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Wai Yin Wong, Preservation of Echogenicity in Type II Amiodarone-Induced Thyrotoxicosis: Possible Histopathological Basis, The Journal of Clinical Endocrinology & Metabolism, Volume 95, Issue 11, 1 November 2010, Pages 4846–4847, https://doi.org/10.1210/jc.2010-1049
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Extract
Sonographic hypoechogenicity of the thyroid in autoimmune and infective thyroiditis is well known (Fig. 1), whereas the sonographic appearance of type II amiodarone-induced thyrotoxicosis (AIT-II) has not been described.
The ultrasound and scintigraphy findings of 16 consecutive patients diagnosed with AIT-II were reviewed. Thyroid echogenicity was normal in all patients (Fig. 2). Technetium-99m pertechnetate uptake was invariably reduced.
AIT-II results from follicular damage and thyroid hormone leakage, a pathogenesis similar to subacute thyroiditis (SA). Subtle differences in histology defining the two conditions may explain the discrepant sonographic appearance. Normal thyroid echogenicity is due to reflection of acoustic waves at the thyrocyte-colloid interface. Histology reports detailing AIT-II are scarce because surgical management is the exception rather than the rule. Nonetheless, available reports describe the coexistence of colloid-distended follicles and disrupted follicles filled with foamy histiocytes (1, 2).
Follicular disruption with intrafollicular infiltrates is also seen in SA. In addition, the interstitium contains prominent inflammatory infiltrates and noncaseous granulomas (3). Reduction in thyrocyte-colloid interfaces and a hypercellular interstitium accounts for the hypoechogenicity of SA.
