The case of the relapsing pituitary enlargement with galactorrhea

Hypothyroidism may cause reversible pituitary enlargement from thyrotroph and lactotroph hyperplasia.

Issue: May 2008

ByStephanie L. Lee, MD, PhD, ECNU

A 36-year-old woman was referred to the endocrine clinic with the diagnosis of severe hypothyroidism and extremely elevated TSH levels. The patient complained of persistent fatigue, amenorrhea and weight gain of 15 lb over the last two years. She admitted to intermittent non-compliance with her thyroid medication and had not taken her thyroid medication for at least the last six months.

Her past medical history was unremarkable except she had been diagnosed with hypothyroidism and a pituitary tumor at another hospital 10 years prior to this visit. She denied any treatment for the pituitary tumor. She had no allergies and was not taking any medications or drugs of abuse at the time of her initial appointment. Her physical exam showed normal secondary sex characteristics. Her visual fields on confrontation were normal. Her head and neck exam revealed periorbital edema and an enlarged thyroid of 30 gm with a firm, rubbery texture without nodules. Her breast exam was significant for expressible galactorrhea. Her deep tendon reflexes had a markedly delayed relaxation phase.

Stephanie L. Lee

Laboratory studies revealed a prolactin 42 (reference <20 ng/mL), LH 0.2 mIU/mL , FSH 0.5 mIU/mL, estradiol <37 pg/mL, TSH 297 (reference 0.3 – 4.5 uU/mL), free T₄ 0.1 (reference 0.9-1.8 ng/dL). MRI of the pituitary revealed pituitary enlargement with displacement and tenting of the optic chiasm but no evidence of cavernous sinus invasion (see figures 1A, 1B, and 2C). Two MRI scans of the pituitary 10 years before were obtained and demonstrated a similar pituitary enlargement on the initial scan (figure 2A) with a TSH of 603 uU/mL and the a normal pituitary when imaged again six months later (figure 2B) after L-thyroxine therapy with a TSH of 3.6 uU/mL.

The patient was treated with levothyroxine therapy 112 mcg daily with normalization of her TSH to 1.2 uU/mL and prolactin to 8.2 ng/dL. The patient’s fatigue resolved and her menses resumed after two months of L-thyroxine therapy. Repeat pituitary MRI images revealed a normal appearing pituitary gland (figure 2D).

Figure 1A: MRI of the pituitary gland, coronal view

Figure 1. MRI of the pituitary gland. Coronal (A) and sagittal (B) views showing an enlarged pituitary gland (blue arrow) with tenting of the optic chiasm (red arrow). Posterior pituitary is seen on the sagittal view (yellow arrow).

Pituitary and sella enlargement have been recognized for three decades. Thyrotrope hyperplasia correlates with TSH levels. The clue to extreme thyrotrope and pituitary hyperplasia is this patient was the extremely elevated TSH to >200 uU/mL. The regression of the pituitary hyperplasia is completely reversible and may occur within days of high dose L-thyroxine therapy. In addition, the elevated hypothalamic TRH level induced by hypothyroidism can stimulate prolactin secretion as observed in this patient.

It is important to recognize that hypothyroidism may cause reversible pituitary enlargement from thyrotroph and lactotroph hyperplasia with an elevated prolactin level that can be misinterpreted as a pituitary macroadenoma and lead to the misdiagnosis of a prolactinoma. This is the first example of relapsing enlargement of the pituitary due to erratic medical compliance and repeated episodes of severe hypothyroidism (figure 2A, 2B, 2C, 2D).

Figure 2A: Pituitary hyperplasia with hypothyroidism

Figure 2B: Normalization of the pituitary gland during periods of euthyroidism

Figure 2C: Pituitary hyperplasia with hypothyroidism

Figure 2D: Normalization of the pituitary gland during periods of euthyroidism

Figure 2. Reversible pituitary enlargement and hypothyroidism. Pituitary hyperplasia with hypothyroidism (panels A, C) and normalization of the pituitary gland during periods of euthyroidism (panels B and D). Pituitary (blue arrow). Optic chiasm (red arrow).

Photos courtesy of Boston Medical Center

Stephanie L. Lee, MD, PhD, is an Associate Professor of Medicine at Boston University School of Medicine and Director of Endocrine Clinic, and the Robert Dawson Evans Clinician at the Boston Medical Center.

For more information:

Bigos ST, Ridgway EC, Kourides IA, Maloof F. Spectrum of pituitary alterations with mild and severe thyroid impairment. J Clin Endocriol Metab. 1978;46:317-325.

Pioro EP, Scheitnauer BW, Laws ER, et al. Combined thyrotroph and lactotroph cell hyperplasia simulating prolactin-secreting pituitary adenoma in long-standing primary hypothyroidism. Surgical Neurology. 1988;29: 218-226.

Saris NJ, Bucker-David F, Toppan JL, Scapulas MC. MRI-demonstrable regression of a pituitary mass in a case of primary hypothyroidism after a week of acute thyroid hormone therapy. J Clin Endocrinol Metab. 1997;82:808-810.

Yamada T, Tsukui T, Ikejeri K, et al. Volume of sella turcica in normal subjects and in patients with primary hypothyroidism and hyperthyroidism. J Clin Endocrinol Metab. 1976;72:817-822.

Stephanie L. Lee, MD, PhD, is an Associate Professor of Medicine at Boston University School of Medicine and Director of Endocrine Clinic, and the Robert Dawson Evans Clinician at the Boston Medical Center.