title: Hypogonadism in Wegener's granulomatosis.
abstract: OBJECTIVE
  Current developments in the management of Wegener's granulomatosis (WG) focus on adoption of therapeutic strategies to avoid complications of both the disease and its therapy. Systematic analyses with respect to the reproductive system in WG are missing.
  
  
  METHODS
  Data of a cross-sectional study of sexual hormones in 19 male WG patients were analysed. Disease extension was classified according to the ears, nose, and throat (E), lungs (L), and kidneys (K) classification (ELK classification) and to the disease extent index (DEI). Laboratory investigation included measurement of gonadotrophins, oestradiol, and total serum testosterone. Hypogonadism was defined by an increase in follicle-stimulating hormone (FSH) beyond twice the upper reference range in the presence of low serum testosterone. Thirty-eight age-matched men served as controls.
  
  
  RESULTS
  Hypogonadism was found in 52.6% of the patients but was not detectable in any of the controls (p<0.0001). No significant correlation to any clinical factor of systemic vasculitis, current or past medication was detected. In particular, testosterone or FSH levels were not correlated with current or cumulative use of cyclophosphamide or corticosteroids (p = 0.417, p = 0.293; p = 0.893, p = 0.317).
  
  
  CONCLUSIONS
  Data of our study revealed an unexpected high rate of hypogonadism irrespective of cyclophosphamide use, and subclinical involvement of the testes by the vasculitis itself might be an alternative explanation. Screening during the course of the disease is reasonable as hypogonadism might severely affect patients' quality of life. Further prospective studies with respect to gender-specific changes in the reproductive system are warranted.
authors.affiliation: Department of Endocrinology, Diabetes and Rheumatology, Rheumatology Section, University Hospital Düsseldorf, D 40225 Düsseldorf, Germany. richter@rheumanet.org
authors.forename: J G
authors.initials: JG
authors.lastname: Richter
authors.forename: A
authors.initials: A
authors.lastname: Becker
authors.forename: C
authors.initials: C
authors.lastname: Specker
authors.forename: M
authors.initials: M
authors.lastname: Schneider
mesh_terms: D000368:Aged; D018501:Antirheumatic Agents / Q000009:adverse effects / Q000627:therapeutic use; D015519:Bone Density / Q000502:physiology; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D003520:Cyclophosphamide / Q000009:adverse effects / Q000627:therapeutic use; D004958:Estradiol / Q000097:blood; D005640:Follicle Stimulating Hormone / Q000097:blood; D006062:Gonadotropins / Q000097:blood; D014890:Granulomatosis with Polyangiitis / Q000097:blood / Q000150:complications*; D006801:Humans; D007006:Hypogonadism / Q000097:blood / Q000453:epidemiology* / Q000209:etiology*; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D012307:Risk Factors; D013739:Testosterone / Q000097:blood; D014657:Vasculitis / Q000188:drug therapy
chemical_list: D018501:Antirheumatic Agents; D006062:Gonadotropins; D013739:Testosterone; D004958:Estradiol; D003520:Cyclophosphamide; D005640:Follicle Stimulating Hormone