ABSTRACT
Endometriosis is a common gynecologic disorder characterized by the presence of endometrial
tissue outside the uterine cavity. Although no single theory can explain all cases
of endometriosis, the most commonly accepted theory is Sampson's theory of retrograde
menstruation. Retrograde menstruation occurs in 76 to 90% of women. The much lower
prevalence of endometriosis suggests that additional factors determine susceptibility
to endometriosis. Endometriosis is associated with changes in both cell-mediated and
humoral immunity. Impaired natural killer cell activity resulting in inadequate removal
of refluxed menstrual debris may play a role in the development of endometriotic implants.
Moreover, although the peritoneal fluid of women with endometriosis contains increased
numbers of immune cells, these seem to facilitate rather than inhibit the development
of endometriosis. Macrophages that would be expected to clear endometrial cells from
the peritoneal cavity appear to enhance their proliferation by secreting growth factors
and cytokines. Although it is unclear whether these immunologic alterations induce
endometriosis or are a consequence of its presence, they appear to play an important
role in allowing endometriosis implants to persist and progress and contribute to
the development of associated infertility and pelvic pain. Danazol and gonadotropin-releasing
hormone (GnRH) agonists are commonly used for the medical treatment of endometriosis.
These medications seem to down-regulate cellular and humoral immune responses concomitant
with their effect on endometriotic implants. Immunomodulatory effects of danazol and
GnRH agonists are likely to contribute to the observed clinical improvement associated
with their use.
KEYWORDS
Endometriosis - immune response - cytokines - treatment of endometriosis
