Benign Mesothelioma

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

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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.

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.

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.


Figure 30.2. Adenomatoid tumor of rete testis. A proliferation of duct-like andglandular-like structures in a brous stroma is shown.

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).


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).


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


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).


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).

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).


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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Figure 30.6. Solitary brous tumor of the pleura. The diagnostic positivity forCD 34 is shown.

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Benign Mesothelioma