Endocrine Abstracts

Introduction: The reactive pituitary gland enlargement is a non-neoplastic growth of at least one pituitary lineage, which can often be essential or secondary to prolonged deficit of a gland target. It may be difficult to differentiate from functional pituitary adenomas. Herein we report a case of pituitary hyperplasia secondary to congenital primary hypothyroidism diagnosed at the age of 38 years.

Observation: A 38-year-old female patient presented with spaniomenorrhea, mental retardation and delayed stature. On physical examination,she had a height of 134 cm, a weight of 54 kg, adult pubertal status, galactorrhea, skin infiltration and non-palpable thyroid gland. Her hormonal profile showed raised thyrotropin stimulating hormone (TSH) (>100 mIU/L, range: 0.35-5), low FT4 (<0.40 ng/dL, range: 0.7-1.5) and hyperprolactinemia (142 μg/L). Further investigation showed negative antiperoxydase antibodies and the scintigraphy confirmed an ectopic sublingual thyroid gland. The patient was put on levothyroxine replacement therapy. Four months later, she presented with a normal TSH level but a persistent hyperprolactinemia (69 μg/L). A pituitary magnetic resonance imaging (MRI), requested in order to explore this hyperprolactinemia, showed diffuse pituitary enlargement with stalk deviation.

Conclusion: In our review of the literature, primary uncontrolled hypothyroidism has been described as a precursor to pituitary hyperplasia. It results from the loss of thyroxine feedback inhibition and the subsequent overproduction of thyrotropin-releasing hormone (TRH). L-thyroxine replacement therapy prevents enlargement of pituitary gland and may regress the change, but is not the only outcome of pituitary enlargement. Other coexisting disturbances must be considered when the treatment is not successful.