BLACK THYROID - PATHOLOGY CLINIC

A finding of a black thyroid gland (figure 1) is unusual and disconcerting. Among the possible causes of black thyroid are minocycline-induced pigmentation, hemochromatosis, ochronosis, mucoviscidosis, ceroid storage disease, bruising, and hemorrhage. In addition, medullary thyroid carcinomas have been reported to produce melanin in rare cases. Minocycline, a derivative of tetracycline, can also cause pigmentation in the skin, nails, oral mucosa, teeth, eyes, bones, cardiac valves, coronary vessels, substantia nigra, and atherosclerotic plaques. In the thyroid, minocycline accumulates in the follicular epithelium and colloid in benign, and even hyperplastic tissue as a result of the oxidative interaction between the drug and the enzyme thyroid peroxidase (figure 2). These black pigment deposits remain in epithelial cells for long periods of time.

Ultrastructurally, pigment (neuromelanin) is confined to lysosomes. This granular pigment stains like melanin on Fontana-Masson staining; it can also be bleached. In aspiration cytology specimens, the degenerative changes in follicular epithelial ceils found in black thyroid glands can cause nuclear hyperchromatism and chromatin clumping (figure 3). Pigment present in follicular epithelial cells in fine-needle aspirate can also be mistaken for hemosiderin-laden macrophages. It is interesting that thyroid adenomas and carcinomas fail to incorporate black pigment (figure 1). Although the concentration of minocycline-related pigment can interfere with thyroid function, it appears to be unrelated to tumorigenesis. Pigment-containing follicular epithelium has reduced thyroglobulin and ubiquitin immunoreactivity. Because of the possible antithyroid effects of minocycline, it seems advisable to monitor thyroid function in patients who are on long-term minocycline therapy.

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