Erectile dysfunction

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Abstract

Erectile dysfunction (ED) in SSc was first described in 1981 [1]. These authors described 5 male SSc patients who presented with impotence as a significant initial feature of their disease. Endocrine, urological, and psychiatric evaluations failed to reveal an alternative cause for impotence. None of the patients was taking medications known to alter sexual function. All of these patients had preservation of libido throughout their illness, but absent or greatly diminished erectile function. None had evidence for large vessel vascular disease. Subsequently, Nowlin and colleagues [2] performed a study of ten SSc patients who were evaluated for sexual function. Five of these reported complete impotence and three-partial potence. Endocrinological evaluation, including measurements of serum testosterone, prolactin, estradiol, folliclestimulating hormone, and luteinizing hormones, was normal in all patients. Since these early reports, several other descriptions of ED in male patients with SSc have been reported [3-8]. In most of these reports, comprehensive evaluations for other causes of impotence were unrevealing, and ED was felt to be attributed directly to SSc. The prevalence of ED in SSc has varied from 27% to 81% [2, 4, 9].

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Lally, E. V., Burnett, A. L., & Bivalacqua, T. J. (2012). Erectile dysfunction. In Scleroderma: From Pathogenesis to Comprehensive Management (pp. 395–398). Springer US. https://doi.org/10.1007/978-1-4419-5774-0_31

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