Best Practice & Research Clinical Obstetrics and Gynaecology

Vol. 20, No. 5, pp. A7eA16, 2006

doi:10.1016/j.bpobgyn.2006.07.003
available online at http://www.sciencedirect.com

Adenomyosis
Answers to Multiple Choice Questions
for Vol. 20, No. 4

1. (a) T (b) F (c) F (d) T (e) T

Cullen is generally believed to have described adenomyosis first as reports of
earlier descriptions are inconsistent, disputed and difficult to authenticate. The cur-
rent definition of adenomyosis has changed considerably and the current one was
proposed and accepted by Bird as late as 1972. The history of adenomyosis is
very difficult to disentangle due to the fact that for much of its history there has
been little differentiation between adenomyosis and endometriosis. Sampson’s orig-
inal work from the 30’s still informs the main ideas about the origins of endometri-
osis, particularly possible aberrant menstrual bleeding. Since the 1950’s imaging and
in vitro tests have repeatedly shown abnormal junctional zone responses to sex
steroids directing metaplasia in aberrant directions as a highly likely cause of
adenomyosis.

2. (a) F (b) F (c) F (d) T (e) F

The frequency of uterine adenomyosis in perimenopausal women undergoing hys-
terectomy is around 20-30% independently of the type of surgical indication. These
studies are biased by the fact that hysterectomies are rarely performed at younger
ages and that the study population is selected based on pathologic conditions. Thus,
the reported results should only refer to this group of women, and cannot be
generalised to all women of the same strata of age. With the use of transvaginal
ultrasonography and magnetic resonance imaging, adenomyosis is often found in
symptomatic or infertile women in their 20s and 30s. However, the prevalence in
the general female population is unknown. Diagnostic criteria have only been rea-
sonably consistent over the last 10-15 years and therefore all information about
prevalence of adenomyosis over the years is intrinsically flawed. Lack of defined di-
agnostic criteria has indeed historically led to considerable over-diagnosis of adeno-
myosis, with rates as high as 80% in some series. Though there are well described
diagnostic criteria on TVS and MRI for adenomyosis, there is still considerable
debate as to their accuracy and as such prevalence rates remain unknown in the
general population.
1521-6934/$ - see front matter
A8 Appendix

3. (a) T (b) F (c) T (d) T (e) F

The risk of adenomyosis increases with number of births and spontaneous abor-
tions. Foci of adenomyosis may be included in the myometrium due to the aggressive
action of the trophoblast, and viable endometrium may be displaced during parturition.
Alternatively, the hormonal milieu of pregnancy may favour the development of islands
of ectopic endometrium. No consistent relation between adenomyosis and age at sur-
gery or menopausal status emerged from the analyses of the available surgical series.
Surgical trauma on the pregnant uterus seems to disrupt the endo-myometrial border,
facilitating dislocation, implantation, embedding, and survival of endometrium within
the myometrial wall. In particular, repeated sharp curettage at induced abortion seems
to increase the risk of adenomyosis. Data on caesarean section are inconsistent. An
increase in risk of adenomyosis after D&C has been observed; however this may be
interpreted in terms of indication bias as women who require D&C may more fre-
quently have a diagnosis of endometrial hyperplasia, a risk factor for adenomyosis.
The estimated odds ratio for the disease is 2.5 (95% CI 1.2-5.2) in women with endo-
metrial hyperplasia in comparison with those without adenomyosis. Also Bergholt
et al., in their series of 549 hysterectomy specimens, confirmed a significant positive
association between endometrial hyperplasia and adenomyosis (OR 3.0, 95% CI 1.2-
8.3). With the exception of the studies of Kunz et al. based on MRI but without
histological confirmation, no significant association has been demonstrated between
adenomyosis and endometriosis. The two conditions have different epidemiological
characteristics, e.g. parity seems to have an opposite effect on adenomyosis and
endometriosis. These findings suggest that the two disorders are different clinical
and nosological entities with no shared aetiological mechanisms.

4. (a) F (b) T (c) T (d) F (e) T

Unlike most human epithelial surfaces there is no submucosa, the endometrial
glands are in direct contact with the myometrium. Both MRI and high resolution
TVS readily identify the junctional zone as distinct in appearance to the endometrium
and other areas of the myometrium. Though basic histological examination of the
myometrium is homogenous there are many cytological and molecular differences
identified in the inner and outer myometrial cells including differences in nuclear:cyto-
plasmic ratio, water content and intermolecular interactions. Both the endometrium
and junctional zone are derived from Mullerian origin and the outer myometrium is
deived from mesodermal origin. As they are of identical embryological origin, both
the endometrium and junctional zone have similar oestrogen and progesterone recep-
tors to which they respond.

5. (a) T (b) T (c) F (d) T (e) F

In vitro and vivo studies all indicate that allocation of cells to the true endometrium
or myometrium is determined by metaplastic events in the junctional zone. MRI ap-
pearances of the junctional zone change cyclically, largely in keeping with endometrial
changes, being most marked during days 8-16. The COCP suppresses ovulation and
the normal cyclical changes required for endometrial and junctional zone proliferation,
and therefore makes the junctional zone less distinct on MRI and US. As changes in the
junctional zone are felt to be vital to successful implantation, the MRI changes reflect
this and become ‘‘brighter’’ on MRI and therefore less distinguishable from the outer
layers on MRI. Multiple ‘‘functional’’ studies of junctional zone subendometrial
 Appendix A9

contractility have shown increase in the follicular phase (aiding upwards sperm trans-
port and thus fertilization) and then decreases under the influence of progesterone in
the luteal phase to facilitate timing for subsequent implantation.

6. (a) T (b) F (c) T (d) F (e) T

MRI diagnosis of adenomyosis requires a thickened junctional zone as part of the
criteria. Hyperplasia of myocytes in the junctional zone does explain the thickened ra-
diological findings on MRI but not the histological appearances of myometrial hyperpla-
sia which are found distant to the junctional zone in adenomyosis. Studies in women
with endometriosis have not only shown a higher prevalence of thickened junctional
zone but also increased basal tone, frequency and amplitude of uterine contractions.
These observations have led to the hypothesis that aberrant junctional-zone peristalsis
plays an integral part in the pathogenesis of endometriosis by facilitating retrograde
menstruation. Only submucous fibroids are derived from junctional myocytes, hence
their increased ability to impair menstrual and reproductive function. In humans, inter-
stitial and intravascular trophoblast invasion goes beyond the endometrium and in-
volves the junctional zone but not the outer myometrium. Indeed, defective deep
placentation, characterized by absence or inadequate physiological transformation of
the junctional-zone spiral arteries, is a pathological hallmark of a spectrum of obstet-
rical disorders ranging from pre-eclampsia to placental abruption and fetal growth
restriction.

7. (a) T (b) F (c) T (d) F (e) F

Both adenomyosis and endometriosis grow and regress in an oestrogen-dependent
fashion. Adenomyosis is associated with 69% of cases of endometriosis, whereas pelvic
endometriosis is observed only in 6-20% women with adenomyosis.
Oestrogen metabolism is altered in the endometrium of adenomyosis patients. Ad-
enomatous hyperplasia is present in 35% of adenomyosis cases. About 33-38% of
women with endometrial carcinoma have adenomyosis, and 60% of uteri with endo-
metrial carcinoma contained coexistent adenomyosis compared to 39% in control
uteri. Since adenomyosis is more common in multiparous women, mechanical events
at parturition have been believed to be the main pathogenesis of adenomyosis. How-
ever, 20% of adenomyosis cases occur in women without a history of pregnancy. He-
reditary occurrence of adenomyosis has been reported but is considered to be a rare
cause. Like tissue in other oestrogen-dependent diseases, adenomyotic tissue contains
oestrogen, progesterone and androgen receptors, but in reduced quantities when
compared with corresponding normal myometrium. Continuous oral contraceptive
pills may provide symptomatic relief from menorrhagia and dysmenorrhea. However,
to date, no evidence has been reported showing that continuous administration of oral
contraceptive pills cause regression of adenomyosis.

8. (a) F (b) T (c) F (d) T (e) T

Several polymorphisms in oestrogen receptor genes have been identified as possi-
ble causes of adenomyosis, due to aberrant expression of oestrogen receptor activity.
Most studies of oestrogen and progesterone receptors have been found that there is
generally a reduction in both steroid receptor levels in adenomyosis and endometri-
osis. Adenomyotic tissue is independently capable of synthesizing oestrogens from
androgen and oestrone precursors as it expresses aromatase and oestrone sulphatase.
A10 Appendix

P450aromatase detection in endometrial biopsy specimens is essentially a marker for

oestrogen-dependant disease including adenomyosis, endometriosis and leiomymata.
Taken together, though eutopic and ectopic endometria more or less resemble one
another histologically, the endometria of diseased patients are remarkably different
from the endometria of disease-free women with regard to oestrogen metabolism.

9. (a) F (b) T (c) T (d) T (e) T

GnRH agonists provide regression of adenomyotic lesions as a secondary effect
after suppressing the hypothalamusepituitary axis and providing a hypo-oestrogenic
status, rather than in the tissue itself. Danazol however seems to have its principle
effect directly on the endometrial receptor expression. Danazol directly inhibits the
growth of endometrial and endometriotic cells by inhibiting multiple steroidogenetic
enzyme activities, including cytochrome P450s, aromatase, oestrone sulphatase, and
dehydrogenases. Adenomyotic tissue contains progestagen receptors and the clinical
improvement seen with LNG IUCDs is believed to be via these receptors. Though
there is little evidence of regression of abnormal endometrial tissue or changes in ste-
roid receptor activity in adenomyosis on the COCP, the majority of women still report
some improvement in menstrual symptoms.

10. (a) F (b) F (c) T (d) T (e) T

Despite the use of in vitro techniques to study the characteristics of the various
cells that comprise adenomyosis, production of a good in vitro model for the complex
stromaleglandular interactions in this disorder has proved elusive. The data suggests
that the two conditions have a different aetiology as endometriosis occurs only in pri-
mates whereas adenomyosis occurs in diverse species. A genetic basis is suggested by
the fact it occurs in greater prevalence in certain strains of mice although experimental
data also suggests that exposure of neonates to hormonal imbalance might alter the
development of the myometrium where disruption to the mesenchymal layers of
the uterine wall gives rise to disordered structure and function of the myometrium
which provides the abnormal architectural framework for aberrant growth of the en-
dometrium and its penetration deep into the myometrium. Disruption to the vascula-
ture here also seems likely to predispose to adenomyosis.

11. (a) F (b) T (c) F (d) F (e) T

Microscopically, adenomyosis has a haphazard distribution within the myometrium,
and by definition the ectopic endometrium must be located past the ‘last’ glands of the
basalis. The adenomyotic glands and stroma most often are of the proliferative type,
but may contain secretory to menstrual changes. It is circumferentially surrounded
by bundles of hypertrophic smooth muscle cells (‘collar’). As a result, foci of adeno-
myosis are seen 2 mm or deeper in the myometrium or more than one microscopic
field at 10X magnification from the endomyometrial junction. The stromal fibroblasts
clearly differ cytologically from the adjacent smooth muscle cells. Unless stringent
‘‘depth’’ criteria are used there are huge discrepancies in quoted pathological rates
of adenmyosis due to deep myometrial penetration by normal endometrium.

12. (a) T (b) T (c) T (d) T (e) T

Uteri removed because of symptoms contain higher rates of adenomyosis than
those without symptoms. The diagnosis rates vary from 10% to 80% between
 Appendix A11

pathologists, 12% to 58% between hospitals, and 20% to 67% at autopsy. Also, the
more sections taken from a given specimen, the higher the frequency (one study
31% with three routine sections of hysterectomy specimens 61% with six sections).
Using stringent diagnostic criteria e e.g. deeper than 25% of myometrial thickness e
yields lower adenomyotic rates than if more superficially located glands are consid-
ered. An adenomyoma is a circumscribed, nodular aggregate of smooth muscle,
endometrial glands, and (usually) endometrial stroma. It may be located within the
myometrium or it may involve or originate in the endometrium and grow as a polyp.
These must be differentiated from so-called adenomyosis or rates will vary.

13. (a) F (b) T (c) T (d) F (e) F

The first and most popular hypothesis is that adenomyosis originates from the deep
part (basalis or junctional zone) of the endometrial mucosa invaginating between
bundles of smooth muscle fibres of the myometrium. This situation is enhanced by
a structurally weakened myometrium or by the influence of ovarian hormones via
the over-expression of sex-steroid receptors. (Oestradiol receptor expression in
the adenomyotic foci is greater than in the normal endometrium and is associated
with expression of the apoptosis-suppressing gene product, bcl-2, throughout the
menstrual cycle and both may promote both the invagination process). Adenomyosis
is indeed often associated with polyps, anovulation, hyperplasia without cytological
atypia, and uterine leiomyomata, all of which are produced by hyper-oestrogenic
states. Another theory suggests that invagination of the basalis would proceed along
the intramyometrial lymphatic system. A third theory, suggests metaplasia from de
novo ectopic intramyometrial endometrial tissue likely to originate form myocytes
in the superficial junctional zones due to a common embryological origin from the
mullerian ducts of endometrium and subjacent myometrium.

14. (a) T (b) F (c) T (d) F (e) T

The most frequent symptoms of adenomyosis are menorrhagia (50%), dysmenor-
rhoea (30%), and metrorrhagia (20%). About one-third of adenomyosis cases are
asymptomatic. Several authors have found that the frequency and severity of symp-
toms tend to correlate with the extent and depth of adenomyosis unlike endometri-
osis where the symptoms are commonly at odds with the amount of disease found.
Prior Caesarean section has not been found to be an independent risk factor for Cae-
sarean section despite the theoretical seeding of the myometrium. Tamoxifen in
treated postmenopausal women seems to reactivate pre-existing adenomyosis, which
leads to an increase in myometrial volume and uterine size, with adenomyosis re-
ported in 60% of 14 postmenopausal women on chronic tamoxifen therapy in one
study. Adenomyosis is a condition associated with excessive oestrogenic activity and
aberrant oestrogen receptor activity. The only logical explanation for this is agonistic
effects in the tissue.

15. (a) T (b) F (c) T (d) F (e) T

Nearly 90% of adenomyotic uteri occur in multiparous women but there is no clear
evidence to say whether the condition is more prevalent in white than in black women.
The vast majority of cases (80%) are reported in women aged 40 - 50 years old and are
often associated with the most severe symptoms. Obesity however, does not appear
to be a predisposing factor. Up to 80% of adenomyotic uteri contain associated
A12 Appendix

pathology. The most frequent one is leiomyomata; endometrial polyps, hyperplasia

(without and with atypia) as well as adenocarcinoma are encountered more frequently
in patients with adenomyosis than in the general population.

16. (a) T (b) T (c) F (d) F (e) F

In one study, 60% of uteri with endometrial carcinoma contained coexistent adeno-
myosis compared to 39% in control uteri and other authors have found increased rates
in association with carcinoma of the endometrium. Endometrial adenocarcinomas as-
sociated with adenomyosis tend to occur in younger patients, are FIGO stage I and
grade 1, well differentiated, type I endometrioid, hormone-sensitive adenocarcinomas,
though type II non-endometrioid adenocarcinomas are reported. From a pathological
point of view, when adenomyosis is associated with adenocarcinoma it is difficult to
distinguish between an adenocarcinoma that invades the myometrium and that of car-
cinoma exhibiting intramucosal extension into foci of adenomyosis - women with en-
dometrial adenocarcinoma extending directly (without myometrial invasion) into foci
of adenomyosis have an excellent prognosis and need no further treatment, whereas
myometrial invasion adjacent to foci of adenomyosis may require further therapy de-
pending on the depth of myometrial invasion.

17. (a) F (b) F (c) F (d) F (e) T

MRI seems more sensitive overall than TVUS for diagnosis, particularly when
adenomyosis is associated with leiomyomata, though ultimately, the definite diagnosis
of adenomyosis is only made on the histological examination of several transmural
sections of the uterine body and fundus of a hysterectomy specimen. Adenomyosis
is refractory to sex steroid therapy despite the well documented over-expression of
sex steroid receptors (oestrogen and progesterone) in adenomyotic tissue. Though
not easy to explain there appears to be an overriding oestrogen effect making the
effect of exogenous progestagens limited with a concomitant poor clinical effect. Anti-
oestrogenic therapeutic agents such as GnRH agonists (GnRHa) and the anti-
gonadotrophin danazol induce regression of adenomyosis. However (GnRHa) therapy
is given only for 6 months, following which the symptoms of dysmenorrhoea and men-
orrhagia reappear quickly. As things stand, the best therapeutic means for adenomyo-
sis is total abdominal hysterectomy.

18. (a) T (b) T (c) T (d) F (e) T

Uterine peristaltic waves are confined to the subendometrial myometrium and this
is characterized by a predominantly circular arrangement of the muscular fibres, as
opposed to the outer myometrium with a predominantly longitudinal arrangement and
the middle layer, composed of a three-dimensional mesh of short muscular bundles
that constitute the bulk of the human myometrium. The subendometrial myometrium
extends from the lower part of the cervix through the uterine corpus into the cornua,
where it continues as the muscular layer of the Fallopian tubes. The embryological for-
mation of this layer is recognized by a kind of a fundo-cornual raphe that results from
the fusion of the two Mullerian ducts and their mesenchymal elements to form the
primordial uterus. The bipartition of the circular subendometrial myometrium in
the upper part of the uterine corpus and its separate continuation through the cornua
into the respective tubes is the morphological basis of directed sperm transport into
the tube ipsilateral to the dominant follicle. Though many factors are considered
 Appendix A13

important, uterine peristaltic activity is principally controlled by cyclical levels of oes-

tradiol and progesterone that correspond to the cyclically changing oestradiol and
progesterone receptor expression in the subendometrial layer. It has been shown
using dynamic hysterosalpingoscintigraphy (HSSG) that changes in utero-tubal flow
velocity occur at the same frequency as the peristaltic contractions and it is therefore
reasonable to assume that the uterine peristaltic activity with cervico-fundal contrac-
tion waves provides the forces that are required for the transport of spermatozoa
from the external os of the cervix into the tubes within minutes.

19. (a) T (b) F (c) F (d) T (e) T

Women with endometriosis show a significant increase in uterine peristaltic activity
in comparison to women free of disease. This change in the contractile activity of the
uterus in women with endometriosis has a profound effect on the uterine retrograde
transport capacity. In women with endometriosis the intrauterine pressure is increased
in comparison to women without the disease and hyperperistalsis with increased intra-
uterine pressure is considered to exert a considerable auto-traumatization of the
uterus. Hyperperistalsis that is present during the menstrual period of the cycle in
women with endometriosis abrades fragments of basal endometrium, whereas functio-
nalis and spongiosa (and not basalis) are only normally shed in women without the dis-
ease. It has be shown that in 80% of women with endometriosis, and in only 10% of
women without endometriosis, fragments of basal endometrium could be detected in
the respective menstrual blood specimens. Data from the literature strongly suggest
that the principal mechanism of endometriosis/adenomyosis is the paracrine interfer-
ence of endometrial oestrogen with the cyclical endocrine control of subendometrial
peristalsis exerted by the ovary. Both endometriotic and adenomyotic tissues possess
the ability to undergo metaplasia to peri-stromal myometrium because they are both
derived from the sub-endometrial layer which maintains its embryological pluripotent
nature.

20. (a) F (b) T (c) T (d) T (e) T

Though undoubtedly associated with subfertility, the occurrence of superficial non-
tubo-ovarian endometriosis is not readily explained as a causal factor. This is backed
up by the fact that surgical and medical eradication of the endometriotic lesions do
not improve or normalize fertility in such patients, suggesting that peritoneal endo-
metriotic lesions without tubo-ovarian involvement may not constitute a major cause
of subfertility. The most plausible explanation for the impact of adenomyosis on fertil-
ity is the impairment of the uterine mechanism of rapid and sustained directed sperm
transport in consequence of the destruction of the normal architecture of the archi-
myometrium - the peristromal muscular cells of the adenomyotic lesions, a muscular
tissue develops that is irregularly arranged, in contrast to the normal subendometrial
myometrium with its circular muscle fibres. Moreover, this muscular tissue is respon-
sive to the endocrine and paracrine stimuli that regulate uterine peristalsis resulting in
increased intrauterine pressure and in dysperistalsis during the late follicular phase.
The basal endometrium is, by virtue of the expression of P450 aromatase throughout
the menstrual cycle, a tissue capable of converting androgen into oestrogen and pro-
ducing various substances that are mainly active in a paracrine way, such as oxytocin,
prostaglandins, growth factors and cytokines. A possible direct impact of the ad-
enomyotic lesions with their secretory products is on ovarian function. A number
of studies have demonstrated a diminished ovarian reserve, an impaired granulosa
A14 Appendix

celleoocyte environment, and an impaired oocyte quality and fertilization rate in pa-
tients with endometriosis and adenomyosis. There is a correlation between the per-
centage of immature oocytes among those retrieved in IVF cycles and the depth of
adenomyotic infiltration and a reduced rate of blastocyst formation in the presence
of extended adenomyosis. With respect to immunological factors the inflammatory
defence is one of the fundamental functions of the endometrium in the early process
of reproduction. Endometriotic and adenomyotic lesions display, as ectopic lesions, the
same immunological potential as the parent tissue. While immunoreactive cells such as
‘bone-marrow-derived white blood cells’ and macrophages are cyclically shed with
menstruation, they cannot be externalized, at least from extrauterine ectopic lesions.
They remain in situ and cause immunological and inflammatory processes.

21. (a) F (b) F (c) T (d) F (e) T

There are no symptoms that are pathognomonic of adenomyosis. Pathological di-
agnoses of adenomyosis is commonly made in hysterectomy specimens of women
with no symptoms (approximately 30%) referable to adenomyosis and also the com-
mon symptoms said to be associated with adenomyosis (menorrhagia, dysmenor-
rhoea, and an enlarged tender uterus) are common to a number of other
gynaecological disorders in women. Adenomyosis commonly co-exists with a number
of other pelvic pathologies. Series of cases where only adenomyosis was found on his-
topathology have found between 51% and 60% of patients complained of heavy bleed-
ing with or without other symptoms. Several authors have found increasing blood loss
with both superficial and increasingly deep adenomyosis and there does not appear to
be a consistent relationship. Similar results have been found correlating increasing
dysmenorrhoea with increasing depth and density of adenomyotic involvement of
the myometrium by most authors.

22. (a) T (b) F (c) F (d) F (e) F

One study showed that the depth of adenomyosis into the myometrium found on
endomyometrial resection biopsy correlated with the amount of heavy bleeding re-
ported. They treated the adenomyosis with endometrial ablation or resection and
found that patients with superficial adenomyosis (<2 mm penetration) had better
treatment results with a greater long-term likelihood of no periods or light periods.
Women with deeper penetration tended to continue to have heavy bleeding. Studies
have repeatedly shown no relationship between symptoms such as menorrhagia, dys-
menorrhoea, abdominal pain and uterine weight. Though age is an obvious confound-
ing factor there is a large body of evidence to suggest a causal link with subfertility and
adenomyosis still occurs in younger women who are subfertile. Several studies to date
indicate that the pregnancy complication rates due to adenomyosis are low. Adenocar-
cinoma arising from adenomyosis is a generally good prognostic factor as the carcino-
mas tend to be low grade, early stage and of endometrioid type.

23. (a) T (b) F (c) T (d) F (e) F

The scientific evidence gathered over recent years and the major technical improve-
ments in the manufacture of high-quality small-bored scopes have answered the ques-
tion of how diagnostic hysteroscopy can be implemented successfully in an office
environment. Atraumatic insertion technique (mini-hysteroscope <4mm), and the
use of watery distension medium are essential for successful office hysteroscopy.
 Appendix A15

With these conditions local anaesthesia is rarely needed and the common use of direct
vagino-cervico hysteroscopy generally precludes the need for speculum or tenaculum.

24. (a) T (b) F (c) T (d) F (e) T

Although hysteroscopy is unable to offer a pathognomonic sign for adenomyosis,
some investigators have described the hysteroscopic uterine appearance of patients
with adenomyosis. There is some evidence that findings such as irregular endometrium
with endometrial defects, hypervascularization, strawberry pattern or cystic haemor-
rhagic lesions are possibly associated with adenomyosis.

25. (a) F (b) T (c) F (d) T (e) T

Uterine enlargement without signs of fibroids and asymmetric thickening of the
anterior and posterior myometrial walls are indirect sonographic signs originally de-
scribed with transabdominal sonography (TAS), but TAS does not afford sufficient im-
age resolution for visualization of the myometrium to reliably diagnose adenomyosis.
The TVS image characteristics of adenomyosis most commonly seen are heteroge-
neous and hypoechogenic, poorly described areas in the myometrium (with or without
anechoic lacunae or cysts of varying size), increased echo texture of the myometrium,
linear striations radiating out from the endometrium into the myometrium, and an in-
distinct endomyometrial junction with a pseudo-widening of the endometrium. The
TVS appearance of adenomyomas as opposed to leiomyomas are suggested by the
presence of an elliptical rather than globular shaped lesion with poorly defined bor-
ders, lack of calcification, and lack of edge shadowing. Doppler sonography may facil-
itate the differentiation between myomas and adenomyosis - vessels around myomas
produce a well-defined rim with a few vessels entering the body of the mass, whereas
in adenomyosis vessels follow their normal perpendicular course in myometrial areas.
TVS appears to be a sufficiently accurate tool for the diagnosis of adenomyosis in
clinically suspicious cases (sensitivity > 70%, specificity > 80%), but not in unselected
premenopausal women especially with myomas.

26. (a) T (b) F (c) T (d) T (e) F

Adenomyosis typically presents as either diffuse or focal thickening of the junctional
zone or an ill-defined myometrial nodule of low signal intensity on T2-weighted im-
ages. Occasionally, the islands of ectopic endometrial tissue can be demonstrated as
punctate foci of high intensity on T2-weighted images. When menstrual hemorrhage
occurs, these foci also show high intensity on T1-weighted images.

27. (a) T (b) F (c) F (d) T (e) T

Adenomyomatous polyps may present as a polypoid mass protruding into the uterine
cavity. Subserosal masses showing exophytic growth are often seen in leiomyomas. Adeno-
myotic cysts usually manifest as unilocular hemorrhagic cyst within the myometrium. Adeno-
myomas may present as well-circumscribed masses of low intensity. If there is haemorrhage
to form a myometrial cyst these show as hyperintense areas on T1-weighted images.

28. (a) F (b) T (c) T (d) F (e) T

Differentiation between adenomyosis and uterine leiomyoma is usually easy on MR
imaging. MR imaging is useful in predicting therapeutic effect of GnRHa therapy. One
A16 Appendix

series have reported that adenomyosis presenting as focal thickening of the JZ with
hyperintense foci on T2-weighted images have a better clinical response compared
to more diffuse change. In cases with endometrial cancer in the uterus with adeno-
myosis, evaluation of myometrial invasion may become difficult since benign invasion
of the basal endometrium into the myometrium in benign adenomyosis is often difficult
to be distinguished from true myometrial invasion by endometrial cancer. Diagnosis of
adenocarcinoma arising from adenomyosis on MR imaging may be difficult, since MR
features of this entity include a myometrial nodule simulating leiomyoma or diffusely
infiltrating process that can not be distinguished from preexisting adenomyosis.
Benign invasion of the basal endometrium into the myometrium identified as ‘‘linear
striations’’ or ‘‘pseudowidening’’ of the endometrium on T2-weighted MR images may
simulate infiltrative malignancy.

29. (a) T (b) T (c) T (d) T (e) F

Levonorgestrel acts directly on the adenomyotic deposits. Down-regulation of oes-
trogen receptors, which are present in both glandular and stromal endometrial tissues,
occurs shortly after placement of the device causing the adenomyotic deposits to re-
duce in size, and as a result of these shrinking deposits, uterine contractility improves
and the uterine size decreases. Symptoms overall tend to improve as well. The major-
ity of cases series of excision of adenomymata have shown an overall benefit to the
patient though location of the lesions can be difficult. Multiple case reports of success-
ful pregnancies after this treatment have also been published. In a large comparative
study of complications of vaginal hysterectomy in patients with leiomyomata and in pa-
tients with adenomyosis, it was found that women with adenomyosis had a significantly
higher risk of bladder injury, while there was no difference in blood loss and operating
time when the uterine weight was taken into account. The definite reason for the in-
creased risk of bladder injury is unknown, but it may be due to the greater difficulty in
identifying the supravaginal septum and the vesicovaginal and vesicocervical planes.
Conservative surgery can be proposed in the majority of patients with recto-vaginal
adenomyomata . The surgery may require excision of the nodular fibrotic tissue
from the posterior vagina, rectum, posterior cervix, and uterosacral ligaments, as
well as excision of rectal deposits. Hysterectomy is rarely required.

30. (a) T (b) T (c) F (d) T (e) F

Co-existent pathology is extremely common in adenomyosis making nearly all pub-
lished studies difficult to interpret in terms of efficacy. Several series have reported
better symptomatic control with combined endometrial ablation and LNG-IUS for
women with adenomyosis. Trials of a danazol releasing IUD as well as improving symp-
toms have not reported danazol related side effects as serum levels of danazol remain
universally undetectable. The results from UAE for adenomyosis only are very encour-
aging as long a MRI seems to be used to make the diagnosis. Results with co-existent
fibroids are more variable. MRgFUS may well represent an alternative treatment for
focal adenomyosis but results so far come from a very small number of cases only.