Menses-associated pain in the pelvis, lower abdomen, or lower back
- Primary dysmenorrhea: functional menses-associated pain due to amplification of normal menstrual physiologic processes
- Secondary dysmenorrhea: menses-associated pain due to other pelvic pathology, such as endometriosis or Müllerian anomaly
- Primary dysmenorrhea
- Typically begins 6 to 24 months post-menarche
- More likely as more cycles become ovulatory
- Secondary dysmenorrhea
- More common later in adolescence and in young adults
- Most common gynecologic condition among women of reproductive age, affecting 45–95% of menstruating women
- Up to 62% of adolescents with dysmenorrhea have endometriosis.
- Early menarche
- Increased duration or amount of menstrual flow
- Cigarette smoking
- Alcohol consumption
- Family history of dysmenorrhea
- Higher body mass index
- Dysmenorrhea more common in patients with a positive family history
- Hereditary predisposition to endometriosis; polygenic mode of inheritance, multifactorial, with expression varying with interaction with environmental factors
- Even when not in pain, women with primary dysmenorrhea have upregulation of proinflammatory cytokine genes and downregulation of anti-inflammatory response genes.
- Ovulation is followed by increased progesterone release by the corpus luteum in the second half of the menstrual cycle. With the drop in progesterone late in the menstrual cycle, arachidonic acid and other omega-6 fatty acids are released, triggering an inflammatory response cascade involving prostaglandins (PGs) and leukotrienes (LTs).
- Uterine PGs and LTs cause myometrial contractions and endometrial artery vasoconstriction, resulting in uterine ischemia with ensuing pain.
- PGF2alpha is thought to stimulate the myometrium and cause vasoconstriction.
- Dysmenorrhea severity is directly proportional to endometrial PGF2alpha concentrations.
- Vasopressin, also elevated among women with dysmenorrhea, may play a secondary role by potentiating uterine contractions and ischemic pain.
- PGs and LTs can affect other body systems/organs, leading to dysmenorrhea-associated symptoms such as nausea/vomiting, diarrhea, and headache.
- Inappropriate local aromatase activity in endometriosis lesions leads to a local rise in estrogen, which induces cyclooxygenase (COX)-2 transcription and PGE2 synthesis. Aberrant cytokine expression also mediates inflammation/pain.
- Secondary dysmenorrhea may be caused by a Müllerian abnormality.
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