A case of thyrotropin-producing pituitary adenoma, accompanied by an increase in anti-thyrotropin receptor antibody after tumor resection

Abstract

We describe a rare, but interesting, case of TSH-producing adenoma (TSHoma), accompanied by increases in both anti-TSH receptor antibody (TRAb) and thyroid-stimulating antibody (TSAb) after tumor resection. A 21-yr-old woman was referred to our department for further evaluation of pituitary tumor. In a nearby hospital, she had been diagnosed as having pituitary tumor. Her serum free T4, free T3, and TSH levels were all elevated concomitantly. On the basis of a diagnosis of pituitary adenoma with TSH production, transsphenoidal resection of the pituitary adenoma was performed. Two weeks after the operation, the blood concentrations of TSH were undetectable, whereas both TRAb and TSAb levels were elevated. TSAb levels gradually increased further from 2 weeks to 3 months after the operation, accompanied by an increase in TSH and free T4 levels. TSH is an important hormone in maintaining physiology and regulating immunomodulators in thyrocytes, as it can influence a variety of immune-regulating cytokine-like activities and inhibit expressions of Fas antigen, intracellular adhesion molecule-1, and class II trans-activator. Changes in TSH would modulate the immune circumstances in the thyroid, and then induce TRAb and TSAb. Autoimmune parameters with thyroid function should be observed carefully when managing patients with TSHoma.

Coexistence of Thyroid-Stimulating Hormone-Secreting Pituitary Adenoma and Graves' Hyperthyroidism

“…Therefore, a rapid reduction in the TSH levels after trans-sphenoidal tumor resection, pituitary irradiation, or octreotide administration may induce apoptosis and activate autoimmune responses against the thyroid gland as a result of increased expression of various cell surface markers (Fas, intercellular adhesion molecule-1, MHC class II) on thyrocytes [8]. In line with these hypotheses, Kageyama et al [19] reported the case of a 21-year-old woman with TSHoma who had increases in both anti-TSH receptors antibody and thyroid-stimulating antibody after tumor resection.…”

“…Fas antigen is functionally expressed on the surface of thyrocytes, and TSH inhibits Fas antigen-mediated apoptosis of thyrocytes resulting in the promotion of growth of the thyroid gland [15]. Intercellular adhesion molecule-1 and class II MHC have been implicated as contributing factors for numerous diseases, including autoimmune thyroid diseases, and TSH could downregulate their interferon-γ-mediated expression [16,17,18,19]. Therefore, a rapid reduction in the TSH levels after trans-sphenoidal tumor resection, pituitary irradiation, or octreotide administration may induce apoptosis and activate autoimmune responses against the thyroid gland as a result of increased expression of various cell surface markers (Fas, intercellular adhesion molecule-1, MHC class II) on thyrocytes [8].…”

Thyroiditis Developing Post Initiation of Octreotide in a Case of TSH Secreting Tumor

“…Thyroiditis in our patient developed post therapy when the TSH levels declined from above 10 mIU/L to 1.8 mIU/L post therapy. Previously, anecdotal cases of development of Graves' disease after surgery of pituitary tumor have been described (when TSH levels declined) (7,8,16,17). The immunomodulatory role of TSH was implicated for the development of Graves' disease post surgery in these cases.…”

“…The prevalence of circulating antithyroid autoantibodies is similar to that found in the general population. However, there are anecdotal case reports of patients developing Graves' disease after pituitary surgery (7,8). The immunomodulatory role of TSH with the decline in TSH levels post surgery has been implicated for autoimmune thyroid disease.…”

A case of TSH-producing adenoma treated with octreotide in combination with thiamazole for the control of TSH and thyroid hormones after trans-sphenoidal neurosurgery

“…While serum TSH concentration was decreased to a normal range in response to treatment with the somatostatin analog, octreotide, the concentrations of free T3 and free T4 were not normalized and tachycardia continued. Some cases of TSHoma complicated by Graves' disease have been reported [10][11][12]. TSH is known to repress the expression of interferon-γ-induced Fas antigen [13], intercellular adhesion molecule (ICAM)-1 [14] and class II trans-activator, which is a non-DNAbinding regulator of major histocompatibility complex (MHC) transcription on the thyroid cell surface [11].…”