An elevation of stem cell factor in patients with hyperthyroid Graves' disease.

Graves' disease is an autoimmune disorder characterized by the presence of antibodies against thyrotropin receptor (TRAb). Stem cell factor (SCF), derived from bone marrow, is known to promote lymphohematopoiesis. To investigate the relation between the alteration in plasma levels of SCF, thyroid hormone status, and TRAb measured by thyrotropin binding inhibition (TBI), 13 untreated, 21 treated, and 4 relapsed hyperthyroid Graves' disease patients, 21 patients with Hashimoto's thyroiditis, 6 patients with subacute thyroiditis, and 11 control subjects were examined. In untreated hyperthyroid Graves' disease patients, serum levels of thyroxine (T4) and triiodothyronine decreased rapidly by methimazole treatment, and TBI decreased progressively, but variably. Simultaneously, the elevated plasma levels of SCF decreased gradually and progressively. The plasma levels of SCF correlated curvilinearly with the serum levels of T4. In 4 patients with relapsed hyperthyroid Graves' disease, TBI was marginally positive in 3 patients and negative in 1, but plasma levels of SCF were elevated significantly in all 4 patients. In patients with subacute thyroiditis and Hashimoto's thyroiditis with or without T4 replacement, plasma levels of SCF did not differ from that of controls. These findings indicate that the elevation of plasma levels of SCF relates to the longstanding thyrotoxic state and that short-term thyrotoxicosis does not significantly affect plasma levels of SCF. It remains to be determined whether the elevation in plasma levels of SCF is induced by excess thyroid hormone, reflecting the hypermetabolic state, or whether the elevation of plasma levels of SCF contributes to stimulation of lymphocytes producing TRAb.

[1]  N. Nagata,et al.  Cyclic change of cytokines in a patient with cyclic thrombocytopenia , 1996, British journal of haematology.

[2]  C. Manegold,et al.  Serum levels of stem cell factor are increased in asymptomatic human immunodeficiency virus-infected patients and are associated with prolonged survival. , 1995, Blood.

[3]  T. Erbas,et al.  Serum levels of interleukin 6 and tumor necrosis factor-alpha in hyperthyroid patients before and after propylthiouracil treatment. , 1995, European journal of endocrinology.

[4]  B. Hogan,et al.  Embryonic expression of a haematopoietic growth factor encoded by the SI locus and the ligand for c-kit , 1990, Nature.

[5]  K. Zsebo,et al.  Identification, purification, and biological characterization of hematopoietic stem cell factor from buffalo rat liver-conditioned medium , 1990, Cell.

[6]  David A. Williams,et al.  Stem cell factor is encoded at the SI locus of the mouse and is the ligand for the c-kit tyrosine kinase receptor , 1990, Cell.

[7]  P. Leder,et al.  The hematopoietic growth factor KL is encoded by the SI locus and is the ligand of the c-kit receptor, the gene product of the W locus , 1990, Cell.

[8]  C. March,et al.  Molecular cloning of mast cell growth factor, a hematopoietin that is active in both membrane bound and soluble forms , 1990, Cell.

[9]  C. March,et al.  Identification of a ligand for the c-kit proto-oncogene , 1990, Cell.

[10]  N. Copeland,et al.  Mast cell growth factor maps near the steel locus on mouse chromosome 10 and is deleted in a number of steel alleles , 1990, Cell.

[11]  L. Degroot,et al.  The causes of autoimmune thyroid disease. , 1989, Endocrine reviews.

[12]  K. Burman,et al.  Immune mechanisms in Graves' disease. , 1985, Endocrine reviews.

[13]  M. Wheeler,et al.  Extrathyroidal sites of autoantibody synthesis in Graves' disease. , 1984, Clinical and experimental immunology.

[14]  S. Galli,et al.  The kit ligand, stem cell factor. , 1994, Advances in immunology.

[15]  R. Volpe The role of cytokines in the development of autoimmune thyroid disease. , 1993, Thyroid : official journal of the American Thyroid Association.

[16]  D. Williams,et al.  Biological activities and potential therapeutic uses of steel factor. A new growth factor active on multiple hematopoietic lineages. , 1992, The American journal of pediatric hematology/oncology.

[17]  T. Aizawa,et al.  Pituitary-thyroid feedback regulation in patients with Graves' disease during antithyroid drug therapy. , 1982, The Journal of clinical endocrinology and metabolism.