title: Type V phosphodiesterase inhibitor treatments for erectile dysfunction increase testosterone levels.
abstract: OBJECTIVE
  Lack of sexual activity due to erectile dysfunction (ED) decreases testosterone (T) levels through a central effect on the hypothalamic-pituitary axis. In this paper we studied the effect of different type V phosphodiesterase (PDE5) inhibitor treatments for ED on the reversibility of this endocrine pattern.
  
  
  METHODS
  Open-label, retrospective study.
  
  
  METHODS
  Seventy-four consecutive patients were treated on demand with sildenafil (Sild) (50 mg) and tadalafil (Tad) 20 mg.
  
  
  METHODS
  The success in sexual intercourse was recorded and total (tT) and free testosterone (fT) levels were studied before and after 3 months of treatment.
  
  
  RESULTS
  Basal level of tT and fT were at the bottom of the normal range and LH levels were at the top of the high normal range. After treatments, this endocrine pattern was reversed in both groups. However, the T increase in Sild-treated patients was significantly lower than in those treated with Tad (4.7 +/- 2.7 vs. 5.1 +/- 0.9, P < 0.001). fT levels followed a directly proportional pattern, while the inverse was found when LH production was studied. The intercourse rate reflected this effect: in fact, the Sild group showed a 4.9 +/- 2.9/month full sexual intercourse rate while in the Tad group a significantly higher rate of sexual intercourse was found (6.9 +/- 4.6/month, P = 0.04). However, drug consumption was comparable between the groups (Sild 4.9 +/- 2.9 vs. Tad 4.4 +/- 2.8 pills/month, P = 0.72).
  
  
  CONCLUSIONS
  As it is unlikely that the two drugs have a different direct effect on the pituitary-testis axis, this effect is probably due to the higher frequency of full sexual intercourse in the Tad-treated group, because of the drug's longer half-life.
authors.affiliation: Department of Experimental Medicine, University of L'Aquila, L'Aquila, Italy.
authors.forename: Eleonora
authors.initials: E
authors.lastname: Carosa
authors.forename: Paolo
authors.initials: P
authors.lastname: Martini
authors.forename: Fulvia
authors.initials: F
authors.lastname: Brandetti
authors.forename: Savino M
authors.initials: SM
authors.lastname: Di Stasi
authors.forename: Francesco
authors.initials: F
authors.lastname: Lombardo
authors.forename: Andrea
authors.initials: A
authors.lastname: Lenzi
authors.forename: Emmanuele A
authors.initials: EA
authors.lastname: Jannini
mesh_terms: D015106:3',5'-Cyclic-GMP Phosphodiesterases; D000328:Adult; D000368:Aged; D002243:Carbolines / Q000627:therapeutic use*; D054706:Cyclic Nucleotide Phosphodiesterases, Type 5; D007172:Erectile Dysfunction / Q000097:blood* / Q000188:drug therapy*; D006801:Humans; D007986:Luteinizing Hormone / Q000097:blood; D008297:Male; D008875:Middle Aged; D010726:Phosphodiesterase Inhibitors / Q000627:therapeutic use*; D010727:Phosphoric Diester Hydrolases; D010879:Piperazines / Q000627:therapeutic use*; D011687:Purines; D012189:Retrospective Studies; D000068677:Sildenafil Citrate; D013450:Sulfones; D000068581:Tadalafil; D013739:Testosterone / Q000097:blood*
chemical_list: D002243:Carbolines; D010726:Phosphodiesterase Inhibitors; D010879:Piperazines; D011687:Purines; D013450:Sulfones; D013739:Testosterone; D000068581:Tadalafil; D007986:Luteinizing Hormone; D000068677:Sildenafil Citrate; D010727:Phosphoric Diester Hydrolases; D015106:3',5'-Cyclic-GMP Phosphodiesterases; D054706:Cyclic Nucleotide Phosphodiesterases, Type 5; C517381:PDE5A protein, human