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Commentary

Commentary

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The authors provide an evaluation of mean platelet volume (MPV) and vitamin D (VD) values in the moderate and severe erectile dysfunction (ED) patients in data accompanied by well executed graphic representations [Citation1]. Although the number of study patients is one of the important limitations, the findings of Culha et al. demonstrated significant positive correlation between ED severity and VD levels and negative correlation between ED severity and MPV levels, representing a critical clinical finding. Therefore, in parallel with other studies, we need to understand potential positive effect of VD on ED and ensure that patients are receiving treatments that are supported by the highest level of evidence.

In the last decade, growing evidence highlighted that there is an association between VD deficiency and atherosclerotic cardiovascular (ASCV) diseases. Database information of more than 7000 VD deficient patients showed an association between VD deficiency and many cardiovascular disease states, including hypertension, coronary artery disease, ED and ASCV risk factors, such as hypertension, diabetes mellitus, and hyperlipidemia [Citation2]. Recent research suggests that nearly every cell of our body has receptors for VD, indicating a much more diverse role for this vitamin, than we previously recognized. Strikingly, over 3000 genes are responsive to VD [Citation3] and its biological effects are mediated through binding to the VD receptor and inducing either genomic or non-genomic down-stream effects [Citation4–6].

Many factors affect the prevalence of VD deficiency including geographical location, diet, supplement use, clothing, obesity, smoking, concerns about sun damage and maybe most importantly the nature of the environment. Having said that, the optimal VD levels needed for preventing ASCV diseases, targeted serum levels VD and dosage to remain a challenge! The VD dose that is administered and its duration in order to achieve a therapeutic serum level are of utmost importance. Total serum 25(OH)D concentration is an indicator of VD status. In terms of VD serum level, the Institute of Medicine publication recommended a target serum 25(OH)D of >20 ng/mL [Citation7]. However this report was based almost exclusively on skeletal considerations and was criticized by VD experts [Citation8,Citation9]. On the other hand, the Endocrine Society defines VD deficiency as a 25(OH)D < 30 ng/mL [Citation6]. The Endocrine Society recommends adult VD supplements of up to 4,000 IU/day [Citation6]; and that obese children and adults be given at least two to three times more VD for their age group to satisfy their body’s VD requirement. Certainly, 10,000 IU/day for adults 19 year and older may be needed to correct VD deficiency [Citation6].

Mean platelet volume (MPV), which is a determinant of platelet function, is an independent risk factor for cardiovascular diseases [Citation1]. Remarkably, patients with hypogonadism are susceptible to increased platelet activation and increased MPV values which contribute to increased risk of cardiovascular complications [Citation10]. VD (actually is a potent steroid hormone) is positively correlated with testosterone elevates when testosterone was supplemented in androgen deficient men [Citation11]. Amazingly, the reverse situation is also true, suggesting that VD supplementation might increase testosterone levels [Citation12]. Recently, Canguven et al. demonstrated that VD treatment improves testosterone levels and erectile function in middle-aged men [Citation13].

The story is old and well-known. Seven blind men examine an elephant focusing on seven different aspects. The result is seven completely different descriptions of the very same object of interest. As in ASCV diseases, we should integrate our knowledge within a bigger picture. According to several evidence-based studies, measurement of VD in ED patients is logical with supplementation initiated, as required. VD supplementation potentially represents a low-cost, low-risk method to treat and reduce rates of ED.

Disclosure statement

No potential conflict of interest was reported by the authors.

References

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  • Carlioglu A, Durmaz SA, Kibar YI, et al. Mean platelet volume in a patient with male hypogonadotropic hypogonadism: the relationship between low testosterone, metabolic syndrome, impaired fasting glucose and cardiovascular risk. Blood Coagul Fibrinolysis. 2015;26:811–815.
  • Francis RM, Peacock M, Aaron JE, et al. Osteoporosis in hypogonadal men: role of decreased plasma 1,25-dihydroxyvitamin D, calcium malabsorption, and low bone formation. Bone. 1986;7:261–268.
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