Endometriosis
Sept. 9, 1997. 1st year resident S. M. CHOI M.D.
Etiology
transtubal regurgitation during menstruation
cells to develop into endometrial tissue
affected by endometriosis
develop as a result of reduced immunologic clearance of viable endometrial cells
from the pelvic cavity
endometriosis : may impair fertility by reducing sperm motility, increasing sperm
phagocytosis, or interfering with fertilization by increased secretion of cytokines such as a-TNF
: may promote the growth of endometrial cells by secretion of growth and
angiogenetic factors such as EGF, MDGF, fibronectin, adhesion molecules such as
integrins.
patient
appearance of subtle endometriosis implants, cysts, and adhesions
·Subfertility, dysmenorrhea, dyspareunia, chronic pelvic pain, asymptomatic
adhesion formation, fibrotic thickening and collection of shed menstrual blood in
endometriotic implants, resulting in painful traction with the physiologic movement
of tissue
adhesions that block tubo-ovarian motility and ovum pickup, it is associated with
subfertility
luteinized unruptured follicle syndrome, recurrent abortion, altered immunity, and
intraperitoneal inflammation) have been proposed, the association between fertility
and minimal or mild endometriosis remains controversial
associated with an increased rate of spontaneous abortion - up to 40% compared
with a normal spontaneous abortion rate of 15-25%. The association of
endometriosis and spontaneous abortion is difficult to assess adequately because of
the lack of prospective studies with well - defined control groups.
premenstrual spotting, and galactorrhea and hyperprolactinemia
pelvis in a cyclic pattern
bleeding, constipation, obstruction
examination
and unilateral ovarian enlargement.
tubes reduced
lesions that are obtained laparoscopically
information
nonmucinous epithelial ovarian carcinoma
follicular phase and the menstrual phase in each patient and when the ratio of
menstrual versus follicular values (>1.5) was used instead of one CA125
endometriosis after therapy
ovaries, cul-de-sac, and broad ligament
or small cysts containing old hemorrhage surrounded by a variable degree of
fibrosis
like), serous or clear vesicles, white plaques or scarring, yellow-brown peritoneal
discoloration of the peritoneum, and subovarian adhesion.
of endometriosis, not only for subtle lesions but also for typical lesions reported to
be histologically negative in 24% of cases
. Superficial endometriosis
. Ovarian endometriotic cysts
- contain a thick, viscous dark brown fluid (chocolate fluid)
- because this fluid may also be found in other conditions, such as a hemorrhagic
corpus luteum cysts or neoplastic cysts, biopsy and preferably removal of the
ovarian cyst for histologic confirmation are necessary.
·Microscopically, endometriotic implants consist of endometrial glands and stroma
with or without hemosiderin-laden macrophages
·Containing endometrial stroma with hemosiderin-laden macrophages or hemorrhages
may represent a very early event in the pathogenesis of endometriosis.
glandular activity
, presence, extent, and type of adnexal adhesions, degree of cul-de-sac obliteration.
correlation of pain or infertility and it has considerable intraobserver and
interobserver variability.
endometriosis, respectively
age, but in typical lesions these parameters and the depth of infiltration increased
with age
been reported to occur in women and in baboons, indicating that endometriosis is a
dynamic condition
enlarge during the first trimester but regress thereafter establishment of a
'pseudopregnant state' with exogenously administered estrogen and progestins was
based on the belief that symptomatic improvement may result from decidualization of
endometrial implants during pregnancy.
·Unfortunately, elimination of the endometriotic implants by surgical or medical
treatment often provides only temporarily relief. Therefore, the goal should be to
eliminate the endometriotic lesions and, more importantly, to treat the sequelae (pain
and subfertility) often associated with this disease
morbidity, and the possibility of recurrence of adhesions postoperatively.
adhesions and to restore normal anatomy.
course of medical treatment to reduce vascularization and nodular size are
recommended
and there is a negligible risk of renewed growth of residual endometriosis to reduce
this risk, hormonal replacement therapy should be withheld until 3months after
surgery.
. Pain : laser laparoscopy may be effective for the treatment of mild to severe
endometriosis pain, minimal endometriosis, laser treatment may limit progression of
disease
. Subfertility : success of surgery in relieving infertility is directly related to the
severity of endometriosis. Preop. medical treatment may be useful to reduce the
extents of endometriosis in patients with advanced disease. Postop. medical
treatment is rarely indicated because it prevents pregnancy, and higher pregnancy
rates occur during the first 6 to 12 months after conservative surgery.
·Estrogen is known to stimulate the growth of endometriosis, hormonal therapy has
been designed to suppress estrogen synthesis, thereby inducing atrophy ectopic
endometrial implants or interrupting the cycle of stimulation and bleeding.
months) was originally used to induce 'pseudopregnancy' caused by the resultant
amenorrhea and decidualization of endometrial tissue. Unfortunately, there is no
convincing evidence that medical therapy with oral contraceptives offers definitive
therapy. Instead, endometrial implants survive the induced atrophy with reactivation
in most patients following termination of treatment.
Any low dose combination oral contraceptive pill containing 30-35mcg ethinyl
estradiol used continuously can be effective in the management of endometriosis
objective of the treatment is induction of amenorrhea, which should be continued
for 6 to 12 months
Posttreatment pregnancy rate up to 50%
followed by atrophy.
response and bleeding patterns
indicated in infertile women because it induce profound amenorrhea and
anovulation, and a varying length of times is required for ovulation to resume
after discontinuation of therapy
hypoestrogenemia
antigonadotropic properties
acne, seborrhea, and oily hair/skin
receptors
androgen, low estrogen environment
start with 400mg daily (200mg twice a day) and increase the dose to achieve
amenorrhea and relieve symptoms
flashes, atrophic vaginitis, reduced breast size, reduced libido, fatigue, nausea, muscle
cramps, emotional instability
function, pregnancy
in low FSH and LH level -- induced and reversible state of pseudomenopause
regimen)
after 5years
nonspecific cycle fecundity enhancement, including controlled ovarian hyperstimulation
with intrauterine insemination, gamete intrafallopian transfer, and in vitro fertilization.
immediate interest in pregnancy
followed by administration of cyclic low-dose combination oral contraceptives to
prevent recurrence
continuous oral contraceptives to prevent progression of disease.