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Thyroiditis: Clinical Features and Management
Thyroiditis encompasses a diverse group of disorders characterized by thyroid inflammation. They are best classified by onset/duration (acute, subacute, chronic) and by pain (painful vs. painless).
Classification Overview
| Type | Also Known As | Cause | Pain |
|---|
| Acute suppurative | Bacterial thyroiditis | Staph, Strep, Enterobacter | Yes |
| Subacute granulomatous | De Quervain's, viral thyroiditis | Viral (mumps, coxsackie, COVID-19) | Yes |
| Subacute lymphocytic | Silent / painless thyroiditis | Autoimmune | No |
| Postpartum thyroiditis | - | Autoimmune | No |
| Hashimoto's | Chronic autoimmune / chronic lymphocytic | Autoimmune | Rarely |
| Riedel's | Fibrous thyroiditis | Unknown (IgG4-related?) | No |
| Drug-induced | - | IFN, amiodarone, checkpoint inhibitors | Variable |
- Harrison's Principles of Internal Medicine 22E, p. 3081 (Table 396-3)
1. Acute (Suppurative) Thyroiditis
Clinical Features
- Rare; caused by bacterial infection (Staphylococcus, Streptococcus, Enterobacter) or fungal organisms in immunocompromised patients
- In children/young adults: often due to a piriform sinus (4th branchial pouch remnant, predominantly left-sided)
- Thyroid pain, often referred to the throat or ears
- Small, tender, asymmetric goiter; fever, dysphagia, erythema over thyroid, lymphadenopathy
- ESR and WBC elevated; thyroid function usually normal
- FNA shows PMN infiltration; culture identifies organism
Management
-
Antibiotics guided by Gram stain and FNA cultures
-
Surgery to drain abscess (localized by CT/ultrasound) if needed
-
Complications if untreated: tracheal obstruction, septicemia, mediastinitis, jugular venous thrombosis
-
Harrison's, p. 3081
2. Subacute Granulomatous Thyroiditis (De Quervain's)
Epidemiology
- Most common cause of a painful thyroid gland
- Accounts for ~5% of clinical thyroid disorders
- Peak incidence 30-50 years; women affected 3-5x more than men
- Often follows viral prodrome (mumps, coxsackie, influenza, adenovirus, echovirus, SARS-CoV-2)
Pathophysiology
Follicular disruption → release of stored T4/T3 → thyrotoxicosis → hormone depletion → hypothyroidism → recovery (see diagram below)
Figure: Clinical course of subacute thyroiditis (Harrison's 22E, Fig. 396-3). ESR peaks early; free T4 rises then falls; TSH is suppressed initially then rises during the hypothyroid phase before recovering.
Clinical Features
- Painful, enlarged thyroid (often exquisitely tender), sometimes asymmetric
- Pain referred to jaw or ear
- Malaise, low-grade fever, sore throat (may mimic pharyngitis)
- Symptoms of thyrotoxicosis or hypothyroidism depending on phase
- In 10%: acute, severe onset with marked hyperthyroid symptoms
- In 33%: asymptomatic except for goiter
Three clinical phases:
- Thyrotoxic phase (weeks 1-6): raised T4/T3, suppressed TSH, low radioiodine uptake (<5%)
- Hypothyroid phase (weeks 6-12): low T4, elevated TSH
- Recovery phase (weeks 12-18+): normalization of all tests
Investigations
- ESR markedly elevated (often >50 mm/h)
- Low radioiodine uptake or 99mTc pertechnetate uptake (distinguishes from Graves' disease)
- T4:T3 ratio lower than in Graves' (stored hormone release rather than de novo synthesis)
- Thyroid antibodies negative
- FNA (if needed): giant cells, granulomas
Management
| Phase | Treatment |
|---|
| Pain / inflammation | NSAIDs (aspirin, ibuprofen) for mild cases |
| Severe pain | Prednisolone 10-20 mg/day x 7 days, then taper over 4 weeks |
| Thyrotoxic phase | Beta-blockers (propranolol, atenolol) - NOT antithyroid drugs (no new hormone synthesis) |
| Hypothyroid phase | Levothyroxine if symptomatic or prolonged |
-
Most patients recover fully within 6 months
-
Permanent hypothyroidism in ~15% (especially if coincident thyroid autoimmunity)
-
Recurrence uncommon but possible
-
Harrison's, p. 3082; Goldman-Cecil Medicine, p. 2440; Bailey and Love's Surgery 28e, p. 893
3. Hashimoto's Thyroiditis (Chronic Autoimmune Thyroiditis)
Epidemiology
- Most common cause of hypothyroidism in iodine-sufficient regions
- Peak age 45-65 years; female predominance 10:1 to 20:1
- Strong genetic component: CTLA4, PTPN22, IL2RA polymorphisms
Pathogenesis
Breakdown of self-tolerance to thyroid antigens (thyroglobulin, thyroid peroxidase) → CD8+ cytotoxic T-cell mediated destruction + CD4+ Th1 cytokine-mediated apoptosis + antibody-dependent cytotoxicity → progressive follicular destruction and fibrosis
Histology
Fig. 24.11: Hashimoto thyroiditis - dense lymphocytic infiltrate with germinal centers; residual follicles lined by oncocytic (Hürthle) cells. (Robbins & Cotran Pathologic Basis of Disease)
Gross: diffusely enlarged, firm, pale yellow-tan gland, well-demarcated. Microscopy: lymphocytes + plasma cells, lymphoid follicles with germinal centers, oncocytic (Hürthle cell) metaplasia, fibrosis (does NOT extend beyond the gland - differentiates from Riedel's).
Clinical Features
- Painless goiter - diffuse, symmetric, firm, "bosselated" texture
- Gradual onset of hypothyroid symptoms: fatigue, weight gain, cold intolerance, constipation, impaired concentration, dry skin, hair loss
- Early phase: sometimes hashitoxicosis (transient thyrotoxicosis from follicular disruption)
- Eventually: primary myxoedema (end stage, no goiter)
- Associated autoimmune diseases: T1DM, Addison's disease, SLE, myasthenia gravis, Sjögren's syndrome
- Increased risk of thyroid lymphoma (most lymphomas arise on a background of lymphocytic thyroiditis)
Investigations
- TSH elevated; free T4 low (or normal in subclinical hypothyroidism)
- Anti-TPO antibodies positive in >90% (anti-thyroglobulin also elevated)
- Ultrasound: heterogeneous, hypoechoic gland
- FNA: oncocytes + heterogeneous lymphocytes (characteristic)
Management
-
Levothyroxine replacement for overt hypothyroidism (titrate to normalize TSH)
-
Subclinical hypothyroidism (elevated TSH, normal T4): treat if TSH >10 mIU/L, or if symptomatic, pregnant, or planning pregnancy
-
Monitor thyroid function annually if not on replacement
-
Goiter causing compressive symptoms: levothyroxine may reduce size; surgery rarely needed
-
Robbins & Cotran, p. 998-999; Bailey and Love's, p. 893
4. Postpartum / Sporadic Silent (Painless) Thyroiditis
Epidemiology
- Postpartum thyroiditis: up to 10% of pregnancies; 20x more common postpartum than Graves' disease
- More frequent with positive anti-TPO antibodies in 1st trimester or personal/family history of autoimmunity
- Sporadic (non-postpartum) silent thyroiditis: age 30-60, female > male (1.5:1)
- Both are variants of the same autoimmune destruction-induced thyroiditis
Clinical Features
- Painless goiter (nontender)
- Classic sequence: thyrotoxic phase (1-3 months) → euthyroid (1-2 months) → hypothyroid phase (up to 12 months)
- Not all patients complete the full sequence: ~25% experience only thyrotoxicosis; ~50% only hypothyroidism
- Thyrotoxic phase: tachycardia, palpitations, heat intolerance (milder than Graves')
- Hypothyroid phase: fatigue, constipation, cold intolerance, impaired concentration
Diagnosis
- Toxic phase: raised free T4/T3, suppressed TSH; T3:T4 ratio <20 (distinguishes from Graves')
- Anti-TPO antibodies positive; TSH-receptor antibodies negative (key distinction from Graves')
- Low/absent radioiodine uptake; ultrasound: heterogeneous, hypoechoic; Doppler flow markedly decreased (vs. increased in Graves')
Management
-
Self-limiting course
-
Thyrotoxic phase: beta-blockers (atenolol 25-50 mg/day) for moderate/severe symptoms; antithyroid drugs NOT effective
-
Hypothyroid phase: levothyroxine if symptomatic or severe; taper after 6-12 months to reassess recovery
-
Pregnancy: continue levothyroxine throughout pregnancy if initiated
-
Prognosis: up to 50% remain chronically hypothyroid; recurs after 70% of subsequent pregnancies; higher risk with high anti-TPO titers
-
Goldman-Cecil Medicine, p. 2439-2440
5. Riedel's Thyroiditis
-
Very rare (0.5% of goiters)
-
Thyroid replaced by cellular fibrous tissue that infiltrates surrounding structures (trachea, muscles, parathyroids, recurrent laryngeal nerve)
-
Presents as a rock-hard, fixed goiter with compressive symptoms (dysphagia, stridor, hypothyroidism)
-
Associated with IgG4-related systemic disease and other fibrosclerotic conditions
-
Management: surgery to relieve compression; corticosteroids; tamoxifen (antifibrotic); levothyroxine for hypothyroidism
-
Bailey and Love's, p. 893
Drug-Induced Thyroiditis
Common culprits and their patterns:
| Drug | Pattern |
|---|
| Amiodarone | Type 1 (iodine-excess Graves'-like) or Type 2 (destructive thyroiditis) |
| Interferon-alpha | Hashimoto-like or Graves'-like |
| Immune checkpoint inhibitors (anti-PD-1/CTLA-4) | Destructive thyroiditis (painless) |
| Tyrosine kinase inhibitors | Hypothyroidism or thyroiditis |
| Lithium | Hypothyroidism / goiter |
Summary Table: Key Distinguishing Features
| Feature | Acute Suppurative | Subacute (De Quervain's) | Hashimoto's | Postpartum/Silent |
|---|
| Pain | Severe | Moderate-severe | None | None |
| Fever | Yes | Yes (low-grade) | No | No |
| Goiter | Asymmetric, tender | Tender, firm | Firm, bosselated | Soft, nontender |
| ESR | Elevated | Markedly elevated | Normal | Normal |
| RAI uptake | Normal | Very low (<5%) | Normal/low | Very low |
| TPO antibodies | Negative | Negative | Positive (>90%) | Positive |
| TSH-RAb | Negative | Negative | Negative | Negative |
| Self-limiting? | With antibiotics | Yes (~6 months) | No (chronic) | Usually (may persist) |