title: Incomplete thyrotroph suppression determined by third generation thyrotropin assay in subacute thyroiditis compared to silent thyroiditis or hyperthyroid Graves' disease.
abstract: Serum TSH concentrations were determined by both second and third generation assays in three types of thyrotoxicosis associated with subacute thyroiditis, silent thyroiditis, and hyperthyroid Graves' disease at the time of each patient's initial visit to the clinic. Serum TSH concentrations as measured by the second generation assay with an analytical sensitivity of 0.04 mU/L were below the detection limit in every patient. In contrast, serum TSH concentrations as measured by the third generation assay with an analytical sensitivity of 0.009 mU/L were below the detection limit in 18 of 21 (86%) patients with Graves' disease, 18 of 20 (90%) with silent thyroiditis, but only 4 of 18 (22%) with subacute thyroiditis. Changes in serum TSH concentrations were studied in healthy volunteers given daily 75 micrograms of T3; their serum TSH concentrations on the second generation assay fell below the detection limit within 3 days in every subject. However, the TSH concentration measured by the third generation assay remained above the detection limit in 6 of 8 normal subjects even on the 14th day of therapy. The reason for incomplete TSH suppression in most subacute thyroiditis patients may be that these patients had notable neck pain, and their initial visit to the clinic may have occurred earlier after the onset of disease than with patients who have had silent thyroiditis or Graves' disease. Thus, the serum TSH concentration had not decreased sufficiently below the detection limit at the time blood was drawn. The data suggest also that the highly sensitive TSH assay, if the level is above the detection limit, can be used to suppose that the short duration of the initiation of thyrotoxicosis indicates a case of subacute thyroiditis.
authors.affiliation: First Department of Medicine, Osaka Medical College, Takatsuki, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Ito
authors.forename: J
authors.initials: J
authors.lastname: Takamatsu
authors.forename: S
authors.initials: S
authors.lastname: Yoshida
authors.forename: Y
authors.initials: Y
authors.lastname: Murakami
authors.forename: S
authors.initials: S
authors.lastname: Sakane
authors.forename: K
authors.initials: K
authors.lastname: Kuma
authors.forename: N
authors.initials: N
authors.lastname: Ohsawa
mesh_terms: D000208:Acute Disease; D000328:Adult; D005260:Female; D006111:Graves Disease / Q000097:blood* / Q000473:pathology; D006801:Humans; D006980:Hyperthyroidism / Q000097:blood* / Q000473:pathology; D007158:Immunologic Techniques; D008297:Male; D008875:Middle Aged; D009994:Osmolar Concentration; D010903:Pituitary Gland, Anterior / Q000378:metabolism* / Q000473:pathology; D012016:Reference Values; D013966:Thyroiditis / Q000097:blood* / Q000473:pathology; D013972:Thyrotropin / Q000037:antagonists & inhibitors* / Q000097:blood; D013974:Thyroxine / Q000097:blood; D013997:Time Factors; D014284:Triiodothyronine / Q000494:pharmacology
chemical_list: D014284:Triiodothyronine; D013972:Thyrotropin; D013974:Thyroxine