CHRONIC LYMPHOCYTIC (HASHIMOTO) THYROIDITIS

Overview and Epidemiology

• Most common cause of primary hypothyroidism in iodine-replete regions.
• Autoimmune in nature, characterized by antibodies against thyroid antigens (e.g., thyroid peroxidase, thyroglobulin).
• Female : Male ratio is about 8 : 1.
• Genetic Predisposition: Often associated with other endocrine autoimmune disorders.
• Onset: Usually becomes clinically evident between 20 and 40 years of age.

Pathology

1. Histologic Features
   • Diffuse lymphocytic infiltration (T and B cells).
   • Destruction of thyroid follicles.
   • Formation of lymphoid germinal centers.
2. Physical Exam
   • Asymptomatic, firm, symmetric goiter (borders scalloped, pseudopodia, bosselated surface).
   • Often discovered incidentally or when hypothyroid symptoms appear.

Clinical Course

• Progression from subclinical to overt hypothyroidism over time (gradual loss of thyroid function).
• Serologic Findings:
  • Elevated thyroid peroxidase (TPO) and thyroglobulin antibodies.
  • Primary hypothyroidism → elevated TSH.

Management

• Levothyroxine replacement to correct hypothyroidism.
• Thyroid biopsy usually unnecessary (diagnosis based on antibody tests + TSH).
• Surgery only indicated for specific reasons, e.g., a large symptomatic goiter.

FIBROUS (RIEDEL) THYROIDITIS

Overview

• Rare, primarily affects males.
• Chronic proliferative fibrosing process involving the thyroid gland, potentially extending to trachea, esophagus, fasciae, muscles.
• May be part of a systemic fibrosing disorder (e.g., also retroperitoneal or mediastinal fibrosis).

Pathology

1. Microscopic Features
   • Marked diffuse fibrosis with infiltration by macrophages and eosinophils.
   • Remnant thyroid acini compressed by dense fibrous stroma.
2. Gross Appearance
   • “Woodlike,” stony-hard thyroid texture.
   • Gland often enlarged asymmetrically, firmly adherent to adjacent structures (but not skin).

Clinical Features

• Neck pressure, tightness, dysphagia, hoarseness.
• May have elevated thyroid autoantibodies (TPO, thyroglobulin), but often euthyroid.
• TSH may be normal or slightly abnormal.
• Diagnosis confirmed by thyroid biopsy.

Management

• Medical Therapy: Glucocorticoids or tamoxifen can halt or reverse fibrotic progression in some cases.
• Surgery: May be required for symptomatic tracheal compression.

SUBACUTE THYROIDITIS (DE QUERVAIN THYROIDITIS)

Overview

• Also called subacute granulomatous thyroiditis, acute nonsuppurative thyroiditis.
• Abrupt onset of hyperthyroid symptoms (fever, fatigue, myalgias), with a very tender thyroid enlargement.
• Five times more frequent in women.

Pathology and Pathogenesis

1. Likely Viral-Related
   • Many have a recent history of upper respiratory infection.
   • Viral insult → follicular damage → release of stored T4/T3 → transient hyperthyroidism, later hypothyroid phase.
2. Histology
   • Inflammatory reaction with lymphocytes, neutrophils, necrosis of follicular cells.
   • Disruption of thyroid follicles.

Clinical Features

• Thyroid gland is painful, tender (sometimes severely).
• Enlargement often asymmetric, 1.5–2× normal size.
• Pain can radiate to jaw/ears; dysphagia may occur.

Laboratory Findings

• Elevated free T4, total T3, and thyroglobulin.
• Suppressed TSH.
• Low radioactive iodine uptake (typically <2%) because the inflamed gland cannot concentrate iodine.
• Elevated ESR (>50 mm/h), possible leukocytosis.

Phases

1. Hyperthyroid Phase: 2–8 weeks of high T3/T4 release from damaged follicles.
2. Hypothyroid Phase: Post-inflammation, as stored hormone is depleted before regeneration.
3. Recovery: Normal function usually returns eventually.

Management

1. Pain Control
   • NSAIDs or short-course glucocorticoids (2–8 weeks).
2. Symptomatic Relief
   • β-blockers for tremor, palpitations, anxiety.
3. Hypothyroid Phase
   • Levothyroxine if clinically symptomatic, usually for 6–8 weeks.
   • Normal thyroid function typically resumes.