Endometriosis endometriosis, suggesting that hormonal disparity may have

Endometriosis is
a gynecological disease of women which is a benign estrogen dependent condition
seen in reproductive age group and characterized by the endometrial implants
outside the uterine cavity. 10% to 15% of women in
reproductive age group has been assessed to be affected by it 1. The very common site of
endometriotic implants is the pelvic cavity, especially the pelvic and ovarian
peritoneum, but implants can also be located in the posterior cul-de-sac,
rectovaginal septum, intestine, and bladder. The endometriotic implants have
also been reported in the pericardium, pleura, liver, kidney, bladder, brain,
lower limbs, and nasal cavity 2. The women who have
endometriosis are at greater risk for getting ovarian cancer than the overall
female population, and they might also be at an increased risk of getting
breast and other cancers as well as autoimmune and atopic disorders 2. In women with endometriosis,
there is a reduced monthly fecundity rate (2-10%) related with fertile couples (15-20%). 28

 

 

HISTORY

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Over the
previous 20 years there has been a rising interest in the history of
endometriosis. In 1899 Russel was the first person who mentioned about an ovary
which contained the mucosa of uterus, but the first person to demonstrate the
specific endometrial activities was Sampson, such as desquamation during the
time of menstruation and decidualization in pregnancy. Afterwards he presented
a theory the pathogenesis of this disease. 9

 

EPIDEMIOLOGY OF
ENDOMETRIOSIS

Numerous reproductive influences
have remained persistently interrelated with likelihood for endometriosis, suggesting
that hormonal disparity may have a substantial effect on the possibility of
developing endometriosis.

For Instance, early age at
menarche 10, 11, 12, 13, 14 and short menstrual cycle length 13,14 are interconnected
with an increased threat, while parity 13 and current use of oral
contraceptives 15 are related with a reduced threat. Circulating estradiol
and estrone, which stimulate ectopic and eutopic endometrial tissue, are greater
amongst women at an earlier age of menarche and in nulliparous women 16-20. Though not a reproductive risk
factor, a reliable inverse connection has also been witnessed amongst body mass
index (BMI) and endometriosis 10, 11–12, 14, 58, 59 and may also relate to hormonal
disparities between heavy women and slender women. Unfortunately, the
evaluation of tubal ligation, parity, and oral contraceptive use in relation to
endometriosis risk has been troubled by methodologic issues. Tubal ligation has
been hypothesized to drop endometriosis possibility through hindering
retrograde menstruation from reaching the pelvic cavity. Yet, the connection
between tubal ligation and endometriosis is difficult to understand since
endometriosis is illustrated by infertility, and women who seek a tubal
ligation are more liable to be parous than the overall population 21, 22. The mean age at diagnosis is 25–29
years, but it is often greater in women who present with infertility rather
than pelvic pain. 23 Though the mechanism is undetermined,
circulating estrogens are known to
be lesser in women who smoke 37 and could impede the growth and persistence of endometriotic
tissue. The association between alcohol
and caffeine consumption is similarly
mixed and may depend on fertility status. Among infertile women, several
studies have reported increased risk with higher alcohol or caffeine intake 54, 55. The association between physical activity and
endometriosis is unclear 33, higher intake of long-chain omega-3 fatty acids has been
associated with reduced endometriosis risk 44.

 

 

 

 

 

 

 

 

Risk
factors for endometriosis

Factors associated with increased risk   References   
       Factors associated with decreased risk     References

 

Earlier age at menarche                          10-14                 Parity                                                        13

Shorter menstrual cycle length               13, 14                Current oral contraceptive use                  15

Taller height                                            58, 59                Smoking                                                   53

Alcohol use                                              54                     Higher body mass index                           10-12, 14

Caffeine intake                                         55                     Regular exercise                                       56

Nulliparous                                              16-20                Fish and omega-3 fatty acids                    57                                                                                        

 

 

 

 

 

 

 

 

 

 

 

PATHOGENESIS OF ENDOMETRIOSIS

Coelomic metaplasia Theory

The coelomic metaplasia theory mentions that the peritoneal
epithelium could be “converted” into endometrial tissue, possibly due to the
persistent inflammatory process or chemical irritation from menstrual blood
which has been refluxed. The “coelomic metaplasia theory”, is founded on the remark
that coelomic epithelium is the mutual antecedent of endometrial and peritoneal
cells, consequently permitting conversion of one kind of cell into alternative type.

The
embryonic rests theory                                            

This theory postulates that the “müllerian remnants” can be
segregated into endometrial material. The environments in which such thing would
even happen are not well-defined nevertheless, after endometrium is existent,
it will start to fabricate symptoms in a cyclical way.

The Retrograde
theory

Sampson was the first
person to explain about the retrograde theory. This theory postulates that,
during menstrual cycle there is the backflow of the menstrual blood which
passes through the oviduct and gets embedded into the pelvic cavity as an
endometriotic implants. 3 The pathogenesis of endometriosis can be virtually explained through
retrograde menstruation. The endometrial implants are rarely discovered in such secluded sites as the lung or
even the nose. Furthermore, endometriosis also appears, rarely, in men taking hefty
doses of estrogen. Hence this theory doesn’t properly explain the full
pathogenesis of this disease.

 

 

Lymphatic Spread Theory

The
ectopic locations of the endometrium could link us to the likelihoods of
implantation of endometrium through the lymphatic system, it explains the
lymphatic spread theory.  Sampson also proposed
that through the lymphatic circulation, the fragments of endometrial tissue can
travel to reach ectopic sites where they get embedded to form endometriotic
lesions 3. This theory explains the finding of endometrial and endometriotic
tissue in lymph nodes and lymphatic vessels and lymph in some patients 3,24.
The incidence of endometriosis in lungs and other uncommon/distant locations
such as nose, brain may also be well explained by lymphatic spread 25.
Following endometrial transportation through the lymphatic circulation to
ectopic sites, anomalies of the eutopic endometrium from women with
endometriosis may allow development of endometriotic lesions.

 

 

 

 

 

Combined
Theories of Pathogenesis

Endometriosis
is not fully enlightened via any of the single theories outlined above;
therefore, different concepts have been merged to understand the pathogenesis
of the disease and also to explain different types of endometriosis. For
example, the composite theory proposed by Javert 26 combines implantation,
lymphatic dissemination, and direct extension theories of endometriosis.
Similarly, Nisolle and Donnez 27 argued that the histogenesis of
endometriosis differs depending on the location and type of endometriotic
lesion. Ovarian and deep infiltrating endometriotic (DIE) lesions can be
explained by metaplasia, whereas peritoneal lesions may be the result of
implantation 27. A prevailing theory is that women
who acquire endometriosis might have an altered immune system which is less
likely to distinguish and attack ectopic endometrial implants. These women may
even have a high concentration of inflammatory cells in the peritoneum which
might contribute to the growth and stimulation of the endometrial implants.
Endometrial implants cause symptoms by disrupting normal tissue, forming
adhesions and fibrosis, and causing severe inflammation. Interestingly, the
severity of symptoms does not necessarily correlate with the amount of
endometriosis. Women with widely disseminated endometriosis or a large
endometrioma may experience little pain, whereas women with minimal dis- ease
in the cul-de-sac may suffer severe chronic pain. (figure from  Dominique de ziglar, Bruno borghese)