Metastases to the thyroid presenting as a metabolically inactive incidental thyroid nodule with stable size in 15 months.

Though the thyroid gland has a rich vascular supply, incidence of metastatic disease from distant organs is rare. Here we present an unusual case of metastases to the thyroid with several interesting features. A 63-year-old male with history of adenocarcinoma of the right lobe lung (5 years prior to presentation), treated with surgery and chemotherapy, followed by new adenosquamous lung cancer in the left lobe of the lung (one year prior to presentation), treated surgically followed by adjuvant chemotherapy, was referred to Endocrinology section for evaluation of an incidental thyroid nodule on CT chest. Ultrasound (US) of the thyroid revealed a complex, predominantly hypoechoic lesion measuring 1.8 cm within the lower pole of the right thyroid lobe and a subcentimeter lesion in the left lobe of the thyroid. Review of prior CT chests showed that the lesion in the right lobe was stable for 15 months, with no evidence of a hypermetabolic lesion on PET scan. The subcentimeter lesion was not seen on prior CT scans. US guided fine needle aspiration (FNA) and pathology of the lobectomy of the thyroid confirmed adenosquamous carcinoma. Interesting features in this case are that the thyroid metastases occurred without any evidence of synchronous lesions elsewhere, the size was stable over 15 months, and the lesions were metabolically inactive.

Signaling through CD14 attenuates the inflammatory response to Borrelia burgdorferi, the agent of Lyme disease.

Lyme disease is a chronic inflammatory disorder caused by the spirochetal bacterium, Borrelia burgdorferi. In vitro evidence suggests that binding of spirochetal lipoproteins to CD14, a pattern recognition receptor expressed on monocytes/macrophages and polymorphonuclear cells, is a critical requirement for cellular activation and the subsequent release of proinflammatory cytokines that most likely contribute to symptomatology and clinical manifestations. To test the validity of this notion, we assessed the impact of CD14 deficiency on Lyme disease in C3H/HeN mice. Contrary to an anticipated diminution in pathology, CD14(-/-) mice exhibited more severe and persistent inflammation than did CD14(+/+) mice. This disparity reflects altered gene regulation within immune cells that may engender the higher bacterial burden and serum cytokine levels observed in CD14(-/-) mice. Comparing their in vitro stimulatory activity, live spirochetes, but not lysed organisms, were a potent CD14-independent stimulus of cytokine production, triggering an exaggerated response by CD14(-/-) macrophages. Collectively, our in vivo and in vitro findings support the provocative notion that: 1) pattern recognition by CD14 is entirely dispensable for elaboration of an inflammatory response to B. burgdorferi, and 2) CD14-independent signaling pathways are inherently more destructive than CD14-dependent pathways. Continued study of CD14-independent signaling pathways may provide mechanistic insight into the inflammatory processes that underlie development of chronic inflammation.