Placental Site Nodule Research Articles

Evaluation of Pregnancy-Related Cells in Endometrial Cytology

To determine the significance of pregnancy-related cells in endometrial smears.Pregnancy-related cells in 4429 endometrial smear samples were retrospectively analyzed and evaluated for clinicopathologic and cytomorphologic features.Of the 4429 endometrial smears taken for cancer screening, pregnancy-related cells were detected in 12 cases (0.3%). They were estimated cytologically as negative or suspicious and confirmed as cases ofspontaneous abortion (8 cases), placental site nodule (3 cases), and partial hydatidiform mole (1 case). Decidual cells were observed in all cases, and some of these showed atypia. Trophoblasts were observed in 5 (41.7%) of the 12 cases. Syncytiotrophoblasts were observed in 1 case (8.3%) and nonsyncytiotrophoblasts in 5 (41.7%) of the 12 cases. Pregnancy-related cells were observed in an endometrial smear in 7 cases; other cases were missed during cytologic examination and were retrospectively identified.Pregnancy-related cells are likely to be missed because they are difficult to identify or are surrounded by a cluster of endometrial cells. The decidual cell is a key cell for the cytologic diagnosis of pregnancy-related cells. Determining the existence of pregnancy-related cells in endometrial smears is important for the further assessment of patients and the differential diagnosis of several endometrial lesions.

Cyclin E and p16 Immunoreactivity in Epithelioid Trophoblastic Tumor???An Aid in Differential Diagnosis

Epithelioid trophoblastic tumor (ETT) is a relatively uncommon trophoblastic tumor that can be confused with several trophoblastic and nontrophoblastic lesions, notably the placental site nodule and invasive squamous carcinoma of the cervix. In this report, we analyzed the immunoreactivity of two cell cycle-regulated proteins, cyclin E and p16, in ETTs, placental site nodules and cervical squamous carcinomas to determine whether they are useful in their differential diagnosis. Other trophoblastic lesions were also evaluated. Using an H-score based on both percentage of positively stained cells and immunointensity, we found that ETTs demonstrated a much higher cyclin E staining score than placental site nodules (P<0.0001) permitting distinction of ETTs and placental site nodules with a sensitivity of 94.7% at a specificity of 91.7% using a cutoff H-score value of >40. Only two placental site nodules had scores above the cutoff and both showed morphologic features that placed them in an intermediate position between a typical placental site nodule and an ETT, so-called "atypical PSN." p16 immunoreactivity, was not detected in any of the ETTs and placental site nodules, whereas it was strongly and diffusely positive in the vast majority of cervical squamous carcinomas examined (83/87 cases) (P<0.001). Therefore, cyclin E expression is useful in distinguishing an ETT from a placental site nodule and p16 expression is useful in distinguishing an ETT from a cervical squamous carcinoma. The majority of other types of trophoblastic lesions showed diffuse and intense nuclear immunoreactivity for cyclin E whereas none were positive for p16.

Expression Pattern of the Activating Protein-1 Family of Transcription Factors in Gestational Trophoblastic Lesions

The human placenta is an endocrine tissue with a unique capacity for rapid, but tightly controlled, proliferation and invasion. Gestational trophoblastic diseases (GTDs) are placental pathologies with endocrine activity and partially malignant potential and include hydatidiform moles, placental site nodules, and tumors such as placental site trophoblastic tumor and choriocarcinomas. The activating protein-1 (AP-1) family of transcription factors is composed of the cellular homologs of the Jun and Fos oncoproteins, which are immediately involved in cellular proliferation, differentiation, and invasion processes and in the regulation of endocrine genes. The expression pattern of the AP-1 family in the normal human placenta has been recently described, where most of the factors were found in the extravillous (invasive) trophoblast. Their systematic expression in GTD has not been studied thus far. For this reason in this study, we investigated the expression pattern of the AP-1 family in GTDs and compared it with the expression in normal placenta using immunohistochemistry with specific polyclonal antibodies against all members of the AP-1 family (JunB, JunD, c-Jun, c-Fos, FosB, Fra-1, Fra-2). Immunohistochemistry was performed on normal human placentas (positive control) and on 28 cases of GTD including 7 choriocarcinomas and 21 hydatidiform moles. In the normal placenta and in hydatidiform molar samples, most AP-1 factors (especially c-Jun, JunD, and Fra2) were expressed in the intermediate (extravillous) trophoblast. In addition, in molar lesions, strong expression was found in trophoblasts proliferating from the surface of villi. There was only a weak expression of JunB and Fra2 in small fractions of villous cyto- and syncytiotrophoblast nuclei. In choriocarcinomas, there was a strong expression for c-Jun, JunD, Fra1, and Fra2. The specific localization to extravillous trophoblasts and their expression pattern in GTDs indicate that the AP-1 family of transcription factors might be implicated in regulating proliferation and invasion of trophoblasts and play a role in the pathogenesis of GTDs.

Expression pattern of the AP-1 family of transcription factors in Gestational Trophoblastic Diseases (GTD)

The human placenta is an endocrine tissue with a unique capacity for rapid, but tightly controlled proliferation and invasion. Gestational trophoblastic diseases (GTD) are placental pathologies with endocrine activity and partially malignant potential and include hydatidiform moles (HM), placental site nodules (PSN) and tumors such as placental site trophobastic tuor (PSTT) and choriocarcinomas (CC). The AP-1 family of transcription factors (activating protein-1) is composed of the cellular homologs of the Jun and Fos oncoproteins, immediately involved in cellular proliferation, differentiation and invasion processes as well as in the regulation of endocrine genes. We have recently described the expression pattern of the AP-1 factors in the normal human placenta. Their systematic expression in GTD has not been studied so far. For this reason in the present study we investigated the expression pattern of AP-1 family in GTD and compared it to the expression in normal placenta by using immunohistochemistry with specific polyclonal antibodies against all members of the AP-1 family (JunB, JunD, c-Jun, c-Fos, FosB, Fra1, Fra2). Immunohistochemistry was performed on nomal human placentas (positive control) and on 20 cases of GTD including four choriocarcinomas, one PSTT, one PSN and fourteen hydatidiform moles. In the normal placenta and in hydatidiform molar samples most AP-1 factors (especially c-Jun, JunD and Fra2) were expressed in the intermediate (extravillous) trophoblast. In addition, in molar lesions strong expression was found in trophoblast proliferating from the surface of villi. There was only weak expression of JunB and Fra2 in small fractions of villous cyto- and sycytiotrophoblast nuclei. In choriocarcinomas, PSN and especially in PSTT there was a strong expression for c-Jun, JunD, Fra1 and Fra2. The specific localization to extravillous trophoblast and their expression pattern in GTD indicates that the AP-1 family of transcription factors is probably implicated in regulating proliferation and invasion of trophoblast.

Radiographic and hysteroscopic findings of a placental site nodule

To report a case of placental site nodule discovered on hysterosalpingogram and evaluated by sonohysterography and hysteroscopy in a patient presenting with infertility. Case report. Academic reproductive endocrinology center. A 30-year-old gravida 1 para 1 receiving evaluation for secondary infertility. Hysterosalpingogram, sonohysterography, and operative hysteroscopy with excision. Diagnosis and treatment of intrauterine lesion. Pathology of the excisional biopsy from operative hysteroscopy revealed a placental site nodule. We report one of the first radiographic and hysteroscopic findings of a placental site nodule. This case demonstrates that in addition to the most common causes of uterine filling defects seen on hysterosalpingogram and sonohysterography, rarer lesions like placental site nodule also need to be considered in the differential diagnosis. Placental site nodule is a benign lesion that requires correct diagnosis to distinguish it from other more serious placental findings, but long-term follow-up is unnecessary. Therapy consists of diagnosis and expectant management.

Expression pattern of the CCAAT/enhancer-binding protein C/EBP-beta in gestational trophoblastic disease.

The CCAAT/enhancer-binding protein (C/EBP) family consists of several factors that are important regulators of intracellular processes and hormone action. C/EBP-beta, the most important member of the C/EBP family, was shown recently to be expressed in the normal human placenta where it is localized in villous syncytiotrophoblast and in the extravillous (intermediate) trophoblast but not the villous cytotrophoblast. The purpose of this study was to investigate the expression pattern of C/EBP-beta in gestational trophoblastic disease (GTD) which has not been studied so far. We used immunohistochemistry on a total of 15 cases of GTD including nine complete hydatidiform moles, one placental site nodule (PSN), one placental site trophoblastic tumor (PSTT), and four choriocarcinomas. All our tested specimens showed positivity for C/EBP-beta. The strongest C/EBP-beta expression could be observed in villous syncytiotrophoblast and in the trophoblast proliferations on the villous surface of hydatidiform moles; villous cytotrophoblast was negative. The PSN also showed positive nuclear staining but the expression was not as strong as it was in the hydatidiform moles and the total amount of stained cells was the lowest of all GTD. The PSTT also showed immunoreactivity but with a weaker and more heterogeneous staining than in the choriocarcinomas. The specific expression pattern of C/EBP-beta in GTD indicate that C/EBP-beta could potentially be an additional marker of such lesions.

P63 expression is useful in the distinction of epithelioid trophoblastic and placental site trophoblastic tumors by profiling trophoblastic subpopulations.

Human trophoblast is composed of a heterogeneous population of cells, which give rise to a variety of trophoblastic tumors and tumor-like lesions. In this report, we analyzed the expression pattern of the p63 gene, a transcription factor belonging to the p53 family, in different trophoblastic subpopulations and in trophoblastic lesions. p63 has various isoforms that are classified into two groups designated TA and DeltaNp63 isoforms. The TA isoforms have a p53-like suppressor function, whereas the DeltaNp63 isoforms exert an oncogenic effect. Based on immunohistochemistry and RT-PCR, it appears that cytotrophoblast expresses the DeltaNp63 isoform whereas chorionic-type intermediate trophoblast in the fetal membranes, placental site nodules, and epithelioid trophoblastic tumors expresses the TAp63 isoform. Intermediate trophoblast in the implantation site and placental site trophoblastic tumors does not express p63. Based on the expression patterns of p63 and the previously described expression patterns of other trophoblastic markers, including HLA-G, cytokeratin 18, hPL, and Ki-67, we developed an immunohistochemical algorithm to diagnose trophoblastic lesions. A validation set of 22 trophoblastic lesions and 34 nontrophoblastic tumors were classified correctly using this algorithm. In conclusion, the findings in this study demonstrate that different trophoblastic subpopulations and their related trophoblastic lesions are characterized by distinctive patterns of p63 expression. Recognizing these distinctive expression patterns helps to further elucidate the biology of trophoblast and can also provide a useful tool for the differential diagnosis of trophoblastic lesions.

Postpartaler Uterustumor unklarer Dignität: „Placental Site Nodule“ - eine Falldarstellung

Postpartale Uterustumoren können unterschiedlicher Herkunft sein und eine entsprechend variable Dignität aufweisen. Wir beschreiben den Fall eines unmittelbar postpartal aufgetretenen Uterustumors, welcher trotz mehrfacher Kürettagen persistierte und im Verlauf eine Endomyometritis verursachte. Der Tumor zeigte eine mäßige β-HCG-Produktion, war intermediär sensibel auf Methotrexat und führte nach einem halben Jahr Beobachtungszeit zu starker vaginaler Blutung. Sonographisch zeigt sich der Tumor als schalldicht, inhomogen und mit der Doppler-Untersuchung konnte eine verstärkte Durchblutung im Tumor nachgewiesen werden. Erst durch die laparoskopisch durchgeführte Abtragung des Uterushorns, in welchem der Tumor lokalisiert war, konnte der Befund vollständig entfernt werden. Die histologische Diagnose, welche auch nach mehrfacher Kürettage und Biopsie der Läsion nicht gestellt werden konnte, ergab einen „Placental Site Nodule (PSN)“, ein benigner Tumor aus der Familie der Intermediärtrophoblast (IT)-Tumoren.

Gestational trophoblastic disease. Non-villous forms of gestational trophoblastic disease

The non-villous forms of gestational trophoblastic disease (GTD) include a wide range of morphologic different lesions and cover a wide range of differential diagnosis. Choriocarcinomas (CCA) represent the most malignant form displaying a dimorphic pattern with proliferation of syncytio- and zytotrophoblast. An early start of chemotherapy is of great prognostic impact. Placental site nodule (PSN) and exaggerated placental site (EPS) are non-neoplastic lesions of the intermediate trophoblast without tumorous appearance, whereas placental site trophoblastic tumor (PSTT) and epitheloid trophoblastic tumor (ETT) represent tumorous neoplasms with a potential for local invasion and metastases. PSNs are incidental findings of highly polymorphic cells. In EPS chorionic villi are almost present, endometrial glands and spiral arteries are completely engulfed by intermediate trophoblastic cells without necroses. In PSTT the monomorphic, occasional multinucleated giant cells separating individual muscle fibers and charactersitically blood vessel walls are extensively replaced by trophoblastic cells and fibrinoid material. The ETT consists large necrotic areas with hyalinisation. Typically small blood vessels with preserved walls are located within the center of glycogen-rich monomorphous proliferation of trophoblastic cells.

Extrauterine Lesions of Intermediate Trophoblast

Lesions of intermediate trophoblast arising in the uterus include exaggerated placental site, placental site nodule, placental site trophoblastic tumor (PSTT), and epithelioid trophoblastic tumor. Only 12 examples of extrauterine lesions of intermediate trophoblast (ELIT) have been previously reported; 7 new cases are described herein. Six lesions were located in the fallopian tube or paratubal region and one in the ovary. The patients were 25 to 47 (average 36) years of age. The lesions ranged from 0.6 to 4 cm in diameter; four were cystic. The four placental site nodules (three tubal, one paratubal) were composed of small, sharply circumscribed nodules of intermediate trophoblast with no mitotic activity. The three PSTTs (two tubal, one ovarian) exhibited irregular stromal infiltration by intermediate trophoblast, mitotic activity, and necrosis. Chronic salpingitis was seen in the six tubal/paratubal cases, and endometriosis was seen in four cases. Immunoreactivity for human placental lactogen, human chorionic gonadotropin, and cytokeratin in two cases was consistent with an origin from intermediate trophoblast. ELITs presumably arise from previous ectopic pregnancies, a history of which was present in two of these patients. Follow-up, available on two of the three patients with PSTT, was uneventful at 6 and 12 years, but study of additional cases is necessary to reliably determine the behavior of extrauterine PSTTs.

HLA-G immunoreactivity is specific for intermediate trophoblast in gestational trophoblastic disease and can serve as a useful marker in differential diagnosis.

HLA-G is a nonclassical MHC class I antigen that has been shown to be a specific marker for normal intermediate trophoblast (IT). In this study HLA-G immunoreactivity assessed with an HLA-G specific antibody (4H84) was detected in all 14 cases of choriocarcinoma, 14 placental site trophoblastic tumors, 13 epithelioid trophoblastic tumors, 16 placental site nodules, and nine exaggerated placental sites. In contrast, HLA-G immunoreactivity was not detected in 34 nontrophoblastic uterine neoplasms. HLA-G immunoreactivity was present in all the IT cells of exaggerated placental sites and placental site trophoblastic tumors and in 70-100% of IT cells in placental site nodules and epithelioid trophoblastic tumors. The pattern of distribution of HLA-G in different subpopulations of IT confirms the relationship of various trophoblastic lesions to different types of IT (exaggerated placental site and placental site trophoblastic tumor to implantation site IT and placental site nodule and epithelioid trophoblastic tumor to chorionic-type IT) and suggests that choriocarcinoma is related to villous-type IT because the majority of mononucleate cells in this neoplasm were HLA-G immunoreactive. In conclusion, HLA-G immunoreactivity appears to be specific for IT in gestational trophoblastic disease and can serve as a useful marker in the differential diagnosis of these lesions.

Molecular basis of gestational trophoblastic diseases.

Gestational trophoblastic disease (GTD) encompasses a diverse group of lesions with specific pathogenesis, morphological characteristics and clinical features. The modified World Health Organization-classification of GTD includes complete and partial hydatidiform mole, invasive mole, choriocarcinoma, placental site trophoblastic tumor, epithelioid trophoblastic tumor, exaggerated placental site, and placental site nodule. The various forms of gestational trophoblastic disease can be defined and related to discrete pathologic aberrations occurring at different stages of trophoblastic differentiation. Some of these lesions are true neoplasms, whereas others represent abnormally formed placentas with a predisposition for neoplastic transformation of the trophoblast. Except hydatidiform moles in which the cytogenetic studies have been extensively reported, the pathogenesis of other trophoblastic lesions is poorly understood. Recent studies have shed light on the molecular mechanisms of trophoblastic function, especially as it relates to trophoblastic disease. This review will focus on these advances with special emphasis on the pathogenesis of each specific form of GTD. In addition, the morphology and clinical behavior of each of these entities will be briefly discussed.

The pathology of intermediate trophoblastic tumors and tumor-like lesions.

An intermediate trophoblast is a distinctive trophoblastic cell population from which four trophoblastic lesions are thought to arise: exaggerated placental site (EPS), placental site nodule (PSN), placental site trophoblastic tumor (PSTT), and epithelioid trophoblastic tumor (ETT). EPSs and PSTTs are related to the differentiation of the intermediate trophoblast in the implantation site (implantation site intermediate trophoblast), whereas PSNs and ETTs are related to the intermediate trophoblast of the chorion laeve (chorionic-type intermediate trophoblast). EPSs and PSNs are nonneoplastic lesions, whereas PSTTs and ETTs are neoplasms with a potential for local invasion and metastasis. Microscopically, intermediate trophoblastic lesions can be confused with a variety of trophoblastic and nontrophoblastic tumors, but an appreciation of the morphologic features and immunophenotype allows their diagnosis to be relatively straightforward in most instances. Correct diagnosis is important because each of these lesions may require different therapeutic approaches.

Old ectopic pregnancy remnants with morphological features of placental site nodule occurring in fallopian tube and broad ligament

Placental site nodule (PSN) is an asymptomatic benign proliferation of intermediate trophoblast from a previous gestation that failed to involute. It is most commonly found in the endometrium or endocervix; however, placental site nodule has recently been reported to occur at sites of ectopic gestation. This is the first case of PSN in the broad ligament in direct contact with the fallopian tube. The patient underwent surgery for an adenocarcinoma of the opposite tube. Microscopically and immunohistochemically, the lesion showed the characteristics of a proliferation of intermediate trophoblast.

Placental site nodule and characterization of distinctive types of intermediate trophoblast

Both placental site nodule and exaggerated placental site are described as being composed of intermediate trophoblast (IT), yet their morphological features and clinical presentation differ significantly. This study was undertaken to evaluate the morphological and immunohistochemical features of trophoblastic cells in placental site nodules and compare them with the trophoblastic cells in exaggerated placental sites as well as in different anatomic locations in the developing placenta to evaluate these differences. Forty-two placental site nodules, 20 abortus specimens ranging from 3 to 13 weeks, 8 second- and 10 third-trimester placentas, and 12 exaggerated placental sites were studied by conventional light microscopy and immunohistochemistry. This analysis showed that the trophoblastic cells in the placental site nodule closely resemble those in the chorion laeve. We have designated these cells “chorionic-type IT cells.” They are composed of two populations of cells, one with eosinophilic and the other with clear (glycogen-rich) cytoplasm. The eosinophilic cells tended to be larger with more pleomorphic nuclei, whereas the clear cells were smaller with more uniform nuclei. Chorionic-type IT cells in the chorion laeve and placental site nodule were diffusely positive for placental alkaline phosphatase but were only focally positive or negative for human placental lactogen (hPL), Mel-CAM (CD146), and oncofetal fibronectin. In contrast, hPL, Mel-CAM, and oncofetal fibronectin were diffusely expressed in IT cells in the placental site, both normal and exaggerated. The chorionic-type IT cells in placental site nodule and chorion laeve showed mild proliferative activity as indicated by an increased Ki-67 labeling index (3% to 10%). In contrast, the Ki-67 labeling index in normal and exaggerated implantation sites was zero. The morphological and immunohistochemical features of chorionic-type IT cells contrast with the IT cells in the implantation site that we have designated “implantation site IT cells.” Both types of IT cells develop from a population of trophoblastic cells in the trophoblastic columns that we have tentatively termed “villous IT cells.” Four of 42 placental site nodules were larger (>5 mm) than the remainder and showed transitional features between a typical placental site nodule and an epithelioid trophoblastic tumor, a recently described distinctive gestational trophoblastic tumor. There were no recurrences among the placental site nodules regardless of size. All placental site nodules were immunoreactive for inhibin-α and cytokeratin 18, whereas 33 squamous cell carcinomas of the cervix, which can at times be confused with placental site nodules, were negative. In conclusion, there appear to be three subpopulations of IT cells with distinctive morphological and immunohistochemical features. Different subpopulations can be related to different trophoblastic lesions: implantation site IT cells to an exaggerated placental site and its neoplastic counterpart, placental site trophoblastic tumor and chorionic-type IT cells to a placental site nodule and its neoplastic counterpart, epithelioid trophoblastic tumor.

Immunohistochemical localization of inhibin-alpha in the placenta and gestational trophoblastic lesions.

The immunohistochemical distribution of inhibin-alpha in formalin-fixed, paraffin-embedded tissues was evaluated in placentas (2 to 40 weeks of gestation), implantation sites, and a variety of trophoblastic lesions. In the first trimester placenta, inhibin-alpha was strongly and diffusely expressed in syncytiotrophoblast. Implantation site intermediate trophoblast in normal and exaggerated placental sites was either negative or only weakly and focally positive for inhibin-alpha. With increasing gestational age, the staining intensity and distribution of inhibin-alpha decreased in syncytiotrophoblast but increased in the implantation site intermediate trophoblast. Chorionic-type intermediate trophoblast, present in the chorion laeve of the term placenta, was weakly but diffusely positive for inhibin-alpha. Cytotrophoblast remained negative for inhibin-alpha throughout gestation. In trophoblastic lesions, inhibin-alpha immunoreactivity was detected in all 17 hydatidiform moles (7 complete and 10 partial), 32 placental site nodules, 23 placental site trophoblastic tumors, 15 epithelioid trophoblastic tumors, and 16 choriocarcinomas. Inhibin-alpha immunoreactivity was confined to the syncytiotrophoblast in hydatidiform moles and choriocarcinoma. As with the normal placenta, inhibin-alpha was not detected in cytotrophoblast. To evaluate the utility of inhibin-alpha in the differential diagnosis of gestational trophoblastic lesions, we tested 32 squamous cell carcinoma of the cervix, 11 low-grade endometrial stromal sarcomas, 12 endometrial (7 well differentiated and 5 moderately differentiated) carcinomas, 7 epithelioid leiomyomas, and 10 leiomyosarcomas for the expression of inhibin-alpha. None of these lesions was positive. These data indicate that inhibin-alpha is expressed by all populations of trophoblast except cytotrophoblast and in all gestational trophoblastic lesions. Accordingly, immunohistochemical detection of inhibin-alpha is useful in the differential diagnosis of gestational trophoblastic lesions.

Trophoblast lesions and trophoblast tumors

The clinico-pathologic characteristics and the histological/immunohistological differential diagnosis of villous trophoblastic lesions (complete, partial, and invasive hydatiform moles), gestational choriocarcinoma and trophoblastic tumors and pseudotumors of the placental site (placental-site trophoblastic tumor, exaggerated placental site reaction, placental site nodule) are reviewed in context with aspects of cytogenetics, epidemiology and molecular pathogenesis.

Placental site nodules and plaques: a clinicopathological and immunohistochemical study of 25 cases with ultrastructural findings

Placental site nodules or plaques (PSN-Ps) are nodular benign lesions of the intermediate trophoblast (IT) cells in the endometrium, endocervix, superficial myometrium or fallopian tube, occurring after a remote intrauterine pregnancy. We present a study of 25 cases of PSN-Ps These lesions occurred in patients aged 18 to 44 years. Most were discovered incidentally in endometrial curettage specimens. The specimens were received as part of clinical investigations for menorrhagia, per vaginal bleeding or pelvic pain. None of the PSN-Ps was visible grossly. Microscopically, they were mostly multiple, well-circumscribed, oval or plaque-like cellular nodules. The IT cells typically had abundant vacuolated or eosinophilic cytoplasm. The nuclei were irregular, large, hyperchromatic, often degenerate-looking and either mononucleated, multinucleated or multiclefted. Hyalinization surrounding individual or groups of IT cells, or located in the centre of the nodules, was a constant feature in all cases. The lesional cells were strongly immunoreactive to CAM 5.2, 34 beta E12, AE1/AE3, EMA and vimentin. Some cases showed focal positivity to HCG and HPL. PLAP staining was consistently negative. Ultrastructurally, the IT cells showed prominent nuclear variation in size and shape. The abundant, vacuolated cytoplasm contained some rough endoplasmic reticulum and loosely arranged filaments. This study describes the clinicopathological and immunophenotypic features of 25 cases of PSN-Ps including the ultrastructural findings of one case.

Extrauterine (tubal) placental site nodule

The clinicopathological and immunohistochemical features of the second case of placental site nodule (PSN) of extrauterine, tubal location are presented. The lesion was incidentally found in the right tube during a cesarean section and eventual tubal ligation in a 23-year-old women gesta 2 para 1, after an uneventful 39-week intrauterine pregnancy. Grossly, the right Fallopian tube had a 1 cm dilatation filled by necrotic material. Microscopically, the lumen of the Fallopian tube was effaced and replaced by a rim of pleomorphic intermediate trophoblastic (IT) cells with pseudoinvasive parietal features which were positive for human placental lactogen, placental alkaline phosphatase, epithelial membrane antigen and CAM5.2. The Ki67 index was 3%. Due to its bizarre microscopic appearance, this lesion should be included in the differential diagnosis with malignant conditions. Both origins from a previous subclinical extrauterine tubal pregnancy and a possible migration of IT from a uterine implantation are considered.

Placental site nodule occurring in a fallopian tube

The placental site nodule (PSN), a recently described benign lesion of intermediate trophoblast, is usually an incidental finding in younger women. It is a well-circumscribed, round to oval lesion that is extensively hyalinized and immunohistochemically stains for cytokeratin, placental alkaline phosphatase (PLAP), human placental lactogen (HPL) and, focally, for human chorionic gonadotropin (HCG) and epithelial membrane antigen (EMA). Thus far, the cases reported have been found in endometrial curettage or hysterectomy specimens. The pathogenesis of PSN is yet to be ascertained; however, there is wide acceptance of the fact that it represents a remnant of the placental implantation site. If this is indeed the case, it should not be surprising to find PSN occurring at sites of ectopic gestation. We describe herewith a case in which PSN was found in a fallopian tube segment resected in a postpartum tubal ligation.