Autoimmune-mediated inflammation of the thyroid gland with release of thyroid hormone resulting in transient hyperthyroidism, frequently followed by a hypothyroid phase before recovery of normal thyroid function.
Occurs sporadically, postpartum, or during cytokine, biologic agent, or lithium therapy.
Some patients progress to permanent hypothyroidism early, others years or decades later.
The diagnosis can be confirmed by a 4-, 6-, or 24-hour radioiodine uptake of <1% during the hyperthyroid phase of the illness.
Treatment, if needed, includes beta-blockers for the hyperthyroid phase and levothyroxine for the hypothyroid phase of the illness.
The condition is characterized by an autoimmune-mediated lymphocytic inflammation of the thyroid gland resulting in a destructive thyroiditis with release of thyroid hormone and transient thyrotoxicosis (hyperthyroidism).   This is frequently followed by a hypothyroid phase and full recovery.
The accepted nomenclature is controversial as many view painless thyroiditis as a variant presentation of chronic lymphocytic (Hashimoto) thyroiditis, because Hashimoto thyroiditis results in permanent hypothyroidism and permanent hypothyroidism may occur shortly after the hypothyroid phase of painless thyroiditis or during prolonged follow-up.    The condition is particularly common in the postpartum period. However, the term postpartum thyroiditis also includes patients who experience only transient hypothyroidism due to an exacerbation of Hashimoto thyroiditis.  Autoimmune thyroid disease, which includes painless and Hashimoto thyroiditis and Graves disease, may arise during cytokine, biologic agent, and lithium therapy.     Finally, a destructive thyroiditis may occur in other settings where pathophysiology, evaluation, and treatment differ from painless thyroiditis. These include acute (suppurative),  subacute (granulomatous, de Quervain),  palpation,  radiation-induced,  and amiodarone-induced thyroiditis. 
Department of Endocrinology
Newcastle upon Tyne Hospitals NHS Foundation Trust
Newcastle upon Tyne
PP has been an invited speaker on thyroid topics for the British Endocrine Society, the European Congress of Endocrinology, the Hellenic Endocrine Society, the Caledonian Society of Endocrinology, and the American Association of Clinical Endocrinologists Gulf Chapter. He has received an honorarium for speaking at the American Association of Clinical Endocrinologists Gulf Chapter.
Dr Petros Perros would like to gratefully acknowledge Dr Douglas S. Ross, the previous contributor to this monograph. DSR declares that he has no competing interests.
Centre for Endocrine and Diabetes Sciences
Cardiff University School of Medicine
University Hospital of Wales
JL declares that he has no competing interests.
Professor of Surgery
Virginia Commonwealth University
RM declares that he has no competing interests.
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