ADENOMYOSIS
Adenomyosis is a condition where endometrial glands and stroma are found within the uterine wall (myometrium). This is the intramural equivalent of extrauterine endometriosis. This is somewhat misleading because endometriosis and adenomyosis coexist in the same patient in about 15% of women while they are clinically different diseases. The only common feature is the presence of ectopic endometrial glands and stroma. Adenomyosis is thought to affect 10% to 15% of all women and may be as high as 60% in women 40 to 50 years old. The predominant age of patients with adenomyosis is between 35 and 50 years, and there appears to be a mild familial predisposition (polygenic or multifactorial inheritance) pattern.
Although no true cause is known, adenomyosis is derived from aberrant
glands of the basalis layer of the endometrium. These grow by direct extension
into the myometrium. These glands rarely undergo the same cyclic changes as
does the normal uterine endometrium. Histologically the glands exhibit an
inactive or proliferative pattern. Surrounding most foci of glands and stroma
are localized areas of hyperplasia of the smooth muscle of the uterus,
resulting in the typical globular enlargement of organ noted clinically.
The pathogenesis of adenomyosis is unknown but it is theorized that a
disruption of the barrier between the endometrium and myometrium is an
initiating step. It has been postulated that high levels of estrogen, high
parity, or a history of postpartum endometritis constitute risk factors for the
development of adenomyosis, but these remain speculative. Local endometrial
invasion may be seen following cesarean delivery, myomectomy, or curettage.
Many cases of adenomyosis are asymptomatic but up to one-half of patients
report menorrhagia or dysmenorrhea, often with increasing severity. On physical
examination, a symmetric “woody” enlargement of the uterus (up to 2 to 3 times
normal) may be found and uterine tenderness that varies with the cycle (worst
just before menstruation) may be present. Because of the similarity of
symptoms, adenomyosis must be differentiated from uterine leiomyomata (most
often resulting in asymmetric uterine changes), endometriosis, or intrauterine
pathology (polyps, hyperplasia, or cancer). The diagnosis of adenomyosis is
generally established on the basis of history and physical examination with
imaging (ultrasonography or magnetic resonance imaging [MRI]) reserved to rule
out other possible pathologic conditions. Either transvaginal ultrasonography
or MRI may demonstrate abnormalities. (On ultrasound, the uterus will have a
heterogeneous texture, without focal abnormalities.) Magnetic resonance imaging
(T2-weighted or contrast-enhanced T1- weighted) will be more specific than
ultrasonography and less subject to variation based on the observer, but
neither is required to establish a clinical diagnosis. The characteristic
history of painful, heavy periods, accompanied by a generous, symmetric, firm or
“woody” uterus suggests, but does not confirm, the diagnosis. Only histologic
examination can confirm the diagnosis. (Diagnostic criteria require glands to be
identified more than 2.5 mm below the basalis layer of the endometrium.) An
endometrial biopsy is seldom of help in establishing the
diagnosis of adenomyosis, although it may be useful to rule out a possible
endometrial cancer when that is a consideration. Adenomyosis is most often
diagnosed incidentally by the pathologist examining histologic sections of
surgical specimens.
Analgesics (nonsteroidal antiinflammatory drugs), cyclic hormone therapy, or gonadotropin-releasing hormone (GnRH) agonists may all be used as therapy for the symptoms of adenomyosis. There is no satisfactory medical cure for adenomyosis. All medical therapy is aimed at ameliorating the symptoms or delaying the progression of the condition. Symptoms generally resolve with the loss of menstrual function at menopause. Hysterectomy is the definitive treatment for adenomyosis and unless associated with endometriosis, surgical therapy is curative. Uterine artery embolization to control syptoms has been suggested but remains experimental.
