ML. Gheorghiu*a (Dr), SM. Lider Burciulescub (Dr), S. Vladoiuc (Mrs), AM. Prunariud (Dr), R. Aldeae (Dr)

a Carol Davila University of Medicine and Pharmacy, C.I. Parhon National Institute of Endocrinology, Bucharest, ROMANIA ; b Carol Davila University of Medicine and Pharmacy, Bucharest, ROMANIA ; c C.I. Parhon National Institute of Endocrinology, Bucharest, ROMANIA ; d Carol Davila University of Medicine and Pharmacy, C.I. Parhon National Institute of Endocrinology, Bucharest, Bucharest, ROMANIA ; e Campulung County Hospital, Campulung, ROMANIA


Introduction: The differential diagnosis for sellar and suprasellar lesions is broad and includes neoplastic masses such as pituitary adenoma, metastases, Rathke’s cleft cyst, craniopharyngioma, and meningioma but also vascular or inflammatory lesions (sarcoidosis, autoimmune hypophysitis). We present a patient with a vanishing pituitary mass of unknown etiology and intemittent central adrenal insufficiency.

Observations: Patient aged 47 y.o. presented sudden secondary amenorrhea and galactorrhea discovered incidentally during mamography. The local endocrinologist diagnosed central hypothyroidism (low FT4, TSH 5.6 mIU/L), autoimmune thyroiditis and mild hyperprolactinemia (PRL 2.5xULN) and initiated thyoxine replacement. Several months later MRI revealed a 1.1cm pituitary mass with low contrast uptake, in contact with the internal carotid artery and optic chiasm, left deviation of pituitary stalk. PRL was still elevated, cabergoline (CAB) 0.5 mg /week was initiated.

Two months later she was diagnosed in our clinic with central hypothyroidism and hypogonadism, normal corticotroph axis and partial GH insufficiency. PRL was normal on 0.25 mg CAB/week. Based on blood tests we excluded sarcoidosis and germinoma, pituitary antibodies were negative. She started estro-progestin replacement.

After 7 months of low dose CAB, MRI showed a minimally increased and inhomogeneous pituitary gland with no visible mass. The patient was discovered with asymptomatic central adrenal insufficiency: serum cortisol 3.53 µg/dL (N=4-19), ACTH 9 pg/mL (N=3-66), low UFC. No source of exogenous glucocorticoids (GC) was identified. She received GC replacement; 3 months later cortisol levels were normally stimulated by synthetic ACTH (19 µg/dL). GC therapy was withdrawn.

Five months later she once again had asymptomatic low cortisol levels: 0.99 ug/dl, ACTH 9.95 pg/mL, with no exogenous GC administration.

Discussion: Through the unexpected morphological and biochemical evolution, our case raises several questions. The vanishing pituitary mass may be interpreted as a lymphocytic hypophysitis in a patient with autoimmune thyroiditis, but also as a non-functioning pituitary adenoma (NFPA) shrank by the CAB treatment, or an asymptomatic apoplexy in a NFPA; however, the intermittent asymptomatic adrenal insufficiency suggests a local active process such as inflammation, although an exogenous GC intake cannot be definitely ruled out. A frequent follow-up is mandatory.

The author has declared no conflict of interest.