Sabato 27 ottobre 2012 - Pacini Editore

PoStER
(see Fig. 1) placental site reactions and 1 placental site nodule
were seen.
Conclusions: In the present study our aim is to identify any maternal
condition which may redispose to endometritis or placental
retention and therefore to cavity revision in the post-partum.
Gestational diabetes, in addition to the knowm effects on the
fetus 2 , is known to be a significant risk factor for endometritis
3 . We also show that latent dysmetabolic/dysglicemic
conditions (6/10 patients - 60%) identified as diabetic placentoplathies,
isolated or in combination with other causes like
chorionamnionitis or hypoxic-ischemic injury also increase
endometritis risk. This finding is important as pregnant women
who were not clinically diabetic during pregnancy may still be
at risk in the post-partum. These latent conditions are identifiable
with an accurate histological evaluation of the placenta. If
we consider causes associated with the retention of parts of the
chorionic disk we see how the hypoxic-ischemic injury is present
in 8/10 (80%) cases. This means that even focal hypoxia
with hypoxic-ischemic injury can involve and lacerate the cotyledons,
and thus lead to an increased risk of placental retention.
Furthermore half of the cases of placenta accreta showed HII.
This may be in keeping with the pathogenetic theories which
attribute the extravillous trophoblast’s excessive motility to
be secondary to differences in oxygen tension 4 . Hypoxia may
therefore further stimulate extravillous trophoblast to infiltrate
the uterine wall.
We also noted in 5 of the 24 cases anomalous trophoblastic reactions.
In particular, 4 of the cases showed exaggerated placental
site reactions 5 and 1 a placental site nodule 6 7 . These are rare benign
conditions, due to the growth of elements like intermediate
trophoblast with proliferation in the endometrium or even, more
rarely, at the level of myometrium.
In conclusion the histologic examination of the placenta may
throw light on possible causes of post-partum complications. In
particular diabetic placentopathies and HII should be noted in the
placental histology report.
references
1 Benirschke K, Kaufman P. Pathology of the Human Placenta. New
York: Springer 2000.
2 Simpson ER, MacDonald PC. Endocrinology of pregnancy. In: Williams
RH, ed. Textbook of endocrinology, 6 th ed. Philadelphia, London,
Toronto: Saundrs 1981.
3 Diamond MP, Entman SS, Salyer SL, et al. Increased risk of endometritis
and wound infection after cesarean section in insulin-dependent
diabetic women. Am J Obstet Gynecol 1986;155:297-300.
4 Genbacev O, Zhou Y, Ludlow JW, et al. Regulation of human placental
development by oxygen tension. Science 1997;277:1669-72.
5 . Shih IM, et al. The pathology of intermediate trophoblastic tumors and
tumor-like lesions. Int J Gynecol Path 2001;20.31.
6 Santos LD, Fernando SS, Yong JL, et al. Placental Site Nodules and
Plaques: A Clinicopathological and Immunhistochemical Study of 25
Cases with Ultrastructural Findings. Pathology 1999;31:328-36.
7 Young RH, Kurman RJ, Scully RE. Placental site nodules and
plaques. A clinicopathologic analysis of 20 cases. Am J Surg Pathol
1990;14:1001-9.
Endometrial stromal sarcoma: a case report
R. Giannatiempo1 , M. Postiglione1 , L. Nugnes1 , R. Franco2 ,
A. Russo1 , A. Nicastro1 , D. Oppressore1 1 UOS Anatomia ed Istologia Patologica /Ospedale Evangelico Fondazione
Betania, Napoli, Italia;; 2 AF Anatomia Patologica/ INT Fondazione G. Pascale,
Napoli, Italia
Case presentation. A 37-year-old lady presented with increased
bleeding per vagina during periods since 1 year. She was a para2,
live2, with last child birth 8 years back and no history of contraceptive
use. She had attained menarchy at the age of her previous
cycles were normal. A pelvic scan taken 1 year back has showed
normal-sized uterus with a fibroid 3.7 cm×3.4 cm in the anterior
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myometrium. Endometrial thickness was 8 mm. A dilatation and
curettage was performed and microscopy showed a disordered
proliferate endometrium. She was given symptomatic treatment
for menorrhagia.
One year later she reported to our outpatient clinic with complaints
of a mass in the lower abdomen and lower abdominal
pain for three months. The patient was apparently asymptomatic
one year previously, but then she noticed a mass in the lower
abdomen that gradually increased in size. She provided a history
of a rapid increase in size for the past three months. She also had
associated lower abdominal pain, which was dull and aching in
type, dragging in nature and continuous with no aggravating or
relieving factors. She was thinly built. On abdominal examination,
an irregular midline mass rising from the pelvis was present.
The upper and lateral borders of the mass could be made out; the
lower margin could not be ascertained. The mass was firm to
hard in consistency with restricted mobility and non tender with
no free fluid.
Pelvic examination revealed the abdominal pelvic painless mass
reaching the umbilical point, some parts of this mass are soft but
the mass dependence on the uterus was not established.
Abdominal and vaginal ultrasound showed a 10 cm about heterogeneous
but a well-circumscribed mass, consisting of cystic and
solid parts whose relationship with the uterus is not well defined.
No vegetation was noted either inside or outside of the mass. The
ovaries was not visualized.
Magnetic resonance imaging (MRI) was indicated to specify
the seat of the mass and its relationship with the neighborhood
organs.
Laboratory investigations including serum was normal.
Endometrial aspiration was performed changes in view of the
rapid enlargement of the uterus within the past 4 months. Microscopy
showed endometrial glands in the secretory phase with
neoplastic cells, suggestive of low-grade endometrial stromal
sarcoma
A total abdominal hysterectomy with bilateral salpingooopherectomy
was performed.
The findings were a uniformly enlarged uterus with normal-looking
tubes and ovaries The tumor had infiltrated the myometrium
anteriorly. There were no metastatic deposits. The lymph nodes
were not enlarged.
Gross finding showed a polypoid and protrude tumor involving in
the myometrium and tend to bulge above the surrounding myometrium.
The tumor has a well circumscribed contour, measuring
10 ×9 × 8 cm and has a fleshy yellow surface. This tumor is
intramural with no connection to the endometrium.
Characteristically uniform oval and spindle-shaped cells, suggestive
of low-grade ESS, infiltrating the entire thickness of the
myometrium, were noted. In microscopic findings, the tumor
consists of cells that closely resemble normal proliferative-phase
endometrial stromal cells with areas of epithelial-like structures
that have an appearance reminiscent of an ovarian sex cord stromal
tumor. The tumor cells have uniform, small, darkly staining
round or oval nuclei with granular chromatin and inconspicuous
nucleoli. Mitotic activity is less than 3MF/10HPF.
The epithelial-like cells grow in cords and trabeculae, they are
cuboidal with scanty amphophilic cytoplasm and nuclei resemble
those of the surrounding stromal cells.
The tumor presents expansive, non infiltrative margins that compress
the surrounding myometrium.
The tumor was immunoreactive to CD10 and hormonal receptors:
oestrogen receptor (ER) and progesterone receptor (PR).
Immunostaining for AML,EMA desmine, cytokeratin AE1/AE3,
cytokeratin 18, HMB45 were negative.
A section from the right fallopian tube showed neoplastic cells
in dilated lymphatic spaces. The cervix and ovaries were normal
The case was confirmed to be a low-grade endometrial stromal
sarcoma stage 3, and she was referred to a regional cancer center.