Which chemicals mediate the cause of dysmenorrhea?

Dysmenorrhea, commonly known as painful menstruation, is primarily mediated by the release of prostaglandins and leukotrienes. Prostaglandins, which are lipid compounds derived from fatty acids, play a crucial role in the contractions of the uterine muscles. Elevated levels of prostaglandins are associated with increased uterine activity, leading to pain and cramping often experienced during menstruation. These compounds can also cause inflammation, which may contribute further to discomfort.

Leukotrienes, which are another group of inflammatory mediators, can exacerbate the inflammatory response during menstruation. The combination of these two types of chemicals increases the sensitivity of pain receptors in the uterus and surrounding tissues, leading to the symptoms characteristic of dysmenorrhea.

In contrast, while corticosteroids can have anti-inflammatory effects, they are not typically involved in the physiological processes that cause dysmenorrhea. Estrogens and progesterones, although influential in regulating the menstrual cycle, do not directly lead to the painful contractions associated with dysmenorrhea. Similarly, testosterone and androgens are more relevant in the context of male physiology or specific disorders in women and do not mediate menstrual pain. Thus, the focus on prostaglandins and