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Case Reports
. 2007 Jan;38(1):95-102.
doi: 10.1016/j.humpath.2006.06.011. Epub 2006 Sep 25.

Pathology of the thyroid in severe acute respiratory syndrome

Affiliations
Case Reports

Pathology of the thyroid in severe acute respiratory syndrome

Lan Wei et al. Hum Pathol. 2007 Jan.

Abstract

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.

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Figures

Fig. 1
Fig. 1
Thyroid of a patient with SARS showing disruption of the lining epithelium with extensive exfoliation into the luminal cavity of a dilated follicle (arrow 1), formation of epithelial cell clusters with no lumen or colloid (arrow 2), and with markedly congested capillaries in the connective tissues between follicles (arrow 3) (hematoxylin-eosin stain; bar, 50 μm).
Fig. 2
Fig. 2
Loss of follicles with increased fibrous tissue (arrow) in interfollicular region in a patient with SARS (hematoxylin-eosin stain; bar, 50 μm).
Fig. 3
Fig. 3
TUNEL stain of normal (A) and SARS (B) thyroid samples. (A) Few TUNEL-positive cells in a normal thyroid (bar, 50 μm). (B) Distinct apoptosis in the follicular epithelium and the interfollicular region in a patient with SARS (insert figure, apoptosis in follicular epithelium; bar, 20 μm) (bar, 50 μm).
Fig. 4
Fig. 4
Calcitonin immunostaining. (A) Calcitonin-positive cells present predominantly in interfollicular region of a normal thyroid (bar, 50 μm). (B) Absence of calcitonin-positive cells in the thyroid of a patient with SARS (bar, 50 μm).

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