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30Benign Mesotheliomas, Mesothelial
Proliferations, and Their PossibleAssociation with Asbestos
Exposure
Giovan Giacomo Giordano and Oscar Nappi
Over the past several years the spectrum of mesothelial
pathology has greatly increased (1). Nevertheless, benign
mesotheliomas andmesothelial proliferations represent a rather
broad category, encom-passing clearly dened lesions, aspecic
reactive patterns, and prolif-erating lesions that cannot yet be
specically dened. As any otherhuman tissue, mesothelial epithelium
and submesothelial mesen-chymal tissue react to injuries with
reproducible patterns (24). In par-ticular, benign epithelial
lesions can express one or more of severalgrowth patterns, which
can be divided into papillary, adenomatoid,micro- or macrocystic,
and solid or nodular (Table 30.1); malignantepithelial
mesotheliomas also exhibit a similar microarchitecture. Therange of
benign submesothelial (mesenchymal) proliferations is muchmore
restricted and basically includes reactive brous and broscle-rosing
changes and the solitary brous tumor (formerly called benignbrous
mesothelioma).
Several contributions concerning differential diagnostic
criteriabetween mesothelial reactive changes and malignant
mesotheliomason small specimens (5,6) and cytologic material (7)
have been pub-lished; immunohistochemically, a strong linear
membrane reactivityfor EMA and a nuclear reactivity for p53 are
considered suspicious formalignancy, but to a lesser extent both
can be found also in reactiveproliferations (8). The evaluation of
anamnestic data and clinical pre-sentation always have to be
considered.
Malignant Mesothelioma In Situ
For mesothelial proliferations showing frankly atypical
cytologic fea-tures without stromal invasion, the term malignant
mesothelioma in situhas been introduced; these changes are often
found in proximity of inva-sive mesothelioma or, rarely, before its
development, and have beenconsidered morphologic precursors (9).
Considering the poor effective-ness of any treatment of invasive
mesotheliomas, the recognition of
469
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a stage 0 mesothelioma, on the basis of validated and
universallyaccepted criteria, should represent a critical step in
the management ofthis tumor. Unfortunately, in our experience, so
far, reliable criteria forthis diagnosis have not been codied.
Therefore, since mesothelial reac-tive proliferations often show
several degrees of cellular atypia, a diag-nosis of malignant
mesothelioma in situ should be made with extremecaution considering
the radical surgical therapy following this diagno-sis. At the
present time we think that only if there is a history of
asbestosexposure without evidence of recognized recent inammatory
pathol-ogy and a multifocal or rather extensive mesothelial surface
cell prolif-erations with consistent nuclear atypias, a diagnosis
of malignantmesothelioma in situ should be suggested; otherwise,
the term atypicalmesothelial hyperplasia should be used for these
lesions (6) and a follow-up with periodic observations could be
preferable. Nevertheless, it isnoteworthy that cases of supercial
atypical mesothelial changes asso-ciated with inltrating
mesothelioma have been reported having aninmmunoreactivity for EMA
and p53 similar to that of invasivemesothelioma (8); these features
could represent an additional supportfor a diagnosis of malignant
mesothelioma in situ.
Epithelial Benign Mesotheliomas and Mesothelial
Proliferation
Papillary Pattern
A papillary pattern is not uncommon in epithelial benign and
malig-nant mesothelial proliferations. Papillary-like cell
aggregates are foundalso in cytologic samples from serosal
effusions secondary to malignantas well as benign mesothelial
pathology.
Well-differentiated papillary mesothelioma is an entity
characterizedby a papillary growth pattern.
Well-Differentiated Papillary MesotheliomaWell-differentiated
papillary mesothelioma (WDPM) is a rare andintriguing tumor (1012).
It is currently considered a low-grade malig-nant tumor, more so
than a fully benign tumor, in light of the widespectrum of lesions
that are morphologically similar but biologicallydifferent,
including benign proliferations and aggressive lesions thatmerge
with true malignant mesothelioma.
470 Chapter 30 Benign Mesotheliomas and Mesothelial
Proliferations
Table 30.1. Epithelial growth patterns of mesothelium as
expressedin benign proliferationsEpithelial growth pattern Benign
mesothelial proliferations
Papillary R A, WDPMAdenomatoid R A, ATSolid-nodular R A,
NHMH(Micro-macro) cystic R A, AT, PMMRA, reactive aspecic; WDPM,
well-differentiated papillary mesothelioma; AT, adeno-matoid tumor;
NHMH, nodular histiocytic/mesothelial hyperplasia; PMM,
peritonealmulticystic mesothelioma.
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The large majority of the cases arise in the peritoneum of women
30to 40 years of age. However, sporadic cases also have been
describedin the peritoneum of male patients, as well as in the
pericardium,pleura, and tunica vaginalis (13).
Clinically, the usual presentation is pain and serous effusion.
Macro-scopically, the lesion generally exhibits a supercial,
sometimes multi-focal vegetative proliferation. Microscopically, a
papillary proliferationcharacterized by papillae with a brovascular
stalk lined by bland,single mesothelial cells, is present (Fig.
30.1); no mitosis is usuallydetected; in some case, psammomas
bodies have been described. Pap-illary proliferation is supercial
but occasionally adenomatoid-likemicrotubules in underlined stroma
have been observed.
Immunohistochemically, proliferating cells are reactive for
cytoker-atin (CK) and mesothelial markers (calretinin, HMBE-1).
Carcinoem-bryonic antigen (CEA) is always negative. Especially on
small biopsies,WDPMs have to be differentiated from aspecic
reactive mesothelialhyperplasia, epithelial malignant mesothelioma
with a prominent papillary pattern, and serous papillary carcinoma
of the ovary andperitoneum. Clinical presentation is important in
differentiatingWDPM from reactive mesothelial hyperplasia that
usually is not massforming and from malignant mesothelioma in which
the cytomorpho-logic features are also signicant. Immunoreactivity
for B72.3, Ber-Ep4,CA19.9, and Leu-M1 and negativity for calretinin
and HMBE-1 areuseful markers in differentiating WDPM, as well as
malignant
G.G. Giordano and O. Nappi 471
Figure 30.1. Well-differentiated papillary mesothelioma of
peritoneum. Thiseld shows several papillary projections with a
brovascular stalk lined bybland, at, single mesothelial cells. In
the underneath stroma, a proliferationof duct-like structures is
seen. Inset: a papillary structure with a broad stalkseen at high
power.
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mesotheliomas, from papillary serous carcinoma of the peritoneum
orof the ovary; CEA immunoreactivity is also an excellent
negativemarker for mesothelial neoplasias but is not always
detected in papil-lary carcinoma (14,15).
Adenomatoid (Pseudoglandular, Tubular) Pattern
The adenomatoid pattern is also frequently expressed by
proliferatingepithelial mesothelium as well as epithelial
mesothelial tumors. Some-times associated with a microcystic
pattern, this pattern is typically rep-resented by adenomatoid
tumors. The so-called mesothelioma of theatrioventricular node also
shows a similar pattern but it does not havea mesothelial
origin.
Adenomatoid TumorAdenomatoid tumor (AT) is a benign mesothelial
tumor with a domi-nant tubular pattern. This tumor usually arises
from the mesotheliumof the paratesticular region (16), from the
serosal surface of the uteruswall (17) and, much less frequently,
from that of the ovary, salpynx, andbroad ligament. Exceptionally,
it can arise also from the pleura (18) andpericardium (19).
Macroscopically, AT is usually a small nodule, oftenfound
incidentally if it is less than 1cm. Microscopically, its
growthpattern is characterized by bland, at, epithelioid cells
arranged intubules, gland-like structures, microcysts, or cords
(Fig. 30.2). Not infre-quently, a cytoplasmatic vacuolization is
present with a signet ringlikefeature. A mesothelial origin of the
AT has been denitively conrmedby ultrastructural and
immunohistochemical studies (20,21); this tumoralways is
immunoreactive for CK/cocktail, EMA, and calretinin.
472 Chapter 30 Benign Mesotheliomas and Mesothelial
Proliferations
Figure 30.2. Adenomatoid tumor of rete testis. A proliferation
of duct-like andglandular-like structures in a brous stroma is
shown.
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Sometimes AT has to be histologically differentiated from
adenocar-cinomas, vascular tumors, and on rare occasions, from
malignantepithelial mesotheliomas with a dominant tubular/glandular
pattern.Appropriate immunohistochemical reactions, such as CEA and
otherpossible markers for specic adenocarcinomas as well as
endothelialmarkers, usually help to clarify the diagnosis in
selected cases.
Rarely, cases of AT having an inltrating local pattern have
beenreported, but the behavior of AT is usually indolent and
benign.
Mesothelioma of the Atrioventricular NodeThe so-called
mesothelioma of the atrioventricular node is not a
truemesothelioma. This denition is a misnomer based on historical
obser-vations regarding the similarity of the proliferative cells
with mesothe-lial cells and the lesions pattern with that of an
adenomatoid tumor.Today, it has been accepted that it arises from a
congenital heterotopiaof endodermal tissue (2224). The large
majority of these tumors hasbeen detected during autopsy (some
sporadic cases have been reportedin transplanted hearts) and most
of them, although inconspicuous,range in size from a few
millimeters to 1 to 2cm and have been consid-ered the cause of
death in cardiac arrest or ventricular brillation (23).
Macroscopically, this tumor often exhibits micropolycystic
featuresin the area of the atrioventricular node. Microscopically,
microcysticspaces are lined by bland, at, mesothelioid cells that
are immunore-active for CK; positivity for CEA also has been
reported.
Cystic/Microcystic Pattern
Although cases of AT with a dominant microcystic pattern have
beenreported, the best example of a lesion characterized by this
pattern isthe peritoneal multicystic mesothelioma.
Peritoneal Multicystic MesotheliomaPeritoneal multicystic
mesothelioma (PMM) arises almost exclusivelyfrom the peritoneum
(2,25); exceptional cases have been described inthe testis (26) and
pleura (27). Like adenomatoid tumor, the histogen-esis of PMM has
also been controversial, the true mesothelial originhaving been
conrmed only recently by ultrastructural and immuno-histochemical
studies. Cystic mesotheliomas, arising from serosal peri-toneal
membranes, can apparently involve the parenchyma of
singleperitoneal and pelvic organs. The common clinical setting is
the pelvicperitoneum of young female patients; on the basis of the
size of theproliferation, it can be accidentally detected, present
vague symptoms,or show a palpable abdominal mass and pain; ascitis
is rarely present.It can be also multifocal with synchronous or
metachronous prolifer-ating lesions in several parts of the abdomen
and pelvis. Macroscopi-cally, one cyst (in this case, terms such as
cystic mesothelioma andmesothelial cyst seem more appropriate) or
several cysts with thin walls and variable size are present; cysts
usually have a uid content(2,25).
G.G. Giordano and O. Nappi 473
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Microscopically, the internal cystic surface is lined by bland,
at,endothelioid cells (Fig. 30.3); immunoreactivity for
cytokeratin/cocktail, calretinin, or HMBE-1 is diagnostically
present. A common,sometimes difcult, differential diagnosis is with
(multi)cystic lymph-angiomas; nevertheless, immunoreactivity for
endothelial markers and immunonegativity for cytokeratin usually
permit a correct diagnosis.
Basically, PMM is a benign tumor, but radical surgery is
mandatorybecause of the possibility of recurrences; follow-up is
needed alsobecause of multifocality. Cases of malignant cystic
mesothelioma havebeen reported, but in the majority of cases
cytologic and clinical features generally clarify the diagnosis. It
is important to rememberthat in the spectrum of mesothelial
proliferations, cystic is not alwayssynonymous with benign
(2,25).
Solid/Nodular Pattern
Within reactive hyperplastic changes of the mesothelium, a
solidpattern can be focally or extensively present. Moreover, there
are somepeculiar clinical settings in which this pattern is
characteristicallyobserved:
Inguinal or umbilical hernia sacs, following chronic injury or
incar-ceration of mesothelium (Fig. 30.4): This feature, not
infrequentlyfound in hernia sacs of children but also adults, has
been dened asnodular mesothelial hyperplasia and has sometimes led
to a misdi-agnosis of malignancy (28).
474 Chapter 30 Benign Mesotheliomas and Mesothelial
Proliferations
Figure 30.3. Peritoneal multicystic mesothelioma. Several cystic
structuresinternally lined by at mesothelioid cells are shown.
Inset: mesothelioid cellsstained with cytokeratin (CK).
-
Cardiac excrescences variously interpreted and called
histiocytoidhemangioma-like lesions (HHLL) (29) or
mesothelial/monocyticincidental cardiac excrescence (MICE) (30):
These are characterizedby nests of round mesothelioid cells usually
detected during cardiacsurgery; some authors have considered these
lesions to be artifactu-ally determined by aspirated mesothelial
cells during cardiotomysuction (31).
Nodular aggregates found in transbronchial biopsies: These can
represent a potential source of misdiagnosis, especially versus
neuroendocrine tumors (32).
The immunohistochemical evidence that many, if not most, of
theround mesothelioid cells present in these lesions are
immunoreactivefor CD 68, a hystiocytic marker, and not for
cytokeratin, which is pos-itive only in other cells, has suggested
that in most cases of the above-mentioned pathologic ndings, a
mixed proliferation of histiocytes andmesothelial cells is present;
alternatively, such evidence suggests thatthe mesothelial cells are
entrapped and not proliferating. Consequently,a diagnosis of
nodular histiocytic/mesothelial hyperplasia has beensuggested for
all of them (33).
Mesenchymal Benign Mesothelial Tumors andMesothelial
Proliferations
Benign mesothelial lesions characterized by proliferations of
mesenchy-mal tissue are basically represented by reactive
submesothelial broscle-rotic proliferations and the localized brous
tumor. Submesothelial
G.G. Giordano and O. Nappi 475
Figure 30.4. Nodular mesothelial hyperplasia in the inguinal
hernia sac. Anodular aggregation of mesothelioid cells in the
stroma is seen.
-
brosclerotic proliferations are relatively common reactions of
serosalmembranes to chronic injuries. Pleural plaques (PPs) and
chronic brouspleurisy, with the so-called brothorax at the
extremity of the spectrum,are the best clinically dened of them.
Pleural plaques are rm, some-times calcied lesions, present in the
parietal pleura, microscopicallycharacterized by hypocellular
collagen-rich mesenchymal proliferationwith a distinctive
basket-weave pattern. They can present as single ormultiple lesions
ranging from a few millimeters to several centimeters.A relation
with asbestos exposure is widely accepted and sufcientlydocumented;
in selected cases, association with malignant mesothe-lioma has
been described as well. Other pneumoconioses have beenreported to
be associated with PP; in our experience, in spite of
differentreported considerations, clinical presentation, number of
lesions, andmicroscopic morphology of these cases substantially
overlap those thatare secondary to asbestos exposure.
Chronic Fibrous Pleurisy
Chronic brous pleurisy (CFP), especially in case of small
biopsies, pre-sents serious problems of differential diagnosis with
sarcomatousmesotheliomas if a consistent spindle cell proliferation
is present, orwith desmoplastic malignant mesotheliomas (DMMs) if,
as occursmore frequently, the lesion is sclerotic and paucicellular
(Fig. 30.5).
476 Chapter 30 Benign Mesotheliomas and Mesothelial
Proliferations
Figure 30.5. Fibrosing pleurisy (FP) (left) and desmoplastic
malignantmesothelioma (DMM) (right) are shown side by side. The two
lesions areimpressively similar; DMM (upper right) shows some
degree of nuclear atypia.Cytokeratin is strongly expressed in DMM
(lower right) but a focal and weakpositivity is also present in FP
(lower left).
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Reliable criteria of malignancy, in absence of frank sarcomatous
over-growths, are currently being considered (6): absence of a
zonal effect(consisting of a supercial high cellularity and deep
paucicellularity,usually present in chronic brotic reactions);
invasion of surroundingtissues (adipose tissue, skeletal muscle,
lung parenchyma); the so-called bland necrosis, typical of DMM and
consisting of circumscribedareas in which necrosis is demonstrated
by a poorly stained eosin; andabsence of an elongated capillary
vessel perpendicular to the serosalsurface as an expression of the
reactive granulation tissue usuallypresent in CFP.
Immunohistochemistry is usually of little help; it is remarkable
that,after an injury causing denudation of mesothelial layers,
submesothelialbroblasts that normally expressed vimentin only
acquire immunoreac-tivity for low molecular weight cytokeratin. For
this reason, in the pres-ence of mesenchymal mesothelial
proliferations, the positivity forcytokeratin should not be
considered as diagnostic of desmoplasticmesothelioma (2,6).
Nevertheless, a clear immunonegativity, or aweakly focal positivity
for cytokeratin, favors the diagnosis of brosingpleurisy, and the
immunopositivity of brosclerosing proliferation inl-trating lung
parenchyma or striated muscle favors that of DMM.
Localized Fibrous Tumor of the Pleura
Localized brous tumor (LFT) of the pleura, although
variouslynamed, has been thought for many decades to arise from
surfacemesothelial cells and, therefore, to be a benign
mesothelioma. Today, itis considered a pleural localization of a
potentially ubiquitous lesion ofmesenchymal origin (34). It can
arise in the pleura of patients of bothsexes and of any age. In
about 50% of cases, the tumor is asymptomaticand incidentally
found; otherwise, cough, pain, and dyspnea arecommon symptoms.
Typically, LFT is separated from the (generally visceral) pleura by
a peduncle, resulting in a polypoid mass, which can also reach
great size (up to 40cm) and consistent weight. The cutsurface is
rmly brous.
Microscopically, several features have been described:
sclerosing,myxoid, and hemangiopericytomatous. Typically LFT is
immunoreac-tive for CD 34 (35); the positivity for this marker is
needed to con-rm the diagnosis (Fig. 30.6). Bcl-2 (36) and CD 99
(37), both positivein the majority of cases, are considered useful
to distinguish LFT fromsarcomatoid malignant mesothelioma, which is
only sporadicallyimmunoreactive for them (37,38).
Some cases of LFT have a malignant behavior; histological
criteriafor selecting them are similar to those of other
mesenchymal neo-plasias: an increase in cellularity, nuclear
atypias, an inltrative pattern,and a greater mitotic index (more
than 4 high-power elds). Solitarybrous tumors have been described
everywhere, including the peri-cardium (39), vaginalis testis (16)
and the peritoneum (40).
G.G. Giordano and O. Nappi 477
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Possible Relation of Benign Mesotheliomas andMesothelial
Proliferations to Asbestos Exposure
To the best of our knowledge, excluding some sporadic and
question-able reported cases, in none of the benign mesotheliomas
described,above does the asbestos exposure play a statistically
signicant role;the only mesothelial reactive change generally
considered secondaryto asbestos exposure is the brosis
macroscopically expressed bypleural plaques (2).
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