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.

Comparison of serum thyrotrophin concentrations determined by a third generation assay in patients with various types of overt and subclinical thyrotoxicosis

“…Thus, it is suggested that serum TSH was influenced by the period of thyrotoxicosis in our patients. Although we could find no significant correlation between the serum TSH level and the duration of illness, Ito et al . (1997 ) reported that the serum TSH levels declined with disease duration in patients with subacute thyroiditis.…”

“…Thyrotoxicosis due to destructive thyroiditis such as subacute thyroiditis and painless thyroiditis is known to be caused by a release of thyroid hormones following destruction of thyroid follicular cells, which has a close relationship with viral infection in the former and thyroid autoimmunity in the latter. Recently, Ito et al . (1997 ) reported that serum TSH concentrations determined by a third‐generation assay in patients with subacute thyroiditis were incompletely suppressed.…”

Clinical Characteristics of 852 Patients with Subacute Thyroiditis before Treatment

“…We found that abnormal laboratory findings, such as elevations of FT4, FT3, Tg, CRP, and aminotransferases, reached their peak levels within 7 days after onset, whereas fully suppressed TSH could be detected later, in agreement with a previous report (18). The duration of elevated FT4 was much longer in SAT than in other types of destructive thyroiditis, including painless thyroiditis and acute suppurative thyroiditis, whereas the duration and levels of liver dysfunction in SAT were similar to those in painless thyroiditis (19,20 …”

Incidence rate and clinical features of hyperthyroidism in a long‐term iodine sufficient area of Sweden (Gothenburg) 2003–2005

“…Generally, OH had lower TSH levels than SH, consistently seen in all sub‐groups. The level of TSH suppression in patients with GD or thyroiditis may, however, be attributed to the duration of disease and a delayed recovery of the pituitary–thyroid axis . An alternative explanation in GD suggests that TRab may control TSH secretion through an ultra‐short feed‐back loop in the pituitary .…”

“…The level of TSH suppression in patients with GD or thyroiditis may, however, be attributed to the duration of disease and a delayed recovery of the pituitarythyroid axis. 30 An alternative explanation in GD suggests that TRab may control TSH secretion through an ultra-short feedback loop in the pituitary. 31 This study suggests also that the degree of thyroid hormone elevation matters for the level of TSH suppression.…”