ABSTRACT

Hot flash, peripheral vasodilatation and severe sweating has been reported in approximately two thirds of the patients who receive androgen deprivation treatment (ADT) for prostate cancer. Besides, this has been reported to be the most important adverse event leading to impairment of quality of life in 30 to 40% of the patients. Although the exact pathophysiology of hot flash has not been determined yet, it is thought to be the result of cathecolamine release from the hypothalamus. Temperature differences in the body are coordinated in the thermoregulation center in the anterior hypothalamus, and body temperature conservation or waste is accomplished by dermal vasonconstriction or vasodilatation. Various neurotransmitters are released when the balance of this thermoregulation center is modified by hormonal changes. Stimuli like sudden changes in the temperature of the environment, hormones and neurotransmitters, hot drinks, and changing body position increase catecholamine release and thereby trigger hot flashes. Chronic low testesteron levels decrease secretion of opioid peptides from the hypothalamus, which in turn result in increased intrahypothalamic catecholamines. Although variety of neurotransmitters play role in hot flashes, the primary neurotransmitter known to result in temperature loss by modifying the balance of thermoregulation center is noorepinephrine. Seretonine is another important neurotransmitter that plays role in hot flash. Central active clonidine, megesterol acetate, gabapentine, selective seretonine reuptake inhibitors (venflaksasin), cyproterone acetate, dietilstilbesterol (DES) or acupuncture can be utilized in the treatment of hot flashes. The pathophysiology and currrent treatment alternatives for hot flash has been reviewed in this paper.