Elsevier

Human Pathology

Volume 38, Issue 1, January 2007, Pages 95-102
Human Pathology

Original contribution
Pathology of the thyroid in severe acute respiratory syndrome

https://doi.org/10.1016/j.humpath.2006.06.011Get rights and content

Summary

The severe acute respiratory syndrome (SARS) epidemic started in November 2002 and spread worldwide. The pathological changes in several human organs of patients with SARS have been extensively described. However, to date, little has been reported about the effects of this infection on the thyroid gland. Femoral head necrosis and low serum triiodothyronine and thyroxine levels, commonly found in patients with SARS, raise the possibility of thyroid dysfunction. We have undertaken this study to evaluate for any potential injury to the thyroid gland caused by SARS on tissue samples obtained from 5 SARS autopsies. The terminal deoxynucleotidyl transferase-mediated dUPT nick end–labeling assay was performed to identify apoptotic cells. The follicular epithelium was found to be damaged with large numbers of cells exfoliated into the follicle. The terminal deoxynucleotidyl transferase-mediated dUPT nick end–labeling assay demonstrated many cells undergoing apoptosis. Follicular architecture was altered and showed distortion, dilatation, and collapse. No distinct calcitonin-positive cells were detectable in the SARS thyroids. In conclusion, both parafollicular and follicular cells were injured. This may provide an explanation both for low serum triiodothyronine and thyroxine levels and the osteonecrosis of the femoral head associated with patients with SARS. Apoptosis may play a role in the pathogenesis of SARS associated coronavirus infection in the thyroid gland.

Keywords

SARS
Thyroid
Calcitonin
TUNEL

Cited by (0)

This study was supported by grants from Peking University and the Ministry of Science and Technology, People's Republic of China, entitled “Histopathology, tissue collection and the pathogenesis of SARS” (2003AA208105) and “Pathogenesis and clinical pathology of SARS” (2003AA208107). The support of the Lifu Foundation is also gratefully acknowledged.

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