Looking Beyond the MRI

Reversible Pituitary Hyperplasia in a Patient with Severe Primary Hypothyroidism

By Cristina S. Candido-Vitto, MD


Magnetic resonance imaging of the brain does not always distinguish between pituitary hyperplasia versus an adenoma.  This case report describes a female adolescent with severe primary hypothyroidism with brain MRI findings suspicious for a pituitary tumor displacing the optic chiasm.  The pituitary gland enlargement resolved after treatment with Levothyroxine.


A 14-year-old, previously healthy female adolescent presented to her pediatrician for new-onset daily headaches. No other associated symptoms were noted except for mild fatigue. She was seen by a pediatric neurologist who ordered a brain MRI with attention to the sella that showed an enlarged pituitary gland measuring 1.6 x 1.6 x 1.1 cm effacing the undersurface of the optic chiasm, which was read by the radiologist as consistent with a pituitary adenoma (Figure 1).





Fig. 1  Initial brain MRI with attention to the sella showing an enlarged pituitary gland measuring 1.6 x 1.6 x 1.1 cm, effacing the undersurface of the optic chiasm.

Visual problems, galactorrhea, gastrointestinal symptoms, and weight changes were absent.  The patient was premenarchal.  The mother mentioned that the patient’s growth had been slower the past year.


The patient’s height (10th to 25th percentile) and weight (25th to 50th) were normal.  Her vital signs were normal with heart rate of 68 bpm.  The visual fields were normal.   Her thyroid gland was smooth, easily palpable but not enlarged.  She was Tanner IV for breast and pubic hair development.  The rest of the exam was normal.


Laboratory tests showed severe primary hypothyroidism with a significantly elevated Thyroid Stimulating Hormone (TSH) of > 150 mIU/L (normal range of 0.5 – 4.3) and low Free T4 of 0.4 ng/dL (normal range of 0.9 – 1.4).  Prolactin was slightly high at 33.1 ng/ml (normal range of 3.2 – 20). A basic metabolic profile was normal.   The patient was then referred to the Cottage Pediatric Endocrinology Clinic



Fig 2  Repeat brain MRI five months after thyroxine replacement showing a significant interval decrease in the size of the pituitary gland at 1.1 x 1.0 x 0.9 cm, no longer effacing the optic chiasm.


Further laboratory testing showed positive thyroid peroxidase antibodies at 145 IU/ml (normal of <35 IU/ml) and thyroglobulin antibodies at 542 IU/ml (normal of <20), consistent with Hashimoto’s thyroiditis.  IGF-1 was normal at 479 ng/ml (normal range of 222-650) and IGFBP3 5.1 mg/L (normal range of 3.3-10).


Early morning ACTH was 63 pg/ml (normal range of 9–57) with cortisol at 16.4 mcg/dl. LH was 5.87 mIU/ml (normal range of 0.04 – 10.8), and FSH 1.18 mIU/ml (normal range of 0.8 to 8.5) with estradiol of 51 pg/ml.  The patient was initially started on 44 mcg of Levothyroxine, which was subsequently increased to 88 mcg daily after two weeks.


The patient’s headaches and mild fatigue resolved after a few weeks of Levothyroxine replacement.  Repeat thyroid function tests were normal.  Prolactin went down to normal at 11.5 ng/ml.  A repeat brain MRI five months later showed a significant interval decrease in the size of the pituitary gland from 1.6 x 1.6 x 1.1 cm to 1.1 x 1.0 x 0.9 cm, no longer effacing the optic chiasm (Figure 2).  A study on the pubertal physiologic hypertrophy of the pituitary gland describes the average diameter of the pituitary gland in female adolescents as between 0.8 to 1 cm.1


Pituitary hyperplasia secondary to primary hypothyroidism has been described in literature. 1-5 The lack of negative feedback from low levels of circulating thyroid hormones contributes to thyrotroph cell as well as lactotroph hyperplasia.2 The degree of pituitary gland enlargement in severe primary hypothyroidism is variable and has been reported in some extreme cases showing both sellar and suprasellar masses that compress surrounding structures.  Patients, in addition to symptoms of hypothyroidism, may present with menstrual irregularities, neurologic and visual deficits, hyperprolactinemia, and secondary adrenal insufficiency requiring hydrocotisone replacement.3  The demonstration of a presumed pituitary adenoma on brain MRI studies, as well as CT scans, has led to some inadvertent transsphenoidal surgeries.2  This case highlights the unreliability of magnetic resonance imaging in distinguishing between a pituitary adenoma versus pituitary hyperplasia.


The pituitary gland enlargement and accompanying symptoms in severe primary hypothyroidism may be completely reversible with thyroid hormone replacement.  This time period varies from within only a week to a few months from starting treatment.1-5 Thyroid function testing in the investigation of pituitary masses, as well as careful assessment and monitoring of MRI imaging of the sella with appropriate treatment, may prevent progression of neurologic symptoms as well as unnecessary surgery.




  • Doraiswamy PM, Potts JM, Figiel GS, Boyko OB, Krishnan KR. 1991. MR imaging of physiologic pituitary gland hypertrophy in adolescence. Radiology. 178(1):284-5.
  • Sarlis NJ, Brucker-Davis F, Doppman JL, Skarulis MC. 1997. MRI-demonstrable regression of a pituitary mass in a case of primary hypothyroidism after a week of acute thyroid hormone therapy.  Clin Endocrinol Metab. 82(3):808-11
  • Passeri E, Tufano A, Locatelli M, Lania AG, Ambrosi B, Corbetta S. 2011.  Large pituitary hyperplasia in severe primary hypothyroidism. J Clin Endocrinol Metab. 96(1):22-3.
  • Xu AJ, Li T. 2010. Pituitary hyperplasia secondary to primary hypothyroidism in children: report of 8 cases. Zhongguo Dang Dai Er Ke Za Zhi. 12(1):17-20.
  • Joshi AS, Woolf PD. 2005. Pituitary hyperplasia secondary to primary hypothyroidism: a case report and review of the literature. Pituitary. 8(2):99-103

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