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.
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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