title: Does ACTH improve the diagnostic performance of adrenal vein sampling for subtyping primary aldosteronism?
abstract: OBJECTIVE
  Adrenal vein sampling (AVS) is used for determining treatment options for primary aldosteronism (PA), but is a difficult procedure. Adrenocorticotropic hormone (ACTH) infusion or bolus has been reported to improve AVS success rates by increasing cortisol secretion, but effects on lateralization are controversial. We therefore assessed the effects of ACTH in regard to AVS success and lateralization in our unit, after a change in protocol to ACTH-stimulated AVS.
  
  
  METHODS
  AVS was performed after overnight recumbency in patients with PA confirmed by fludrocortisone suppression testing. Bilateral sequential sampling was performed before and after an intravenous bolus of 250 mcg of ACTH. Lateralization was defined as an aldosterone/cortisol ratio in one adrenal vein at least twice peripheral, combined with a contralateral adrenal ratio no higher than peripheral (contralateral suppression).
  
  
  RESULTS
  In 47 AVS procedures, the median adrenal/peripheral cortisol gradient increased on the left (11·6 vs 18·2 μg/100 ml, P < 0·001) and right (15·6 vs 31·5 μg/100 ml, P < 0·001) after ACTH. A total of 34 of 47 studies were diagnostic pre-ACTH (six failing because of low aldosterone levels bilaterally and seven failing to cannulate one or both sides) vs 44 of 47 (P = 0·011) studies diagnostic post-ACTH (failure to cannulate one or both sides in 3). Concordance between diagnostic studies pre- and post-ACTH was 91%, but two bilateral cases became unilateral after ACTH and one unilateral case before ACTH was bilateral afterwards.
  
  
  CONCLUSIONS
  ACTH improved cortisol gradients and aldosterone secretion, resulting in a reduction in the proportion of nondiagnostic studies. There was a low proportion of discordance between pre- and post-ACTH diagnoses, the significance of which is unclear.
authors.affiliation: Endocrine Hypertension Research Centre, Greenslopes and Princess Alexandra Hospitals, University of Queensland School of Medicine, Brisbane, Qld, Australia.
authors.forename: Martin J
authors.initials: MJ
authors.lastname: Wolley
authors.affiliation: Endocrine Hypertension Research Centre, Greenslopes and Princess Alexandra Hospitals, University of Queensland School of Medicine, Brisbane, Qld, Australia.
authors.forename: Ashraf H
authors.initials: AH
authors.lastname: Ahmed
authors.affiliation: Endocrine Hypertension Research Centre, Greenslopes and Princess Alexandra Hospitals, University of Queensland School of Medicine, Brisbane, Qld, Australia.
authors.forename: Richard D
authors.initials: RD
authors.lastname: Gordon
authors.affiliation: Endocrine Hypertension Research Centre, Greenslopes and Princess Alexandra Hospitals, University of Queensland School of Medicine, Brisbane, Qld, Australia. m.stowasser@uq.edu.au.
authors.forename: Michael
authors.initials: M
authors.lastname: Stowasser
mesh_terms: D000311:Adrenal Glands / Q000098:blood supply*; D000324:Adrenocorticotropic Hormone / Q000008:administration & dosage*; D000450:Aldosterone / Q000097:blood / Q000378:metabolism; D001800:Blood Specimen Collection / Q000379:methods*; D002404:Catheterization; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood / Q000378:metabolism; D006929:Hyperaldosteronism / Q000175:diagnosis*; D008297:Male; D008875:Middle Aged; D014680:Veins
chemical_list: D000450:Aldosterone; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone