This toxic fluid content can cause dire alterations to the normal surrounding endometriotic cells, potentially impacting the embryo, the ability of an embryo to implant successfully, and the responsiveness of the endometrium. Endometrioma can potentially lead to premature ovarian failure, decreased ovarian function, or problems with ovulation. Studies have also found that endometriomas occur two times more frequently in the left ovary (67%) than in the right one (33%), possibly due to the presence of the sigmoid colon on the left side. Risks
Endometriomas can increase the risk of ovarian cancer in reproductive women, decrease normal ovarian function, and cause pain in the pelvis during or after periods or during sexual intercourse. Although most endometriomas are found to be benign, the possibility of malignant tumors still exists, and surgery is needed to confirm malignancy and determine what future treatment must be administered. Another factor that endometrioma can impact is the ovarian reserve, or the number of quality follicles left in the ovary to produce viable eggs. Ovaries with endometriomas showed significantly less follicular density as compared to healthy ovaries, leading to a decrease in fertility. Treatment
Medication
Nonsteroidal anti-inflammatory drugs (NSAIDs) are frequently used first in patients with pelvic pain, particularly if the diagnosis of endometriosis has not been definitively (excision and biopsy) established. The goal of directed medical treatment is to achieve an anovulatory state. Typically, this is achieved initially using hormonal contraception. This can also be accomplished with progestational agents (i.e., medroxyprogesterone acetate), danazol, gestrinone, or gonadotropin-releasing hormone agonists (GnRH), as well as other less well-known agents.
Thus, each male offspring has a 50% chance of being affected by XLI, while each female offspring has a 50% chance of being a carrier for this condition. Any individual that inherits the mothers normal copy of the STS gene will be unaffected and will have an extremely low chance of having a child affected with this condition.Due to random segregation of the chromosomes during gametogenesis, each pregnancy will be subject to the same probabilities, regardless of the number of previously affected or unaffected offspring. The above recurrence risks are based on the assumption that an affected male or carrier female will have children with an unaffected or non-carrier individual. The risks of having affected offspring would clearly increase in the case of a union between a male with XLI and a carrier female. Physiology/biochemistry
The STS enzyme (EC 3.1.6.2), also referred to as Arylsulfatase C, is expressed throughout the body, with highest expression in the skin, liver, lymph nodes, and placenta, and lower expression in breast tissue and brain  STS catalyzes the hydrolysis of sulfated steroids, such as estrone sulfate and dehydroepiandrosterone sulfate (DHEAS), to non-sulfated steroids estradiol and androstenediol, respectively. Prenatally, the enzyme is involved in placental estrogen production. The enzyme is also involved in adrenal steroid production as well as conversion of sulfated steroids in other tissues.There seems to be a particularly important role for the enzyme in skin. Deficiency of the enzyme leads to the characteristic dry and scaly skin seen in ichthyosis.