De Quervain's thyroiditis pathophysiology: Difference between revisions

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{{De Quervain's thyroiditis }}
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==Overview==
==Overview==



Revision as of 18:29, 1 August 2017

De Quervain's thyroiditis Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating De Quervain's thyroiditis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications, and Prognosis

Diagnosis

Diagnostic Criteria

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

Chest X Ray

CT

MRI

Echocardiography or Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary prevention

Secondary prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]

Overview

Pathophysiology

Pathogenesis

The exact pathogenesis of de Quervain's thyroiditis is unclear. Cytotoxic T cell recognition of viral and cell antigens presented in a complex leading to thyroid follicular cell damage has been proposed as the pathogenesis of de Quervain's thyroiditis. De Quervain's thyroiditis is usually preceded by a viral prodrome. Various viral infections are associated with the de Quervain's thyroiditis including mumps, adenovirus, Epstein–Barr virus, coxsackievirus, cytomegalovirus, influenza, echovirus, and enterovirus.

Genetics

  • De Quervain's thyroiditis is associated with the histocompatibility antigen (HLA) B35.
  • In some cases of De Quervain's thyroiditis HLA B15/62 positivity was also reported.

Pathology

The primary pathology of de Quervain's thyroiditis is:

  • Destruction of the follicular epithelium
  • Loss of the follicular integrity


References