title: Adjunctive GnRH-a treatment attenuates depletion of ovarian reserve associated with cyclophosphamide therapy in premenopausal SLE patients.
abstract: BACKGROUND
  We measured antimullerian hormone (AMH), a marker of ovarian reserve, in women with lupus treated with cyclophosphamide (CYC) (group I), CYC plus gonadotropin-releasing hormone agonist (GnRH-a) (group II) or neither (group III). We hypothesized that AMH would be diminished in women exposed to CYC versus women receiving adjunctive GnRH-a treatment or no CYC exposure.
  
  
  METHODS
  Forty-eight premenopausal lupus patients were retrospectively divided into three treatment groups: CYC alone (group I, n = 11), CYC + GnRH-a (group II, n = 10) and neither (group III, n = 27). Serum AMH levels between groups were compared using a nonparametric test (Wilcoxon rank-sum). Multiple linear regression adjusting for age was performed.
  
  
  RESULTS
  AMH (ng/mL) levels at the last collection were significantly lower in group I versus group III (mean ± SD: 0.18 ± 0.20 group I vs 1.33 ± 1.59 group III; p = 0.015), and versus group II (mean ± SD: 0.86 ± 1.06; p = 0.018). When centered on age 30 years, average AMH levels for group I, group II and group III were 0.20, 0.44 and 1.00, respectively. When adjusted for age, AMH between all groups was significantly different (p<0.0001).
  
  
  CONCLUSIONS
  Posttreatment AMH levels were significantly higher among patients receiving CYC + GnRH-a compared to CYC alone, suggesting that GnRH-a coadministration mitigates CYC-induced ovarian injury.
authors.affiliation: Department of Internal Medicine, Division of Rheumatology, University of Michigan, Ann Arbor, MI 48109-5358, USA. wmarder@umich.edu
authors.forename: W
authors.initials: W
authors.lastname: Marder
authors.forename: W J
authors.initials: WJ
authors.lastname: McCune
authors.forename: L
authors.initials: L
authors.lastname: Wang
authors.forename: J J
authors.initials: JJ
authors.lastname: Wing
authors.forename: S
authors.initials: S
authors.lastname: Fisseha
authors.forename: D S
authors.initials: DS
authors.lastname: McConnell
authors.forename: G M
authors.initials: GM
authors.lastname: Christman
authors.forename: E C
authors.initials: EC
authors.lastname: Somers
mesh_terms: D000328:Adult; D054304:Anti-Mullerian Hormone / Q000097:blood; D015415:Biomarkers / Q000097:blood; D015331:Cohort Studies; D003520:Cyclophosphamide / Q000009:adverse effects* / Q000627:therapeutic use; D003692:Delayed-Action Preparations / Q000627:therapeutic use; D005260:Female; D005300:Fertility Agents, Female / Q000627:therapeutic use; D059247:Fertility Preservation; D005500:Follow-Up Studies; D007987:Gonadotropin-Releasing Hormone / Q000819:agonists*; D006801:Humans; D007166:Immunosuppressive Agents / Q000009:adverse effects* / Q000627:therapeutic use; D007247:Infertility, Female / Q000139:chemically induced / Q000517:prevention & control; D016729:Leuprolide / Q000627:therapeutic use*; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D010053:Ovary / Q000187:drug effects* / Q000503:physiopathology; D017697:Premenopause; D020011:Protective Agents / Q000627:therapeutic use*; D012189:Retrospective Studies
chemical_list: D015415:Biomarkers; D003692:Delayed-Action Preparations; D005300:Fertility Agents, Female; D007166:Immunosuppressive Agents; D020011:Protective Agents; D007987:Gonadotropin-Releasing Hormone; D054304:Anti-Mullerian Hormone; D003520:Cyclophosphamide; D016729:Leuprolide