Abstract
Systemic Sclerosis (SSc) is a connective tissue disorder featuring vascular alterations and an immunological activation leading to a progressive and widespread fibrosis of several organs such as the skin, lung, gastrointestinal tract, heart, and kidney. Men with SSc are at increased risk of developing erectile dysfunction (ED) because of the evolution of early microvascular tissutal damage into corporeal fibrosis. The entity of penile vascular damage in SSc patients has been demonstrated by using Duplex ultrasonography and functional infra-red imaging and it is now clear that this is a true clinical entity invariably occurring irrespective of age and disease duration and constituting the ‘‘sclerodermic penis”. Once-daily phosphodiesterase type-5 (PDE5) inhibitors improve both sexual function and vascular measures of cavernous arteries by improving surrogate markers of endothelial dysfunction, that is, plasma endothelin-1 and adrenomedullin levels, which may play a potential role in preventing progression of penile fibrosis and ED. Also, the beneficial effect of long-term PDE5i add-on therapy to SSc therapy in the treatment of Raynaud's phenomenon is described.
Highlights
Systemic Sclerosis (SSc) is a connective tissue disorder featured by vascular alterations and immunological activation leading to progressive and widespread fibrosis of several organs such as skin, lung, gastrointestinal tract, heart, and kidney [1, 2]
Irrespective of the classification of the disease, SSc is typically associated with Raynaud’s phenomenon (RP) that is characterized by microvascular damage, high plasma adrenomedullin and ET-1 levels, reduced production of NO [8,9,10,11]
After careful review of clinical and instrumental data already published in our previous papers, we suggest that there is a relationship between erectile dysfunction (ED) and SSc vascular damage evaluated by capillaroscopic pattern and vascular domain of Medsger Disease Severity Scale (DSS) [30]
Summary
Systemic Sclerosis (SSc) is a connective tissue disorder featured by vascular alterations and immunological activation leading to progressive and widespread fibrosis of several organs such as skin, lung, gastrointestinal tract, heart, and kidney [1, 2]. Disease is mediated through microvascular dysfunction secondary to a number of factors including endothelial damage, overexpression of specific adhesion molecules, and perivascular inflammatory cell infiltration [6]. These changes make endothelium unable to carry out its functions in the regulation of vascular tone, coagulation, adhesions and migration of blood cells, transportation of nutrients, achieved through production of a complex array of molecules including vasodilators (e.g., nitric oxide: NO), vasoconstrictors (e.g., endothelin-1: ET1), and cell adhesion molecules (e.g., selectins and integrins) [7]. The prevalence of ED in men with SSc has been reported as high as 80% [18] and it can be considered an end-organ disease involving both macro and microvascular damage
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