Subacute ThyroiditisAnd Related Disorders

Richard M. Jordan, MD, Regional Dean, School of MedicineTexas Tech Health Sciences Center at Amarillo

Dr. Smith’s Backyard

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 And Related Disorders

Definitions

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%

Subacute Thyroiditis

Normal Histology of the Thyroid

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(DeQuervain’s, Granulomatuous

Suppressed Radioactive Iodine Update in Hyperthyroid Phase

Sedimentation Rate approximately > 50 mm/h

Treatment – NSAIDS or Steroids, Beta Blocker in Hyperthyroid Phase

Subacute 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%

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

Treatment of Painless Thyroiditis

Painless Thyroiditis vs Factitious Thyrotoxicosis

Painless Thyroiditis Factitious Thyrotoxicosis Goiter Small Usually Absent

Thyroglobulin Elevated Undetectable

Occupation Not Specific Access to Thyroid Hormone 

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

Post Partum 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

Postpartum Graves’ DiseaseGoiter 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 Versus Graves’ Disease

Hyperthyroid Phase – Beta Blocker

Hypothyroid Phase – Thyroid Hormone

Selenium During Pregnancy in TPO Positive Patients

Postpartum Thyroiditis Treatment

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

Amiodarone and Thyroid Function

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

Distinguishing Type 1 from Type 2 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

Treatment of Amiodarone-Induced Hyperthyroidism

Interferon Alfa-10% Hypothyroidism, Painless Thyroiditis, or Graves Disease

Interleukin 2% Painless Thyroiditis Lithium-Painless Thyroiditis But

Hypothyroidism more common Denileukin Difitox

Etiology of Chemical or Destructive Thyroiditis