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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