Subacute Thyroiditis / De Quervain’s Thyroiditis (Part II)

• Clinical Manifestations:
  • The clinical manifestations:
    • May be preceded by an upper respiratory tract infection, or a prodromal phase of:
      • General malaise
      • Generalized myalgia
      • Pharyngitis
      • Low-grade fevers
    • Pain or swelling in the thyroid region develops later:
      • Accompanied by higher fevers
    • Up to 50% of patients have symptoms of thyrotoxicosis
    • Pain may be moderate or severe
    • Rarely symptoms are entirely lacking
    • Similarly:
      • Tenderness may be moderate or severe (or even exquisite):
        • Or conversely, may rarely be lacking
    • One of the lobes may be involved initially and later spread to the opposite lobe:
      • “Creeping thyroiditis”
    • Both lobes may be involved from the outset
    • The systemic reaction:
      • May be minimal or severe
        • Fevers may reach 40°C
    • Rarely, subacute thyroiditis may present as:
      • A non-tender solitary nodule:
        • In these cases, the diagnosis has been made after fine-needle aspiration biopsy:
          • Atypical presentations are often misdiagnosed as papillary cancer
    • Patients can generally localize the pain to the thyroid region over one or both lobes
    • They may refer to their symptoms as a “sore throat,”:
      • But upon specific questioning it becomes apparent that pain is in the neck, not within the pharynx.
    • Typically, pain radiates from the thyroid region:
      • Up to the angle of the jaw or to the ear on the affected side(s).
      • The pain may also radiate to the anterior chest or may be centered over the thyroid only
      • Moving the head, swallowing, or coughing may aggravate pain
    • Although an occasional patient may have no systemic symptoms, most complain of:
      • Myalgia
      • Fatigue
      • Fevers
      • Malaise:
        • Can be extreme and can be associated with arthralgias

• On physical exam:
  • Most patients appear uncomfortable and flushed on inspection:
    • With variable elevations in temperature
  • Palpation usually reveals:
    • An exquisitely tender, hard, ill-defined nodular thyroid:
      • The tender region may encompass an entire lobe and mild tenderness may be present in the contralateral lobe
  • The overlying skin is occasionally warm and erythematous
  • Cervical lymphadenopathy is rarely present
  • Although the majority of patients are only mildly to moderately ill:
    • Subacute thyroiditis may have a dramatic presentation:
      • With marked fever (greater than 40°C)
      • Severe thyrotoxicosis
      • Obstructive symptoms:
        • Resulting from pronounced thyroid inflammation and edema
  • During the active / painful phase of subacute thyroiditis:
    • The erythrocyte sedimentation rate is:
      • Markedly elevated:
        • In fact, a normal erythrocyte sedimentation rate essentially rules out subacute thyroiditis as a tenable diagnosis
    • The white blood count is normal to mildly increased
    • There is often a normochromic, normocytic anemia
    • During the inflammatory phase there are increases in:
      • Serum ferritin
      • Soluble intercellular adhesion molecule-1
      • Selectin
      • Interleukin-6 levels
      • C-reactive protein
      • Alkaline phosphatase and other hepatic enzymes may be elevated in the early phase:
        • It has been suggested that subacute thyroiditis may actually represent a multi-system disease also affecting the thyroid
    • In the thyrotoxic phase:
      • The serum T4 concentration is disproportionately elevated relative to the serum T3 concentration:
        • Reflecting the intra-thyroidal T4:T3 ratio
        • In addition:
          • The acute illness decreases the peripheral deiodination of T4 to T3:
            • Resulting in lower serum T3 concentrations than expected.
      • Serum TSH concentrations are low to undetectable
      • It is important to note in subacute thyroiditis:
        • Antibodies directed against thyroglobulin and thyroid peroxidase:
          • Are either absent or present in low titer:
            • These develop several weeks after disease onset and tend to disappear thereafter
  • The radioactive iodine uptake:
    • During the thyrotoxic phase is:
      • Low:
        • Most often less than 2% at 24 hours:
          • As with the erythrocyte sedimentation rate:
            • A normal radioactive iodine uptake essentially rules out subacute thyroiditis as a tenable diagnosis
    • Ultrasound:
      • May show generalized, multiple, or single regions of hypoechogenicity

• Pathology:
  • The primary events in the pathology of subacute thyroiditis are:
    • Destruction of the follicular epithelium
    • Loss of follicular integrity:
      • However the histopathologic changes:
        • Are distinct from those found with Hashimoto’s thyroiditis
  • The lesions are:
    • Patchy in distribution and are off:
      • Varying stages of development
    • With infiltration of mononuclear cells in affected regions
    • Partial or complete loss of colloid
    • Fragmentation and duplication of the basement membrane
    • Histiocytes congregate around masses of colloid:
      • Both within the follicles and in the interstitial tissues:
        • Producing giant cells:
          • Often these giant cells consist of:
            • Masses of colloid surrounded by large numbers of individual histiocytes:
              • So they more accurately should be termed pseudo-giant cells
    • The term granulomatous thyroiditis:
      • A synonym for subacute thyroiditis:
        • Should likewise be changed to pseudo-granulomatous thyroiditis:
          • However, true giant cells and granulomas do appear in this disease as well
    • During recovery:
      • The inflammation recedes and there is a variable amount of fibrosis and fibrotic band formation
      • In addition:
        • Follicular regeneration occurs:
          • Without caseation, hemorrhage, or calcification
      • Recovery is generally complete:
        • Only in the rare instance:
          • Is there complete destruction of the thyroid parenchyma that leads to:
            • Permanent hypothyroidism

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