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Endocrinological Oncology |
Laboratory of Molecular and Cellular Biology (N.J.S.) and Molecular and Cellular Endocrinology Branch (F.B-D., M.C.S.), National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), and Department of Radiology (J.L.D.), Warren G. Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland 20892
Address correspondence and requests for reprints to: Nicholas J. Sarlis, MD, PhD, Steroid Hormones Section, Laboratory of Molecular and Cellular Biology (LMCB), National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health, Bldg 8/Rm B2 A11, 8 Center Drive, MSC 0805, Bethesda, Maryland 20892-0805; E-mail: njsarlis{at}box-n.nih.gov
Although magnetic resonance imaging (MRI) characteristics of pituitary gland hyperplasia in primary hypothyroidism have been previously described, the time span necessary for the regression of the hyperplasia in response to acute thyroid hormone (TH) therapy has not been defined.
A 26-yr-old woman underwent 131I ablation 11 yr before admission. Intermittent poor compliance to levothyroxine (LT4) therapy led to inappropriately high serum thyroid-stimulating hormone (TSH) for her triiodothyronine (T3) and thyroxine (T4) levels. The patient was investigated to rule out TSH-secreting pituitary adenoma or resistance to TH. On admission, the patients clinical features and thyroid function tests, as well as thyrotropin-releasing hormone (TRH) and acute T3 suppression tests, were in favor of profound primary hypothyroidism. MRI revealed symmetrical enlargement of the pituitary gland with distinct morphological characteristics of a macroadenoma. The patient began high-dose TH therapy and was rescannned six days later. The follow-up scan revealed a dramatic shrinkage of the pituitary gland. Four weeks later, serum T4 and TSH were within the normal range, and repeat MRI scan of the pituitary at that time showed a normal gland.
This case is the first to document dramatic shrinkage of pituitary hyperplasia in long-standing primary hypothyroidism within one week of acute TH therapy. MRI alone is unable to reliably differentiate between a TSH-secreting pituitary adenoma and hypothyroidism-induced pituitary hyperplasia. Dynamic endocrine testing as well as repeat pituitary MRI after a brief TH trial may provide a firm diagnosis in similar cases.
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