A 50-year-old woman who had undergone lung lobectomy because of
lung adenocarcinoma presented with
thyrotoxicosis, neck swelling, and cervical
lymphadenopathy one month after the operation. The total serum
triiodothyronine (T3) and
thyroxine (T4) levels were markedly elevated to 514 ng/dL and 26.4 microg/dL, respectively, and serum
thyrotropin (TSH) was suppressed to less than 0.005 microU/mL. Although the thyroid gland had been normal before surgery, chest computed tomography (CT) scan revealed a markedly enlarged thyroid gland only 1 month after surgery. 123I uptake for 24 hours was suppressed to 4% in the thyroid gland with no uptake elsewhere including the lung. Fine-needle aspiration cytology (FNAC) of the thyroid showed invasion of poorly differentiated
adenocarcinoma cells, cytologically identical to the cells obtained from sputum and those infiltrating the resected sections of the
lung adenocarcinoma. Immunohistochemical studies of resected lung tissues did not show positive staining for
thyroglobulin,
carcinoembryonic antigen (CEA), or
surfactant protein A. Clinically, the
thyrotoxicosis had spontaneously improved, followed by a hypothyroid state with shrinkage of the thyroid gland after
chemotherapy. Despite repeated
chemotherapy and the administration of
thyroxine for
hypothyroidism, the patient died of
respiratory failure 9 months after the onset of
thyrotoxicosis. From these findings and the
clinical course, thyroid
metastasis, developing subacutely from
lung adenocarcinoma, was diagnosed. We speculate that aggressive invasion of
tumor cells into the thyroid gland resulted in highly destructive
thyrotoxicosis.