Thyroiditis clinical features, management

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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

TypeAlso Known AsCausePain
Acute suppurativeBacterial thyroiditisStaph, Strep, EnterobacterYes
Subacute granulomatousDe Quervain's, viral thyroiditisViral (mumps, coxsackie, COVID-19)Yes
Subacute lymphocyticSilent / painless thyroiditisAutoimmuneNo
Postpartum thyroiditis-AutoimmuneNo
Hashimoto'sChronic autoimmune / chronic lymphocyticAutoimmuneRarely
Riedel'sFibrous thyroiditisUnknown (IgG4-related?)No
Drug-induced-IFN, amiodarone, checkpoint inhibitorsVariable
  • 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)
Clinical course of subacute thyroiditis - three phases: thyrotoxic, hypothyroid, and recovery, showing ESR, free T4, and TSH trends over 18 weeks
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:
  1. Thyrotoxic phase (weeks 1-6): raised T4/T3, suppressed TSH, low radioiodine uptake (<5%)
  2. Hypothyroid phase (weeks 6-12): low T4, elevated TSH
  3. 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

PhaseTreatment
Pain / inflammationNSAIDs (aspirin, ibuprofen) for mild cases
Severe painPrednisolone 10-20 mg/day x 7 days, then taper over 4 weeks
Thyrotoxic phaseBeta-blockers (propranolol, atenolol) - NOT antithyroid drugs (no new hormone synthesis)
Hypothyroid phaseLevothyroxine 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

Hashimoto thyroiditis histology: dense lymphocytic infiltrate with germinal centers, residual follicles lined by pink oncocytic (Hürthle) cells, and fibrosis
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:
DrugPattern
AmiodaroneType 1 (iodine-excess Graves'-like) or Type 2 (destructive thyroiditis)
Interferon-alphaHashimoto-like or Graves'-like
Immune checkpoint inhibitors (anti-PD-1/CTLA-4)Destructive thyroiditis (painless)
Tyrosine kinase inhibitorsHypothyroidism or thyroiditis
LithiumHypothyroidism / goiter

Summary Table: Key Distinguishing Features

FeatureAcute SuppurativeSubacute (De Quervain's)Hashimoto'sPostpartum/Silent
PainSevereModerate-severeNoneNone
FeverYesYes (low-grade)NoNo
GoiterAsymmetric, tenderTender, firmFirm, bosselatedSoft, nontender
ESRElevatedMarkedly elevatedNormalNormal
RAI uptakeNormalVery low (<5%)Normal/lowVery low
TPO antibodiesNegativeNegativePositive (>90%)Positive
TSH-RAbNegativeNegativeNegativeNegative
Self-limiting?With antibioticsYes (~6 months)No (chronic)Usually (may persist)
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