ESPE Abstracts (2014) 82 FC13.5

ESPE2014 Free Communications Thyroid (6 abstracts)

The Ultrastructural Changes in Thyroid Cells in the Course of Damage in Hashimoto’s Thyroiditis

Iwona Ben-Skowronek a , Leszek Szewczyk a & Elzbieta Korobowicz b


aMedical University Department of Paediatric Endocrinology and Diabetology, Lublin, Poland; bMedical University Department of Pathomorphology, Lublin, Poland


Background: The development of the Hashimoto’s thyroiditis is the result of the damage to thyrocytes, apoptosis, and autoimmune cytotoxic action of lymphocytes.

Objective and Hypotheses: The aim of the study is to present ultrastructural changes in thyroid cells in the course of damage in Hashimoto’s thyroiditis.

Method: The study involved 40 children: 20 children with Hashimoto’s thyroiditis and 20 children as a control group. Specimens for ultrastructural investigations were obtained during thyroidectomy. Ultrathin sections were contrasted with uranyl acetate and lead citrate and examined under the EM 900 Zeiss Germany Electron Microscope.

Results: In the control group, the thyroid follicular cells were cuboidal or cylindrical and were lying on a thin basement membrane. Varied degrees of apoptosis were observed in the Hashimoto’s thyroiditis patients. The basement membrane of the follicles was thickened by deposition of numerous collagen fibres. The thyrocytes had irregular cell nuclei and an increased number of mitochondria in the basal pole. Different stages of thyrocyte necrosis were visible at the sites of contact between lymphocytes or plasma cells and thyrocytes. The nuclei of dying thyroid cells were deformed, the cisterns of the endoplasmic reticulum were swollen, and the cell membrane disrupted.

Conclusion: Ultrastructural examinations of thyroid sections sampled from patients with Hashimoto’s thyroiditis suggest the following stages of process thyrocyte damage: thickening of the basement membrane caused by collagen deposition, thyrocyte apoptosis, stimulation of lymphocytes and plasma cells to cytotoxic reactions, and necrosis of thyrocytes damaged by the cytotoxic reaction.

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