ABSTRACT
Endometrial stromal sarcoma metastases usually occur within the pelvis and rarely involve the great vessels or the heart. We present the case of a 55-year-old woman who was referred for endovascular therapy to treat presumed thrombosis of the inferior vena cava. The suspected thrombus was recalcitrant to endovascular removal with use of an AngioVac venous drainage device. Results of an intraprocedural transvenous biopsy revealed the mass to be the intravascular extension of an endometrial stromal sarcoma. The patient underwent surgical excision of the tumor, and, shortly thereafter, a hysterectomy and salpingo-oophorectomy. This complex case highlights both the rarity of malignancy masquerading as caval thrombus and the importance of multispecialty collaboration.
Subject(s)
Endometrial Neoplasms/pathology , Heart Neoplasms/pathology , Sarcoma, Endometrial Stromal/secondary , Vascular Neoplasms/secondary , Vena Cava, Inferior/pathology , Biopsy , Diagnostic Errors , Endometrial Neoplasms/surgery , Female , Heart Atria/pathology , Heart Neoplasms/surgery , Humans , Hysterectomy , Middle Aged , Neoplasm Invasiveness , Ovariectomy , Phlebography/methods , Predictive Value of Tests , Salpingectomy , Sarcoma, Endometrial Stromal/surgery , Tomography, X-Ray Computed , Treatment Outcome , Vascular Neoplasms/surgery , Vena Cava, Inferior/diagnostic imaging , Vena Cava, Inferior/surgery , Venous Thrombosis/diagnosisABSTRACT
Abstract Alterations in glutathione (GSH) metabolism are associated with neurodegeneration in Alzheimer's disease (AD), and GSH depletion follows application of exogenous fibrillar amyloid beta (Abeta) peptides in experimental systems; these results are commonly cited as evidence of oxidative damage in AD. We used MC65 human neuroblastoma cells that conditionally express carboxy-terminal fragments of the Abeta precursor protein (Abeta/CTFs) to directly test the hypothesis that GSH is part of the cellular response to stressors associated with Abeta/CTF accumulation and not simply a marker of oxidative damage. Our data showed that Abeta/CTFs accumulated by post-translational processes and were associated with progressive increases in oxidative damage and cytotoxicity. Ethycrinic acid (EA) or diethyl maleate (DEM), reagents that deplete GSH through non-specific thiol adduction, gave rise to dose-dependent cytotoxicity that was independent of Abeta/CTF expression and minimally responsive to alpha-tocopherol (AT). In contrast, buthionine sulfoximine (BSO), a selective inhibitor of GSH synthase, not only augmented Abeta/CTF-associated cell death but unexpectedly potentiated Abeta/CTF accumulation; both outcomes were completely suppressed by AT. These data suggest that antioxidants may serve as 'Abeta targeting' therapies that suppress toxic protein aggregation rather than simply acting as downstream radical scavengers.
