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The Pathogenesis of Endometriosis — 257
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57. Birnbaum LS. The mechanism of dioxin toxicity: relationship to
risk assessment. Environ Health Perspect. 1994;102(suppl 9):157–
167.
58. Hinsdill RD, Couch DL, Speirs RS. Immunosuppression in mice
induced by dioxin (TCDD) in feed. J Environ Pathol Toxicol.
1980;4:401–425.
59. Guo SW. The link between exposure to dioxin and endometriosis:
a critical reappraisal of primate data. Gynecol Obstet Invest.
2004;57:157–173.
60. Igarashi TM, Bruner-Tran KL, Yeaman GR, et al. Reduced expression of progesterone receptor-B in the endometrium of women
with endometriosis and in cocultures of endometrial cells exposed
to 2,3,7,8-tetrachlorodibenzo-p-dioxin. Fertil Steril. 2005;84;67–
74.
61. Guo SW, Wu Y, Strawn E, et al. Genomic alterations in the
endometrium may be a proximate cause for endometriosis. Eur
J Obstet Gynecol Reprod Biol. 2004;116:89–99.
62. Sato N, Tsunoda H, Nishida M, et al. Loss of heterozygosity on
10q23.3 and mutation of the tumor suppressor gene PTEN in
benign endometrial cyst of the ovary: possible sequence progression from benign endometrial cysttoendometrioidcarcinomaand
clear cell carcinoma of the ovary. Cancer Res. 2000;60:7052–7056.
63. Wu Y, Strawn E, Basir Z, et al. Genomic alterations in ectopic and
eutopic endometrial ofwomenwithendometriosis. Gynecol Obstet
Invest. 2006;62:148–159.
64. Groothuis PG, Koks CA, De Goeij AF, et al. Adhesion of
human endometrialfragments to peritoneumin vitro. Fertil Steril.
1999;71:1119–1124.
65. Demir Weusten AY, Groothuis PG, Dunselman GA, et al. Morphological changes in mesothelial cells induced by shed menstrual
endometrium in vitro are not primarily due to apoptosis or necrosis. Hum Reprod. 2000;15:1462–1468.
66. Kyama CM, Overbergh L, Debrock S, et al. Increased peritoneal
and endometrialgene expression of biologicallyrelevant cytokines
and growth factors during the menstrual phase in women with
endometriosis. Fertil Steril. 2006;85:1667–1675.
67. Nap AW, GroothuisPG,DemirAY, etal.Tissueintegrityisessential
for ectopic implantation of human endometrium in the chicken
chorioallantoic membrane. Hum Reprod. 2003;18:30–34.
68. Oosterlynck DJ, Cornillie FJ, Waer M, et al. Women with
endometriosis show a defect in natural killer activity resulting in
a decreased cytotoxicity to autologous endometrium. Fertil Steril.
1991;56:45–51.
69. Somigliana S, Vigano P,Gaffuri B, GuarneriD, Busacca M,Vigbali
M. Human endometrial stromal cells as a source of soluble intercellular adhesion molecule (ICAM)-1 molecules. Hum Reprod .
1996;11:1190–1194.
70. Tseng JF, Ryan IP, Milam TD, et al. Interleukin-6 secretion in
vitro is up-regulated in ectopic and eutopic endometrial stromal
cells from women with endometriosis. J Clin Endocrinol Metab.
1996;81:1118–1122.
71. VelascoI, RuedaJ, Acien P. Aromataseexpression in endometriotic
tissues and cell cultures of patients with endometriosis. Mol Hum
Reprod . 2006;12:377–381.
72. Halme J, Becker S, Wing R. Accentuated cyclic activation of peritoneal macrophages in patients with endometriosis. AmJObstet
Gynecol. 1984;148:85–90.
73. Rana N, Gebel H, Braun DP, Rotman C, House R, Dmowski
WP. Basal and stimulated secretion of cytokines by peritoneal macrophages in women with endometriosis. Fertil Steril.
1996;65:925–930.
74. Sharpe-Timms KL, Piva M, Ricke EA, Surewicz K, Zhang YL,
Zimmer RL.Endometriosissynthesizesandsecretes ahaptoglobinlike protein. Biol Reprod. 1998;58:988–994.
75. Sharpe-Timms KL, Zimmer RL, Ricke EA, Piva M, Horowitz GM.
Endometriotic haptoglobin binds to peritoneal macrophages and
alters their function in women with endometriosis. Fertil Steril.
2002;78:810–819.
76. Ryan IP, Tseng JF, Schriock ED, Khorram O, Landers DV, Taylor RN. Interleukin-8 concentrations are elevated in peritoneal
fluid of women with endometriosis. Fertil Steril. 1995;63:929–
932.
77. KhorramO, Taylor RN, Ryan IP,Schall TJ, Landers DV.Peritoneal
fluid concentrations of the cytokine RANTES correlate with the
severity of endometriosis. Am J Obstet Gynecol. 1993;169:1545–
1549.
78. Akoum A, Lemay A, McColl S, Turcot Lemay L, Maheux R. Elevated concentration and biologic activity of monocyte chemotactic protein-1 inthe peritoneal fluidof patients with endometriosis.
Fertil Steril. 1996;66:17–23.
79. Oosterlynck D, Meuleman M, Waer M, Koninckx P. Transforming growth factor-B activity is increased in peritoneal fluid
from women with endometriosis. Obstet Gynecol. 1994;83:287–
292.
80. Hsu CC, Yang BC, Wu MH, Huang KE. Enhanced interleukin-4
expression in patients with endometriosis. Fertil Steril. 1997;67:
1059–1064.
81. Marchino GL,Gennarelli G, Enria R,Bongioanni F, LipariG, Massobrio M. Diagnosis of pelvic endometriosis with use of macroscopic versus histologic findings. Fertil Steril. 2005;82:12–15.
82. Nisolle M, Donnez J. Peritoneal endometriosis, ovarian endometriosis, and adenomyotic nodules of the rectovaginal septum
are three different entities. Fertil Steril. 1997;68:585–596.
83. Sakamoto A. Subserosal adenomyosis: a possible variant of pelvic
endometriosis. Am J Obstet Gynecol. 1991;165:198–201.
84. Wu Y, Kajdacsy-BallaA, Strawn E, et al. Transcriptional characterizations of differences between eutopic and ectopic endometrium.
Endocrinology. 2006;147:232–246.

Section 10.2. Thoracic Endometriosis
https://t.me/med1917
Georgios E. Hilaris and Camran Nezhat
The purpose of this section is to provide practicing gynecologic
endoscopic surgeons with up-to-date evidence on the etiopathogenesis, diagnosis, and treatment of thoracic endometriosis and
to heighten the level of clinical suspicion of the syndrome. This
syndrome possibly represents an underreported cause of catamenial spontaneous pneumothorax. A multidisciplinary approach
by a thoracic and gynecologic surgicalteamoffersthebestchances
for an accurate diagnosis and treatment of women with this syndrome.
INTRODUCTION
Endometriosis, defined as the presence of endometrial glands
and stroma outside the endometrial cavity, is a common disease
that affects approximately 2% to 15% of women of reproductive
age.[1,2] Consequently, thoracic endometriosis is the presence of
endometrial glands and stroma in the thoracic cavity.
Thoracic endometriosis syndrome (TES) encompasses
mainly four clinical entities: catamenial pneumothorax (CP),
catamenial hemothorax (CHt),catamenialhemoptysis(CH),and
lung nodules, withthe first beingbyfar the mostcommonclinical
presentation.[3]
The diagnosis of thoracic endometriosis has improved substantially over the past two decades because of advances in endoscopic techniques (video-assisted thoracoscopic surgery [VATS]
as well as laparoscopy) coupled with a higher level of clinical
suspicion.
Its etiology and pathogenesis, however, are still not well understood. Hence,optimal management of thoracicendometriosis
remains to be elucidated, with medical, surgical, or combined
approaches being reported in the international literature thus
far.
EPIDEMIOLOGY
The true incidence of TES remains unclear. Since Barnes [4]
described the first case of thoracic endometriosis in 1953, there
have been more than 250 cases of thoracic endometriosis and CP
reported in the international literature.[5–13] In recentpublished
series, however, up to one third (30%) of women hospitalized
with a diagnosis of spontaneous pneumothorax had CP.[12,14]
Thus, it is plausible that thoracic endometriosis is an underreported cause of secondary spontaneous pneumothorax in an age
group of women in whom most cases of pneumothorax were so
far thought to be primary.[15]
Like other sites of extragenital endometriosis, thoracic
endometriosis seems to affect a slightly older population than
does pelvic disease. The mean age at presentation of women with
thoracic endometriosis is 35 ± 0.6 years, with a range from 15
to 54 years. Interestingly, pelvic endometriosis precedes thoracic
endometriosis symptoms, occurring between 24 and 29 years –
that is, approximately 5 to 7 years earlier.[3] Similar data come
from a recent review of CP cases in 229 patients in whom the
mean age at onset of symptoms was 34.2 ± 6.9 years, with a
range from 15 to 47 years.[13]
Fifty percent to 84% of women diagnosed with thoracic
endometriosis haveassociatedpelvicendometriosis. The percentage, though, of women with pelvic disease who develop thoracic
endometriosis is largely unknown.[3]
Most lesions are solitary, with the right hemithorax (mainly
pleura and far less commonly the lung parenchyma) being
involved in up to 92% of cases and the left hemithorax in 5%
of cases; the remaining 3% have bilateral involvement.[13]
CP is the most frequent clinical presentation of patients with
TES, occurring in approximately 80% of the cases; CHt occurs
in 14% and CH in 5%. Least common are endometriotic nodules.[3,16]
ETIOLOGY AND PATHOGENESIS
Based on the anatomic location of the endometriotic lesions,
thoracic endometriosis can be classified into pleural and bronchopulmonary (parenchymal). The former, which is the most
common type, gives rise to CP and CHt, whereas the latter gives
rise to CH and the exceedingly rare lung nodules.[16,17]
There is general agreement that thoracic endometriosis is the
only cause of CHt, CH, and endometriotic lung nodules. Conversely, CP, although most frequently associated with thoracic
endometriosis, may also have other etiologic mechanisms.[15]
Three theories have been proposed to explain the presence
of thoracic endometriotic lesions: coelomic metaplasia, lymphatic or hematogenous embolization from the uterus or pelvis,
and retrograde menstruation with subsequent transperitoneal–
transdiaphragmatic migration of endometrial tissue.[3,14] The
first theory cannot be supported by the almost 9:1 right-sided
predominance of endometriotic pleural implants. On the other
hand, thelymphovascular embolization theory could explainnot
only the parenchymal or bronchopulmonary endometrioticnodules but also other extrapelvic locations.[1,3] In fact, a review
of autopsy data showed that cadavers with bronchopulmonary
endometriosis usually had bilateral lesions whereas pleural and
diaphragmatic lesions were almost always right sided.[18]
The theory of transdiaphragmatic passage of endometrial
debris and/or air is now the most favored explanation for
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thoracic endometriosis. It best supports both the anatomic location of endometriotic lesions (found in the right pleura in more
than 90% of the cases) and the exceedingly more common presentation of CP versus other, less common entities of TES.[19]
This last theory is based on the concept that peritoneal fluid circulation within the abdomen follows a characteristic clockwise
pattern that promotes flow of fluids (air, cell aggregates, pus)
from the pelvis to the right subdiaphragmatic area through the
right paracolic gutter. Transdiaphragmatic passage of peritoneal
fluid into the right pleural cavity may occur through congenital or acquired defects and fenestrations [3,13,20] and may be
the key pathognomonic feature of thoracic endometriosis. During menses, refluxed endometrial tissue or air may pass through
these defects into the pleural space, favored by both the thoracoabdominal pressure gradient and the “piston-like” action of
the solid liver bulk.[20]
As in the case of pelvic endometriosis, heterotopic endometrial implants adhere, proliferate, and follow hormonal cyclic
changes. Recurrent bleedingand subsequent fibrosismay weaken
the implantation site on visceral pleura that in subsequent cycles
may rupture or bleed, causing pneumothorax or hemothorax,
respectively. Bronchopulmonary implants, on the other hand,
may erode the parenchyma or bronchi, causing hemoptysis and
fibrosis, as in the case of lung nodules.
Based onthe last two theories, itis not surprising that women
with bronchopulmonary endometriosis tend to have a history of
uterine manipulation or trauma (e.g., hysteroscopy, dilation and
curettage); this supports the lymphovascular embolization theory, whereas those with pleural disease most often have a history
of pelvic endometriosis.[16,17]
CLINICAL FEATURES
The most common presentation of TES is CP, which accounts
for almost 80% of cases. Less frequent clinical entities include
CHt (14% of cases), CH (5% of cases), and lung nodules.[3,16]
CP is defined as a recurrent pneumothorax occurring within 72
hours from the onset of menstruation.[14] Though CP is typically cyclic, noncyclic recurrences occurring in the immediate
premenstrual period [21,22] or ovulatory phase [23] have also
been reported.
In most cases, CP is right sided [3,13], with the left side being
rarely involved.Bilateral CP ispossible but extremely rare.[24,25]
Patients with CP present with symptoms of spontaneous
pneumothorax that are usually nonspecific, such as pleurisy,
cough, and shortness of breath. Patients may also have referred
peri-scapular or neck-irradiating pain due to diaphragmatic irritation. In most cases, symptoms are mild to moderate; severe
presentations are rare.[15]
CHt is an uncommon manifestation of TES accounting for
approximately 14% of cases. As with CP, CHt is almost always
unilateral and right sided, although left-sided hemothorax has
been reported.[26]Again, symptoms are nonspecific and include
pleuritic pain, shortness of breath, and cough. The presence of
bloody effusion is variable. Computed tomography (CT) of the
chest may show multiloculated effusions, nodular lesions of the
pleura, or bulky pleural masses.[6]
CH and lung nodules are both clinical entities of bronchopulmonary TES and very rare manifestations. Hemoptysis is
a quite variable manifestation, with neither massive hemoptysis
nor deaths being described so far.Anassociationwith menses may
not always be appreciated, and diagnostic delays of up to 4 years
fromthe onset of symptoms havebeen reported.[27] CH and lung
nodules are interrelated entities. Thus, patients who present with
CH frequently have associated lung nodules on imaging studies
and vice versa.[15]
CP, CHt, CH, and lung nodules represent the main clinical
entities in TES. However, they are not the only manifestations
of TES. Specifically, in diaphragmatic-only endometriosis cases,
catamenial phrenic nerve irritation causing a catamenial painonly syndrome, namely cyclic shoulder, neck, epigastric, or right
upper quadrant pain, may be theonly presentationofTES.[28,29]
Overall, a high level of clinical suspicion is of paramount
importance in TES. A detailed history might make the difference
in promptly establishing a correct diagnosis and avoiding delays
in treatment, which are commonly reported.
DIAGNOSIS
The mostvaluable tool inthe diagnosis ofthoracic endometriosis
is a high level of clinical suspicion.[5] A cyclic (i.e., catamenial)
constellation of symptomscan be consideredpathognomonic for
the disease. However, diagnosis is often delayed for more than 8
months from the onset of symptoms.[17].
Chest radiograph, CT, magnetic resonance imaging, thoracocentesis, and bronchoscopy are most useful in the differential
diagnosis ofthe patient presentingwith pneumothorax,hemothorax, hemoptysis, or lung nodules and help rule out malignancy,
infection, and other pathologies. They all, however, have limited
diagnostic yield in the diagnosis of TES per se, with variable and
inconsistent findings.[5,17]. Interestingly, in the case of bronchopulmonary endometriosis, bronchoscopy-directed biopsies
of suspected lesions usually fail to provide a tissue diagnosis,
whereas brush cytology frequently shows distinctive features of
endometrial cells.[30]
Performance of imaging studies or bronchoscopy during
menses may assist in the diagnosis of pleural or bronchopulmonary disease. Repeat imaging studies or bronchoscopy during
midcycle typically documentsthedisappearanceofthe previously
reported findings, thus strengthening the clinical suspicion.[31]
VATS is at present the gold standard for both the definitive diagnosis and surgical treatment of CP.[5,12,13,15] In the
largest review of CP cases, more than 50% (52.1%) of patients
with CP assessed with VATS were diagnosed as having thoracic
endometriosis. Diaphragmatic abnormalities (fenestrations or
endometriosis, alone or combined) are nowadays the most commonly described lesions (38.8%), followed by endometriosis of
the visceral pleura (29.6%). In the remainder of cases, discrete
lesions, such as bullae, blebs, and scarring (23.1%), or no findings (8.5%) are noted.[13,14,21]
Diaphragmatic fenestrations range from a few millimeters to
2 cm.[14,32] Endometrial deposits in both the diaphragm and
pleura have similar appearance and range from a few millimeters
to 1 cm. Their color ranges from violet to brown, depending on
the day of the menstrual cycle.[5,15,33]
Performanceof a combined VATS and laparoscopy procedure
in a single session is another diagnostic approach.[5] This way,
the thoracic cavity as well as the pelvis and subdiaphragmatic

260 — Georgios E. Hilaris and Camran Nezhat
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region can be assessed. It may be particularly helpful in cases of
inconclusive VATS, which may be the result of the presence of
endometriosis in the abdominal-only aspect of the diaphragm,
causing catamenial phrenic nerve irritation and pain.[29]
Although exploratory thoracotomy was performed extensively in the past, it is now reserved for select cases of prior thoracoscopic (VATS) failure or large lesions.
TREATMENT OPTIONS
Treatment of thoracic endometriosis can be medical, surgical, or
a combination of both.
Medical Treatment
Medical treatment has long been considered the first step in the
management of thoracic endometriosis. Danazol, progestational
agents, oral contraceptive pills, and GnRH analogues have all
been widely used.[15] All have equal effectiveness in alleviating
symptoms, and the decision on which one to use is influenced by
cost, compliance, and side effect profiles.[2] Among the agents
studied however, GnRH agonists have been found to be more
effective in controlling recurrences of CP, particularly when used
for prolonged periods of as long as 1 year.[34–36]
Nevertheless, in the largest series of TES, which included 110
patients, medical treatment was far less effective than surgical
treatment, with recurrence rates exceeding 50% regardless of the
agent used. Specifically, recurrence rates at 6 and 12 months were
50% and 60% for medicaland5%and25%for surgical treatment,
respectively.[3] Thisis anticipated because at best, current agents
can suppress endometriotic implant growth and activity only as
long as they are being used.
Medical treatment often serves merely as a diagnostic tool. A
positive response to medical treatment in women with suspected
TES may be considered diagnostic, and surgical treatment may
be sought.[31]
Surgical Treatment
Thoracentesis and chest tube placement are obviously first-step
therapeutic interventions in the emergency room until further
action is taken.
VATSis currently the gold standard forthe surgical treatment
of TES, especially CP. Laparoscopy aids in the surgical treatment
of implants on the abdominal aspect of the diaphragm.
When endometriotic implants are the sole findings during
VATS and are in the range of a few millimeters, they can be carefully fulgurated using bipolar diathermy or CO
laser, regardless
2
of their location (i.e., parietal, visceral, or diaphragmatic pleura)
(Figures 10.2.1 and 10.2.2). Larger endometriotic implants of
the visceral pleura may be excised using sharp dissection.[5]
Nonetheless,biglesionsordeepparenchymal endometriotic nodules are best treated with parenchymal-sparing procedures, such
as wedge resection [14] or subsegmentectomy [37], via a minithoracotomy. Occasionally, lobectomy may be required.[38]
Diaphragmatic lesions (endometriotic implants or perforations) are probably best treated by resection using endoscopic
stapler devices, provided that the resected surface is relatively
small.[14,20] Larger diaphragmatic perforations can be sutured,
Figure 10.2.1. Endometriotic deposits in parietal and visceral pleura.
even though significant recurrences have been reported with the
use of sutures.[39] The useofmeshtoreplacelargediaphragmatic
excisions has been described in three women who at 45 months’
follow-up suffered no recurrences [21], although other authors
have not confirmed these results.[40]
Another important therapeutic intervention is pleurodesis
(mechanical, chemical, pleurectomy, or talcum). It can be performed alone or in conjunction with implant and/or perforation excision. In a literature review of 79 VATS-treated patients,
28 underwent pleurodesis alone, with a median recurrence-free
interval of 61 months (10 days to 264 months).[13] Pleurodesis,
especially in younger patients, should always be carried out concomitantly with VATS exploration. This way,an accurate diagnosis and treatment can be instituted and recurrences avoided. The
pleural cavity and the diaphragm should be carefully explored.
Otherwise, endometriotic implants or perforations may be overlooked.
If the abdominal aspect of the diaphragm is involved by
endometriotic implants, an experienced team of gynecologic
and thoracic surgeons can fulgurate or excise small lesions.
Hydrodissection, laser fulguration, or excision can be carried out
successfully.[29] However, if larger implants or defects are
present, they should be approached via VATS, as the liver bulk
Figure 10.2.2. Endometriotic implants in parietal pleura.

Thoracic Endometriosis — 261
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and limited subdiaphragmatic space may not allow complete
resection.[28]
There is limited information in the literature regarding surgical treatmentof CHtand CH. Pleurectomyfor CHt has been successfully reported intwocases.[6,41] A singlecase of CH, successfully treated with bronchoscopy-directed Nd:YAG laser destruction of an endobronchial implant, has also been reported.[42]
Finally, hysterectomy and BSO is the treatment of last resort
when other options have failed. Nonetheless, TES may recur if
the intrathoracic disease has not been properly addressed and
hormone replacement treatment is initiated.[3]
Combined Treatment
Based on the suboptimal recurrence rates following either medical or surgical treatment, some investigatorsprefer surgical treatment followed by hormonal suppression in the postoperative
period.[14,20,33,43]
CONCLUSION
TES is a challenging clinical entity. A high index of clinical suspicion is of paramount importance as both diagnosis and treatment may often be delayed for years. Endometriosis has variable and often subtle clinical and macroscopic features that can
be best appreciated by experienced gynecologic endoscopic surgeons. Hence, a multidisciplinary approach from a thoracic and
gynecologic surgical team carries the highest chance of making
an accurate diagnosis and providing the appropriate treatment
strategies.
REFERENCES
1. Olive DL, Schwartz LB. Endometriosis. N Engl J Med.
1993;328:1759–1769.
2. Hilaris GE, Nezhat CR. Endometriosis and pelvic pain. In: Wetter
PA, Kavic MS, Levinson CJ, Kelley WE Jr, McDougall EM, Nezhat
C, eds. Prevention and Management of Laparoendoscopic Surgical
Complications. Miami:The Society of LaparoendoscopicSurgeons;
2005.
3. Joseph J, Sahn SA. Thoracic endometriosis syndrome: new observations from an analysis of 110 cases. AmJ Med.1996;100:164–170.
4. Barnes J.Endometriosisofthepleuraandovaries.JObstetGynaecol
Br Emp. 1953;60:823.
5. Hilaris GE, Payne CK, Cannon W, Osias J, Nezhat CR.
Synchronous rectovaginal, urinary bladder and pulmonary
endometriosis. JSLS. 2005;9:78–82.
6. Ziedalski TM, Sankaranarayanan V, Chitkara RK. Thoracic
endometriosis: a case report and literature review. J Thorac Car-
diovasc Surg. 2004;127:1513–1514.
7. Poyraz AS, Kilic D, Hatipoglu A, Demirhan BA.A very rare entity:
catamenial pneumothorax.Asian Cardiovasc Thorac Ann.2005;13:
271–273.
8. Peikert T, Gillespie DJ, Cassivi SD. Catamenial pneumothorax.
Mayo Clin Proc. 2005;80:677–680.
9. Yoshioka H, Fukui T, Mori S, Usami N, Nagasaka T, Yokoi K.
Catamenial pneumothorax in a pregnant patient. Jpn J Thorac
Cardiovasc Surg. 2005;53:280–282.
10. Devue K, Coenye K, Verhaeghe W. A case of catamenial pneumothorax caused by thoracic endometriosis. Eur J Emerg Med.
2005;12:92–94.
11. Hiraoka N, Odama S, Unoura K, et al. Five cases of female pneumothorax with endometriosis on the blebs [in Japanese]. Nihon
Kokyuki Gakkai Zasshi. 2005;43:53–58.
12. Marshall MB, Ahmed Z, Kucharczuk JC, Kaiser LR, Shrager JB.
Catamenial pneumothorax: optimal hormonal and surgical management. Eur J Cardiothorac Surg. 2005;27:662–666.
13. Korom S, Canyurt H, Missbach A, etal.Catamenialpneumothorax
revisited: clinical approach and systematic review of the literature.
J Thorac Cardiovasc Surg. 2004;128:502–508.
14. Alifano M, Roth TH, Camilleri Broet S, Schussler O, Magdeleinat
P, Regnard JF. Catamenial pneumothorax. A prospective study.
Chest. 2003;124:1004–1008.
15. Alifano M, Trisolini R, Cancellieri A, Regnard JF. Thoracic endometriosis: current knowledge. Ann Thorac Surg . 2006;81:
761–769.
16. Jubanyik KJ, Comite F. Extrapelvic endometriosis. Obstet Gynecol
Clin North Am. 1997;24:411–440.
17. Nezhat CR, Berger GS, Nezhat F, Buttram VC Jr., Nezhat CH, eds.
Endometriosis: Advanced Management and Surgical Techniques.
New York: Springer-Verlag.
18. Kovaric JL, Toll GD. Thoracic endometriosis with recurrent spontaneous pneumothorax. JAMA. 1966;196:595.
19. Kirschner PA. Porousdiaphragmsyndromes.ChestSurgClinNorth
Am. 1998;8:449–472.
20. Alifano M, Cancellieri A, Fornelli A, Trisolini R, Boaron M.
Endometriosis-related pneumothorax: clinico-pathologicalobservations from a newly diagnosed case. J Thorac Cardiovasc Surg.
2004;127:1219–1221.
21. Bagan P, Le Pimpec Barthes F, Assouad J, Souilamas R, Riquet M.
Catamenial pneumothorax: retrospective study of surgical treatment. Ann Thorac Surg. 2003;75:378–381.
22. Yamazaki S, Ogawa J, Koide S, Shohzu A, Osamura Y. Catamenial
pneumothorax associated with endometriosis of the diaphragm.
Chest. 1980;77:107–109.
23. Brown RC. A unique case of catamenial pneumothorax. Chest .
1989;95:1368.
24. Laws HL, Fox LS, Younger B. Bilateral catamenial pneumothorax.
Arch Surg. 1977;112:627–628.
25. Wilhelm JL, Scommegna A. Catamenial pneumothorax: bilateral occurrence while on suppressive therapy. Obstet Gynecol.
1977;50:227–231.
26. Joseph J, Reed CE, Sahn SA. Thoracic endometriosis recurrence
following hysterectomywith bilateral salpingo-oophorectomy and
successful treatment with talc pleurodesis. Chest . 1994:106:1894–
1896.
27. Cassina PC, Hauser M, Kacl G, Imthurn B, Schroder S, Weder
W. Catamenial hemoptysis. Diagnosis with MRI. Chest. 1997;111:
1447–1450.
28. Redwine DB. Diaphragmatic endometriosis: diagnosis, surgical
management, and long-term results of treatment. Fertil Steril.
2002;77:288–296.
29. Nezhat C, Seidman DS, Nezhat F, Nezhat C. Laparoscopic surgical management of diaphragmatic endometriosis. Fertil Steril.
1998;69:1048–1055.
30. Kuo PH, Wang HC, Liaw YS, Kuo SH. Bronchoscopic and
angiographic findings in tracheobronchial endometriosis.Thorax.
1996;51:1060–1061.
31. Hope-Gill B, Prathibha BV. Catamenial haemoptysis and
clomiphene citrate therapy. Thorax. 2003;58:89–90.
32. Cowl CT, Dunn WF, Dechamp C. Visualization of diaphragmatic
fenestration associated with catamenial pneumothorax. Ann Tho-
rac Surg. 1999;68:1413–1414.
33. Alifano M, Venissac N, Mouroux J. Recurrent pneumothorax associated with thoracic endometriosis. Surg Endosc. 2000;
14:680.

262 — Georgios E. Hilaris and Camran Nezhat
https://t.me/med1917
34. Tripp HF, Thomas LP, Obney JA. Current therapy of catamenial
pneumothorax. Heart Surg Forum. 1998;1:146–149.
35. Tripp HF, Obney JA. Consideration of anatomic defects in the
etiology of catamenial pneumothorax. J Thorac Cardiovasc Surg .
1999;117:632–633.
36. Slabbynck H, Laureys M, Impens N, De Vroey P, Schandevyl W.
Recurring catamenial pneumothorax treated with a Gn-RH analogue. Chest. 1991;100:851–851.
37. Terada Y, Chen F, Shoji T, Itoh H, Wada H, Hitomi S. A case
of endobronchial endometriosis treated by subsegmentectomy.
Chest. 1999;115:1475–1478.
38. Kristianen K, Fjeld NB. Pulmonary endometriosis causing
haemoptysis. Report of a case treated with lobectomy. Scand J
Thorac Cardiovasc Surg. 1993;27:113–115.
39. Fonseca P. Catamenial pneumothorax: a multifactorial etiology. J
Thorac Cardiovasc Surg. 1998;116:872–873.
40. Sakamoto K, Ohmori T, Takei H. Catamenial pneumothorax
caused by endometriosis in the visceral pleura. Ann Thorac Surg.
2003;76:290–291.
41. Byanyima RK. Menstruation in an unusual place: a case of thoracic endometriosis in Kampala, Uganda. Afr Health Sci. 2001;1:
97–98.
42. Puma F,CarloniA, CasucciG,PulighedduC,Urbani M, Porcaro G.
Successful endoscopic Nd-YAG laser treatment of endobronchial
endometriosis. Chest. 2003;124:1168–1170.
43. Blanco S, Hernando F, Gomez A, Gonzalez MJ, Torres AJ, Balibrea JL. Catamenial pneumothorax caused by diaphragmatic
endometriosis. J Thorac Cardiovasc Surg. 1998;116:179–180.

Section 10.3. Laparoscopic Treatment of Endometriosis
https://t.me/med1917
Bulent Berker, Thomas H. S. Hsu, Keith L. Lee, Ceana Nezhat, Farr Nezhat,
and Camran Nezhat
Endometriosis is a common gynecologic condition found in
women of reproductive age. The condition is associated with
chronic pelvic pain and infertility, which may result in reduced
quality of life, psychologic morbidity, and work absenteeism. It is
characterized by the presence of uterine endometrial tissue outside the normal location – mainly on the pelvic peritoneum, but
also on the ovaries and in the rectovaginal septum, and more
rarely in the pericardium, pleura, and even the brain.[1,2] The
prevalence of pelvic endometriosis approaches 6% to 10% in the
general female population; in women with pain, infertility, or
both, the frequency is 35% to 50%.[3] The disorder is most commonly diagnosed in women of reproductive age, although time
to diagnosis may be very long because of variability in symptoms
and signs and confusion with other disorders. Among gynecologic disorders, endometriosis is surpassed in frequency only by
leiomyomas.[4]
The gold standard for diagnosis of pelvic disease is surgical
assessment by laparoscopy or laparotomy, and many scoring systems have been developed to assess extent of disease. The American Society for Reproductive Medicine revised classification system for endometriosis (ASRM 1996) is the most widely accepted
staging system.[5] Patients who have endometriosis present with
different clinical complaints at variousstagesof the disease. Treatment depends on age of the patient, extent of the disease, severity
of the symptoms, and desire for fertility. Intervention usually is
indicated for pain,infertility,or impaired functionof the bladder,
ureter, or intestine. Medical and surgical forms of management
are available.
HISTORICAL PERSPECTIVES
Rokitansky [6] described pelvic endometriosis of the fallopian
tubes, ovaries, and uterus in 1860. Before 1960, therapy often
required hysterectomy and bilateral salpingo-oophorectomy
(BSO).[7] Conservative operations to relieve pain and preserve
fertility have been modified significantly since the introduction
of suchtherapy. After recognition ofthe negative impactof surgical trauma and postoperative adhesions on success rates, microsurgical techniques were developed and applied with improved
results.[8] Nevertheless, recurrences were not eliminated.[9]
Recent advances in endoscopic surgical techniques and the
increased sophistication of surgical instruments have offered
new operative methods and techniques for the gynecologic
surgeon.[10] The addition of a small video camera to the laparoscope (videolaparoscopy) greatly enhanced the popularity of
operative endoscopy because of the possibility of operating in a
comfortable, upright position and using the magnification capabilities of the camera.[11,12] Nezhat et al. started performing
laparoscopic GI and GU surgeries in the mid- to late 1980.[13]
Currently, laparoscopy is perceived as a minimally invasive surgical technique that both provides a panoramic view of the pelvic
organs and allows surgery at the time of diagnosis. Both laparotomy and operative laparoscopy are effective for the treatment
of endometriosis in that they reduce the incidence of implants,
relieve dysmenorrhea and pelvic pain, and improve fertility
potential.[14–18] Unlike radical operations, conservative procedures frequently are not curative.[19,20]
CURRENT SURGICAL MANAGEMENT
OF ENDOMETRIOSIS
The optimum management of endometriosis remains as problematic as ever. Endometriosis may be either asymptomatic or
associated with minor symptoms and lesions that are sometimes
self-limiting. It may also be associated with very severe symptoms and major pathologic lesions involving the vital structures
of the pelvis. Different levels of symptomatology and pathology require different levels of therapeutic intervention.[21] The
extent of surgery is dependent on the preoperative symptoms
and the severity of disease. Most clinicians use the revised ASRM
scoring systemfor endometriosis, which comprises four groups –
minimal (stage I), mild (stageII), moderate (stageIII), and severe
(stage IV) – according to the operativefindings.[22] Patients with
minor disease mayinadvertentlybe subjected toexcessive investigations and invasive treatment, whereas those with major lesions
might be underinvestigated such that appropriate treatment is
delayed for years.
Since 1980, surgical instruments and techniques with varying degrees of efficacy have been introduced, including lasers,
video cameras, monitors, electric generators, hydrodissection,
microelectrodes, microsurgery, and operative laparoscopy.[23]
The introduction of laser technologies revolutionized the surgical field of medicine. The combination of the cutting and hemostatic properties of lasers was useful for many surgical interventions, including laparoscopy and hysteroscopy, to improve their
effectiveness and safety. However, application of surgical lasers
, argon, potassium titanyl phosphate [KTP], neodymium:
(CO
2
yttrium–aluminum–garnet [Nd:YAG]) is limited by relatively
high cost and the necessity for special training. There are definite advantages to using a high-powered CO
the Ultrapulse 5000 L [Coherent Instruments]) as a long knife
through the operative channel of the laparoscope. Because this
laser (especially
2
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264 — Bulent Berker, Thomas H. S. Hsu, Keith L. Lee, Ceana Nezhat, Farr Nezhat, and Camran Nezhat
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laser does not penetratewater, it can beusedwith hydrodissection
[23] to selectively treat sensitive areas in the bowel, bladder,
ureters, and blood vessels. Laparoscopic diagnosis and excision
of all forms of endometriosis are effective and may now be
considered the “gold standard” of clinical care for women with
endometriosis-related pain and infertility. Therecognizedadvantages of operative laparoscopy include faster patient recovery
and reduced cost.[24] Various treatment modalities are available for use at laparoscopic surgery. These include laser, scissors withmonopolar electrocautery and bipolar coagulation, and
harmonic scalpel, all of which allow resection and cauterization
and vaporization of endometriosis. In a recent prospective study,
laparoscopic excision of endometriosissignificantly reduced pain
and improved quality of life for up to 5 years.[25] Promising
results have been obtained with more radical surgery, including
extensive excision ofdeep disease and also removal ofportions of
bowel and bladder containing significant endometriosis. There
may be a continuing role for hysterectomy in the management of
endometriosis, but the evidence for concomitant oophorectomy
is less convincing. In addition, as gynecologists become more
proficient, pregnancy rates after operative laparoscopy should
improve and surpass the results after laparotomy.
Laparoscopy versus Laparotomy
It is difficult to imagine any aspect of care for a gynecologic patient
today – examination, surgical correction, monitoring of treatment efficacy – without endoscopy. The endoscopic approach is
of vital importance for the differential diagnosis of gynecologic
diseases, especially in unclear clinical situations in which other
methods fail to reveal either the true diagnosis or extent of the
pathology – for example, pelvic pain, adhesions, infertility, and
endometriosis.[26] Indeed, it has been suggested that endoscopy
be the approachofchoice to all gynecologic conditions because of
its acknowledged advantages, including minimal trauma, superb
visualization, low incidence of complications, reduction of adhesion formation, and favorable postoperative course along with
rapid recovery and cosmetic effect.[27,28]
The results of endoscopy and laparotomy are judged by
many factors.[29] Three studies compared postoperative adhesion formation and re-formation after a standardized laser
injury and laser adhesiolysis by both surgical approaches.[30–
32] Laparoscopy caused fewer postoperative adhesions compared
with laparotomy.Aftermicrosurgicalsalpingoplastyoradhesiolysis by laparotomy, adhesionrecurrence rates were40%to72%and
new adhesions occurred in more than 50% of patients.[33–37]
However, when comparable operations are carried out laparoscopically, recurrence of postoperative adhesions appears to be
less common [38] and new adhesions were either absent or less
than 20%.[39] Lundorff and colleagues[36] evaluated the formation of adhesions after laparoscopy and laparotomy in patients
treated for tubal pregnancy. Those authors stratified 105 women
with tubal pregnancy by age and risk factors and prospectively
randomized them to treatment by laparoscopy or laparotomy.
Second-look laparoscopy revealed more adhesions in the laparotomy group.[36]
Data from animal [30–32] and clinical studies [33–37] suggest that laparoscopic operations are more effective for adhesiolysis, cause fewer new adhesions than does laparotomy, and
reduce impairment of tubo-ovarian function.[36] The efficacy of
laparotomy or laparoscopy has not been evaluated for restoring
fertility or reducing pelvic pain. However, it has been reported
that pain relief and pregnancy rates after operative laparoscopy
are comparable to or better than those after laparotomy [9,13–
17,24,29,36,40–42] for endometriosis (mild to severe), hydrosalpinges, and ectopic pregnancy.
Gomel [43]described the therapeuticefficacy of laparoscopic
adhesiolysis in 1975. In a follow-up publication, he stated that
“in trained hands, laparoscopic salpingo-ovariolysis is a lowrisk procedure associated with a surprisingly good success rate.”
In his series of 92 patients with moderate to severe adnexal
adhesive disease, the intrauterine pregnancy rate was 62.5%.[44]
Subsequent studies confirmed that the results of laparoscopy
were better than those obtained by laparotomy, especially in
the case of severe endometriosis.[16,17,29,40–43] Even extensive endometriosis can be treated more effectively at laparoscopy
and with better results than at laparotomy.[14,15]
Fayez and Collazo [41] noted pregnancy rates of 58% after
laparoscopy and 36% after laparotomy. Chong and colleagues
[45] assessed the relative efficacy of CO
laser surgery by
2
laparoscopy and laparotomy in treating infertile patients with
severeendometriosis; the mean revised American Fertility Society
(rAFS) scores were 59 (laparoscopy) and 58 (laparotomy), with
similar pregnancy rates. In two studies, CO
laser laparoscopy
2
was compared with laparotomy as a treatment for all stages
of endometriosis associated with infertility.[16,17] Operative
laparoscopy was found to be safe and effective for all stages of
endometriosis. The endoscopic approach should be considered
only if the results with laparoscopy are equal to or better than
those with laparotomy.[14,23,45] The reduced hospital cost and
recovery period obtained with the laparoscopic approach cannot
compensate for failure to achieve the optimal treatment.
The outcome of laparoscopy was compared with that
of laparotomy in conservative surgical treatment for severe
endometriosis.[46] A nonrandomized group of 216 patients
underwent conservative surgical treatment for severe endometriosis by either laparoscopy (n = 67) or laparotomy (n = 149).
The results from laparoscopy and laparotomy were equal for the
treatment of infertility and chronic pelvic pain associated with
severe endometriosis. However, a trend toward a higher pregnancy rate and less dyspareunia was observed after operations
done for severe endometriosis by laparotomy compared with
laparoscopy.
Laser laparoscopywas comparedwith traditional laparoscopy
or laparotomy in thetreatment of 309infertile womenwith moderate or severe endometriosis.[47] These patients were treated
with one of four options: operative laparoscopy with the CO
laser vaporization or resection, operative laparoscopy with electrocoagulation and sharp dissection, laparotomy with electrocoagulation and sharp dissection, and medical treatment with
danazol. Pregnancy rates in the laparoscopy group were equal to
or higher than those in the laparotomy group for both the entire
population and the endometriosis-only subset. When the CO
laser was used as an adjuvant option, the rates were better, especially in patients with advanced disease and with endometriosis
as the only infertility factor.
Operative laparoscopy is as efficacious in the treatment of
recurrent endometriosis as it is in the treatment of the primary disease, and simplifies management of the disease for
the clinician. It is currently believed that infertile women with
2
2

Laparoscopic Treatment of Endometriosis — 265
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recurrent endometriosis should be included in assisted reproduction programs. However, the poor results of these techniques
and their cost make operative laparoscopy the treatment of
choice in such women. Likewise, operative laparoscopy seems
to offer notable advantages with respect to repeated courses of
medical therapy, which are necessary for patients with pelvic
pain associated with recurrent endometriosis. Busacca and colleagues [48] compared two consecutive surgical series for the
cure of endometriosis. The patients were 81 women with recurrent endometriosis, 41 reoperatedon at laparotomyfrom 1986 to
1991 and40 reoperated onat laparoscopy from 1992to 1996. The
cumulative probability of recurrence of dysmenorrhea (34 and
43, respectively), and the frequency of recurrence of pelvic pain
and dyspareunia and of clinical findings suggestive of the disease
were not significantly different in the two groups. The rate of
recurrence of dyspareunia was higher in the patients operated
on at laparotomy as was the number requiring a third operation. However, this could be the result of the longer follow-up of
this group. No significant difference was observed between the
cumulative pregnancy ratesat 24 monthsin the two groups(45 in
the laparotomy and 54 in the laparoscopy group). The investigators concluded that operative laparoscopy seems as efficacious as
conservative surgery at laparotomy in the treatment of recurrent
endometriosis.
Conservative Operations
The goals of conservative operative procedures are to remove
all implants, resect adhesions, relieve pain, reduce the risk of
recurrence and postoperative adhesions, and restore the involved
organs toanormalanatomicandphysiologiccondition.Forinfertile patients, restoration of the normal tubo-ovarian relationship
is essential to enhance fertility. These goals may be achieved by
using various surgical instruments (scalpel, scissors, lasers, or
electrodes) and a variety of techniques (laparoscopy, laparotomy,
combined endoscopy and minilaparotomy).
The usefulness of conservative surgery for pain relief is
unclear, but it appears that immediate postoperative efficacy is at
least as high as with medical treatment, and long-term outcomes
may be considerably higher.[49] Women who desire pregnancy
and whose disease is responsible for their symptoms of pain or
infertility should have conservative operations. Although seldom
curative, such procedures improve the likelihood of pregnancy
and offer at least temporary pain relief. Approximately 25% of
patients undergoingconservative operations will require a subsequent operation because of recurrence of endometriosis or progression of residual (microscopic) disease.[50] The rate of repeat
interventions is related directly to the extent of disease and the
ability to conceive postoperatively. Among those who achieve
pregnancy after the initial operation, only 10% require another
operation.[50,51] Conservative methods are cytoreductive, and
recurrence of symptoms most likely is caused by the progression
of existing microscopic disease thatwasnot seen during theinitial
operation.[52–54]
Controversyremainsregarding the benefit of surgical ablation
of minimal-to-mildendometriosis at the time of laparoscopy.An
extensive meta-analysis of published studies showed that either
no treatment or surgery is superior to medical treatment for
the management of minimal and mild endometriosis associated with infertility.[55] A randomized,controlledCanadian trial
studied 341 infertile women to ascertain whether laparoscopic
operations enhanced fecundity in infertile women with minimal or mild endometriosis.[56] The women were assigned randomly during diagnostic laparoscopy to undergo either resection
or ablation of visible endometriosis or diagnostic laparoscopy
only. Among the 172 women who had resection or ablation
of endometriosis, 29% became pregnant 36 weeks after the
laparoscopy and had pregnancies that continued for 20 weeks
or longer, compared with 17.2% of the 169 women in the diagnostic laparoscopy group. Laparoscopic resection or ablation of
minimal and mild endometriosis significantly improved fecundity in infertilewomen.Another randomized trial oflaparoscopic
ablation versus no treatment in 101 infertile women with minimal or mild disease demonstrated similar cumulative pregnancy
rates during the first postoperative year (19.6% vs. 22.2%).[57]
Another prospective study assessed the efficacy of CO
2
laser
laparoscopyin treating 176infertile women with minimalto mild
endometriosis according to the ASRM classification in terms of
pregnancy rates.[58] The patients were treated with one of four
methods: 49 underwent operative laparoscopy with newly developed CO
laser vaporization or resection, 45 were treated by oper-
2
ative laparoscopy with simple monopolar electrocoagulation, 43
who had undergone only diagnostic laparoscopy did not receive
any treatment, and 39 received danazol 800 mg/day for 3 months
after diagnostic laparoscopy. Advanced laparoscopic operations
with a laser were more efficient than were other modalities in
treating infertile women with minimal to mild endometriosis in
terms of pregnancy rates. Tulandi and al-Took [59] found no difference in the pregnancy rates of 101 infertile women with mild
endometriosis treated laparoscopically either by excision or by
electrocoagulation. The role of resection or ablation of moderate to severe disease is clear. Both fecundity and relief of pelvic
pain are improved with surgery in patients with advanced-stage
disease as compared with medical therapy or observation. One
report suggested that fertility may be particularly improved with
ablative procedures in patients with deep infiltrating endometriotic lesions.[60]
Radical Operations
Radical ablative surgery for endometriosis is indicated chiefly
for symptoms of pain that fail to respond to conservative treatment. The sites of involvement must be carefully assessed and
surgery planned taking account of the wishes of the patient concerning her fertility. Procedures include oophorectomy, salpingooophorectomy, hysterectomy, appendicectomy, and the excision
of deeply infiltrating endometriosis possibly involving bowel
resection. The most important arbiteroftherapeuticsuccessisthe
removal of the ovaries, hysterectomy and BSO offering the ultimate cure for this chronic condition.[61] Hysterectomy and BSO
are indicated for patients with severe symptoms who have not
responded to medical or conservative surgical treatment and are
not interested in pregnancy. Fibrosis obliterates tissue planes and
sometimes causes a suspicion of malignancy because of extensive involvement of the intestinal and urinary tracts. In advanced
disease, the ovaries may be encased and densely adherent to the
pelvic side wall. Ovarian dissection entails the risk of injury to
the ureter, major blood vessels, and bowel. A retroperitoneal
approach can isolate the ureter throughout its course to ensure
complete removal of ovarian tissue and prevent ovarian remnant

266 — Bulent Berker, Thomas H. S. Hsu, Keith L. Lee, Ceana Nezhat, Farr Nezhat, and Camran Nezhat
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syndrome.[62] Bilateral oophorectomy is done for the purpose
of the elimination of the estrogenthat sustainsand stimulates the
ectopic endometrium.[63] Although conserving one ovary has
resulted in reasonable cure rates [19,64,65], failure rates of 13%
and 40% at 3 and 5 years, respectively, have been reported after
laparotomy when ovarian function is preserved.[66]
Definitive surgery, which includes hysterectomy and BSO, is
reserved for use in women with intractable pain who no longer
desire pregnancy. In less severe cases, one ovary may be retained
to preserve ovarian function, although improvement will be less
definitive. The decision to perform bilateral oophorectomy at
the time of surgery for endometriosis is dependent upon many
factors, one of which is the opinion of the surgeon concerned.
A postal survey performed in Australia revealed a conservative
approach, with only 27.5% of surgeons electing to perform a
hysterectomy in conjunction with bilateral oophorectomy.[67]
Namnoum and colleagues [68] had determined the risk of reoperation and/or recurrence of symptoms after hysterectomy for
the treatment of endometriosis. Among 138 women, 39 had a
hysterectomy with ovarian preservation and 109 had all ovarian
tissue removed. Of those whose ovaries were preserved, 62% had
recurrent pain and 31% required intervention. The authors concluded that the women with ovarian preservation had six times
the risk of developingrecurrent pain and an eightfold greater risk
of reoperation. At present, there is no consensus on this subject.
Oophorectomy should be considered only once it is clear that the
ovaries are acauseof the pelvic pain.To determine this,it is sometimes helpful to administer a 2-month course of gonadotropinreleasing hormone (GnRH) agonists to induce amenorrhea and
a short-term cessation of ovarian function. Preoperative and
postoperative medical therapy has a limited role in surgery,
whereas women who have undergone oophorectomy should be
treated with estrogen replacement, even at the risk of some
recurrence.
HORMONE REPLACEMENT
Oophorectomy with or without hysterectomy is still a frequently
chosen therapeutic option in women with extensive, infiltrating, or recurrent pelvic endometriosis who do not want children. In such patients, foci of endometriosis are often left in
deep pelvic sites or on other organs, such as the bowel, ureters,
and bladder. In fact, the difficulty of eradicating these lesions
completely is the main reason for performing definitive surgery.
Moreover, the women concernedare generally still far fromphysiologic menopause and therefore require hormone replacement
therapy (HRT) for many years. In such cases, gynecologists often
have reservations about instituting standard HRT because of the
fear that the estrogens may induce a recurrence of the disease
and its symptoms.[69] Although HRT involves some risks, after
hysterectomy and BSO, patients often require HRT to relieve
menopausal symptoms.Administeringtheminimaleffectivedose
of estrogen is associated with only a small risk of recurrence.[66]
The hormonal dependence of endometriosis is evident, as the
disease is rarely found before menarche, after menopause, or
during pregnancy, and it regresses during medical treatments
that induce hypoestrogenemia. Endometriosis after menopause
is rare, althoughthe influence of HRT in the pathogenesis ofpostmenopausal growth of endometriosis is still unclear. In the last
20 years, the recurrence of endometriosis in menopausal women
has increased because of the use of HRT.[70] Several investigators advise against the use of HRT in patients with a history of
endometriosis, a contraindication based on retrospective uncontrolled studies as well as theoretic and experimental considerations. No prospective controlled studies have been performed.
Indeed, the majority of retrospective studies have employed types
of HRT that are not presently in general use.
However, there is evidence that estrogen might stimulate the
growth ofendometriosis duringmenopause.[71,72] Studies concerning HRT after BSO or after total hysterectomy and BSO for
endometriosis are scant. Most of them are retrospective, and
the follow-up evaluations and diagnosis lack standardization.
Most of them employ therapeutic regimes that are no longer
used. The only randomized prospective study concerning HRT
in endometriosis involved21womenstudiedover12months,and
the results suggested that tibolone may be a safe HRT in women
with residual endometriosis.[69]
To estimatetherisk of recurrence after administration ofHRT
in women who had endometriosis and who underwent BSO,
Matorras et al. [73] conducted a prospective randomized trial.
To circumvent the theoretical risk of malignancy, the HRT they
used consisted of sequentialadministration of bothestrogensand
progesterone, even in patients without a uterus. Of the women
with a histologic diagnosis of endometriosis in whom BSO was
performed, 91.8% had a total hysterectomy.Theauthorsobserved
a trend of a higher recurrencerate among patients receiving HRT
versus controls. There was no recurrenceamong women who did
not receive HRT, versus a 3.5% rate (four out of 115), or 0.9%
per year, in women who received HRT. Among women receiving
HRT, the followingrisk factorswere detected: peritoneal involvement of 3 cm or greater (2.4% vs. 0.3% recurrence per year)
and incomplete surgery (22.2% vs. 1.9% per patient). In their
study, the Matorras group reported that patients with a history
of endometriosis in whom total hysterectomy and BSO were performed hadalow risk ofrecurrencewhen HRT was administered.
In patients such as these, HRT is a reasonable option. However,
in caseswith peritonealinvolvement of 3 cm or greater, therecurrence rate makesHRTa controversial option. IfHRTis indicated,
it should be monitored closely.
The recurrence rate with HRT in women who have had
total hysterectomy and BSO is very low (0.5% per year); thus,
HRT should not be contraindicated. Even so, these patients
should be informed of and accept this recurrence rate. When
a total hysterectomy has not been performed because of technical difficulties, the recurrence risk contraindicates the use of
HRT. The beneficial effects of HRT do not compensate for the
high recurrence rate of endometriosis. In cases with severe peritoneal involvement, although HRT is not totally contraindicated,
the rate of recurrence is relatively high (9.1% per patient). If
HRT is indicated, patients should be monitored closely, especially with vaginal ultrasound. If there is any suspicion of recurrence, HRT should be stopped.[73] The theoretic risks related
to HRT in women with endometriosis are not limited to the
possibility of disease recurrence. Although the likelihood may
be only slight, there are reports of malignant change many
years after surgery in women receiving HRT.[61] Extragonadal
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