P-41 THYROTROPHS HYPERPLASIA IN SEVER UNTREATED PRIMARY HYPOTHYROIDISM A RARE CAUSE OF MISLEADING PITUITARY ENLARGEMENT
Authors: Al Waeli Dheyaa Kadhim , Mohammed Adel Gassab , Albaghdadi Firas Abdullah 
Published: January 2025

Introduction

Pituitary gland hyperplasia (PGH) due to primary hypothyroidism (PH) still underdiagnosed. It is reversible with proper thyroxine therapy. Unfortunately, patients may be referred to unnecessary pituitary surgery without thyroid function test (TFT) assessment. We present a case of a 13 years old female scheduled for pituitary surgery for macro adenoma diagnosed by PMRI but fortunately, endocrine assessment revealed intense PH, proper treatment produced dramatic resolution in PGH.

Increase number of Pituitary gland (PG) cells causes PGH leads to abnormally enlarged PG on pituitary MRI (PMRI) (1). There is hypercellularity, polymorphism with large acini and intact reticulum (2). Firstly described at 1851 in cretins (3). It could be physiological in pregnancy or pathological due to primary hypothyroidism (PH), primary hypoadrenalism or primary gonadal insufficiency (4). Typical PMRI showed diffuse, regular, isointense enlargement of PG with homogenous uptake of gadolinium (5).

Clinical Case

We present a 13 years old female scheduled for PG surgery due to large mass, fortunately referred for endocrinological evaluation which showed very high TSH and low free T4 with normal other endocrine & vision assessment. Diagnosis of PH established and thyroxine therapy started with monitoring response to treatment by TSH and repeat the PMRI after 7 months which showed dramatic reduction in PG size and TSH normalized. At presentation TSH was &gt; 100 mIU/L (0.27-4.2), while Free T4 was 0.08 ng/dL (0.93-1.70 ng/dL). Thyroxine 50 mcg had been started and increased gradually according to TSH level every 6 weeks. After 7months, TSH level became 3 mIU/L and new PMRI showed significant reduction in size of PG.

Low thyroid hormones caused thyrotrophic hyperactivity resulting in PGH (6). Although thyrotrophs form 5-10% of anterior PG, trans conversion of somatotrophs to thyrotrophs with multiplication of thyrotrophs increase cells producing TSH (7). Hyperprolactinemia may occur in about 75% of cases and features of hypothyroidism are usual presentations in children and young patients rather than features due to sellar expansion (8). Thyroxine treatment reduces size of the PG in 85% of cases of PGH (9). Surgery may be indicated to decompress the optic chiasma or to confirm diagnosis when size not reduced or worsened with treatment (10). Although it is difficult to differentiate between tumor and PGH, prominent midline with smooth outlines suggests PGH (11). In PGH, there is a uniform hyperplasia causing homogenous enlargement on unenhanced T1,T2 images and post contrast there is an equal enhancement of hyperplastic PG (12). Biochemical, clinical and radiological follow up is indicated to check response and pick up early complications (13).

Conclusion

Prolonged, intense PH one of causes of PGH and should be kept in mind in every case of homogenously enlarged PG necessitating thyroid function and other pituitary hormones assessment before surgery.Figure 1:MRI picture before and after thyroxine therapyDramatic reduction in the size of pituitary gland after 7 month treatment with thyroxine.