Subacute Thyroiditis And Related Disorders Richard M. Jordan, MD, Regional Dean, School of Medicine Texas Tech Health Sciences Center at Amarillo

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Subacute Thyroiditis And Related Disorders Definitions Subacute Thyroiditis – (DeQuervain’s Thyroiditis, Granulomatous Thyroiditis, Giant Cell Thyroiditis) A Post Viral Syndrome with Thyroid Pain Painless Thyroiditis – (Subacute Lymphocytic Thyroiditis, Silent Thyroiditis) Probable Variant of Autoimmune (Hashimoto’s) Thyroiditis. Excludes Women with Painless Thyroiditis Occurring within 1 Year of Delivery. Postpartum Thyroiditis – Probable Variant of Autoimmune Thyroiditis, Similar to Painless Thyroiditis But Occurring Postpartum. Drug Induced Thyroiditis – Amiodarone, Lithium, Interleukin- 2, Denileukin Diffitoxin, Radiation Induced – Occurs Post Radioactive Iodine Treatment  

Subacute Thyroiditis Preceding Viral Infection with Sore Throat, Fever, Myalgias May occur in Clusters Damage to the Thyroid Follicles with Release of Thyroid Hormone Goiter with Neck Pain – Can Radiate to Jaw or Ear Elevated Sedimentation Rate, Elevated Thyroglubulin Triphasic Course – Hyperthyroidism to Hypothyroidism to Euthyroidism Permanent Hypothyroidism may develop in 10-15%

Normal Histology of the Thyroid

Subacute Thyroiditis (DeQuervain’s, Granulomatuous Acute viral infection Presents with viral prodrome, thyroid tenderness, and hyperthyroid symptoms Pathology Disruption and Collapse of the Thyroid Follicles Infiltration with Inflammatory Cells Neutrophils Lymphocytes Histiocytes Multinucleated “Giant” Cells

Subacute Thyroiditis Suppressed Radioactive Iodine Update in Hyperthyroid Phase Sedimentation Rate approximately > 50 mm/h Treatment – NSAIDS or Steroids, Beta Blocker in Hyperthyroid Phase

Painless Thyroiditis Probable Variant of Autoimmune (Hashimoto’s) Thyroiditis Sedimentation Rate is Normal or Slightly Elevated May have Elevated Antithyroid Peroxidase (TPO) Levels Thyroglobulin Levels Are Elevated Pathology-Lymphocytic Infiltration which Persists in Recovery Clinical Course-Similar to Subacute Thyroiditis; Hyperthyroidism (Usually Mild) Followed by Recovery or Hypothyroidism Permanent Hypothyroidism Develops in 20-50%

Treatment of Painless Thyroiditis Hyperthyroidism-Mild may require no therapy. If Symptomatic give beta-bockers Hypothyroidism-If Symptomatic or TSH>10mU/L give thyroid hormone replacement Monitor for the development of hypothyroidism

Painless Thyroiditis vs Factitious Thyrotoxicosis Painless Thyroiditis Factitious Thyrotoxicosis Goiter Small Usually Absent Thyroglobulin Elevated Undetectable Occupation Not Specific Access to Thyroid Hormone  

Post Partum Thyroiditis Variant of Autoimmune (Hashimoto’s) Thyroiditis Follows Delivery Autoimmune Damage to the Follicles with Release of Thyroid Hormone Painless with Small Goiter Variable Triphasic Course Suppressed Radio Iodine Uptake Sedimentation Rate-<30 mm/h

Postpartum Thyroiditis Prevalence 7 to 10 Percent of All Pregnancies Most Common Variety of Hyperthyroidism Associated with Pregnancy Risk Factors Elevated TPO Antibodies – 50% Will Develop Postpartum Thyroiditis Type I Diabetes Mellitus – 25% Will Develop Postpartum Thyroiditis Postpartum Thyroiditis with Prior Pregnancy Pathology Lymphocytic Infiltration, Disruption of Follicles, Germinal Centers Variant of Hashimoto’s Thyroiditis

Postpartum Thyroiditis Course 25% - Classic Triphasic Response 35% - Only Hyperthyroidism 40% - Only Hypothyroidism Persistent Hypothyroidism After 4 years 25 to 50% have hypothyroidism or Goiter or Both 56% with a Hypothyroid Phase Develop Permanent Hypothyroidism Patients with Postpartum Hypothyroidism Require Yearly Screening

Postpartum Thyroiditis Versus Graves’ Disease Postpartum Graves’ Disease Goiter Small, No Bruit Small to Large, Bruit Present Course Mild, Short Duration Mild to Severe, Long Duration Opthalmopathy Absent May Be Present Iodine Uptake Low Normal to Elevated TSI Absent Present * TSI-Thyroid Stimulating Immunoglobulin

Postpartum Thyroiditis Treatment Hyperthyroid Phase – Beta Blocker Hypothyroid Phase – Thyroid Hormone Selenium During Pregnancy in TPO Positive Patients

Amiodarone and Thyroid Function Hypothyroidism-Iodine Induced Overt Hypothyroidism – 5% Subclinical Hypothyroidism – 25% Hyperthyroidism – 3-5% Type 1- (Jod-Basedow, Iodine-Induced), Underlying MNG, Graves’ Disease Type 2 – Chemical Destructive Thyroiditis

Distinguishing Type 1 from Type 2 Hyperthyroidism I123 Uptake is Usually Suppressed in Both Types Of the I123 Detectable Type 1 is Likely Presence of the Diffuse Goiter, MNG or TSI suggests Type 1 Color Flow Doppler Increased Flow (increased vascularity) – Type 1 Decreased Flow (absent vascularity) – Type 2 Interpretation Difficult

Treatment of Amiodarone-Induced Hyperthyroidism Type 1 Thionamides (Methimazole or PTU) Radioactive Iodine (If I123 Uptake is Detectable) Thyroidectomy (Failure of Other Options) Type 2 Prednisone 40 mg daily for 6 to 12 weeks Uncertain If Type 1 or Type 2 (Usually the Case) Start Prednisone 40 mg and Methimazole 40 Mg daily Measure Thyroid Function in 6 weeks If Improved Taper Methimazole If Unimproved Taper Prednisone

Treatment of Amiodarone-Induced Hyperthyroidism Type 1 Thionamides (Methimazole or PTU) Radioactive Iodine (If I123 Uptake is Detectable) Thyroidectomy (Failure of other options) Type 2 Prednisone 40 mg daily for 6 to 12 weeks Uncertain if Type 1 or Type 2 (Usually the Case) Start Prenisone 40 mg and Methimazole 40 Mg daily Measure Thyroid Function in 6 weeks If Improved Taper Methimazole If Unimproved Taper Prednisone

Etiology of Chemical or Destructive Thyroiditis Interferon Alfa-10% Hypothyroidism, Painless Thyroiditis, or Graves Disease Interleukin 2% Painless Thyroiditis Lithium-Painless Thyroiditis But Hypothyroidism more common Denileukin Difitox