A number of oral therapies have been investigated for the treatment of Peyronie’s disease.

Vitamin E

Mechanism of action: Antioxidant properties. First investigated by Scott and Scardino in 1948, vitamin E was theorized to be of clinical efficacy secondary to its anti-oxidant activities. The use of vitamin E today continues and remains a choice for many practicing urologists, predominantly due to the minimal adverse event profile and the low cost. However, most studies do not address the natural history of the disease, nor have they included a control arm. Gelbard et al. investigated vitamin E therapy in comparison to the natural history of Peyronie’s disease in 86 patients, and revealed no significant difference between the treatment and control groups for curvature, pain, and the ability to have intercourse.

Colchicine

Mechanism of action: Inhibition of collagen synthesis and anti-fibrotic effects. Colchicine was first proposed by Akkus and colleagues in 1994 where, in 19 patients, a progressively increasing dose was given over a three to five month period. Alterations in curvature were noted in 36% of the patients (n = 7) and palpable plaque improvement in 63% (n = 12). Erectile quality was improved in 78% (n = 7); however, no placebo or control arm was used in the studies. In a subsequent control study by Kadioglu, 60 patients were evaluated with Colchicine 1 mg twice a day, with mean follow up of 11 months. Pain improvement in 95% (n = 57), with reduction in curvature in 30% (n = 19) and progressive worsening of curvature in 22% (n = 13), were noted. Adverse events: Severe diarrhea.

Potassium amino benzoid (Potaba, Glenwood)

Potaba is historically used in dermatologic patients — particularly scleroderma, dermatomyositis, and pemphigus.

Mechanism of action: Increasing activity of mono-amine oxidase in tissues, a subsequent decrease in serotonin levels, and thus a reduction in fibrogenesis, with subsequent decreased scar tissue formation.

The use of potassium amino benzoid was described initially by Zarafonatis in 1959. Alarge, pooled European study in 1978 involving 2653 patients, reported a 57% success rate with complete resolution in 9%. However, this study had no study arm or placebo group, nor were any objective parameters assessed. Weidner et al. reported a randomized prospective double-blind trial of potassium amino benzoid at a dose of 3 mg four times per day for one year, versus oral placebo. Statistically, an improvement between the two groups was noted in plaque size that did not correlate with a reduction in the curvature. Adverse events: Severe gastrointestinal side effects.

Tamoxifen citrate (Nolvadex, Astrozenica)

Mechanism of action: The potential benefit is based on its effect on the release of transforming growth factor beta (TGF-P) from fibroblasts, and blocking the TGF-P receptor sites, resulting in decreased fibrogenic activity.

This was first introduced by Ralph et al. in 1992, at a dose of 20 mg given twice a day for three months in 36 patients. The results demonstrated a reduction in pain in 80% of patients (n = 29), reduction in curvature in 35% of patients (n = 13), and a decrease in plaque size in 34% (n = 12). However, a control trial by Teloken et al. in 1999 at a similar dose revealed no significant improvement between the treatment groups compared with the placebo arm.

Carnitine (Camitor, Sigma-Tau)

Mechanism of action: Inhibition of acidyl coenzyme-A. Published initially by Biagiotti et al. in 2001, 48 patients were randomized to receive either carnitine or tamoxifen. The first group received tamoxifen 20 mg twice daily for three months, while the second group received acetyl-L-carnitine at a dose of 1 mg twice daily for three months. While the authors reported a greater benefit with respect to curvature in the carnitine arm, no objective parameters were measured.

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