Graves disease

Graves disease
Updated: 12/13/2018
© Jun Wang, MD, PhD


General features
  • Autoimmune disorder
  • Most common cause of hyperthyroidism
  • Peak incidence between 20 and 40
  • More common in women
  • Risk for life threatening thyrotoxicosis if untreated
Pathogenesis
  • Autoantibody against multiple thyroid proteins, most importantly the TSH receptor 
  • Autoantibody activate TSH receptor to promote thyroid hyperplasia and hyperfunction
Clinical presentations
  • Hyperthyroidism associated with diffuse enlargement of the gland
  • Infiltrative ophthalmopathy with resultant exophthalmos
  • Localized, infiltrative dermopathy, sometimes called pretibial myxedema, which is present in a minority of patients
Infiltrative ophthalmopathy
  • Proptosis in addition to other ocular presentations of hyperthyroidism
  • Activated T-cells cross react with TSH receptor expressed in fibroblasts, causing cytokine production and subsequent edema and fibrosis
  • Increased volume of the extraocular muscles and retro-orbital connective tissues
  • Marked infiltration of the retro-orbital space by mononuclear cells, predominantly T cells
  • Inflammation with edema and swelling of extraocular muscles
Key laboratory findings
  • Low TSH, usually first positive finding
  • High thyroxin or FTI
  • Increased uptake of radioactive iodine
  • Positive activating autoantibodies against TSH receptor
  • Other autoantibodies: Thyroglobulin, thyroid peroxidase, and sodium-iodide symporter
Genetic abnormalities
  • CTLA4, etc
Pathological features
  • Diffuse hyperplasia and hypertrophy of follicular cells 
  • Intact follicles
  • Tall follicular cells with papillae without fibrovascular cores
  • Pale colloid with scalloped margins
Treatment
  • Beta-blockers
  • Inhibitors for thyroid hormone synthesis (propylthiouracil, etc)
  • Radioiodine ablation
  • Surgery



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