Pituitary hyperplasia: a complication of the pseudomalabsorption of thyroxine

Abstract

Objective“The pseudomalabsorption of thyroxine” has been used to describe patients with hypothyroidism who fail to comply with their treatment. We describe a unique case of a 32-year-old with hypothyroidism who developed pituitary hyperplasia and hyperprolactinemia secondary to the pseudomalabsorption of thyroxine.Investigations and treatmentAfter baseline thyroid-function tests were performed, the patient was administered levothyroxine 0.5 mg under the supervision of a registered nurse. Thyroid function testing was repeated at 30, 60, 120, and 180 minutes. Arrangements were made for further daily supervised loading of levothyroxine 0.1 mg.ResultsWith the administration of 0.5 mg levothyroxine, free thyroxine levels increased by 120 minutes, and with daily supervised dosing of 0.1 mg there was normalization of the thyroid hormone levels and a reduction of thyroid-stimulating hormone levels. Maintenance of thyroid-stimulating hormone < 15 mU/L for 2 weeks led to a reduction in prolactin levels and regression in the size of the pituitary on magnetic resonance imaging.ConclusionIf left untreated, these patients face significant morbidity and are at risk of developing pituitary hyperplasia, complications from an increase in pituitary size, hyperprolactinemia, and potentially myxedema coma. Recognizing pituitary hyperplasia and hyperprolactinemia as a complication from the pseudomalabsorption of levothyroxine may prevent the potential of a misdiagnosis of a prolactinoma leading to unnecessary investigations and inappropriate treatment. Patient awareness of this serious complication and the rapid, demonstrable resolution with adequate thyroid hormone replacement may provide motivation to comply with supervised dosing of levothyroxine. It has also been suggested that supervised treatment enables the individual to maintain their patient status, which may be in part the motivation behind this disorder.

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“…The hypersecretion of TSH may result in hyperplasia of thyrotropes in the pituitary gland, as recently reported by Doyle et al in a case of "pseudomalabsorption of LT4" with much elevated TSH (> 700 mIU/L) [27]. The mass effect of pituitary hyperplasia can suppress the secretion of LH [14,15,27]. Due to the same mechanism of lack of feedback suppression, the hypophyseal TRH is also expected to be elevated, which increases the secretion of both TSH and prolactine (PRL) levels; the hyperprolactinemia will in turn suppress the LH [1].…”

“…The hypersecretion of TSH may result in hyperplasia of thyrotropes in the pituitary gland, as recently reported by Doyle et al in a case of "pseudomalabsorption of LT4" with much elevated TSH (> 700 mIU/L) [27]. The mass effect of pituitary hyperplasia can suppress the secretion of LH [14,15,27].…”