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Related Concept Videos

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...
Synthesis and Regulation of Thyroid Hormones01:20

Synthesis and Regulation of Thyroid Hormones

Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...
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...
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...
Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...
Hypothyroidism II: Pathophysiology01:23

Hypothyroidism II: Pathophysiology

Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...

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In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
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Somatostatin receptor expression in thyroid disease.

Helen Atkinson1, James A England, Amy Rafferty

  • 1Department of Otolaryngology Head and Neck Surgery, Castle Hill Hospital, East Yorks, UK. hfatkinson@gmail.com

International Journal of Experimental Pathology
|May 16, 2013
PubMed
Summary

This study investigated somatostatin receptor (SSTR) expression in thyroid tissues. SSTRs 1, 3, 4, and 5 are highly expressed, while SSTR2 is present in thyroid disease, suggesting SSTR2 as a potential therapeutic target.

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Area of Science:

  • Endocrinology
  • Oncology
  • Molecular Biology

Background:

  • Somatostatin analogues are established treatments for acromegaly and neuroendocrine tumors.
  • The expression and therapeutic potential of somatostatin receptors (SSTRs) in thyroid disease remain unexplored.
  • Understanding SSTR expression is crucial for developing targeted therapies for thyroid disorders.

Purpose of the Study:

  • To evaluate the expression of somatostatin (SST) and somatostatin receptors (SSTR1-5) in normal and diseased thyroid tissues.
  • To investigate the potential of SSTRs as therapeutic targets for novel somatostatin analogue treatments in thyroid conditions.

Main Methods:

  • Analysis of 67 thyroid tissue specimens, including normal thyroids, differentiated thyroid carcinomas, follicular adenomas, multinodular goitres, Graves' disease, and Hashimoto's thyroiditis.
  • Immunohistochemical staining for SST and SSTR1-5.
  • Double-blinded observer assessment of receptor positivity and intensity.

Main Results:

  • SSTRs 1, 3, 4, and 5 were highly expressed in normal thyroid tissue.
  • SSTR2a and SSTR2b were absent in normal tissue but present in benign and malignant thyroid conditions (P < 0.02).
  • SSTR2b was the most common receptor in all pathological subtypes, while SSTR5 was frequently expressed in differentiated thyroid cancer.

Conclusions:

  • SSTRs 1, 3, 4, and 5 are widely expressed across normal, benign, and malignant thyroid tissues.
  • The presence of SSTR2 in thyroid pathologies, contrasting with its absence in normal tissue, highlights its potential as a targeted therapeutic focus.
  • Targeted SSTR2-based therapies may offer a promising new treatment avenue for various thyroid diseases.