Serum Thyroglobulin Levels in the Diagnosis and Follow-up of Subacute 'Painful' Thyroiditis

Madeddu, Giuseppe

doi:10.1001/archinte.1985.00360020063012

Cited by 15 publications

(2 citation statements)

References 27 publications

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“…It also stimulates the gested by several authors (8), but there are no published growth of thyroid neoplasms, because these neoplasms ex-prospective clinical studies to confirm these suggestions, press TSH receptors on their plasma membranes; hence, Because high doses of LT4 have some untoward effects on reduction of TSH secretion can arrest tumor extension bone and heart (9,10), the degree of suppression of TSH, (1,2). 1245 roid, and (3) Activation of TSH receptor (11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21). and have no recurrent or metastatic cancer.…”

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confidence: 99%

Degree of Thyrotropin Suppression in Differentiated Thyroid Cancer without Recurrence or Metastases

Kamel

Güllü²,

Ilgin³

et al. 1999

Thyroid

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Forty-eight patients with differentiated thyroid cancer (DTC), who had no evidence of tumor recurrence or metastases on studies such as radioiodine scanning, neck ultrasonography, and with thyrotropin (TSH) and thyroglobulin (Tg) levels less than 1 mU/L and 5 ng/mL, respectively, were included in the study. The mean age was 43 +/- 12 years (range 15-65) and all were receiving levothyroxine (LT4) treatment with a mean dose of 184 +/- 46 microg daily. Patients were divided into two groups; group A included patients that had baseline TSH levels of 0.4 mU/L or more, and group B patients had baseline TSH levels of less than 0.4 mU/L. LT4 doses for all patients were increased, and serum TSH and Tg measurements were reevaluated after 2 months of dose increments. The mean TSH of group A (patients with baseline TSH levels > or = 0.4 mU/L) decreased from 0.67 +/- 0.28 mU/L to 0.16 +/- 0.08 mU/L (p < 0.001), but mean serum Tg level showed no change after dose increments (2.92 +/- 1.36 ng/mL vs. 3.59 +/- 0.93 ng/mL at the second month; p > 0.05). Similar results were also observed in group B (patients with baseline TSH levels < 0.4 mU/L). Mean TSH level decreased from 0.26 +/- 0.07 mU/L to 0.1 +/- 0.05 mU/L (p = 0.006), but no decrease occurred in mean Tg level (3.0 +/- 1.16 ng/mL vs. 3.3 +/- 1.03 ng/mL; p > 0.05). The patients' data were reevaluated according to second-month TSH levels. Patients with a TSH level between 0.11 to 0.4 mU/L were set as "final TSH > 0.1 group," and patients with a TSH level equal or less than 0.1 mU/L were set as "final TSH < or = 0.1 group," and baseline and second-month Tg levels were assessed. The mean second month Tg levels did not differ in these two patient groups (3.7 +/- 0.74 ng/mL for final TSH > 0.1 group vs. 3.3 +/- 1.2 ng/mL for final TSH < or = 0.1 group; p > 0.05). No difference could be found between initial and second-month Tg levels in both groups (2.8 +/- 1.4 ng/mL vs. 3.7 +/- 0.74 ng/mL in final TSH > 0.1 group and 3.11 +/- 1.1 ng/mL vs. 3.3 +/- 1.2 in final TSH < or = 0.1 group; p > 0.05). In conclusion, these results indicate that serum Tg levels cannot be suppressed by maximal TSH suppression in tumor-free DTC patients. The suppression of TSH to less than 0.1 mU/L seems not to be necessary in most patients who have no evidence of active disease.

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confidence: 99%

Degree of Thyrotropin Suppression in Differentiated Thyroid Cancer without Recurrence or Metastases

Kamel

Güllü²,

Ilgin³

et al. 1999

Thyroid

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“…A study by Teixeira et al in a small sample of SAT patients showed that serum TG was markedly higher in patients with SAT than in controls (149 ± 52 ng/ml vs. 10.5 ± 1.0 ng/ml) and that TG remained higher than in healthy subjects up to 4–5 months after the acute phase of the disease [ 13 ]. Madeddu et al showed that TG was elevated in 92% of patients with newly diagnosed SAT and decreased after the introduction of glucocorticoids [ 14 ]. Similarly, Yamamoto et al observed that patients receiving prednisolone showed lower TG concentrations than their salicylate-treated counterparts after 4 weeks of treatment; the authors suggested that the observed decrease in TG concentration could be the result of impaired intrathyroid hydrolysis of colloid due to glucocorticoid use [ 15 ].…”

Section: Destructive Thyroiditis: Subacute Thyroiditismentioning

confidence: 99%

Clinical use of thyroglobulin: not only thyroid cancer

Berlińska,

Świątkowska-Stodulska

2024

Endocrine

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Thyroglobulin (TG) is a dimeric glycoprotein produced exclusively by mature thyroid tissue and stored within the follicular lumen. It is essential for the organification of iodine and the production of thyroid hormones. The concentration of TG in the bloodstream varies between individuals and depends on factors such as thyroid mass, stimulation of the gland by thyrotropin or autoantibodies, and tissue destruction. TG is essential to monitor patients with differentiated thyroid cancer; however, its use is not limited only to this clinical entity. Measurement of circulating TG can provide better insight into numerous clinical scenarios, such as destructive thyroiditis, presence of ectopic thyroid tissue, thyroid trauma, factitious thyrotoxicosis, or iodine nutrition. Lately, TG has found its new clinical use in immune checkpoint-related thyroid dysfunction. TG measurement should be performed carefully in patients with antithyroglobulin antibodies due to possible laboratory interferences. In this review, we offer a summary of current knowledge about the clinical use of TG and the implications it brings to daily practice.

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Thyroglobulin Measurement

Spencer

Petrović²

2010

Thyroid Function Testing

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Serum Thyroglobulin Levels in the Diagnosis and Follow-up of Subacute 'Painful' Thyroiditis

Cited by 15 publications

References 27 publications

Degree of Thyrotropin Suppression in Differentiated Thyroid Cancer without Recurrence or Metastases

Degree of Thyrotropin Suppression in Differentiated Thyroid Cancer without Recurrence or Metastases

Clinical use of thyroglobulin: not only thyroid cancer

Thyroglobulin Measurement

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