preclinical hyperthyroidism maintained by autonomously functioning goiter compartments.

Serum thyroid hormone and TSH concentrations were measured before and after oral TRH (40 mg) administration in 46 women with preclinical hypothyroidism. Preclinical hypothyroidism was defined as serum T4 in the normal range, a normal or elevated basal serum TSH, and an exaggerated serum TSH response to TRH, in the absence of clinical manifestations of hypothyroidism. The results were compared to those in 22 normal women of the same age and body mass index. Overall, the patients had significantly lower mean values for basal T4 [total T4, free T4 index (FT4 index), and free T4] but not for T3; all indices of T4 were lower in those with an elevated basal TSH, but only the FT4 was lower in patients who had normal basal TSH levels and exaggerated TSH responses to TRH. Thyroid reserve, or the increase in serum thyroid hormones after TRH (delta T4, delta FT4, and delta T3) showed an inverse correlation with basal TSH (for delta T4, r = -0.518 and P less than 0.001; for delta FT4, r = -0.442 and P less than 0.05; for delta T3, r = -0.645 and P less than 0.001). Thyroid reserve was lower than normal in those with elevated basal TSH levels, but was normal in those with exaggerated TSH responses to TRH who had normal basal TSH levels. Thus, an elevated basal TSH level, even with basal serum T4 and T3 levels in the normal range, indicates deficient thyroid reserve.