Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: MON 167-198-Hypothalamus-Pituitary Development & Biology
Monday, June 17, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board MON-197
Charalampos Lyssikatos*1 and Martha Quezado2
1National Institutes of Health (NIH), Bethesda, MD, 2NIH- National Cancer Institute, Bethesda, MD
Acromegaly with concurrent ACTH secretion: Cushing syndrome masked by acromegaly

Charalampos Lyssikatos1, Martha Quezado2, Constantine A. Stratatakis1. 1Eunice Shriver Kennedy National Institute of Child Health and Human Development, National Institutes of Health (NIH), Bethesda, MD. 2National Cancer Institute, National Institutes of Health (NIH), Bethesda, MD.

Background: Acromegaly with corticotropin (ACTH) co-secretion is a rare entity; Cushing syndrome manifestations are often masked by the excess growth hormone (GH) production. Nevertheless, a substantial number of GH-producing pituitary tumors are ACTH-stained.

We report a 34-year-old male who was in normal state of health until the age of 29, at which time he noticed a slow increase in the size of his hands and feet, headaches and facial feature coarseness. His body habitus was that of a patient with acromegaly and he lacked any of the classic stigmata of Cushing syndrome (no moon face, webbed neck, nor any striae). GH was 1.91 ng/mL (0.0-0.8); pituitary MRI revealed an 18 x 15 mm pituitary adenoma. Post transphenoidal resection (TSS) of his pituitary adenoma, his IGF-1 remained elevated at 756 ng/mL (107-310) and his repeat pituitary MRI, 2 months later was consistent with a 10 x 12 mm pituitary adenoma, and an IGF-1 of 917 ng/ml (115-307). He underwent a second TSS which finally cured his acromegaly (GH measured 0.47 ng/mL).  His pm and am cortisol measured at 15.3 mcg/dL (5.0-25.0) and 14.9 mcg/dL respectively, prior to his cure from acromegaly but by post op  day 17, midnight and morning cortisols and ACTH were <1.0 mcg/dL (5.0-25.0) and <5.0 pg/ml (0.0-46.0) respectively and the patient was started on replacement glucocorticoids. Histology of the excised pituitary adenoma confirmed a tumor whose cells stained for GH and ACTH.

Conclusion: We conclude that the phenotypic effects of hypercortisolemia may be masked by concurrent GH excess. ACTH co-secretion by a mammo-somatotroph pituitary tumor can be clinically significant but phenotypically unidentifiable.

Nothing to Disclose: CL, MQ

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