الفهرس 
Premature ejaculationOnly 14 pages are availabe for public view
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Abstract
Premature ejaculation is the most common male sexual disorder and is estimated to affect up to 30 % of men worldwide (Rowland et al., 2004). It was defined by The American Urological Association Guideline as ejaculation that occurs sooner than desired, either before or shortly after penetration causing distress to either one or both partners (Montague et al., 2004). It can be classified as global or primary (lifelong) that suggests an organic basis for its pathogenesis and situational or secondary (McMahon et al., 2004). The most widely used treatment for PE is SSRIs with a rank order of efficacy for paroxetine being the best followed by clomipramine,sertraline and fluoxetine ( Waldinger et al., 2004 ).
Trace elements in semen play an important role in male sexuality (Li Yuyan et al., 2007). Magnesium is one of the trace elements present in human semen estimated as < 70 mg/l and much higher than in serum which is 17-24 mg/l (Bartis and Ashwood, 2001). Magnesium is involved in very important processes including gating of calcium channels, transmembrane ion flux, regulation of adenylate cyclase, muscle contraction, neuronal activity, control of vasomotor tone and neurotransmitter release and it has been likened a physiological calcium antagonist (Romani and Maguire, 2002). Magnesium consumed by most of individuals is 20-30% less than the recommended dietary allowance (Papadakis, 1995), so its probable that consumption of more Mg in diet leads to increase in seminal Mg levels (Zavaczki et al., 2003).
In this study the results of measuring magnesium seminal level for group (A) which includes men with PE without any other sexual or organic disorder, group (B) which includes healthy men without PE or any other sexual or psychological disorder, group (C) which includes men with both PE and ED without any other organic or psychological disorder showed a significantly higher values of Mg in group (B) when compared group (A) with lower values and the lowest in group (C) which suggests a possible role of Mg in the pathogenesis of PE.
Low magnesium level stimulates angiotensin-induced aldosterone synthesis and thromboxane-A2 overproduction by phospholipase-A2 activation, engagement of thromboxane-A2 results in Ca2+ influx and elevated calcium in endothelial cells promotes phosphodiesterases and decreases G-cyclase activity and decreased NO production and its release from the endothelium. This will decrease cGMP resulting in decreased nitric oxide (NO) production, as NO is a vascular smooth muscle relaxing factor and thus, decreased levels of NO consequently lead to contraction of smooth muscles of genital tract and thus to rapid emission and premature ejaculation. A decrease of NO can lead also to a contraction of cavernosal smooth muscles causing a state of erectile dysfunction (Nikoobakht et al., 2005; Aloosh et al., 2006).
A decrease of Mg level in semen can lead to a state of PE and a more decrease in Mg might also lead to a combination of PE and ED acting through NO system. As nitric oxide is released from the nerve and endothelial cells in the corpora cavernosa of the penis so it acts first on the smooth muscles of the corpora causing relaxation and further erection, thus, when nitric oxide decreases most of the residual amount will be consumed for having an erection and so ejaculation will be affected causing PE and with a more decrease of nitric oxide PE and ED may both occur. This is supported by fact that in group (C), PE occurred first before ED, explaining the lowest Mg level found. So, further studies should be conducted to evaluate the role of magnesium in the pathogenesis of premature ejaculation and erectile dysfunction and to search for possible connecting factors of PE and ED apart from hypomagnesemia and NO.