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Related Concept Videos

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...
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...
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...

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Related Experiment Video

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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
04:39

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Published on: March 17, 2023

Low-level laser therapy in chronic autoimmune thyroiditis: a pilot study.

Danilo B Höfling1, Maria Cristina Chavantes, Adriana G Juliano

  • 1Radiology Institute (InRad), Hospital das Clínicas, Faculdade de Medicina da Universidade de São Paulo, Avenida Dr. Enéas de Carvalho Aguiar, CEP 05403-001 São Paulo, Brazil. dbhofling@uol.com.br

Lasers in Surgery and Medicine
|July 28, 2010
PubMed
Summary

Low-level laser therapy (LLLT) may improve thyroid function in patients with chronic autoimmune thyroiditis (CAT). This study found reduced levothyroxine (LT4) needs and lower thyroid peroxidase antibodies (TPOAb) after LLLT treatment.

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Area of Science:

  • Endocrinology
  • Immunology
  • Medical Laser Applications

Background:

  • Chronic autoimmune thyroiditis (CAT) is the leading cause of acquired hypothyroidism.
  • Current treatments do not regenerate thyroid tissue damaged by CAT.
  • There is a need for therapies to improve thyroid function in CAT patients.

Purpose of the Study:

  • To evaluate the effectiveness of low-level laser therapy (LLLT) in patients with CAT.
  • To assess changes in thyroid function, autoantibodies, and ultrasound characteristics after LLLT.
  • To determine the impact of LLLT on levothyroxine (LT4) requirements.

Main Methods:

  • Fifteen hypothyroid patients with CAT undergoing LT4 treatment received 10 LLLT sessions.
  • Ultrasound studies (USs) with quantitative echogenicity analysis were performed before and after LLLT.
  • Thyroid function tests and autoantibody levels (TPOAb, TgAb) were monitored for 9 months post-LLLT after LT4 withdrawal.

Main Results:

  • Patients showed a significant reduction in LT4 dosage needs, with 47% discontinuing LT4.
  • Thyroid peroxidase antibody (TPOAb) levels decreased significantly post-LLLT.
  • A significant increase in parenchymal echogenicity (EI) was observed, indicating improved tissue characteristics.

Conclusions:

  • LLLT shows promise in improving thyroid function in CAT patients.
  • LLLT may reduce the need for LT4 medication and decrease TPOAb levels.
  • LLLT appears to positively influence thyroid tissue echogenicity.