Thirty-three patients with
Addison's disease were studied. Twenty-two had idiopathic
Addison's disease; within this group, 14 patients had clinical or subclinical
hypothyroidism, and 16 had increased titres of thyroid
autoantibodies. Five patients had tuberculous, and eight had unclassifiable
Addison's disease; only one patient in the latter group had evidence of thyroid autoimmunity. A stimulation test with 15 mU bTSH/kg was performed in three patients with
Schmidt's syndrome (coexisting
Addison's disease and manifest
primary hypothyroidism), 15 patients with either subclinical
hypothyroidism or increased titres of thyroid
autoantibodies, 10 patients without thyroid involvement, and 10 normal controls. There was no detectable increase of 'free' and total
thyroid hormones in
Schmidt's syndrome. The mean increases after 3-4 h of T4, fT4, T3 and fT3 were 22, 35, 63 and 66%, respectively, in patients without thyroid involvement, and 13, 24, 46 and 45% in patients with subclinical
hypothyroidism. 'Free' but not total
thyroid hormones rose significantly (P less than 0.01) higher in patients without signs of thyroid involvement than in patients with subclinical
hypothyroidism and/or thyroid
autoantibodies.
Thyroid hormone response to bTSH in
Addison's disease with apparently healthy thyroid glands was not different from normal controls. Serum
diiodotyrosine rose in all groups except in
hypothyroidism; hypothyroid patients had, however, basal levels well within the normal range. Thus,
thyroid hormone synthesis appears to be blocked at a point distal to
diiodotyrosine formation in this particular situation. These results support the assumption that TSH elevation in idiopathic
Addison's disease is due to coexisting thyroid autoimmunity and that it reflects incipient thyroid failure.(ABSTRACT TRUNCATED AT 250 WORDS)