Endometriosis is a chronic, estrogen-dependent, inflammatory disease in which endometrial-like glands and stroma implant outside the uterine cavity, most often on the ovaries, uterosacral ligaments, pelvic peritoneum, and, less commonly, the bladder, bowel, diaphragm, or surgical scars. Repeated cyclic bleeding from these ectopic foci provokes fibrosis, adhesions, and neuronal sensitization that can produce severe pelvic pain and subfertility. It affects about 10 % of reproductive-aged individuals worldwide and can begin with menarche and persist until natural or surgical menopause.
Cyclic dysmenorrhea that progressively worsens, deep dyspareunia, chronic non-cyclic pelvic pain, dyschezia, dysuria, and infertility are hallmarks. Pain may radiate to the back or thighs and flare pre-menstrually. Gastrointestinal bloating, constipation, or cyclic rectal bleeding occur with bowel implants; catamenial pneumothorax manifests as shoulder-tip pain and dyspnea when thoracic lesions bleed. Some individuals remain asymptomatic, discovered only during infertility work-up or unrelated surgery.
A first-degree relative with endometriosis triples risk. Early menarche, short menstrual cycles (<27 days), heavy or prolonged menses, low parity, tall thin body habitus, Müllerian anomalies obstructing outflow, and neonatal exposure to diethylstilbestrol increase likelihood, whereas prolonged lactation, regular exercise, and higher parity are protective. Caucasian or Asian ancestry, high red-meat intake, alcohol consumption, and chronic pelvic infection may also contribute.
A presumptive clinical diagnosis is made when typical symptoms coexist with supportive imaging—transvaginal ultrasound detecting ovarian endometriomas or deep nodules, or MRI delineating deep infiltrating disease. Serum CA-125 lacks sensitivity and specificity. Definitive diagnosis requires laparoscopic visualization with histologic confirmation of endometrial glands and stroma, though current guidelines endorse empirical treatment without surgery if features are classic. Diagnostic delay averages seven to eight years, underscoring the need for vigilance.
Management targets pain relief, lesion suppression, and fertility preservation. First-line therapy for pain is continuous combined oral contraceptives or progestin-only agents (oral norethindrone acetate, depot medroxyprogesterone, or a 52 mg levonorgestrel IUD). Second-line options include GnRH agonists or antagonists with add-back therapy, or the oral selective progesterone-receptor modulator dienogest. Non-steroidal anti-inflammatory drugs provide adjunctive analgesia. For ovarian endometriomas ≥3 cm or deep infiltrating disease causing obstruction or intolerable pain, laparoscopic excision with fertility-sparing cystectomy is preferred, preserving ovarian reserve better than ablation. Recurrent pain after surgery is managed with long-term hormonal suppression or repeat surgery in specialized centers; definitive hysterectomy with bilateral salpingo-oophorectomy is reserved for refractory severe disease in those who have completed childbearing. Assisted reproductive technologies, particularly IVF, bypass tubal and peritoneal barriers and offer the highest pregnancy rates for endometriosis-associated infertility. Emerging therapies under study include oral GnRH antagonists with novel add-back regimens, anti-IL-1β monoclonal antibodies, and neuro-angiogenic pathway inhibitors.
Although endometriosis is benign, chronic pain can impair quality of life, and spontaneous pregnancy rates decline with increasing disease stage and age. Roughly 20 %–40 % of infertile women have endometriosis, yet postoperative IVF yields live-birth rates comparable to those of women without the disease when age and embryo quality are controlled. Recurrence of symptoms or lesions occurs in up to 50 % within five years after conservative surgery without ongoing medical suppression. Malignant transformation is rare—mainly clear-cell and endometrioid ovarian cancers arising from endometriomas—with a lifetime risk estimated at 1 %.
Chronic pelvic pain, dyspareunia, anovulatory infertility, ovarian endometriomas with torsion or rupture, dense pelvic adhesions leading to bowel or ureteric obstruction, hydronephrosis, decreased ovarian reserve after repeated surgery, heightened risk of clear-cell or endometrioid ovarian carcinoma, and significant psychosocial distress are recognized sequelae.
Primary prevention is limited, but regular exercise, maintaining a healthy BMI, and avoiding high-alcohol or red-meat diets may reduce incidence, while early use of continuous hormonal contraception after adolescence might delay progression in high-risk individuals. Post-operative recurrence prevention hinges on long-term hormonal suppression, ideally starting within six weeks after conservative surgery.
Daily aerobic exercise, pelvic-floor physiotherapy, and anti-inflammatory diets rich in omega-3 fatty acids and low in red meat can lessen pain flares. Heat therapy, mindfulness-based stress reduction, and cognitive-behavioral therapy help modulate central sensitization. Patients on GnRH analogs must take calcium/vitamin D and undergo periodic bone-density monitoring. Peer-support groups and counseling address psychosocial burdens such as anxiety, depression, and sexual dysfunction. Partners can assist by tracking medication schedules, accompanying to appointments, and fostering open communication regarding intimacy.