Mammosomatotroph Pituitary Adenomas: Incidence, Clinical Features, and Treatment Outcomes

Jonathan W. Rick; Arman Jahangiri; Patrick M. Flanigan; Ankush Chandra; Sandeep Kunwar; Lewis Blevins; Manish K. Aghi

doi:10.1055/s-0038-1633577

Journal of Neurological Surgery Part B: Skull Base, Table of Contents

CC BY 4.0 · J Neurol Surg B Skull Base 2018; 79(S 01): S1-S188
DOI: 10.1055/s-0038-1633577

Oral Presentations

Mammosomatotroph Pituitary Adenomas: Incidence, Clinical Features, and Treatment Outcomes

Authors

Jonathan W. Rick

¹University of California, San Francisco, San Francisco, California, United States
Arman Jahangiri

¹University of California, San Francisco, San Francisco, California, United States
Patrick M. Flanigan

¹University of California, San Francisco, San Francisco, California, United States
Ankush Chandra

¹University of California, San Francisco, San Francisco, California, United States
Sandeep Kunwar

¹University of California, San Francisco, San Francisco, California, United States
Lewis Blevins

¹University of California, San Francisco, San Francisco, California, United States
Manish K. Aghi

¹University of California, San Francisco, San Francisco, California, United States

Abstract

Full Text

Objective Routine immunostainings of pituitary adenomas (PAs) have revealed that many are plurihormonal. Mammosomatotroph adenomas (MSAs), tumors staining for prolactin and growth hormone (GH), is the most frequent hormone combination. These tumors are derived from a common progenitor to both mammotrophs and somatotrophs and consequently can have numerous effects on the endocrine axes. However, these tumors are rare and their presentations, clinical features, and treatment outcomes are not well understood.

Methods The authors performed a retrospective review over 5 years of PAs resected at our institution. Data were collected on variables related to clinical presentation, tumor pathology, radiographic size, and disease recurrence. Tumors were separated into clinical cohorts and pathological classes. Cohorts were compared with respective non-MSA controls. Fisher's exact test, ANOVA, student t-test, and the chi-square test were used to measure statistical significance and Bonferroni corrections were applied as needed.

Results Of 593 PAs, 35 (5.6%) were MSAs staining for GH and prolactin. MSA patients were younger (49.2/39.9 years, p = 0.001) with comparable gender (49.2%/52.1% female; p = 0.9) as non-MSA patients. MSAs were comparably sized to non-MSAs (1.94/1.90 cm, p = 0.5). MSAs were divided into four cohorts: (1) 20% had no hormone symptoms; (2) 17% had symptoms of hyperprolactinemia only; (3) 46% had symptoms of acromegaly only; and (4) 17% had symptoms of both. Cohort 2 MSA patients were more likely to experience reduced libido (83.3%/7.6%; p = 0.0001) than prolactinomas. Cohort 3 MSA patients were more likely to experience hyperhidrosis (68.8%/32.6%; p = 0.012) than acromegalics. Two cohort 2 patients were treated with dopamine agonists for presumed prolactinomas and had biochemical remission without volumetric reduction. Recurrence rates were comparable in MSAs versus non-MSAs (14%/10%; p = 0.4), and when cohorts were compared with respective controls (p = 0.1−0.3).

Conclusion While silent MSAs presented like hormonally negative adenomas, cohort 2/3 patients presented with more severe symptoms than prolactinoma/acromegaly patients. MSA must be considered when evaluating acromegaly or prolactinoma patients, underscoring the importance of hormone analysis and tumor immunostaining. Even when the second axis is not elevated, MSA should be suspected in patients who fail medical management.