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Cytopathologic analysis of paraspinal masses: a study of 59 cases with clinicoradiologic correlation
Paraspinal masses (PSM) are uncommon and present a wide spectrum of differential diagnoses on fine-needle aspiration (FNA). We analyzed 59 cases of PSM on FNA in a 15-yr period, in the context of clinicoradiologic correlation. Radiologic findings, clinical data, and tissue biopsies were reviewed. Patients were 14-83 yr of age (mean 54.7) with a M:F ratio of 1.36:1. Of the 59 cases, 39 (66%) were deemed diagnostic. Of these, 8 (21%) revealed nonneoplastic lesions and 31 (79%) yielded neoplasms: 2 (6%) benign and 29 (94%) malignant. Of the malignant cases, 22 (76%) were metastatic tumors from various sites, while 7 (24%) were cancers from local spread, which included non-Hodgkin's lymphoma (NHL, 5) and myeloma (2). Benign neoplasms were nerve sheath tumors. Metastatic tumors consisted of adenocarcinoma, 9; squamous-cell carcinoma, 3; renal-cell carcinoma, 1; and non-small-cell carcinoma/not otherwise specified (NOS), 9. Twenty-four (41%) cases received further studies: immunoperoxidase (IPOX) alone, 17 (71%); special stains for microorganisms, 2 (8%); IPOX/other special stains, 4 (17%); and flow cytometry analysis, 1 (4%). Eight (14%) cases received follow-up biopsies. Half of these biopsies added information to previously "nondiagnostic" FNAs. Of the previously "diagnostic" FNAs, tissue biopsy yielded no additional information. Cytopathologic diagnoses were consistent with the pre-FNA radiology analyses in 13 (39%) cases. In instances of radiologic and cytopathologic discrepancy (4 cases, 12%), diagnoses made by FNA reversed the initial radiologic impression of neoplasm to infection, and vice versa. PSMs are rare lesions (0.26% of total FNAs done in 15 yr at our institution). The most common lesion encountered is metastatic adenocarcinoma, followed by NHL. Ancillary studies are helpful in difficult cases. In cases of radiologic/cytopathologic discrepancy, FNA diagnoses are more accurate and decisive for patient management. The sensitivity and specificity of a PSM FNA are 88% and 75% respectively. 相似文献
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Duffy AJ Nolan B Sheth K Collette H De M Bankey PE 《The Journal of surgical research》2000,90(1):51-57
BACKGROUND: Altered transendothelial migration and delayed apoptosis of neutrophils (PMN) have been implicated as contributing to infection in patients with gram-negative sepsis. Macrophage inflammatory protein 2 (MIP-2) signals PMN immigration and may alter other PMN functions. We tested the hypothesis that sequential endotoxin challenge in vivo alters PMN apoptosis and chemotactic responses. MATERIALS AND METHODS: Endotoxemia was induced in male Wistar rats (250 g) via intraperitoneal (IP) administration of LPS (4 mg/kg). After 18 h, intratracheal (IT) injection of LPS (400 microg/kg) was performed. Control animals received saline injections. Four hours after IT-LPS, circulating and bronchoalveolar lavage (BAL) PMN were isolated. PMN yields were calculated, and apoptosis was quantified after 18 h in culture by annexin V-fluorescein isothiocyanate FACS analysis. BAL MIP-2 concentrations were determined by ELISA. PMN chemotaxis to MIP-2 and IL-8 was determined using a fluorescent in vitro migration assay. RESULTS: Endotoxemia (IP-LPS) significantly decreases BAL PMN yield in response to an in vivo IT-LPS challenge. IT-LPS inhibits BAL PMN apoptosis to the same extent as sequential IP/IT-LPS. Alveolar MIP-2 concentrations are similar in the two groups. In vitro migration to IL-8 and MIP-2 was inhibited in PMN from endotoxemic versus control animals. CONCLUSIONS: These data demonstrate that endotoxemia inhibits PMN migration despite similar MIP-2 concentrations in the alveolus. Sequential insults do not affect the inhibition of apoptosis. In vitro, PMN from endotoxemic animals display impaired chemotaxis to MIP-2 and interleukin-8. This may result in an inadequate host defense that contributes to increased ICU-acquired pneumonia in septic patients. 相似文献
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Erik G. Hayman Akil P. Patel W. Taylor Kimberly Kevin N. Sheth J. Marc Simard 《Neurocritical care》2018,28(3):276-287
We sought to review the role that cerebral edema plays in neurologic outcome following cardiac arrest, to understand whether cerebral edema might be an appropriate therapeutic target for neuroprotection in patients who survive cardiopulmonary resuscitation. Articles indexed in PubMed and written in English. Following cardiac arrest, cerebral edema is a cardinal feature of brain injury and is a powerful prognosticator of neurologic outcome. Like other conditions characterized by cerebral ischemia/reperfusion, neuroprotection after cardiac arrest has proven to be difficult to achieve. Neuroprotection after cardiac arrest generally has focused on protecting neurons, not the microvascular endothelium or blood–brain barrier. Limited preclinical data suggest that strategies to reduce cerebral edema may improve neurologic outcome. Ongoing research will be necessary to determine whether targeting cerebral edema will improve patient outcomes after cardiac arrest. 相似文献
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Indian Journal of Pediatrics - Bone marrow failure has many different etiologies, including genetic defects which manifest with specific syndromes, as well as acquired conditions as a result of... 相似文献