title: Physiologic reactivity to a laboratory stress task among men with benign prostatic hyperplasia.
abstract: OBJECTIVE
  The sympathetic nervous system and hypothalamic-pituitary-gonadal axis are involved in the pathophysiology of benign prostatic hyperplasia (BPH). The sympathetic nervous system and hypothalamic-pituitary-gonadal axis are also highly reactive to psychological stressors, yet associations between prostate function and reactivity to a psychological stressor have not been examined using standardized psychological stress paradigms. The objective of this study was to examine the associations between psychological stress reactivity and BPH disease parameters.
  
  
  METHODS
  A total of 83 men diagnosed with BPH completed a standardized laboratory stress task, yielding measures of blood pressure, testosterone, and cortisol reactivity. Links were examined between stress reactivity (as indicated by changes in blood pressure, testosterone, and cortisol during the stress task) and measures of BPH disease, including prostate volume, postvoid residual bladder volume, urine flow rate, self-reported lower urinary tract symptoms, and impact and bother scores.
  
  
  RESULTS
  In equations controlling for BPH medications, body mass index, and age, greater diastolic blood pressure reactivity was associated with a greater transition zone volume (P <0.001), greater total prostate gland volume (P <0.05), greater postvoid residual bladder volume (P <0.05), more severe lower urinary tract symptoms (P <0.001), and greater impact scores (P <0.05). Greater cortisol reactivity was associated with greater bother (P <0.05) and impact (P <0.001) scores.
  
  
  CONCLUSIONS
  Physiologic reactivity to a standardized laboratory stressor is associated with objective and subjective BPH disease parameters. These findings contribute to growing data suggesting that stress conditions could be associated with the development or aggravation of prostatic disease.
authors: Department of Rehabilitation Medicine, University of Washington School of Medicine, Seattle, Washington, USA. pullrich@u.washington.edu
authors: Philip M
authors: PM
authors: Ullrich
authors: Susan K
authors: SK
authors: Lutgendorf
authors: Karl J
authors: KJ
authors: Kreder
mesh_terms: D000368:Aged; D001794:Blood Pressure; D017292:Doxazosin / Q000627:therapeutic use; D018120:Finasteride / Q000627:therapeutic use; D006801:Humans; D006854:Hydrocortisone / Q000032:analysis; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009929:Organ Size; D010913:Pituitary-Adrenal System / Q000503:physiopathology; D011467:Prostate / Q000000981:diagnostic imaging / Q000473:pathology; D011470:Prostatic Hyperplasia / Q000150:complications / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology* / Q000523:psychology; D016032:Randomized Controlled Trials as Topic / Q000706:statistics & numerical data; D012463:Saliva / Q000737:chemistry; D013315:Stress, Psychological / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D013739:Testosterone / Q000032:analysis; D014463:Ultrasonography; D001743:Urinary Bladder / Q000473:pathology; D014555:Urination Disorders / Q000209:etiology / Q000523:psychology
chemical_list: D013739:Testosterone; D018120:Finasteride; D017292:Doxazosin; D006854:Hydrocortisone