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Somatostatin receptor expression, which was not a previously described marker for Hurthle cell cancer of the thyroid, was demonstrated by in vivo imaging with 111In-pentetreotide in three patients. This phenomenon not only adds another imaging technique to the nuclear medicine armamentarium for detecting recurrent and metastatic cancer in patients with Hurthle cell cancer but also opens up an alternative therapeutic avenue with somatostatin analogs or their radiolabeled compounds.
Key Words: Hurthle cell cancer; somatostatin receptors; indium111-pentetreotide; thyroid cancer
J Nucl Med 1998; 39.243245
Hurthle cell tumors of the thyroid are neoplasms composed exclusively or predominantly (over 75%) of oncocytic follicular cells. Hurthle cells originate from follicular cells as evidenced by an intact thyroid stimulating hormone (TSH) receptoradenylate cyclase system, which remains functional in the neoplastic state. Hurthle cell tumors are identified by the presence of cells with an abundant granular cytoplasm attributable to a large number of mitochondria ultrastructurally.
Carcangiu et al. (1) classify these neoplasms as malignant, intermediate or benign based on the presence and degree of capsular and vascular invasion, pattern of growth (follicular, trabecular or solid), nuclear atypia and necrosis. Malignant Hurthle cell tumors comprise 18% of Hurthle cell neoplasms of the thyroid and account for 2%-3% of all patients with thyroid cancer.
As in all other types of thyroid cancer, all aspects of patient management including extent of initial surgery, the role of radioactive iodine treatment and appropriate metastatic workup are controversial in Hurthle cell cancer (2-4). The oncocyte phenotypic differentiation in Hurthle cell cancer has not only morphologic significance, but also connotes metabolic and biologic behavior differences which justify categorizing of these tumors as a different clinical entity. The number of patients who die of Hurthle cell cancer is approximately 10 times that of patients dying from papillary or follicular cancers (5). Radioactive iodine uptake of Hurthle cell cancers is minimal and probably due to the uptake in the follicular component (6). As a consequence, the clinical role of radioactive iodine treatment is largely limited to postsurgical ablation. The rationale for ablation is the fact that the Hurthle cell phenotype usually preserves the thyroglobulin production capacity and, thus, thyroglobulin can be used as a tumor marker for metastatic/recurrent disease after radioactive iodine ablation.
A prominent subcellular marker of...