title: Prostate cancer in elderly Croatian men: 5-HT genetic polymorphisms and the influence of androgen deprivation therapy on osteopenia--a pilot study.
abstract: BACKGROUND
  The aim of this study was to determine the relationship between body mass index, biochemical parameters, and 5-hydroxytryptamine (5-HT) genetic polymorphisms and prostate dysfunction in an elderly general male population.
  
  
  RESULTS
  One hundred and seventeen elderly male subjects [60 men without symptoms of prostate hyperplasia, 42 men with untreated benign prostatic hyperplasia (BPH), and 15 men with prostate cancer (PCa)] treated with finasteride or flutamide were included. Multiple comparisons showed significant difference in age, T-score, concentration of phosphorus, calcium, C-reactive protein, and prostate-specific antigen (PSA) between the groups. T-score was the lowest and phosphorus concentration was the highest in the PCa group. Highest PSA, proteins, calcium, and Hekal's formula score were found in the BPH group. Patients with PCa were more frequent GG+GA carriers of 5-HT1B 1997A/G gene polymorphism (p=0.035). Univariate regression analysis showed association of PCa-treated subjects with age (p=0.010) and 5-HT1B genetic polymorphism (p=0.018). Antiandrogen therapy affects T-score (p=0.017), serum phosphorus (p=0.008), glucose (p=0.036), and total proteins (p=0.050). Multivariate-stepwise logistic regression analysis showed the significant association of treated PCa with age (p=0.028) and inorganic phosphorus (p=0.005), and a marginal association with ultrasonographic T-score (p=0.052).
  
  
  CONCLUSIONS
  Antiandrogen therapy might induce bone mineral loss in elderly PCa patients. Preliminary data imply that the genetic variants of the 5-HT1B receptor might be associated with PCa.
authors.affiliation: Department of Chemistry, Biochemistry, and Clinical Chemistry, School of Medicine, University of Zagreb, Zagreb, Croatia. daria.pasalic@mef.hr
authors.forename: Daria
authors.initials: D
authors.lastname: Pašalić
authors.forename: Paulina
authors.initials: P
authors.lastname: Pauković
authors.forename: Selma
authors.initials: S
authors.lastname: Cvijetić
authors.forename: Alica
authors.initials: A
authors.lastname: Pizent
authors.forename: Jasna
authors.initials: J
authors.lastname: Jurasović
authors.forename: Sanja
authors.initials: S
authors.lastname: Milković-Kraus
authors.forename: Slavica
authors.initials: S
authors.lastname: Dodig
authors.forename: Dorotea
authors.initials: D
authors.lastname: Mück-Šeler
authors.forename: Maja
authors.initials: M
authors.lastname: Mustapić
authors.forename: Nela
authors.initials: N
authors.lastname: Pivac
authors.lastname: Lana-Feher-Turković
authors.forename: Mladen
authors.initials: M
authors.lastname: Pavlović
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000726:Androgen Antagonists / Q000009:adverse effects* / Q000627:therapeutic use; D015519:Bone Density; D001851:Bone Diseases, Metabolic / Q000139:chemically induced* / Q000453:epidemiology / Q000235:genetics; D018120:Finasteride / Q000009:adverse effects / Q000627:therapeutic use; D005485:Flutamide / Q000009:adverse effects / Q000627:therapeutic use; D005787:Gene Frequency; D005838:Genotype; D006801:Humans; D008297:Male; D010865:Pilot Projects; D011110:Polymorphism, Genetic; D011470:Prostatic Hyperplasia / Q000453:epidemiology / Q000235:genetics / Q000473:pathology; D011471:Prostatic Neoplasms / Q000453:epidemiology / Q000235:genetics* / Q000473:pathology; D044302:Receptor, Serotonin, 5-HT1B / Q000235:genetics*; D012701:Serotonin / Q000235:genetics
chemical_list: D000726:Androgen Antagonists; D044302:Receptor, Serotonin, 5-HT1B; D012701:Serotonin; D018120:Finasteride; D005485:Flutamide