1.Intralesional and topical treatments for Peyronie's disease: a narrative review of current knowledge.
Antonio MINORE ; Loris CACCIATORE ; Fabrizio PRESICCE ; Andrea IANNUZZI ; Antonio TESTA ; Gianluigi RASO ; Rocco PAPALIA ; Marco MARTINI ; Roberto Mario SCARPA ; Francesco ESPERTO
Asian Journal of Andrology 2025;27(2):156-165
Peyronie's disease (PD) presents a multifaceted challenge in contemporary urological practice, marked by penile deformity, pain, and the potential for erectile dysfunction. We meticulously explored the existing literature of intralesional/topical interventions, aiming to provide clinicians with a nuanced understanding of available options for comprehensive PD management. To conduct this review, we performed a systematic search using the PubMed, Scopus, and ScienceDirect databases, including the keywords of combination of the "Peyronie's disease/plastic induration of the penis (PIP) and intralesional/topical treatments". The study selection was based on adherence to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, resulting in the inclusion of 16 articles. We delve into the effectiveness and safety profiles of collagenase Clostridium histolyticum (CCH), interferon, platelet-rich plasma (PRP), hyaluronic acid, botulinum toxin, stem cell, extracorporeal shock wave therapy (ESWT), and traction therapy, assessing their impact on penile curvature, length improvement, and patient-reported symptoms and outcomes. The best options evaluated are intralesional injections of CCH and penile traction devices, alone or in combination. Despite PD remains a challenge for urologists, the objective of this review is to contribute to the evolving landscape of PD management, fostering informed decision-making, and personalized care for individuals grappling with this challenging condition.
Humans
;
Male
;
Administration, Topical
;
Botulinum Toxins/administration & dosage*
;
Extracorporeal Shockwave Therapy
;
Hyaluronic Acid/administration & dosage*
;
Injections, Intralesional
;
Interferons/administration & dosage*
;
Microbial Collagenase/administration & dosage*
;
Penile Induration/therapy*
;
Platelet-Rich Plasma
;
Stem Cell Transplantation
;
Traction
2.Regulation of magnesium release by cAMP during chemical hypoxia in the rat heart and isolated ventricular myocytes.
Jin Shang KIM ; Antonio SCARPA
The Korean Journal of Physiology and Pharmacology 1999;3(1):59-68
Chemically induced hypoxia has been shown to induce a depletion of ATP. Since intracellular free Mg2+ ((Mg2+)i) appears to be tightly regulated following cellular energy depletion, we hypothesized that the increase in (Mg2+)i would result in Mg2+ extrusion following hormonal stimulation. To determine the relation between Mg2+ efflux and cellular energy state in a hypoxic rat heart and isolated myocytes, (Mg2+)i, ATP and Mg2+ content were measured by using mag-fura-2, luciferin-luciferase and atomic absorbance spectrophotometry. Mg2+ effluxes were stimulated by norepinephrine (NE) or cAMP analogues, respectively. Mg2+ effluxes induced by NE or cAMP were more stimulated in the presence of metabolic inhibitors (MI). Chemical hypoxia with NaCN (2 mM) caused a rapid decrease of cellular ATP within 1 min. Measurement of (Mg2+)i confirmed that ATP depletion was accompanied by an increase in (Mg2+)i. No change in Mg2+ efflux was observed when cells were incubated with MI. In the presence of MI, the cAMP-induced Mg2+ effluxes were inhibited by quinidine, imipramine, and removal of extracellular Na+. In addition, after several min of perfusion with Na+-free buffer, a large increase in Mg2+ efflux occurred when Na+-free buffer was switched to 120 mM Na+ containing buffer. A similar Mg2+ efflux was observed in myocytes. These effluxes were inhibited by quinidine and imipramine. These results indicate that the activation of Mg2+ effluxes by hormonal stimulation is directly dependent on intracellular Mg2+ contents and that these Mg2+ effluxes appear to occur through the Na+-dependent Na+/Mg2+ exchange system during chemical hypoxia.
Adenosine Triphosphate
;
Animals
;
Anoxia*
;
Heart*
;
Imipramine
;
Magnesium*
;
Muscle Cells*
;
Norepinephrine
;
Perfusion
;
Quinidine
;
Rats*
;
Spectrophotometry

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