Iris Publishers- Open access Journal of Urology & Nephrology | Secondary Hypogonadism at Patients Hormonally
Treated for Prostatic Carcinoma from a Cardiologist
Perspectiv
In the cardiologist’s care are often patients treated for erectile dysfunction or prostatic cancer and, vice versa, in the urologist or andrologist´s care patients treated for hypertension, arrhythmias and coronary heart disease. There is needed to respect mutually influences and take them in account at the diagnostic and therapeutic indications. Secondary hypogonadism at patients hormonally treated for prostatic carcinoma leads to loss of both positive testosterone effects on cardiovascular and metabolic system and vitality decrease. Cardiovascular rehabilitation carries benefit not to patients with coronary artery disease only, but to patients treated for prostatic carcinoma too. Prostatic disease treatment by urologist may influence blood pressure values of patient treated by cardiologist. This article provides more detail information’s on the pathological-physiological background of relevant mutual relationships and their practical impact on clinical patient management.
Hormonal treatment of Ca prostate leads to secondary hypogonadism, a marked drop in testosterone levels that occurs in human serum in three forms: free, easily bound to albumin or strongly bound to sex hormone-binding globulin (SHBG). Testosterone receptors are found to be ubiquitous in the human body, and the effects of testosterone are crucial to male life [1].
a. Improving quality and life expectancy
b. Increases sexual desire and improves erectile function
c. Increase muscle mass, muscle strength and bone density, increase blood formation and physical activity
d. Reduce visceral fat volume and risk of fractures
e. Improves the feeling of mental well-being, mood, memory, vitality
Of particular importance are the positive effects of testosterone and its modulators (LHRH hormone releasing luteinizing hormone) on the cardiovascular system [2-4].
a. Modulate myocardial contractility (receptors in myocytes)
b. Vasodilator effects on coronary artery disease, inhibition of endothelial cell apoptosis
c. Antiarrhythmic effects, shortening of the QTc interval
d. Inhibition of atherosclerosis, improvement of insulin resistance, improvement of metabolic syndrome dyslipidemia, decrease of glucose level and TK
e. Immunomodulatory effects (decrease in cytokine levels associated with inflammation and development of atherosclerosis)
f. Low testosterone levels are associated with increased cardiovascular mortality
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