Androgens deficiency
Deficit androgeni e disfunzione erettile
I deficit di androgeni sono piuttosto comuni negli uomini con disfunzione erettile, e sono associati all'età ed all'ipercolesterolemia fra gli altri fattori. E' sempre più chiaro che le disfunzioni sessuali possono essere un sintomo di malattie di base nel sesso maschile, come ad esempio malattie cardiovascolari o diabete. E' stato rilevato un lieve aumento dell'ipogonadismo fra i 45 ed i 50 anni, al di là dei quali si osserva un plateau fino agli 80 anni. I livelli di PSA e creatinina non influenzano il testosterone, ma l'età, il diabete incontrollato, elevati livelli di colesterolo totale e l'anemia sono fattori correlati a livelli di testosterone significativamente ridotti. Anche se viviamo in un'epoca in cui esistono terapie mediche efficaci per via orale per la disfunzione erettile, gli uomini che la accusano dovrebbero sottoporsi ad un controllo completo che comprenda anche esami ormonali. (Urology 2008; 71: 693-7)
MTHFR mutations
Treatment of erectile dysfunction due to C677T mutation of the MTHFR gene with vitamin B6 and folic acid in patients non responders to PDE5i. 2010
J Sex Med. 2010 Jan;7(1 Pt 1):216-23. Epub 2009 Aug 17.
Lombardo F, Tsamatropoulos P, Piroli E, Culasso F, Jannini EA, Dondero F, Lenzi A, Gandini L.
Department of Medical Pathophysiology, University of Rome La Sapienza, Rome, Italy. lombardo@uniroma1.it
Abstract
INTRODUCTION: Epidemiological studies conducted on erectile dysfunction (ED) have demonstrated its close correlation with cardiovascular disease. Since hyperhomocysteinemia is considered an important cardiovascular risk factor, it could also be involved in the pathogenesis of ED. AIM: To study the role of the C677T MTHFR mutation with subsequent hyperhomocysteinemia in the determination of ED. METHODS: We studied 75 consecutive patients presenting with ED. Patients were interviewed using the International Index of Erectile Function. Blood samples were drawn for determination of MTHFR gene C677T mutation, homocysteine (Hcy) and folate levels. Penile color Doppler was also performed. MAIN OUTCOME METHODS: Patients were administered sildenafil citrate for 2 months. The nonresponders were treated with combination of sildenafil, vitamin B6, and folic acid for 6 weeks. Patients were split into three groups, A, B, and C on the basis on their MTHFR genotype, and in a further group defined as "sildenafil nonresponders" (NR). RESULTS: We found 20 patients homozygous for mutant MTHFR 677T, 36 heterozygous, and 19 wild type. Difference in baseline values for Hcy and folic acid was found between groups A and B, and A and C. The NR group (18 patients from group A and B), presented high levels of Hcy and low levels of folic acid. After combination treatment 16 of them (88.9%) revealed an improvement in the IIEF questionnaire. Moreover, it was measured a significant difference between the values of Hcy and folic acid at the baseline and at the end of the study for the nonresponders. CONCLUSIONS: Hyperhomocysteinemia in patients homozygotes for the C677T mutation may interfere with erection mechanisms and thus be responsible for ED. In case of hyperhomocysteinemia associated with low levels of folates, the administration of PDE5 inhibitors may fail if not preceded by the correction of the alterated levels of Hcy and folates.
J Endocrinol Invest. 2004 Oct;27(9):883-5.
Might erectile dysfunction be due to the thermolabile variant of methylenetetrahydrofolate reductase?
Lombardo F, Sgrò P, Gandini L, Dondero F, Jannini EA, Lenzi A.
Unit of Seminology and Immunology of Reproduction, Department of Medical Physiopathology, University of Rome La Sapienza, Rome, Italy. francesco.lombardo@uniroma1.it
Abstract
Hyperhomocysteinemia is considered one of the most important cardiovascular risk factors increasing considerably the risk of stroke and myocardial infarction. With respect to endothelial function, direct effects of hyperhomocysteinemia on vascular endothelial cells have been demonstrated through the reduction of endothelial nitric oxide production. In this paper, we report the case of a young man with homozygote genotype mutated with 5-methylenetetrahydrofolate reductase (MTHFR) thermolabile variant who, in the absence of relational stress, developed an erectile dysfunction (ED) refractory to the vasoactive type-V phosphodiesterase (PDE5) inhibitor therapy. After one month of treatment with 5 mg/day folic acid and 1000 microg/day cyanocobalamin, the patient restarted the assumption of 50 mg sildenafil, obtaining satisfying erections during sexual intercourse. We suggest that hyperhomocysteinemia may interfere with penile blood supply and, thus, be responsible for ED. If this relationship is confirmed, plasma levels and urinary homocysteine (HCy) should be evaluated in selected young patients with vascular ED. Furthermore, careful attention should be given to the risk of ED when dealing with this metabolic disturbance.
Dopamine, Serotonin, Prolactin
dopamine+and+prolactin+and+sexual
dopamine and prolactin and serotonin and sexual
The pathophysiology of hypoactive sexual desire disorder in women. 2010
In general, dopamine, estrogen, progesterone, and testosterone play an excitatory role in sexual desire, whereas serotonin, prolactin, and opioids play an inhibitory role.
Anatomy, Pathophysiology, Molecular Mechanisms, and Clinical Management of Erectile Dysfunction in Patients Affected by Coronary Artery Disease: A Review. 2021
Sexual function is related to numerous neurotransmitters and neuropeptides, and the main ones are dopamine, oxytocin, nitrile oxide (NO), norepinephrine, serotonin (5-hydroxytryptamine), and prolactin.
Drug treatment of paraphilic and nonparaphilic sexual disorders. 2009
RESULTS In vitro and in vivo (animal) studies have revealed that serotonin and prolactin inhibit sexual arousal, while norepinephrine (via alpha(1)-adrenoceptor activation), dopamine, acetylcholine (via muscarinic receptor activation), enkephalins, oxytocin, gonadotropin-releasing hormone, follicle-stimulating hormone, luteinizing hormone, testosterone/dihydrotestosterone, and estrogen/progesterone stimulate it.
