title: Medical therapy in patients with acromegaly: predictors of response and comparison of efficacy of dopamine agonists and somatostatin analogues.
abstract: BACKGROUND
  Acromegaly is associated with increased morbidity and mortality. Treatment options include surgery, radiotherapy, and medical therapy.
  
  
  OBJECTIVE
  The objective of the study was to examine the role of prolactin status, prior surgery, and radiotherapy on the response to medical therapy in patients with acromegaly and assess the relative efficacy of dopamine agonist therapy compared with somatostatin analog therapy.
  
  
  METHODS
  A total of 276 patients with acromegaly received either dopamine agonists (DA) and/or somatostatin analogs (SSA). One hundred seventy-two patients had received surgery and 73 radiotherapy prior to receiving medical therapy. One hundred ninety-eight of 276 received DA, and 143 of 276 received SSA. GH and IGF-I values at baseline and after 12 months on therapy were analyzed.
  
  
  RESULTS
  In the DA group, basal prolactin concentration did not predict response to therapy, GH percent reduction: hyperprolactinemia, 26.7% (-10.4 to 48) vs. normoprolactinemia, 34.8% (0.2-53.2), P = 0.58; IGF-I percent reduction: hyperprolactinemia 30.0% (9.2-43.1) vs. normoprolactinemia 16.8% (4-37), P = 0.45. Prior surgery was not associated with any difference in response to DA: GH percent reduction (P = 0.1) and IGF-I percent reduction (P = 0.08). By contrast, prior radiotherapy was associated with an enhanced efficacy of GH response to DA, P = 0.02. In the SSA group, there was no effect of prior surgery or radiotherapy on response of GH, but radiotherapy was associated with less marked IGF-I percent reduction (P = 0.05). SSA were more potent than DA at decreasing both GH [62.8% (20.7-85%) vs. 42.4% (-6.5 to 68.6), P < 0.008] and IGF-I [SSA 40.4% (0-64.3) vs. 8% (0-40.8), P = 0.05].
  
  
  CONCLUSIONS
  The effects of DA are irrespective of baseline prolactin concentrations. Prior radiotherapy is associated with differences in GH and IGF-I response to DA and SSA therapy.
authors.affiliation: Division of MedicalSciences, Centre for Endocrinology, Diabetes, and Metabolism, University of Birmingham, Birmingham, United Kingdom.
authors.forename: M
authors.initials: M
authors.lastname: Sherlock
authors.forename: E
authors.initials: E
authors.lastname: Fernandez-Rodriguez
authors.forename: A Aragon
authors.initials: AA
authors.lastname: Alonso
authors.forename: R C
authors.initials: RC
authors.lastname: Reulen
authors.forename: J
authors.initials: J
authors.lastname: Ayuk
authors.forename: R N
authors.initials: RN
authors.lastname: Clayton
authors.forename: G
authors.initials: G
authors.lastname: Holder
authors.forename: M C
authors.initials: MC
authors.lastname: Sheppard
authors.forename: A
authors.initials: A
authors.lastname: Bates
authors.forename: P M
authors.initials: PM
authors.lastname: Stewart
mesh_terms: D000172:Acromegaly / Q000097:blood* / Q000188:drug therapy* / Q000532:radiotherapy / Q000601:surgery; D018491:Dopamine Agonists / Q000627:therapeutic use*; D005640:Follicle Stimulating Hormone / Q000172:deficiency; D019382:Human Growth Hormone / Q000097:blood; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D007986:Luteinizing Hormone / Q000172:deficiency; D011388:Prolactin / Q000097:blood; D013004:Somatostatin / Q000031:analogs & derivatives* / Q000627:therapeutic use*
chemical_list: D018491:Dopamine Agonists; D019382:Human Growth Hormone; D013004:Somatostatin; D007334:Insulin-Like Growth Factor I; D011388:Prolactin; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone