Author:
Iwata Shimpei,Tsumura Kenji,Ashida Kenji,Tokubuchi Ichiro,Demiya Mutsuyuki,Kitamura Miyuki,Ohshima Hiroyuki,Yano Mamiko,Nagayama Ayako,Yasuda Junichi,Tsuruta Munehisa,Motomura Seiichi,Yoshida Shigeo,Nomura Masatoshi
Abstract
Abstract
Background
Thyroid stimulating hormone (TSH) receptor and local infiltrate lymphocytes have been considered as major pathological factors for developing thyroid-related ophthalmopathy. Overexpression of insulin-like growth factor-I (IGF-I) receptor has emerged as a promising therapeutic target for refractory patients. However, the relationship between activation of growth hormone (GH)/IGF-I receptor signaling and development or exacerbation of thyroid ophthalmopathy has not been elucidated. Herein we describe a case that provides further clarification into the association between thyroid-related ophthalmopathy and GH/IGF-I receptor signaling.
Case presentation
A 62-year-old Japanese female diagnosed with thyroid-related ophthalmopathy was admitted to Kurume University Hospital. She had received daily administration of GH subcutaneously for severe GH deficiency; however, serum IGF-I levels were greater than + 2 standard deviation based on her age and sex. She exhibited mild thyrotoxicosis and elevation in levels of TSH-stimulating antibody. Discontinuation of GH administration attenuated the clinical activity scores of her thyroid-related ophthalmopathy. Additionally, concomitant use of glucocorticoid and radiation therapies resulted in further improvement of thyroid-related ophthalmopathy. The glucocorticoid administration was reduced sequentially, followed by successful termination. Thereafter, the patient did not undergo recurrence of thyroid-related ophthalmopathy and maintained serum IGF-I levels within normal physiological levels.
Conclusions
We describe here a case in which development of thyroid-related ophthalmopathy occurred upon initiation of GH administration. GH/IGF-I signaling was highlighted as a risk factor of developing thyroid-related ophthalmopathy. Additionally, aberrant TSH receptor expression was suggested to be a primary pathophysiological mechanism within the development of thyroid-related ophthalmopathy. Physicians should be aware of the risks incurred via GH administration, especially for patients of advanced age, for induction of thyroid-related ophthalmopathy.
Publisher
Springer Science and Business Media LLC
Subject
General Medicine,Endocrinology, Diabetes and Metabolism
Reference22 articles.
1. Bahn RS. Graves’ ophthalmopathy. N Engl J Med. 2010;362:726–38.
2. Bartalena L, Baldeschi L, Boboridis K, Eckstein A, Kahaly GJ, Marcocci C, et al. The 2016 European Thyroid association/European group on graves’ orbitopathy guidelines for the management of Graves’ orbitopathy. Eur Thyroid J. 2016;5:9–26.
3. Otto EA, Ochs C, Hansen C, Wall JR, Kahaly GJ. Orbital tissue-derived t lymphocytes from patients with Graves’ ophthalmopathy recognize autologous orbital antigens. J Clin Endocrinol Metab. 1996;81:3045–50.
4. Ueda-Sakane Y, Kanamoto N, Fushimi Y, Tanaka-Mizuno S, Yasuno S, Miura M, et al. Overall safety and efficacy of high-dose and low-dose intravenous glucocorticoid therapy in patients with moderate-to-severe active Graves’ ophthalmopathy. Endocr J. 2016;63:703–14.
5. Fröhlich E, Wahl R. Thyroid autoimmunity: role of anti-thyroid antibodies in thyroid and extra-thyroidal diseases. Front Immunol. 2017;8:521.
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