Adenomyosis: Symptoms, Causes & Treatment

Adenomyosis is defined by the presence of endometrial glands and stroma embedded within the uterine myometrium, with adjacent smooth muscle hyperplasia. Unlike endometriosis — where endometrial tissue implants outside the uterus — adenomyosis is confined within the uterine wall, causing it to enlarge (globular or asymmetric uterus on examination) and develop a tender, boggy consistency. The ectopic endometrial tissue undergoes the same cyclical proliferative and secretory changes driven by estrogen and progesterone, resulting in cyclic intralesional bleeding, fibrosis, and the characteristic symptoms of dysmenorrhea and heavy menstrual bleeding.

Adenomyosis predominantly affects reproductive-age women, historically described in multiparous women over 40, though modern MRI-based studies reveal significant prevalence in younger and nulliparous women. Prevalence estimates range from 20–35% in women of reproductive age, though many cases remain undiagnosed. It frequently coexists with endometriosis (in ~50% of cases), uterine fibroids, and other benign uterine conditions, complicating diagnosis and symptom attribution.

Pathophysiology involves disruption of the endometrial-myometrial junction — likely from prior uterine surgery, inflammation, or congenital factors — allowing endometrial cells to invade the myometrium. This invasion triggers a local inflammatory response, smooth muscle hyperplasia, and altered uterine contractility that contributes to dysmenorrhea, heavy bleeding, and impaired fertility. Estrogen dependence means symptoms typically regress after menopause.

• Severe progressive dysmenorrhea — often worsening with age; key distinguishing feature from primary dysmenorrhea
• Heavy menstrual bleeding (menorrhagia) with clots; risk of secondary iron-deficiency anemia
• Deep pelvic pain and dyspareunia (pain during intercourse)
• Uterine enlargement: diffuse globular enlargement or focal adenomyoma palpable on bimanual examination
• Intermenstrual or premenstrual spotting
• Subfertility or recurrent early pregnancy loss in some patients

• Disruption of the endometrial-myometrial junction allowing gland invasion — associated with uterine surgery (cesarean section, curettage, myomectomy)
• Chronic endometrial inflammation and altered immunological environment
• High cumulative estrogen exposure: early menarche, short cycles, nulliparity, obesity
• Genetic predisposition: family clustering suggests hereditary component
• Possible de novo differentiation of myometrial stem cells into endometrial-like cells

Diagnosis is clinical-radiological: symptoms + physical examination (enlarged, tender uterus) + imaging. Transvaginal ultrasound (TVUS) shows characteristic features: asymmetric myometrial thickening, heterogeneous myometrial echotexture, myometrial cysts, subendometrial echogenic linear striations, poor definition of endometrial-myometrial junction. MRI is the most accurate non-invasive modality: thickened junctional zone >12 mm is highly specific. Definitive histological diagnosis requires myomectomy or hysterectomy specimen. Endometrial biopsy does not diagnose adenomyosis.

Medical therapy (symptom control): NSAIDs for dysmenorrhea; combined oral contraceptives or progestin-only pills reduce bleeding and pain. Levonorgestrel-releasing IUD (LNG-IUS/Mirena): highly effective — reduces heavy bleeding by 80–90% and alleviates pain; first-choice medical option. GnRH agonists (leuprorelin) or antagonists (elagolix) induce medical menopause — effective but limited to 6–12 months due to bone loss; useful as bridge to surgery or in perimenopausal patients. Uterine artery embolization: minimally invasive, preserves uterus — suitable for selected patients. Hysterectomy: the only definitive cure; recommended for severe refractory cases not desiring future fertility.

• Iron-deficiency anemia from chronic heavy menstrual blood loss
• Subfertility and recurrent miscarriage — adenomyosis impairs uterine contractility and implantation
• Significant quality-of-life impairment: work absenteeism, sexual dysfunction, psychosocial distress

• No established primary prevention. Minimizing unnecessary uterine procedures (repeated curettage, myomectomy) may reduce endometrial-myometrial junction disruption
• Avoiding elective cesarean section without medical indication — cesarean section disrupts the junctional zone and may increase adenomyosis risk