Over several years, it has been a matter of debate whether or not the use of a uterine balloon manipulator during laparoscopic hysterectomies for endometrial carcinoma (EC) may cause tumor disruption resulting in a positive peritoneal cytology. More recently, this procedure has been associated with vascular pseudoinvasion in cases of low-risk EC. In this study, we evaluated a series of 21 cases of low-risk EC treated by laparoscopic hysterectomy (LH) to determine the incidence of this finding and to better characterize its histopathologic features. In addition, we reviewed 28 cases of low-risk EC treated by total abdominal hysterectomy (TAH) for comparison. Clinical information was obtained from patients' charts. Hematoxylin and eosin-stained slides were retrospectively reviewed in all cases. The following information was recorded: tumor grade and tumor stage according to the International Federation of Gynecology and Obstetrics, tumor shape (polypoid versus flat), presence or absence of vascular space involvement (VSI), size and location of the vessels with tumor involvement, concomitant presence of artifactual clefts in the myometrium with tumor involvement if applicable, presence or absence of lymph node sampling and the presence or absence of involvement at this site, and results of peritoneal cytology. Seven of 21 (33%) cases of low-risk EC treated by LH in this study showed VSI. None of the cases treated by TAH had VSI (P=0.001). In all of the cases of LH with VSI, the endometrial tumor was polypoid. VSI was detected only in large, thick-walled vessels in the outer myometrium or in ectatic vessels anywhere in the myometrium; no tumor fragments were seen in small vessels. The tumor in the VSI consisted of conspicuous fragments of tumors detached from the vascular wall. The VSI also lacked the inflammatory perivascular infiltrate seen in many cases of bona fide lymphovascular invasion. In addition, all of the cases with VSI also showed fragments of tumor in artifactual clefts in the myometrium. None of the cases of LH in which lymph node sampling and/or peritoneal cytology were obtained showed tumor at this site. In summary, our study confirms that LH is indeed associated with a higher rate of vascular pseudoinvasion when compared with TAH. However, we cannot attribute this phenomenon to mechanical disruption, displacement, and transport of tumor tissue into vascular spaces by the use of a uterine manipulator alone. Instead, we propose that pathologists may be generating postoperative pseudoinvasion by mechanically transporting tumor into vascular spaces during the grossing process. Proper recognition of this artifact is of utmost importance to avoid the overtreatment of patients undergoing LH for low-risk EC.

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Sticky platelet syndrome has been described as a hereditary thrombophilic condition. The aim of this study is to identify the presence of platelet hyperaggregability in patients who have experienced thrombosis. Light-transmittance platelet aggregometry was used to assess for spontaneous platelet aggregation, aggregation in response to full and low-dose (LD) epinephrine (Epi) and adenosine diphosphate, as well as arachidonic acid, and identify a distinct pattern of platelet hyperaggregability. Light-transmittance platelet aggregometry results were correlated with PFA-100® (Dade-Behring, Marburg, Germany) results, when available. An exaggerated response to LD Epi was found in 68% of patients with thrombosis compared to only 36% of healthy controls (P=0.034). Patients with thrombosis, either arterial or venous, demonstrated an exaggerated response to LD Epi nearly twice as frequently as healthy controls, even without significant family history of thrombophilia or other known risk factors for thrombosis. This suggests that platelet hyperaggregability may be multifactorial in nature and not necessarily hereditary.

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Epstein-Barr virus (EBV) is known to play a key role in the development of several lymphoproliferative disorders (LPD), ranging from indolent lesions to highly aggressive lymphomas. Here, we describe an incidentally detected unique case of a localized EBV-positive large B cell LPD within a popliteal artery aneurysmal hematoma of a 91-yearold male. Histopathologic examination of an expanding right thigh mass demonstrated organizing hematoma with microscopic clusters of atypical large lymphoid cells with a nongerminal center B cell immunophenotype, a high proliferation rate by Ki-67 staining, and strong positivity for EBV-encoded RNA (EBER) by in situ hybridization. An 18-month followup revealed no evidence of disease progression. The presence of cytologically malignant EBV-positive large B cells supports a LPD, with a differential diagnosis that includes a spectrum of EBV-associated lesions, including diffuse large B cell lymphoma (DLBCL) of the elderly, DLBCL associated with chronic inflammation, as well as a variety of recently described indolent EBV-associated large B cell proliferations occurring in cardiac fibrin thrombi, atrial myxomas, and other unusual sites. This case is the first report of an indolent fibrinassociated EBV-positive LPD occurring in an aneurysmal hematoma of the extremity. This lesion may represent the indolent end of the spectrum of EBV-associated large B cell proliferations, and recognition of such lesions may prevent unnecessary aggressive treatment.

Objectives To improve diagnostic accuracy in differentiating hematogones from leukemic blasts in cases of precursor B-lymphoblastic leukemia/lymphoma (B-ALL), particularly those that are posttreatment or after bone marrow transplant, and to provide an algorithmic approach to this diagnostic challenge. Methods A seven-color antibody panel including CD10, CD19, CD45, CD38, CD34, CD58, and CD81 was generated to assess the feasibility of a single tube panel and provide an algorithmic approach to distinguish hematogones from B-ALL. Fifty-three cases were analyzed, and results were correlated with histology and ancillary studies. Results There was a significant difference in mean fluorescent intensity (MFI) for CD81 and CD58 when comparing hematogones and B-ALL populations (P < .001). B-ALL cases had a mean (SD) MFI of 24.6 (27.5; range, 2-125) for CD81 and 135.6 (72.6; range, 48-328) for CD58. Hematogones cases had a mean (SD) MFI of 70.2 (19.2; range, 42-123) for CD81 and 38.8 (9.4; range, 23-58) for CD58. Conclusions The flow cytometry panel with the above markers and utilization of the proposed algorithmic approach provide differentiation of hematogones from B-ALL. This includes rare cases of hematogones and B-ALL overlap where additional ancillary studies are necessary.

S100 T-cell lymphomas are infrequent, and except 1 all have been CD4 negative. On the basis of an index case of CD4 S100 T-cell prolymphocytic leukemia (T-PLL), we studied S100 protein expression in 19 additional T-PLLs and 56 other T-cell lymphomas that are usually CD4, including 15 angioimmunoblastic T-cell lymphomas, 24 anaplastic large cell lymphomas (16 ALK and 8 ALK), 7 mycosis fungoides/Sézary syndrome, and 10 peripheral T-cell lymphoma, not otherwise specified (PTCL, NOS). Two additional S100 CD4 PTCL, NOS cases were also reviewed. Thirty percent (6/20) of T-PLLs were S100 compared with 0/56 other T-cell lymphomas with previously unstudied S100 reactivity (40 CD4, 2 CD8, 11 CD4/CD8, 3 unknown) (P=0.0007). There were no significant differences between the S100 and S100 T-PLLs with regard to the male:female ratio (2:1 vs. 1:1), age (71.6±7.7 vs. 65.4±9.3), peripheral blood lymphocyte count (67.2±116.6 vs. 101.1±159.7×10/L), or median survival (463 vs. 578 d, where known). The 2 S100 PTCL, NOS cases occurred in a 7-year-old boy and a 45-year-old woman. Both had involvement of the bone marrow and peripheral blood but were morphologically unlike T-PLL and lacked TCL1 gene rearrangement. These results demonstrate that S100 T-cell lymphomas include a subset that are CD4 and most often, but not exclusively, are T-PLL. Although having diagnostic implications, there were no documented clinical differences between the S100 and S100 T-PLLs.