Download - Subacute Thyroiditis And Related Disorders
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