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Related Concept Videos

Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
The Thyroid Gland01:23

The Thyroid Gland

The thyroid gland is a small, butterfly-shaped gland located in the neck and covers the anterior surface of the trachea. The gland has two lateral lobes connected by a thin tissue mass called the isthmus. Internally, each lobe comprises many small spherical structures known as thyroid follicles, surrounded by a network of blood vessels.
The follicles have a central cavity lined by simple cuboidal to squamous epithelial cells called follicular cells. These cells produce the glycoprotein...
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...
Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...
The Parathyroid Glands00:59

The Parathyroid Glands

The two pairs of parathyroid glands embedded within the posterior surface of the thyroid gland are restricted by a dense capsule around them. These glands comprise two distinct cell populations—parathyroid oxyphil and parathyroid principal cells- pivotal in calcium homeostasis.
Oxyphil cells, whose functions remain elusive, emerge during late puberty, adding a layer of complexity to the parathyroid gland's intricacies. In contrast, principal parathyroid cells undertake a vital role by producing...
Goiter01:27

Goiter

Goiter refers to an abnormal enlargement of the thyroid gland that may appear as a diffuse goiter (uniform enlargement) or nodular (single or multiple nodules). Functionally, it is classified as nontoxic (normal/low hormone levels) or toxic (excess hormone production).PathophysiologyDiffuse thyroid enlargement typically results from prolonged stimulation by thyroid-stimulating hormone (TSH) or TSH-like agents, commonly seen in hypothyroidism or iodine deficiency. In contrast, in hyperthyroid...

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Solid cell nests in Hashimoto's thyroiditis sharing features with papillary thyroid microcarcinoma.

Sofia Asioli1, Lori A Erickson, Ricardo V Lloyd

  • 1Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN 55905, USA.

Endocrine Pathology
|October 8, 2009
PubMed
Summary

Solid cell nests (SCN) in Hashimoto's thyroiditis can mimic papillary thyroid microcarcinoma due to atypical nuclear features. Histological and immunohistochemical markers like p63, TTF-1, and thyroglobulin help differentiate SCN from malignancy.

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Area of Science:

  • Endocrinology
  • Pathology
  • Oncology

Background:

  • Solid cell nests (SCN) are uncommon thyroid findings.
  • SCN associated with Hashimoto's thyroiditis can exhibit nuclear atypia.
  • These atypical features may be misdiagnosed as papillary thyroid microcarcinoma.

Purpose of the Study:

  • To identify distinguishing histological and immunophenotypic features between SCN and papillary thyroid microcarcinoma in Hashimoto's thyroiditis.
  • To improve diagnostic accuracy and prevent misclassification of SCN.

Main Methods:

  • Retrospective review of 12 Hashimoto's thyroiditis cases with numerous SCN (>10 per slide) from 1,420 archival specimens.
  • Histological examination for nuclear features and basement membrane characteristics.
  • Immunohistochemical analysis using p63, TTF-1, thyroglobulin, HBME-1, and calcitonin.

Main Results:

  • SCN showed atypical nuclear features (grooves, overlapping, clearing) and a distinct eosinophilic basement membrane.
  • SCN were strongly positive for p63, weakly positive for TTF-1, and negative for thyroglobulin, HBME-1, and calcitonin.
  • Papillary thyroid microcarcinomas were positive for thyroglobulin, TTF-1, HBME-1, variably positive for p63, and negative for calcitonin.

Conclusions:

  • Histological and immunohistochemical findings can reliably differentiate SCN from papillary thyroid microcarcinoma in Hashimoto's thyroiditis.
  • p63, TTF-1, and thyroglobulin are key markers in distinguishing these entities.
  • Accurate diagnosis is crucial for appropriate patient management.