Soluble interleukin-2 receptor in sera of patients with Graves' disease

C. Balázs, N. R. Farid

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Activation of T lymphocytes has been found to be associated with an increase in soluble interleukin-2 receptor (sIL-2R) levels. The aim of this study was to investigate serum levels of sIL-2R in 20 untreated patients with Graves' disease and to relate these levels to disease activity and to TSH-receptor, anti-thyroglobulin, anti-microsomal and anti-eye muscle antibodies. sIL-2R levels were significantly increased in newly diagnosed Graves' patients compared with controls (667 ± 270 vs 205 ± 45 U/ml) (P <0.001). The sIL-2R levels were higher in patients with active infiltrative ophthalmology than in those without eye symptoms (810 ± 313 vs 525 ± 180 U/ml). All patients were treated with methimazole for at least 12 months. sIL-2R levels were normalized by methimazole treatment in the majority of patients without ophthalmopathy but not in those with ophthalmopathy. In five patients sIL-2R serum levels were studied after interruption of thyrostatic therapy. An increase was observed in three patients and hyperthyroidism subsequently relapsed in two of these. Furthermore, a correlation was found between soluble interleukin-2 receptor levels and TSH-receptor antibodies but not with other immune parameters examined. Serum sIL-2R represents a useful marker of immunological activity in Graves' disease.

Original languageEnglish
Pages (from-to)681-688
Number of pages8
JournalJournal of Autoimmunity
Volume4
Issue number4
DOIs
Publication statusPublished - 1991

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Interleukin-2 Receptors
Graves Disease
Serum
Methimazole
Thyrotropin Receptors
Hyperthyroidism
Ophthalmology
T-Lymphocytes
Muscles
Antibodies
Therapeutics

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

Soluble interleukin-2 receptor in sera of patients with Graves' disease. / Balázs, C.; Farid, N. R.

In: Journal of Autoimmunity, Vol. 4, No. 4, 1991, p. 681-688.

Research output: Contribution to journalArticle

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