Thyroid incidentalomas. Prevalence by palpation and ultrasonography.

BACKGROUND: Thyroid nodules are commonly identified on autopsy examination. There are relatively few descriptions, however, of the frequency with which thyroid nodules are encountered incidentally during the course of other investigations. METHOD: Prospective study to examine the prevalence of thyroid nodules in asymptomatic North American subjects, with palpation findings compared with findings on high-resolution ultrasonography. RESULTS: Palpable nodules were identified in 21 (21%) of 100 subjects, with nine solitary nodules (9%) and 12 multiple nodules (12%). In comparison, only 33 subjects were found to be free of any nodules by ultrasonography. Of the 67 subjects with abnormal ultrasound findings, 22 had solitary nodules (22%) and 45 had multiple nodules (45%). The prevalence of nodules was greater in women (72%) than in men (41%) (P < .02). A concordance rate of 49% was noted between ultrasound and findings by palpation. CONCLUSIONS: The data indicate that thyroid abnormalities are very common incidental findings, emphasizing the need for a conservative approach when such lesions are encountered incidentally.

Allelic loss of chromosome 17p distinguishes high grade from low grade transitional cell carcinomas of the bladder.

Forty-three transitional cell carcinomas of the bladder of differing grades and stages were examined for reduction to homozygosity for chromosomes 9q, 11p, and 17p. Allelic loss of chromosome 9q was seen in 24 of 38 informative grades II, III, and IV tumors providing further evidence for a bladder tumor suppressor gene on this chromosome. In contrast to the grade-independent involvement of chromosome 9q, allelic losses of chromosomes 11p and 17p were seen only in grade III and IV tumors. The results with chromosome 17p were particularly striking and showed that 0 of 10 grade II versus 20 of 31 grade III and IV tumors had allelic losses for this chromosome harboring the p53 tumor suppressor gene often mutated in other human cancers. The data suggest that cumulative genetic damage is sustained in transitional cell carcinomas and that one of the underlying molecular mechanisms distinguishing low grade from high grade tumors involves chromosome 17p.