BMC Endocrine Disorders (Aug 2021)

Thyroid-related ophthalmopathy development in concurrence with growth hormone administration

  • Shimpei Iwata,
  • Kenji Tsumura,
  • Kenji Ashida,
  • Ichiro Tokubuchi,
  • Mutsuyuki Demiya,
  • Miyuki Kitamura,
  • Hiroyuki Ohshima,
  • Mamiko Yano,
  • Ayako Nagayama,
  • Junichi Yasuda,
  • Munehisa Tsuruta,
  • Seiichi Motomura,
  • Shigeo Yoshida,
  • Masatoshi Nomura

DOI
https://doi.org/10.1186/s12902-021-00834-2
Journal volume & issue
Vol. 21, no. 1
pp. 1 – 6

Abstract

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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.

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