Development of postpartum spontaneously resolving transient Graves' hyperthyroidism followed immediately by transient hypothyroidism.
A 25-year-old woman with a history of Graves' disease, in remission for 8.5 years following 6 months of methimazole therapy, first came to our attention 5 months after her first delivery with clinical and biochemical hypothyroidism, markedly elevated titre of anti-thyroid microsomal antibody (MCHA; 1:102400) and mildly elevated activity of thyrotropin-binding inhibitory immunoglobulins (TBII; 29.5%). After short-term (3 months) treatment with L-thyroxine therapy, the development of hyperthyroidism in the first trimester of the second pregnancy, which remitted through the second and third trimesters, was observed. TBII showed a peak value (93.1%) 1 month after the onset of hyperthyroidism, and a normal value (12.4%) 6 d after delivery. One month after the second delivery, the patient developed hyperthyroidism, with an elevation of 99mTc thyroid uptake (5.58%; normal range 0.5-2.5%), which was immediately followed by transient clinical and biochemical hypothyroidism. Concomitant increases in MCHA titre and TBII activity were observed after delivery, and both reached peak levels (1:409600 and 81.0%, respectively) one and a half months after the onset of hypothyroidism. Thyroid-stimulating antibody (TSAb), measured using FRTL-5 thyroid cells, was detected at a weakly positive level (161%) on initial examination, and the serial change in TSAb was almost identical to that in TBII. Patients with Graves' disease may develop Graves' type hyperthyroidism, followed immediately by transient hypothyroidism due to coexisting destructive autoimmune thyroiditis during the early postpartum period, despite increasing TSAb activity.
Shigemasa
C
C
First Department of Internal Medicine, Tottori University School of Medicine, Yonago, Japan.
Mitani
Y
Y
Taniguchi
S
S
Ueta
Y
Y
Urabe
K
K
Tanaka
T
T
Yoshida
A
A
Mashiba
H
H
D000328:Adult; D001323:Autoantibodies / Q000032:analysis; D005260:Female; D006111:Graves Disease / Q000209:etiology* / Q000276:immunology; D006801:Humans; D007037:Hypothyroidism / Q000209:etiology* / Q000276:immunology; D011247:Pregnancy; D011248:Pregnancy Complications / Q000209:etiology / Q000276:immunology; D011644:Puerperal Disorders / Q000209:etiology* / Q000276:immunology; D011989:Receptors, Thyrotropin / Q000276:immunology; D012075:Remission, Spontaneous; D012189:Retrospective Studies
D001323:Autoantibodies; D011989:Receptors, Thyrotropin