Splenic Vascular Tumors: A Histologic, Immunophenotypic, and Virologic Study

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Abstract

Vascular tumors of the spleen include several different entities, some of which are unique to that organ. Twenty-two such proliferations were studied, including 10 hemangiomas, six littoral cell angiomas, four angiosarcomas, and two hamartomas. The hemangiomas included seven with localized tumors and three with diffuse angiomatosis of the spleen. All cases were studied by paraffin section immunohistochemistry with a large panel of antibodies. In addition, all cases were studied for the presence of the Kaposi's sarcoma-associated herpesvirus (KSHV) using the polymerase chain reaction. The morphologic findings were similar to those previously reported. All proliferations were vimentin positive, and one angiosarcoma was focally keratin positive. All cases reacted for CD31, whereas 20 of 22 were positive for von Willebrand's factor and 19 of 22 were positive for Ulex europeaus. CD34 expression in lining cells was identified in 10 of 10 hemangiomas, two of four angiosarcomas, and one of two hamartomas, whereas all six cases of littoral cell angioma were negative. CD68 was expressed in all cases of littoral cell angioma but was also positive in all three diffuse hemangiomas, two of seven localized hemangiomas, and two of four angiosarcomas. CD21 expression was restricted to the lining cells of littoral cell angioma, and CD8 expression was only identified in two of two hamartomas and two of four angiosarcomas. KSHV was not detected in any of the cases. These findings suggest that there are distinct immunophenotypic as well as morphologic features of splenic vascular tumors. Littoral cell angiomas have a characteristic CD34-/CD68+/CD21+/CD8- immunophenotype and hamartomas have a characteristic CD68-/CD21-/CD8+ phenotype. The frequent CD68 expression in diffuse hemangioma suggests an immunophenotypic difference from localized hemangioma of the spleen.

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Most cited references 27

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Epstein-Barr virus receptor of human B lymphocytes is the C3d receptor CR2.

Douglas Fearon, J M Fingeroth, T Tedder … (1984)

Identity of the Epstein-Barr virus (EBV) receptor with the complement receptor type 2 (CR2) was established in three sets of experiments using the monoclonal antibodies, HB-5 and anti-B2, which recognize a Mr 145,000 B-lymphocyte membrane protein that is CR2. First, the rank order for binding of fluoresceinated EBV to four lymphoblastoid cell lines (SB, JY, Raji, and Molt-4) was identical to the rank order for binding of HB-5 and anti-B2 by analytical flow cytometry. Second, pretreatment of cells with HB-5 followed by treatment with goat F(ab')2 fragments to mouse IgG blocked binding of fluoresceinated EBV on SB, a B-lymphoblastoid cell line. Virus attachment was not inhibited by HB-5 alone, second antibody alone, rabbit anti-C3b receptor, or UPC10 (an irrelevant monoclonal antibody). Third, transfer of CR2 from SB to protein A-bearing Staphylococcus aureus particles, to which HB-5 had been absorbed, conferred on them the specific ability to bind 125I-labeled EBV. We conclude that CR2 is the EBV receptor of human B lymphocytes.

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Primary angiosarcoma of the spleen. A clinicopathologic study of 40 cases.

Kim Krishnan, J Meis, Christine S. Falk (1993)

Forty primary splenic angiosarcomas occurring in 21 men and 19 women, 19-84 years old (median 59 years) are reported. Patients presented with splenomegaly (35 of 38, 92%), abdominal pain (33 of 40, 83%), and systemic symptoms such as fatigue (2 of 40, 5%), fever (4 of 40, 10%), and/or weight loss (16 of 40, 40%). Five (13%) experienced splenic rupture associated with hemoperitoneum. Abnormal laboratory findings included cytopenia (31 of 34, 91%), leukocytosis (8 of 21, 38%), and thrombocytosis (1/39, 3%). Most spleens weighed 500-1,000 g (mean, 1,180 g). The cut splenic surfaces showed multiple hemorrhagic nodules that were frequently associated with infarction, although some had a diffuse pattern of involvement. Microscopically, there were a variety of histologic patterns displayed by the vasoformative component. A honeycomb or sponge-like pattern was common in some, whereas others simulated a cavernous hemangioma or normal splenic sinuses (pseudosinusoidal pattern). Papillary endothelial tufts and solid proliferations of spindled to round to epithelioid cells were also seen. Factor VIII-related antigen was detected in 19 of 23 cases, BMA-120 in 18 of 23, UEA-1 receptor in 18 of 23, and vimentin in 23 of 23 as well as CD68 antigen in 1 of 23 cases. S-100 protein and cytokeratin were not found in any of the 23 cases studied. Metastases in 22 of 32 patients (69%) were to the liver (13 patients), bone or bone marrow (7 patients), lymph nodes (1 patient), and brain (1 patient). Three patients had concomitant malignancies and one had a prior history of a mixed B-cell lymphoma 5 years previously that had been treated with chemotherapy. Follow-up in 38 patients revealed that 30 (79%) are dead at a median interval of 6 months (range 0-48 months) and 8 are alive 5-21 months after diagnosis. These findings indicate that splenic angiosarcoma is an aggressive neoplasm with a high metastatic rate and an abysmal prognosis. Recognition of the wide range of histologic patterns is of diagnostic value but no apparent prognostic significance.

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Cytokeratin expression in epithelioid vascular neoplasms.

G R Dickersin, Andrew A. Rosenberg, A Bhan … (1990)

Seven epithelioid and eight non-epithelioid vascular tumors were studied by the avidin-biotin-peroxidase method for the presence of endothelial- and epithelial-associated markers, using Ulex europaeus agglutinin-1 (UEA-1) lectin, and antibodies directed against factor VIII-related antigen, (FVIII-RA), vimentin, keratin, carcinoembryonic antigen, and epithelial membrane antigen. The cases included four epithelioid hemangiomas, two epithelioid hemangioendotheliomas (EHE), one epithelioid angiosarcoma (EAS), four common non-epithelioid capillary hemangiomas, and four non-epithelioid angiosarcomas. Staining for FVIII-RA, UEA-1, and vimentin were observed in all cases. The EAS showed staining for keratin in formalin-fixed, paraffin-embedded sections and in frozen sections. Staining for keratin was also observed in frozen sections of one EHE. Both keratin-positive vascular tumors were confirmed with electron microscopy. Carcinoembryonic antigen and epithelial membrane antigen stains were negative in all cases. Our results show that the epithelioid vascular tumors EHE and EAS, in addition to staining for the endothelial markers and vimentin, may also express the epithelial marker keratin. This is important since these tumors may closely resemble carcinomas by routine light microscopy. This study further underscores the importance of using a broad panel of immunohistochemical markers in the diagnostic workup of soft-tissue neoplasms.