**12. Laparoscopic findings**

Laparoscopy is the gold standard for the diagnosis and staging of endometriosis and allows for curative surgical resection at the same time. Patients found to have endometriosis at the time of laparoscopy should either be treated through surgical ablation, resection, or laser treatment. In addition, biopsy is recommended, as lesions of endometriosis in adolescents often take on a different appearance as compared with the typical powder-burn lesions seen in adults. Interestingly, clear or red endometriotic lesions are much more commonly seen in the adolescent population (76).

Endometriosis 15

advantages for control of pelvic pain associated with endometriosis, including effective contraception, minimal systemic effects, and up to 5 years of benefit, as compared with 6

Dienogest (DNG), a progestin of 19‑nortestosterone derivative, has good oral bioavailability and is highly selective for progesterone receptors. Owing to its antiovulatory, antiproliferative activities in endometrial cells, and its inhibitory effects on the secretion of cytokines, DNG is expected to be an effective treatment for endometriosis. Progesterone

• DNG has moderate affinity to the progesterone receptor. DNG shows low binding to the androgen receptor and almost negligible binding to the estrogen receptor,

• An oral DNG dose of 1 mg/day is required for inhibition of ovulation in cyclic women. • DNG has an inhibitory effect on growth and cytokine production of endometriotic cells. • DNG is as effective as triptorelin (gonadotropin-releasing hormone agonist) for

• DNG is as effective as intranasal buserelin acetate for the relief of pain symptoms

Treatment with a GnRH-a followed by long-term dienogest therapy maintains the relief of endometriosis-associated pelvic pain achieved with GnRH-a therapy for at least 12months. This regimen reduces the amount of irregular uterine bleeding that often occurs during the

Complex mechanisms involving promoter regulation may be responsible for the observed aberrations in (Estradiol Receptor a, b) ERa, ERb, and PR (progesterone Receptor) expression in endometriosis. The stromal cell component of endometriotic tissue may be the primary site of these abnormalities. In endometriotic stromal cells, ERb promoter is pathologically hypomethylated and therefore hyperactive, leading to very high ERb levels. ERb suppresses ERa expression and results in strikingly high ERb-to-ERa ratios in

It is possible that this consequence of PR-B deficiency is only the tip of the iceberg with regard to pathogenesis of endometriosis, and that numerous other molecular aberrations may also contribute to the development of resistance to hormone treatments in women with endometriosis. Selective ERb ligands that target high levels of ERb in endometriotic tissue may be clinically beneficial via disrupting this mechanism.(84) PR deficiency is likely responsible for increased levels of E2 in endometriosis because progesterone fails to induce the E2-metabolizing enzyme HSD17B2 in endometriotic tissue. Some conclusion resonates with gene expression microarray studies performed on eutopic endometrium of women with endometriosis compared with that from disease-free women.(85, 86) These studies on eutopic endometrium identified distinct molecular defects that are consistent with the

ER b agonists act as immunomodulators, enhancing the immunologic response to the explants; a second possible explanation lies an antiangiogenic effect because ER b are

receptor-binding affinity is higher for DNG than for progesterone.

glucocorticoid receptor and mineralcorticoid receptor.

• DNG has strong oral progestational activity but antiandrogenic activity.

consolidation therapy after surgery for the treatment of endometriosis.

months, typical of GnRHa treatment.

associated with endometriosis.(82)

early phase of dienogest therapy.(83)

progesterone resistance hypothesis.

endometriotic cells.
