The early stages are characterised by glandular enlargement, follicular disruption and neutrophilic invasion. Later, macrophages and multinucleate giant cells are seen enveloping fragments of colloid. These resemble granulomas.
Viral antibodies are detectable in about half of cases.
The initial transient hyperthyroidism is produced by the leakage of preformed thyroid hormones from the damaged follicular cells. Follicular disruption also explains the low or absent uptake of radioactive iodine.
The ensuing transient hypothyroidism is due to gland destruction. Regeneration of the follicles, usually from the edges of the most severely affected areas, results in restoration of thyroid function.
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