Abstract
In the middle and late '70s it was reported from Japan that women with autoimmune thyroiditis may develop transient hypothyroidism after delivery [2,3]. At the same time several cases of transient thyrotoxicosis due to painless (silent) thyroiditis were described in North America [23, 28] and later it was recognized that this ‘new’ disease had a predilection for the postpartum period [12]. Although still a matter of some controversy [13, 26, 28], the great majority of these different clinical expressions of thyroid disease after childbirth appear to be due to activation of pre-existing subclinical autoimmune thyroiditis [6, 9]. Similarly, it has been observed that subjects with Graves' thyrotoxicosis may experience a transient postpartum aggravation [7]. From recent population studies it is apparent that these changes occur independently of different background factors, such as race and iodine intake, and accordingly should be more widely recognized [5, 14].