I sometimes use a topical PDE-5 inhibitor called Andro cream which contains Butea superba extract. I don't see how a PDE-5 inhibitor would be effective for Peyronie's but it's an interesting idea and I like to see some theory or studies.
I was under the impression that there were human studies, but I cannot find any. Here is a rodent model:
Titre du document / Document title
L-Arginine and phosphodiesterase (PDE) inhibitors counteract fibrosis in the Peyronie's fibrotic plaque and related fibroblast cultures
Auteur(s) / Author(s)
VALENTE Eliane G. A. ; VERNET Dolores ; FERRINI Monica G. ; ANSHA QIAN ; RAJFER Jacob ; GONZALEZ-CADAVID Nestor F. ;
Résumé / Abstract
Inducible nitric oxide synthase (iNOS) is expressed in both the fibrotic plaque of Peyronie's disease (PD) in the human, and in the PD-like plaque elicited by injection of TGFβ1 into the penile tunica albuginea (TA) of the rat. Long-term inhibition of iNOS activity, presumably by blocking nitric oxide (NO)- and cGMP-mediated effects triggered by iNOS expression, exacerbates tissue fibrosis through an increase in: (a) collagen synthesis, (b) levels of reactive oxygen species (ROS), and © the differentiation of fibroblasts into myofibroblasts. We have now investigated whether: (a) phosphodiesterase (PDE) isoforms, that regulate the interplay of cGMP and cAMP pathways, are expressed in both the human and rat TA; and (b) L-arginine, that stimulates NOS activity and hence NO synthesis, and PDE inhibitors, that increase the levels of cGMP and/or cAMP, can inhibit collagen synthesis and induce fibroblast/myofibroblast apoptosis, thus acting as antifibrotic agents. We have found by immunohistochemistry, RT/ PCR, and Western blot that PDE5A-3 and PDE4A, B, and D variants are indeed expressed in human and rat normal TA and PD plaque tissue, as well as in their respective fibroblast cultures. As expected, in the PD fibroblast cultures, pentoxifylline (non-specific cAMP-PDE inhibitor) increased cAMP levels without affecting cGMP levels, whereas sildenafil (PDE5A inhibitor) raised cGMP levels. Both agents and L-arginine reduced the expression of collagen I (but not collagen III) and the myofibroblast marker, α-smooth muscle actin, as determined by immunocytochemistry and quantitative image analysis. These effects were mimicked by incubation with 8-Br-cGMP, which in addition increased apoptosis, as measured by TUNEL. When L-arginine (2.25g/kg/day), pentoxifylline (10mg/kg/day), or sildenafil (10mg/kg/day) was given individually in the drinking water for 45 days to rats with a PD-like plaque induced by TGF β1, each treatment resulted in a 80-95% reduction in both plaque size and in the collagen/fibroblast ratio, as determined by Masson trichrome staining. Both sildenafil and pentoxiphylline stimulated fibroblast apoptosis within the TA. Our results support the hypothesis that the increase in NO and/or cGMP/cAMP levels by long-term administration of nitrergic agents or inhibitors of PDE, may be effective in reversing the fibrosis of PD, and more speculatively, other fibrotic conditions.
Revue / Journal Title
Nitric oxide ISSN 1089-8603 CODEN NIOXF5
Source / Source
2003, vol. 9, no4, pp. 229-244 [16 page(s) (article)]
Langue / Language
Anglais
Editeur / Publisher
Elsevier, San Diego, CA, ETATS-UNIS (1997) (Revue)
Localisation / Location
INIST-CNRS, Cote INIST : 2015 B, 35400011669950.0060
Also this:
Long-term treatment with Varndenafil reduces the development of the fibrotic plaque in a rat model of Peyronie's disease
Authors: Monica Ferrini, PhD, Istvan Kovanecz, PhD, Gaby Nolazco, MSc, Jacob Rajfer, MD and Nestor Gonzalez-Cadavid, PhD; University of California at Los Angeles, Los Angeles, CA.
Ferrini from UCLA, presented further modifications to the work that she has done centered around the use of PDE-5 inhibitors [sildenafil (Viagra), vardenafil (Levitra), and tadalafil (Cialis)] and the reduction of Peyronie's plaque development. This group administered vardenafil (Levitra) to rats with a PD-like plaque. They found that long-term administration of vardenafil slowed down and reversed the early stages of PD-like plaque development. This preliminary data are intriguing and will require confirmation with a large human study to answer this question.
This could be interesting if someone has access to the whole paper:
Int J Impot Res. 2005 Nov-Dec;17(6):546. <span class="linkbar">Corbin J. Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee 37232-0615, USA. jackie.corbin@vanderbilt.edu
Can PDE5 inhibitors inhibit fibrosis? Is this a direct effect of PDE5 inhibitors on the fibrotic cascade? If this hypothesis is found true, then an entire new algorithm for treatment of ED and other diseases may be realized. Three recent manuscripts this year discuss this question. Dr Jackie Corbin, a renowned PDE5 expert, offers a perspective in light of its potential clinical relevance.
Edited by seekonk, 16 June 2009 - 02:00 PM.
