[Our experience on surgical treatment of papillary thyroid microcarcinoma]. / Nostra esperienza sul trattamento chirurgico del microcarcinoma papillifero della tiroide (PTMC).

The papillary thyroid microcarcinoma (PTMC) is a subtype of the papillary thyroid carcinoma (PTC) 1 cm or less in diameter, bilateral and multifocal in a percentage of 15-20%. We describe our experience on the surgical treatment of 217 patient treated between 2005 and 2008. Our therapeutic algorithm for PTMC includes always total thyroidectomy with surgical exploration of the median cervical compartment and recurrent laryngeal nerve lymph node dissection, reserving the median lymph node dissection only to the cases with pathological lymph nodes and the lateral compartment lymphectomy to the cases that show suspect nodes with or without positive cytology. We usually perform total thyroidectomy rather than partial one, in relation to the high rate of multifocality of papillary microcarcinoma, to reduce rate of recurrencies and to better utilize I131 with diagnostic and curative aims. Complete central compartment dissection is mandatory when pathological nodes are present at surgical exploration. It prevents nodal recurrencies and decrease number of re-operations, that have a greater number of complications or morbidity, including hypoparathyroidism and inferior laryngeal nerve lesions. The rate of nodal metastases is not affected by the site of primitive tumor, but the tumor size does. The rate of nodal metastases varies from 55.7% for tumors 5 mm or less in diameter, to 73.7% for tumors sized from 5 to 10 mm, and is affected from the capsular infiltration, the presence of multiple foci, and the histological type, i.e. sclerosing type. All patients presenting papillary microcarcinoma with invasion of the capsule and extension to the perithyroid tissues, sclerosing histological type, multifocal and/or metastatic to the regional nodes, were treated with radiometabolic therapy and suppressing l-tiroxin administration, according to the guidelines of the Multidisciplinary Group for the Thyroid Cancer of our Institution.

Physiological concentrations of thyrotropin increase cytosolic calcium levels in primary cultures of human thyroid cells.

The activity of TSH, the main regulator of growth and differentiation in the thyroid, has been mainly related to the activation of the adenylyl cyclase cascade. TSH also activates phospholipase-C and -A2; these effects, however, have been reported to require concentrations of the hormone up to 1000-fold higher than those effective on adenylyl cyclase, suggesting that the main physiological mechanism involved in the action of TSH is the activation of this enzyme. Using primary cultures of human thyroids, we here show that physiological concentrations of TSH (0.01-10 mU/L) are also able to increase intracellular Ca2+ levels. Cells were loaded with the fluorescent Ca2+ probe fura-2 and analyzed by single cell Ca2+ recording. The basal Ca2+ level was 105 +/- 30 nmol/L, and physiological concentrations of TSH increased it by 2- to 7-fold. The Ca2+ increase was transient and lasted up to 10 min. It is also shown that the TSH-dependent Ca2+ increase involves both the activation of phospholipase-C and the entry of extracellular Ca2+. TSH (100-10000 mU/L) increased cAMP levels by up to 20-fold in parallel experiments performed on the same cell preparations. These data demonstrate that physiological concentrations of TSH are able to increase cytosolic Ca2+ levels, indicating that this second messenger might directly mediate the action of this hormone in the thyroid.