The correlation between papillary thyroid carcinoma and lymphocytic infiltration in the thyroid gland.

Abstract

Ninety-five patients with papillary thyroid carcinoma (PTC) who received primary surgical treatment in 1983 at Kuma Hospital and were followed until 1992 were the subjects of this study. Initial therapy was tumor resection for 5 patients, lobectomy for 23 patients, total thyroidectomy with unilateral modified neck dissection for 60 patients, and total thyroidectomy with bilateral modified neck dissection for 7 patients. Clinical stage at diagnosis was as follows. Class I included 28 patients with intrathyroidal disease, class II included 60 patients with positive cervical lymph nodes, and class II included 7 patients with tumor invasion into tissue outside of the thyroid gland. Recurrence of the tumor was evaluated according to lymphocytic infiltration in the thyroid gland. Group A consisted of 36 patients with PTC associated with lymphocytic infiltration, 26 with infiltration surrounding the tumor, 3 with infiltration inside of the tumor, and 7 with both. Group B consisted of the remaining 59 patients with PTC with no lymphocytic infiltration. There were no differences in age, sex, initial tumor size, or initial treatment between groups A and B. Antithyroglobulin antibody and/or antimicrosomal antibody were positive in 16 patients from group A and 4 patients from group B (P < 0.001). Class I included 14 patients from each group, class II included 22 patients from group A and 38 patients from group B, and class III included 7 patients, all from group B. Recurrence of the tumor was found in only 1 group A patient (2.8%), but in 11 patients of group B (18.6%). The percentage of patients free from recurrence over the 10 yr of follow-up in group A was significantly higher than that in group B (by Cox-Mantel test, P < 0.01). The time between initial treatment and recurrence was 2-10 yr. In comparing the clinical stage at the time of initial treatment, recurrence was found in 1 class II patient from group A (4.5%) and in 1 class I (7.1%), 6 class II (15.8%), and 4 class III (57.1%) patients from group B. No patients died during the 10 yr of follow-up. In conclusion, 1) lymphocytic infiltration surrounding the tumor or inside the tumor in PTC might be of use as a means for predicting a favorable prognosis; and 2) class II or class III patients with no lymphocytic infiltration had a high rate of recurrence.

Carcinoma papilífero da tireoide associado à tireoidite de Hashimoto: frequência e aspectos histopatológicos

“…Um prognóstico melhor do CP é reportado quando está associado à TH (10,15,17,26) . Desse modo, esperávamos que a presença de cápsula fosse mais frequente no grupo CP + TH, ao invés de no grupo CP, o que não foi verificado.…”

“…Em nosso estudo, fatores de risco como idade, sexo, tamanho do tumor e multifocalidade não apresentaram diferença significativa na comparação entre os grupos CP e CP + TH, o que vai de encontro com autores que observaram melhor prognóstico em casos nos quais havia associação com TH (16,17) .…”

Tyrosine kinase oncoprotein, RET/PTC3, induces the secretion of myeloid growth and chemotactic factors

“…This association was shown to correspond to a favorable clinical outcome in patients with infrequent tumor recurrence, more differentiated tumors and lower mortality rates (Matsubayashi et al, 1995;Loh et al, 1999;Tamimi, 2002). While the origins of papillary thyroid carcinoma-associated lymphocytic thyroiditis are unknown, genetic analysis of papillary thyroid carcinomas has shown that specific chromosomal rearrangements of the RET/PTC gene family are prevalent (Jhiang, 2000).…”

Interleukin 24 is induced by the RET/PTC3 oncoprotein and is an autocrine growth factor for epithelial cells

“…Consistent with this notion, 10-40% of patients diagnosed with Hashimoto's thyroiditis (HT) may show evidence of concurrent thyroid carcinoma (Dailey et al, 1955;Ott et al, 1987). Although the role of these immune infiltrates is uncertain, clinical studies have shown that patients with papillary thyroid carcinoma (PTC) that present with thyroiditis (PTC/ HT) have a better clinical outcome than patients diagnosed with PTC alone (Matsubayashi et al, 1995;Loh et al, 1999;Tamimi, 2002). Understanding the molecular mechanisms that distinguish PTC from PTC/ HT will be critical if we are to take advantage of the anticancer responses that likely explain the difference between these two pathologies.…”