So-Called Peritoneal Implants of Ovarian Carcinomas

Path. Res. Pract. 182, 195-201 (1987)

So-Called Peritoneal Implants of Ovarian Carcinomas Problems in Differential Diagnosis Dieter Dienemann and Heinz Pickartz Institut fOr Pathologie, Klinikum Steglitz, Freie Universitat Berlin, FRG

SUMMARY The aim of this paper is the differential-diagnostic distinction of peritoneal 'implants' of serous ovarian tumours from morphologically similar lesions in the peritoneum. The authors investigated 22 cases of ovarian carcinomas, 'implants' of ovarian carcinomas, reactive mesothelial proliferates, endosalpingiosis, benign and malignant mesotheliomas, as well as papillary carcinomas of the pelvic peritoneum with conventional histological stainings and immunohistochemical methods (immunoperoxidase, ABC method). The cells of almost all mentioned lesions express cytokeratin, only the cells of the reactive mesothelial proliferates are partially keratin-negative. CEA was not detected in any of the lesions. Alpha-i-antitrypsin was present in the cells of some ovarian carcinomas and their implants. Lysozyme was found focally in some ovarian carcinomas and in some reactive mesothelial proliferates. An exact differentiation of peritoneal 'implants' as metastases of ovarian carcinomas or autochthonous neoplasias in the course of multifocal tumour development is not possible on the basis of our immunohistochemical findings.

Introduction Serous ovarian tumours may be accompanied by pathological lesions in the parietal and visceral peritoneum and in the greater omentum, which are often difficult to distinguish from tumour manifestations. An exact staging requires the differentiation of intraperitoneal implantation metastases of the ovarian tumour, so-called peritoneal implants, from other peritoneal lesions. This differentiation is of great importance because the evaluation of a pathological lesion in the greater omentum as a tumour manifestation implies stage pT 3 instead of stage pTl in a primary tumour otherwise restricted to the ovary, which may have therapeutic consequences. Reactive mesothelial proliferates and peritoneal endosalpingiosis can pose considerable differential-diagnostic difficulties. In rare cases the peritoneal manifestations, particularly in the pelvic peritoneum, are as extensive as those of the ovary or even more extensive, and so a peritoneal mesothelioma must be considered in the differ© 1987 by Gustav Fischer Verlag, Stuttgart

ential diagnosis. In addition, in the case of small serous borderline carcinomas with extensive 'implants' the question arises as to whether the latter are actually implantation metastases of the ovarian tumour or whether they represent neoplasms of the peritoneal mesothelium that developed autochthonously in a certain temporal relation to the ovarian tumour. Material and Methods Differential-diagnostically relevant lesions of the peritoneum were examined in 22 women between 22 and 76 years of age (mean age: 47,7 years). The specimens examined were surgical resecta and biopsies, in one case autopsy material. Type and origin of the specimens are listed in Table 1. The morphological findings differentiated by us partially occurred in combination. The different lesions will be described separately as follows: 1. Ovarian carcinomas (11 cases) and one carcinoma of the Fallopian tube. The classification of the ovarian carcinomas according to the WHO is depicted in Table 2. 0344-0338/87/0182-0195$3.50/0

196 . D. Dienemann and H. Pickartz Table 1. OIigin of the investigated tissues Case No. 1 OB 2 OmRJSO 3 LN/OIPB 4 HS 5 PB 6 PB 7 HSO 8 HSO/OmR

Case No. 9 OmRJSO 10 HSIHSO 11 HSO/OmR 12 HSO 13 HSO/OmR 14 HSO/OmR 15 SO

Case No. 16 O/OmR 17 HSO/OmR 18 HSO/OmR 19 SO 20 HlOmR 21 HSOlPr 22 G

OB = ovarian biopsy, OmR = omentum resectum, SO = salpingoophorectomy, LN = lymph node, 0 = ovarectomy, PB = peritoneal biopsy, HS = hysterosalpingectomy, HSO = hysterosalpingoophorectomy, 0 = oophorectomy, H = hysterectomy, Pr = proctectomy, G = gastrectomy

Results

Table 2. Type of examined ovarian tumours Serous papillary carcinoma of borderline type (completely or partly superficial) Serous papillary carcinoma Endometroid papillary carcinoma Clear-cell papillary carcinoma

The immunohistochemical examination was applied using the avidin-biotin complex method according to Hsu et al. lO • After deparaffination and desiccation the sections were incubated for 15 min with pronase. A 20-minute incubation period with a nonspecific serum was done prior to application of the primary antibodies. The reaction with the biotinized secondary antibody and the avidin-peroxidase complex was performed with the ABC kit (Fa. Vector). All specimens were examined for alpha-l-antitrypsin (alpha-1-AT), lysozyme, CEA and cytokeratin. Incubation with the primary antibody against alpha-1-AT (Fa. Dako) was done for a period of 45 min in a dilution of 1 : 800, with the antibody against lysozyme (Fa. Dako) for a period of 45 min in a dilution of 1 : 600 and with the antibody against CEA (Fa. Dako) for a period of 60 min in a dilution of 1 : 200. Incubation with the monoclonal antibody against cytokeratin (Lab systems, supplied by Fa. Camon) was done overnight in a dilution of 1 : 100.

n=6

3

1 1

2. Peritoneal 'implants' (8 cases). - These are papillary-cystic epithelial complexes on or under the peritoneal surface which, according to histologic and cytologic criteria, are suspected as manifestations of an ovarian carcinoma. The implants were present in six cases of serous borderline carcinomas of the ovary and in two cases of invasive ovarian carcinomas of serous and endometroid type. 3. Reactive mesothelial proliferates, partly flat, partly papillary and pseudo papillary (8 cases). In six cases they occurred in combination with invasive and noninvasive ovarian carcinomas. In the remaining two cases they were accompanying lesions of chronic endosalpingitis. 4. Peritoneal endosalpingiosis (4 cases). Two cases were found in the greater omentum that was resected for staging of an ovarian borderline carcinoma. One manifestation in the greater omentum was an accidental finding occasioned by a hysterectomy performed for prolapse. Another case occurred in the hernial sac of a incisional hernia in the absence of a tumour. 5. Mesotheliomas (4 cases). These cases involve two benign papillary mesotheliomas of the peritoneum, one benign cystic mesothelioma of the ovary and one malignant peritoneal mesothelioma (epithelial type) with lymph node metastases and pulmonary metastases as well as invasion of the ovaries. 6. Serous papillary carcinomas of the pelvic peritoneum (2 cases). Paraffin sections of formaldehyde-fixed tissue were examined microscopically. In one case the tissue was fixed in 3% glutaraldehyde, embedded in plastic and examined electron microscopically. The following stainings were applied: H & E, PAS with and without diastase digestion, alcian blue at pH1, alcian blue with hyaluronidase digestion and the Grimelius' argyrophil reaction. For hyaluronidase digestion the deparaffinated sections were incubated at 37 °C for 30 min in a 1% hyaluronidase solution (Fa. Merck). Subsequently, after rinsing with aqua dest. for 10 min, staining was done with a 1 % alcian blue solution at pH1 and for 5 min with a lithium carbonate solution.

As shown in Table 3, the epithelia and mesothelia of nearly all lesions contain a granular, PAS-positive, diastase-sensitive material, apparently glycogen. Medey some of the cells in reactive mesothelial proliferates fail to contain glycogen granules. There was no PAS-positive, diastase-resistant material. In all lesions the cells have as a staining equivalent of the glycocalix a small alcian blue-positive and hyaluronidaseresistant luminal border at the surface. This border was inconstant and comparatively weak in the flat reactive mesothelial proliferates. In one case of serous papillary carcinoma of the pelvic peritoneum "intracytoplasmic" vacuoles that were stainable with alcian blue by ultrastructural examination proved to be intracellular lumina. In the majority of the cases it was possible to stain the stromal intercellular substance with alcian blue because of its content of acid mucopolysaccharides. There was no staining after prior incubation with hyaluronidase. The Grimelius staining in no case revealed cells with argyrophilic granules. Table 3. Results of conventional and immunohistochemical stainings

Peritoneal 'implants' Endosalpingiosis Reactive mesothelial proliferates Ovarian carcinomas Serous carcinomas of the pelvic peritoneum Mesotheliomas

PAS Alc Cker CEA Lys

AlphaI-AT

+ + + + + + -/+ (+) -/+

- /+

+ + + +

+ +

+ +

+

-/(+) -/(+) -/+

Alc = alcian blue, Cker = cytokeratin, Lys = Lysozyme, Alpha1-AT = alpha-l-antitrypsin (+) = weak positive reaction -/+ = mainly negative, focally positive reaction

Peritoneal Implants . 197

Immunohistochemical findings All tumourous and nontumourous epithelia and mesothelia revealed cytokeratin in their cytoplasm. However, in the flat reactive mesothelial proliferates only one part of the cells reacted positive with antibodies against cytokeratin. On the other hand, most of the single-layer mesothelia of the papillary and pseudopapillary proliferates were always strongly positive for cytokeratin. CEA was not detectable in any tumour or in any of the reactive lesions. Lysozyme was only focally located and weakly positive in individual cells of the ovarian carcinomas and single cells of the flat reactive mesothelial proliferates. Alpha-I-AT was only found in the cells of some ovarian carcinomas and their 'implants'. Discussion The lack of neutral mucins in the cells of mesotheliomas and mesothelial proliferates is considered a reliable diag-

nostic criterion differentiating between peritoneal or pleural metastases of mucus producing adenocarcinomas II, 16, 33. Since serous ovarian carcinomas as well as mesotheliomas contain no or on7 small amounts of neutral mucins in their cytoplasm3o,3 - which also holds true for our patient group - the PAS reaction is of no help in the differentiation of ovarian carcinomas, peritoneal 'implants' and mesotheliomas. The intracytoplasmic detection of hyaluronidase-sensitive acid mucopolysaccharide (aMPS) is considered to be a characteristic of malignant mesotheliomas, in contrast to the majority of carcinomas 11, 12,33. This feature is, however, found in no more than 50% of the malignant mesotheliomas l6 , and our own case of a malignant mesothelioma also lacks intracytoplasmatic aMPS. An alcian bluepositive and hyaluronidase-resistant border at the cell surface, on the other hand, was exhibited by all alterations we examined, including mesotheliomas and mesothelial proliferates as well as serous carcinomas, peritoneal 'implants' and cases of endosalpingiosis. Therefore, this phenomenon is also not suitable for the differential diagnosis of the

Fig. 1 a-b. Surface-reactive mesothelial proliferate of the minor pelvis in the surrounding of an ovarian carcinoma. The arrows mark the course of the former peritoneal surface. Predominantly in the basal layers, a small number of the proliferated mesothelia expresses cytokeratin (a H & E X 296, b Immunostaining with anti-cytokeratin antibody x 296).

198 . D. Dienemann and H. Pickartz

mentioned alterations. The rather low staining intensity of the cell surface with alcian blue in the reactive mesothelial proliferates in our material is in accordance with observations made by Kawai et al. l4 . In the past cytokeratin was immunohistochemically demonstrated in mesotheliomas and reactive mesothelial proliferates3, 5, 9, 35 as well as in ovarian tumours of various epithelial types 22 • Our results confirm these findings. The fact that in flat reactive mesothelial proliferates some of the cells do not express keratin may be interpreted as a functional change of mesothelium from surface epithelium to a phagocytic cell. Accordingly, the examination of effusions from the body cavities reveals that some of the mesothelia are keratinnegative35 . Cells from mesotheliomas or reactive mesothelial proliferates are immunohistochemically negative or at most weakly positive for CEA5,9, 16, 19,20,35,36, a fact that can be used for the differentiation of various CEA-positive carcinomas 9, 16, 36. The ovarian tumours and 'implants' investigated here are, however, all CEA-negative.

Fig. 2. Pseudopapillary reactive mesothelial proliferate on the surface of the greater omentum in coexistence with ovarian carcinoma (H & E X 296).

Fig. 3. Benign papillary mesothelioma of the minor omentum in coexistence with gastric carcinoma (H & Ex 118).

In summary, none of the staining procedures and immunohistochemical reactions including the additionally performed immunohistochemical examination for lysozyme and alpha-I-AT permits a safe differentiation between the respective pathological lesions: neither between the cells of reactive mesothelial proliferates and autonomous mesothelial neoplasms on the one hand, and cells of serous ovarian tumours, peritoneal 'implants' and endosalpingiosis on the other, nor between the various lesions themselves. The lack of cytochemical discrimination can be explained by a common histogenesis. Both, the peritoneal mesothelium and the surface epithelium of the ovary, develop from the embryonic coelomic epithelium. Nowadays the surface epithelium of the ovary is considered to be the matrix of the so-called common epithelial tumours of the ovary2. As a consequence, Parmley and Woodruff23 over-extended the general name "ovarian mesothelioma" to all common epithelial tumours of the ovary. This, however, although embryologically justified, seems to be an inadequate simplification since, in most cases, peritoneal mesotheliomas can be distinguished from epithelial ovarian tumours by their morphology '2,33 and also on the basis of an etiological relation with asbestos exposure 12 . According to the strict meaning of the word, peritoneal 'implants' should be implantation metastases of an ovarian tumour. In fact, however, the pathogenesis of the socalled peritoneal implants is unclear31. There are numerous indications for a possible autochthonous development from the extraovarian mesothelium of the pelvis 2 ,26, 27: often, the 'implants' do not develop on but under the serosal surface; 'implants' also occur in the absence of papillary surface formations on non-invasive ovarian carcinoma; the 'implants' can show invasive groth even if the ovarian carcinoma lacks invasive properties (borderline carcinoma) and vice versa; in rare cases, 'implants' also occur in the presence of a benign ovarian tumour. In the same case, the 'implants' can be partly invasive and partly non-invasive 21 . Thus it is possible that ovarian tumours and so-called 'implants' are primary multifocal formations of a histogenetically related epithelium, i.e. the coelomic epithelium, with its special proliferative capacity. The assumed ascension of the carcinogenic agent from the inner ~enitalia via the tubal ostia into the free abdominal cavity ,23 explains the tumor formation both in the area of the ovarian surface epithelium and in the adjacent pelvic mesothelium. On the other hand, this problem is elucidated by the fact that occasionally serous papillary or psammous tumours with the typical morphology of serous ovarian carcinomas occur in the extraovarian peritoneum of the minor pelvis, whereas the ovaries are tumour-free or show only very slight, quantitatively subordinate tumour manifestations ('implants'? )!, 7,13,34. Such tumours should be designated as serous carcinomas of the pelvic peritoneum 7,ro. According to this, serous ovarian tumours, peritoneal 'implants' and serous tumours of the pelvic peritoneum are homologous entities regarding to their embryology, pathogenesis and morphology, although the ovaries are affected by far the most frequently.

Peritoneal Implants . 199

,

.

., Fig. 4 a-b. Papillary-cystic 'implant' of a serous papillary borderline carcinoma of the ovary under the tubal serosa. The cells of the 'implants' express cytokeratin (a H & E X 479, b Immunostaining with anti-cytokeratin antibody x 296).

Fig. 5. Serous carcinoma of the pelvic peritoneum. Large tumour mass, predominantly outside the ovaries (H & E x 296).

Fig. 6. Endosalpingiosis in the greater omentum in coexistence with ovarian carcinoma. Epithelium of tubal type without atypia. Negligible desmoplastic reaction (Alcian blue X 296).

Endosalpingiosis is a small cystic, partly papillary peritoneal epithelial inclusion of the tubal type without any major stromal component. This term make plain the analogy to endometriosis; it was introduced by Sampson28 who initially used it to designate proliferates of the tubal epithelium after salpingectomy. In fact, endosalpinriosis occurs in the entire pelvic peritoneum and omentum3 ,and in addition also in pelvic lymph nodes 15, 17. It is not restricted to the presence of an ovarian tumour, and our experience also shows that it is a relatively frequent incidental finding especially in the greater omentum. In analogy to serous inclusion cysts of the ovary, to peritoneal 'implants' and to serous tumours of the ovary and peritoneum, its development is mainly explained by the capacity of the Mullerian-type mesothelium for proliferation and differentiation, still preserved in older age I8 , 34, which is neither the case for the peritoneal mesothelium in the male38 nor for the pleural and pericardial mesothelium in both sexes 37 • The cystic character of these formations

and their localisation under the peritoneal surface, and also in deeper structures such as lymph nodes, furthermore illustrates the ability of invagination, a feature particularly seen it'l the Mullerian epithelium6, 18. On the basis of the relation observed between endosalpingiosis and salpingitis as well as lavage of the Fallopian tube Zinsser and Wheeler38 , on the other hand, postulate a formation by migration of the tubal epithelium into the abdominal cavity and subsequent implantation. Problems in differential diagnosis can arise if endosalpingiosis occurs in connection with non-invasive or invasive ovarian carcinomas4, 21, 29. In these cases one should try to make a factual and nominal distinction between 'implants' and endosalpingiosis irrespective of their unclear genesis (metastatic or autochthonous formation). In the majority of cases this can be achieved by means of simple morphological criteria: endosalpingiosis is characterized by epithelium of tubal type, the lack of cellular atypias and the quantitatively underdeveloped stroma.

200 . D. Dienemann and H. Pickartz The 'implants' exhibit the morphology of an ovarian tumour with the corresponding cellular atypias and a higher frequency of desmoplastic reactions. In many cases, the mere knowledge of the phenomenon endosalpingiosis helps to prevent a false diagnosis. In the case of one of the serous ovarian carcinomas in our own series, the clear and bland formation of an endosalpingiosis in the greater omentum was classified as a metastasis ('implant') by a previous examiner. Basically, we must assume the possibility of secondary cellular atypias in endosalpingiosis, which may make a differentiation from 'implants' impossible. This was probably the case in a 25-year-old patient from our series who had an incisional hernia after appendectomy and chronic perityphlitis: in the resected hernial sac we found numerous cystic, partly papillary inclusions with epithelial atypias and much psammous calcification, which were morphological suspected to belong to an ovarian carcinoma, whereas there was no clinical indication for the presence of an ovarian or any other peritoneal tumour. In principle, the possibility of carcinoma formation in an endosalpingiosis has to be reckoned with21 , 29, 38, comparable to the situation in the ovary, where ordinary epithelial tumours develop from inclusions of the surface epithelium. Reactive mesothelial proliferates are very frequent secondary findings of the peritoneum, especially in connection with inflammatory precesses or circulatory disorders. Occuring either in a flat form or as solid nodules, they present hardly any differential diagnostic difficulties. Less frequently, however, they occur as delicate papillary formation (24, own findings), so that the papillary structure alone does not necessarily lead to the diagnosis of an autonomous neoplasm. But in the presence of cellular atypia, nodular solid mesothelial proliferates may lead to false diagnoses, as it is shown in the case published by Rosai and Dehnei4 • Psammous calcifications may occur in benign 7 and malignant 12 mesotheliomas, in reactive paRillary mesothelial proliferates 24, in peritoneal 'implants' 1, in serous carcinomas of the pelvic peritoneum7, 13,34, in the tubal mucosa (own observation) and in foci of endosalpingiosis4 , 21, 38. They are particularly frequent in endosalpingiosis, e. 12 of 16 cases examined by Zinsser and Wheeler3 showed these calcifications. This means that in a given case psammous calcifications - irrespective d'f their particularly frequent occurrence in connection with ovarian tumours - are of little differential diagnostic significance, as in general single parameters - including the histochemical reactions studied by us - are only of minor importance in the differential diagnosis of the lesions described here. Knowledge of the tendency of the pelvic mesothelium for proliferation and metaplasia prevents misinterpretation of authochthonous lesions as peritoneal or omental metastases.

f.

Acknowledgments We are indebted very milch to the following pathologists for submittance of specimens: Dr. W. Oehmichen, Monchenglad-

bach (Case No.2); Prof. Dr. Niedobitek and Dr. K. Dumke, Berlin (Cases No.1, 5); Dr. G. Siegismund, Berlin (Case No.4); Dr. V. MaaSen, Berlin (Case No.3). For skillful technical assistance we are grateful to Mrs. 1. Winter, Mrs. R. Wanderer and Mr. L. Oehring. References 1 August CZ, Murad TM, Newton M (1985) Multiple focal extraovarian serous carcinoma. Int] Gynecol Pathol4: 11-23 2 Bassis ML (1960) An embryologically derived classification of ovarian tumors.]AMA 174: 1316-1319 3 Bejui-Thivolet F, Patricot LM, Vauzelle ]L, Viac] (1984) Keratins in malignant mesotheliomas and pleural adenocarcinomas: Comparative immunohistochemical analysis with polyclonal and monoclonal antibodies. Path. Res. Pract. 179: 67-73 4 Burmeister RE, Fechner RE, Franklin RR (1969) Endosalpingiosis of the peritoneum. Obstet Gynecol34: 310-318 5 Corson ]M, Pinkus GS (1982) Mesothelioma: Profile of keratin proteins and carcinoembryonic antigen. Am] Pathol108: 80-88 6 Czernobilsky B, Lancet M (1972) Broad ligament adenocarcinoma of Mullerian origin. Obstet Gynecol 40: 238-242 7 Foyle A, Al-]abi M, McCaughey WTE (1981) Papillary peritoneal tumors in women. Am] Surg Pathol 5: 241-249 8 Genadry R, Poliakoff S, Rottnensch], Rosenshein NB, Parmley TH, Woodruff ]D (1981) Primary papillary peritoneal neoplasia. Obstet Gynecol 58: 730-734 9 Gibbs AR, Harach R, Wagner ]C, ]asan B (1985) Comparison of tumour markers in malignant mesothelioma and pulmonaf6 adenocarcinoma. Thorax 40: 91-95 1 Hsu S-M, Raine L, Fanger H (1981) Use of Avidin-BiotinPeroxidase complex (ABC) in immunoperoxidase techniques: A comparison between ABC and unlabeled antibody (PAP) procedures. ] Histochem Cytochem 29: 577-580 11 Kannerstein M, McCaughey WTE, Churg ], Selikoff I] (1977) A critique of the criteria for the diagnosis of diffuse malignant mesothelioma. Mt Sinai] Med 44: 485-494 12 Kannerstein M, Churg] (1977) Peritoneal mesothelioma. Hum Pathol 8: 83-94 13 Kannerstein M, Churg], McCaughey WTE, Hill DP (1977) Papillary tumors of the peritoneum in women: Mesothelioma or par,illary carcinoma. Am] Obstet Gynecol127: 306-314 4 Kawai T, Suzuki M, Kageyama K (1981) Reactive mesothelial cell and mesothelioma of the pleura. Virchows Arch (Pathol Anat) 393: 251-263 15 Karp LA, Czernobilsky B (1969) Glandular inclusions in pelvic and abdominal lymph nodes. Am ] Clin Pathol 52: 212-218 16 Kwee WS, Veldhuizen RW, Golding RP, Mullink H, Starn], Donner R, Boon ME (1982) Histologic distinction between malignant mesothelioma, benign pleural lesion and carcinoma metastasis. Virchows Archiv (Pathol Anat) 397: 287-299 17 Lange P (1955) Endometriosis-like formations in the lymph nodes of the pelvic wall. Acta Obstet Gynecol Scand 34: 111-119 18 Lauchlan SC (1972) The secondary Mullerian system. Obstet Gynecol Surv 27: 133-146 19 Loosli H, Hurlimann] (1984) Immunohistological study of malignant diffuse mesotheliomas of the pleura. Histopathology 8: 793-803 20 Marshall R], Herbert A, Braye SG, Jones DB (1984) Use of antibodies to carcinoembryonic antigen and human milk fat globule to distinguish carcinoma, mesothelioma, and reactive mesothelium. ] Clin Pathol 37: 1215-1221

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Received August 1, 1986 . Accepted in revised form October 23, 1986

Key words: Ovarian turrmurs - Mesothelial proliferates - Mesothelioma - Peritoneal implants - Endosalpingiosis Dr. D. Dienemann, Institut rur Pathologie, Klinikum Steglitz der Freien Universitat Berlin, Hindenburgdamm 30, D-I000 Berlin 45, FRG