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Resume Introduction L’hyperplasie hypophysaire secondaire a une hypothyroidie peripherique reste rare et sous-diagnostiquee. Observation Un homme, âge de 18 ans, etait adresse pour prise en charge d’une masse hypophysaire. Le bilan revelait une hypothyroidie peripherique profonde et une hyperprolactinemie. L’evolution etait rapidement favorable sous l -thyroxine avec normalisation de la TSH ainsi que de la prolactinemie et disparition de la masse hypophysaire. Conclusion L’hyperplasie hypophysaire thyreotrope secondaire a l’hypothyroidie peripherique, bien que rare, doit etre reconnue afin d’eviter au patient un geste chirurgical inutile et a risque.

Objective To describe a patient who developed a thyrotropin (TSH)-Secreting adenoma in the setting of primary hypothyroidism. Methods We report the clinical, laboratory, and radiologic findings of a patient with a history of primary hypothyroidism who presented with headache, a bitemporal visual field deficit, and elevated TSH despite long-term levothyroxine therapy. We discuss the diagnostic challenges of this case and review the relevant literature. Results A 54-yearold woman with a history of primary hypothyroidism presented with a 3-year history of headache and a week of worsening vision. Imaging revealed a heterogeneous sellar mass elevating the optic chiasm. Her serum TSH was 46.5 mIU/L and free thyroxine concentration was 0.1 ng/dL. The differential diagnosis included pituitary hyperplasia and a TSH-secreting adenoma in a patient with primary hypothyroidism. The pathologic characteristics of the tumor were consistent with the latter. Conclusion In a patient with an elevated TSH concentration and a previous diagnosis of hypothyroidism, it is important to consider other entities besides medication noncompliance. TSH-secreting adenomas can also cause elevated levels of TSH. (Endocr Pract. 2011;17: e135-e139)

Reactive enlargement of the pituitary gland in primary end organ failure may be indistinguishable from primary pituitary lesions in clinical presentation and on magnetic resonance imaging. The diagnosis of pituitary hyperplasia secondary to end organ failure must be based on endocrinologic investigations. Recognition of this condition and distinguishing it from primary pituitary tumors is important and may eliminate unnecessary surgery.

Summary The determination of the type of proliferative process in the pituitary causing clinical symptoms is quite difficult using classical morphologic techniques, including immunocytochemistry and electron microscopy. The problem is unusually difficult when the material received from the surgeon consists of 1–2 mm fragments of tissue removed from the sella turcica. Morphologic criteria were extensively discussed by other investigators in this symposium. This manuscript discusses the application of flow cytometry using formalin-fixed, paraffin-embedded tissues, in the diagnosis of pituitary lesions.

In patients with Addison's disease, whether treated or untreated for the previous 24 hours, hydrocortisone produced only a partial suppression of their elevated adrenocorticotrophic-hormone (A.C.T.H.) levels. This is comparable to untreated myxœdema, in which administration of triiodothyronine fails to inhibit secretion of thyrotrophin (T.S.H.). In myxœdema, however, continued treatment produces normal T.S.H. levels. Inadequate A.C.T.H. suppressibility in patients with Addison's disease while on treatment may be due to the maintenance of a secondary pituitary hyperplasia by inadequate replacement therapy. This may be clinically important, especially in the genesis of Nelson's syndrome.