Thyrotoxicosis etiology

Painless (silent, lymphocytic, postpartum) thyroiditis is a common cause of thyrotoxicosis its etiology is not fully understood and may be heterogeneous autoimmunity may underlie most cases. 

There is also a significantly increased incidence of IgA deficiency in patients with autoimmune or potentially autoimmune disorders, and usually it is not clear which came first. It can be argued that autoimmunity is a complication of immune imbalance subsequent to inborn IgA deficiency (H24). With inborn absence of IgA, exposure to normal human colostrum, plasma, and saliva can result in the production of antibodies to IgA. By the time such patients are discovered the etiological mechanisms are often obscured and IgA treatment is out of the question. The incidence of IgA deficiency is known to be 1-4% in the following conditions Still s disease, systemic lupus erythematosus, rheumatoid arthritis, Sjogren s disease, warm hemolytic anemia, megaloblastic anemia, idiopathic pulmonary hemosiderosis, thyrotoxicosis, and cirrhosis. 

Since its description in 1975, painless (sUent, lymphocytic, postpartum) thyroiditis has been recognized as a common cause of thyrotoxicosis and may represent up to 15% of cases of thyrotoxicosis in North America. The etiology is not fully understood and may be heterogeneous. The triphasic course of this illness mimics that of painful thyroiditis. Most patients present with mild thyrotoxic symptoms. Lid retraction and lid lag are present but exophthalmos is absent. The thyroid gland may be diffusely enlarged but thyroid tenderness is absent. 

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