title: Decline of the red blood cell count in patients receiving androgen deprivation therapy for localized prostate cancer: impact of ADT on insulin-like growth factor-1 and erythropoiesis.
abstract: OBJECTIVE
  To elucidate the mechanism of blood hemoglobin loss in patients with prostate cancer during androgen deprivation therapy (ADT), and to examine the activity of the growth hormone (GH)/insulin-like growth factor-1 (IGF-1) axis during ADT, which plays an important role in hematopoiesis.
  
  
  METHODS
  A total of 83 patients with localized prostate cancer, who received ADT, were prospectively studied on the basis of their blood samples at the baseline and after ADT for 6 months.
  
  
  RESULTS
  Before ADT, the IGF-1 level was correlated with the red blood cell (RBC) count (Spearman's rank correlation coefficient analysis [rs]=0.315, P=.011), hemoglobin (rs=0.278, P=.018), and mean corpuscular volume (rs=0.266, P=.020), but such relationships disappeared after ADT. After ADT, the serum IGF-1 level increased compared with that at the baseline (21+/-6 vs 18+/-5 nmol/L, respectively, P<.001), but no change was observed in the serum GH level (P=.691). There was no difference between erythropoietin and interleukin-6 concentrations before and after ADT (P=.852 and P=.208, respectively). The hemoglobin concentration and RBC count declined after ADT compared with those before treatment (P<.001 for each). Although the mean corpuscular volume declined after ADT (P=.002), the mean cell hemoglobin was comparable between before and after ADT (P=.676).
  
  
  CONCLUSIONS
  Despite the unaffected GH, erythropoietin, and interleukin-6 levels, the serum IGF-1 concentration was elevated by ADT. Even with the increased IGF-1 level, the RBC count and hemoglobin concentration declined after ADT. IGF-1 in the bone marrow erythroid progenitor cells might be functionally inactivated during ADT.
authors.affiliation: Division of Urology, Department of Regenerative and Transplant Medicine, Graduate School of Medical and Dental Sciences, Niigata University, and Department of Urology, Niigata Cancer Center Hospital, Niigata, Japan. harasho@med.niigata-u.ac.jp
authors.forename: Noboru
authors.initials: N
authors.lastname: Hara
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Nishiyama
authors.forename: Itsuhiro
authors.initials: I
authors.lastname: Takizawa
authors.forename: Toshihiro
authors.initials: T
authors.lastname: Saito
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Kitamura
authors.forename: Kota
authors.initials: K
authors.lastname: Takahashi
mesh_terms: D000368:Aged; D000726:Androgen Antagonists / Q000009:adverse effects* / Q000627:therapeutic use; D018931:Antineoplastic Agents, Hormonal / Q000009:adverse effects / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D001707:Biopsy, Needle; D015331:Cohort Studies; D004906:Erythrocyte Count; D004920:Erythropoiesis / Q000187:drug effects; D005500:Follow-Up Studies; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009367:Neoplasm Staging; D011336:Probability; D011446:Prospective Studies; D017430:Prostate-Specific Antigen / Q000097:blood*; D011471:Prostatic Neoplasms / Q000097:blood* / Q000188:drug therapy* / Q000473:pathology; D018570:Risk Assessment; D013002:Somatomedins / Q000032:analysis*; D018709:Statistics, Nonparametric; D016896:Treatment Outcome
chemical_list: D000726:Androgen Antagonists; D018931:Antineoplastic Agents, Hormonal; D015415:Biomarkers; D013002:Somatomedins; D017430:Prostate-Specific Antigen