Sabato 27 ottobre 2012 - Pacini Editore

COmuNiCaziONi ORali
evaluation that was blindly reviewed by two dedicated pathologists
(with satisfactory positive and negative agreement); c) comparison
of histological pattern in FGR with different etiology; d)
multivariate statistical analysis to assess for independent associations.
We adopted a multivariate analysis model that corrects data
for gestational age and placental weight as pathologic lesions are
strongly dependent on the developmental stage.
Potential limitations of the study are related to the: a) current
criteria used to define the maternal underperfusion pattern;
b) monoinstitutional and retrospective design that may have
introduced a selection bias; c) lack of control placentas from
pregnancies either complicated only by PE and not FGR and of
uncomplicated pregnancies.
Conclusions. FGR with different etiology show differences in
type, prevalence and distribution of placental lesions suggesting
a different relevance in the development and clinical evolution
of FGR. Further studies with stringent and validated criteria are
needed to definitely clarify the significance of placental pathology
in FGR with different etiology.
references
1 Brosens I. The “Great Obstetrical Syndromes” are associated with
disorders of deep placentation. Am J Obstet Gynecol 2011;204:193-
201.
2 Romero R, et al. Placental disorders in the genesis of the great obstetrical
disorders. In: Pijnenborg R, Brosens I, Romero R, editors. Placental
Bed Disorders. Cambridge University Press 2010, pp. 271-89.
3 Roberts DJ, et al. The placenta in preeclampsia and intrauterine
growth restriction. J Clin Pathol 2008;61:1254-60.
4 Tomas SZ, et al. Morphological characteristics of placentas associated
with idiopathicintrauterine growth retardation: a clinicopathologic
study. Eur J Obstet Gynecol Reprod Biol 2010;152:39-43.
5 Redline R, et al. Maternal vascular underperfusion: nosology and
reproducibility of placental reaction patterns. Ped and Dev Path
2004;7:237-49.
6 Redline R, et al. Fetal vascular obstructive lesions: nosology and
reproducibility of placental reaction patterns. Ped and Dev Path
2004;7:443-52.
7 Redline R, et al. Amniotic infection syndrome: nosology and reproducibility
of placental reaction patterns. Ped and Dev Path 2003;6:435-48.
8 Aviram A, et al. Placental aetiology of foetal growth restriction: clinical
and pathological differences. Early Hum Dev 2010;86:59-63.
9 Vedmedovska N, et al. Placental pathology in fetal growth restriction.
Eur J Obstet Gynecol Reprod Biol 2011;155:36-40.
10 Kovo M, et al. Placental vascular lesion differences in pregnancyinduced
hypertension and normotensive growth restriction. Am J
Obstet Gynecol 2010;202:561.e1-5.
A case of primary peritoneal malignant mixed
mullerian tumor
E. Di Cola1 , G. Crisman1 , A.R. Vitale2 , T. Curti2 , S. Discepoli2 ,
G. Coletti3 , P. Leocata1 1 Anatomia Patologica, Dipartimento di Scienze della Salute, Università
degli Studi dell’Aquila, L’Aquila, Italia, 2 U.O.C. Anatomia Patologica,
P.O. “SS. Filippo e Nicola”, Avezzano (AQ), Italia; 3 U.O.C. Anatomia
Patologica, Ospedale Civile “San Salvatore”, L’Aquila, Italia
Background. Extragenital malignant mixed mesodermal (Müllerian)
tumors (MMMT) are very rare neoplasms, with aggressive
behaviour. The characteristic histological feature is represented
by a biphasic pattern, consisting of both epithelial and mesenchymal
component. Endometrium represents the most common
site of onset, even though few cases arising from tube, cervix and
vagina have been described. Only 31 cases of primary peritoneal
MMMT have been reported so far, and other extragenital (i.e.,
ureters) sites of onset seem to be even rarer.
The etiology and histopathogenesis of these kind of tumors
remains controversial and the correlation between primary peritoneal
MMMT and the expression for estrogen receptor (ER) and
progesterone receptor (PR) has not been documented yet.
Material and methods. A 86-year-old woman presented to the
317
Fig. 1. a. Epithelial (squamous) differentiation of the lesion (H&E, 20x
magnification). B: mesenchymal (cartilagineous) differentiation of the
lesion. (H&E, 10x magnification).
Fig. 2. a: pan- Cytokeratins positivity of the epithelial component
(paN-CK, 10x magnification). B: Smooth-muscle actin positivity of the
mesenchymal component (Sma, 10x magnification).
Hospital of Avezzano with acute abdomen and anemia. Abdominal
ultrasound examination revealed a large, rounded mass with
ill-defined margins of the lower abdominal wall, displacing adjacent
small-bowel loops.
The patient underwent abdominal surgery and a bulky abdominal,
bleeding mass of 20cm in-diameter, arising from the peritoneum,
has been excised. Moreover, several masses scattered on the parietal
and visceral peritoneum have been detected as well.
The postoperative course showed a mild improvement of the patient’s
clinical however, the situation suddenly worsened and the
patient died shortly after.
Results. Histological examination of the surgical specimens revealed
a tumor mainly composed by an epithelial carcinomatous
component (tubulo-papillary and squamous type) and a smaller
mesenchymal component, characterized by well differentiated
stromal elements including cartilage and smooth muscle, and
undifferentiated stromal cells.
Immunohystochemical stains revealed a biphasic pattern of the
tumor: the epithelial component strongly stained for Cytokeratins,
whereas the stromal component strongly stains for mesenchymal
markers, such as smooth-muscle actin and Vimentin. Any
expression for ER and PR was detected.
Conclusions. We reported a rare case of primary, aggressive
peritoneal MMMT, occurring in an old, post-menopausal woman,
presenting with the classical biphasic pattern (epithelial and stromal
differentiation) with a prevalence of the well-differentiated
adenocarcinomatous component on the squamous carcinomatous
component, in association with heterologous aspects of the
sarcomatous component. The authors suggested that the lack of
expression of hormonal receptors could represent a lack of hormonal
control.
references
1 Ferrie RK, Ross RC. Retroperitoneal mullerian carcinosarcoma. Can
Med Assoc J 1967;97:1290-2.
2 Cokelaere K, Michielsen P, De Vos R, et al. Primary Mesenteric Malignant
Mixed Mesodermal Tumor with Neuroendocrine Differentiation.
Mod Pathol 2001;14:515-20.
3 Choong SYM, Scurry JP, Planner RS, et al. Extrauterine malignant
mixed Mullerian tumor of primary peritoneal origin. Pathology
1994;26:497-8.