MON-235 - Reversible Pituitary Hyperplasia Secondary to Severe Primary Hypothyroidism Due to Undiagnosed Celiac Disease in an Adolescent Girl- A Case Report

Abstract
Pituitary hyperplasia is a rare but important reversible complication of long-standing untreated or inadequately treated primary hypothyroidism in children. Refractory hypothyroidism due to celiac disease leading to pituitary hyperplasia is underrecognized. Early diagnosis can avoid unnecessary pituitary surgery through appropriate endocrine evaluation. We report a case of a 10-year-old girl with autoimmune hypothyroidism and poor biochemical control despite confirmed compliance, who presented with galactorrhea, headache, and vomiting. Further evaluation revealed pituitary hyperplasia secondary to severe hypothyroidism caused by underlying celiac disease. Timely diagnosis and appropriate therapy led to complete clinical, biochemical, and radiological resolution.
Introduction
Primary hypothyroidism is common among in children. Severe and prolonged hypothyroidism may lead to pituitary hyperplasia due to chronic TRH stimulation. This condition can mimic pituitary adenoma presenting with hyperprolactinemia and compressive symptoms. Malabsorption due to celiac disease is a known but underrecognized cause of refractory hypothyroidism. Early recognition is crucial.
Case Presentation
A 10-year-old girl, a known case of primary hypothyroidism for six years, presented with progressive weight gain, intermittent vomiting, headache, and milky breast discharge. She was receiving levothyroxine 100 µg/day with confirmed compliance. Thyroid-stimulating hormone was markedly elevated at 383 IU/L despite dose escalation to 150 µg/day. Examination Tanner-appropriate pubertal development and galactorrhea. Biochemical evaluation showed severe hypothyroidism with mild hyperprolactinemia. Pituitary MRI demonstrated a symmetrically enlarged gland measuring 14 × 10 × 9 mm with homogeneous enhancement, suggestive of pituitary hyperplasia. Given refractory hypothyroidism, malabsorption was suspected. Tissue transglutaminase IgA antibodies were significantly elevated, confirming celiac disease. She was treated with levothyroxine–liothyronine combination along with gluten-free diet. Three months follow-up showed complete resolution of headache, vomiting, and galactorrhea & biochemical improvement. Repeat pituitary MRI demonstrated complete regression of pituitary enlargement. Inadequately treated primary hypothyroidism results in persistent TRH stimulation, causing thyrotroph hyperplasia and secondary hyperprolactinemia. Pituitary enlargement may mimic adenoma clinically and radiologically. Celiac disease should be excluded in children with refractory hypothyroidism despite confirmed compliance.
Conclusion
This case highlights celiac disease as a reversible cause of refractory hypothyroidism and secondary pituitary hyperplasia. Early identification prevents misdiagnosis and unnecessary pituitary surgery.

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