title: Clinically silent somatotroph adenomas are common.
abstract: OBJECTIVE
  Somatotroph adenomas are typically recognized when they secrete GH excessively and cause acromegaly. Both 'silent' somatotroph adenomas (immunohistochemical evidence of GH excess without biochemical or clinical evidence) and 'clinically silent' somatotroph adenomas (immunohistochemical and biochemical evidence but no clinical evidence) have occasionally been reported. The relative frequency of each presentation is unknown. The goal of this study was, therefore, to determine the frequency of clinically silent somatotroph adenomas, a group that is potentially recognizable in vivo.
  
  
  METHODS
  We retrospectively identified 100 consecutive patients who had surgically excised and histologically confirmed pituitary adenomas.
  
  
  METHODS
  Each pituitary adenoma was classified immunohistochemically by pituitary cell type. Somatotroph adenomas were further classified as 'classic' (obvious clinical features of acromegaly and elevated serum IGF1), 'subtle' (subtle clinical features of acromegaly and elevated IGF1), 'clinically silent' (no clinical features of acromegaly but elevated IGF1), and 'silent' (no clinical features of acromegaly and normal IGF1).
  
  
  RESULTS
  Of the 100 consecutive pituitary adenomas, 29% were gonadotroph/glycoprotein, 24% somatotroph, 18% null cell, 15% corticotroph, 6% lactotroph, 2% thyrotroph, and 6% not classifiable. Of the 24 patients with somatotroph adenomas, classic accounted for 45.8%, subtle 16.7%, clinically silent 33.3%, and silent 4.2%.
  
  
  CONCLUSIONS
  Clinically silent somatotroph adenomas are more common than previously appreciated, representing one-third of all somatotroph adenomas. IGF1 should be measured in all patients with a sellar mass, because identification of a mass as a somatotroph adenoma expands the therapeutic options and provides a tumor marker to monitor treatment.
authors.affiliation: Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Pennsylvania School of Medicine, 3400 Civic Center Boulevard, 12-135 Translational Research Center, Philadelphia, Pennsylvania 19104, USA.
authors.forename: Alisha N
authors.initials: AN
authors.lastname: Wade
authors.forename: Jennifer
authors.initials: J
authors.lastname: Baccon
authors.forename: M Sean
authors.initials: MS
authors.lastname: Grady
authors.forename: Kevin D
authors.initials: KD
authors.lastname: Judy
authors.forename: Donald M
authors.initials: DM
authors.lastname: O'Rourke
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Snyder
mesh_terms: D000172:Acromegaly / Q000209:etiology; D000236:Adenoma / Q000473:pathology*; D000328:Adult; D000368:Aged; D005260:Female; D049912:Growth Hormone-Secreting Pituitary Adenoma / Q000150:complications / Q000473:pathology*; D006801:Humans; D007150:Immunohistochemistry; D007334:Insulin-Like Growth Factor I / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D052683:Somatotrophs / Q000473:pathology
chemical_list: D007334:Insulin-Like Growth Factor I