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Journal of vascular and interventional radiology: JVIR 11/2012; · 1.81 Impact Factor
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Roy J Soberman,
Christopher R Mackay,
Christine A Vaine,
Glennice Bowen Ryan,
Anna M Cerny,
Mikayla R Thompson, Boris Nikolic,
Valeria Primo,
Peter Christmas,
Paul Sheiffele,
Lisa Aronov,
David M Knipe,
Evelyn A Kurt-Jones
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ABSTRACT: The CD200R1:CD200 axis is traditionally considered to limit tissue inflammation by down-regulating pro-inflammatory signaling in myeloid cells bearing the receptor. We generated CD200R1(-/-) mice and employed them to explore both the role of CD200R1 in regulating macrophage signaling via TLR2 as well as the host response to an in vivo, TLR2-dependent model, herpes simplex virus 1 (HSV-1) infection. CD200R1(-/-) peritoneal macrophages demonstrated a 70-75% decrease in the generation of IL-6 and CCL5 (Rantes) in response to the TLR2 agonist Pam(2)CSK(4) and to HSV-1. CD200R1(-/-) macrophages could neither up-regulate the expression of TLR2, nor assemble a functional inflammasome in response to HSV-1. CD200R1(-/-) mice were protected from HSV-1 infection and exhibited dysfunctional TLR2 signaling. Finally, both CD200R1(-/-) mice and CD200R1(-/-) fibroblasts and macrophages showed a markedly reduced ability to support HSV-1 replication. In summary, our data demonstrate an unanticipated and novel requirement for CD200R1 in "licensing" pro-inflammatory functions of TLR2 and in limiting viral replication that are supported by ex vivo and in vivo evidence.
PLoS ONE 01/2012; 7(10):e47740. · 4.09 Impact Factor
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Journal of vascular and interventional radiology: JVIR 11/2011; 23(1):11-8. · 1.81 Impact Factor
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Changli Wei,
Shafic El Hindi,
Jing Li,
Alessia Fornoni,
Nelson Goes,
Junichiro Sageshima,
Dony Maiguel,
S Ananth Karumanchi,
Hui-Kim Yap,
Moin Saleem, [......],
Franz Schaefer,
Christian Morath,
Vedat Schwenger,
Martin Zeier,
Vineet Gupta,
David Roth,
Maria Pia Rastaldi,
George Burke,
Phillip Ruiz,
Jochen Reiser
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ABSTRACT: Focal segmental glomerulosclerosis (FSGS) is a cause of proteinuric kidney disease, compromising both native and transplanted kidneys. Treatment is limited because of a complex pathogenesis, including unknown serum factors. Here we report that serum soluble urokinase receptor (suPAR) is elevated in two-thirds of subjects with primary FSGS, but not in people with other glomerular diseases. We further find that a higher concentration of suPAR before transplantation underlies an increased risk for recurrence of FSGS after transplantation. Using three mouse models, we explore the effects of suPAR on kidney function and morphology. We show that circulating suPAR activates podocyte β(3) integrin in both native and grafted kidneys, causing foot process effacement, proteinuria and FSGS-like glomerulopathy. Our findings suggest that the renal disease only develops when suPAR sufficiently activates podocyte β(3) integrin. Thus, the disease can be abrogated by lowering serum suPAR concentrations through plasmapheresis, or by interfering with the suPAR-β(3) integrin interaction through antibodies and small molecules targeting either uPAR or β(3) integrin. Our study identifies serum suPAR as a circulating factor that may cause FSGS.
Nature medicine 01/2011; 17(8):952-60. · 27.14 Impact Factor
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ABSTRACT: The purpose of this article is to estimate the absorbed radiation dose in radiosensitive organs during coronary MDCT angiography using 320-MDCT and to determine the effects of tube voltage variation and heart rate (HR) control on absorbed radiation dose.
Semiconductor field effect transistor detectors were used to measure absorbed radiation doses for the thyroid, midbreast, breast, and midlung in an anthropomorphic phantom at 100, 120, and 135 kVp at two different HRs of 60 and 75 beats per minute (bpm) with a scan field of view of 320 mm, 400 mA, 320 × 0.5 mm detectors, and 160 mm collimator width (160 mm range). The paired Student's t test was used for data evaluation.
At 60 bpm, absorbed radiation doses for 100, 120, and 135 kVp were 13.41 ± 3.59, 21.7 ± 4.12, and 29.28 ± 5.17 mGy, respectively, for midbreast; 11.76 ± 0.58, 18.86 ± 1.06, and 24.82 ± 1.45 mGy, respectively, for breast; 12.19 ± 2.59, 19.09 ± 3.12, and 26.48 ± 5.0 mGy, respectively, for lung; and 0.37 ± 0.14, 0.69 ± 0.14, and 0.92 ± 0.2 mGy, respectively, for thyroid. Corresponding absorbed radiation doses for 75 bpm were 38.34 ± 2.02, 59.72 ± 3.13, and 77.8 ± 3.67 mGy for midbreast; 26.2 ± 1.74, 44 ± 1.11, and 52.84 ± 4.07 mGy for breast; 38.02 ± 1.58, 58.89 ± 1.68, and 78 ± 2.93 mGy for lung; and 0.79 ± 0.233, 1.04 ± 0.18, and 2.24 ± 0.52 mGy for thyroid. Absorbed radiation dose changes were significant for all organs for both tube voltage reductions as well as for HR control from 75 to 60 bpm at all tube voltage settings (p < 0.05). The absorbed radiation doses for the calcium score protocol were 11.2 ± 1.4 mGy for midbreast, 9.12 ± 0.48 mGy for breast, 10.36 ± 1.3 mGy for lung, and 0.4 ± 0.05 mGy for thyroid.
CT angiography with 320-MDCT scanners results in absorbed radiation doses in radiosensitive organs that compare favorably to those previously reported. Significant dose reductions can be achieved by tube voltage reductions and HR control.
American Journal of Roentgenology 12/2010; 195(6):1347-54. · 2.78 Impact Factor
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ABSTRACT: Mixed hematopoietic chimerism is associated with islet allograft tolerance and may reverse autoimmunity. We developed low intensity regimens for the induction of mixed chimerism and examined the effects on autoimmunity in prediabetic nonobese diabetic (NOD) mice.
NOD mice received various combinations of total body irradiation, anti-CD154, anti-CD8alpha, anti-CD4, and anti-Thy1.2 monoclonal antibodies, with or without transplantation of C57BL/6 bone marrow cells and were followed up for development of diabetes, chimerism, and donor skin graft survival. Autoimmunity was assessed by histologic examination of salivary glands and pancreata.
Although conditioning alone prevented or delayed the onset of diabetes, stable mixed chimerism was required for the reversal of isletitis. Mixed chimerism and skin graft tolerance were achieved in NOD mice receiving anti-CD154 with bone marrow transplantation as the means of tolerizing peripheral CD4 T cells to alloantigens. However, isletitis was not reversed in allotolerant mixed chimeras prepared with this regimen.
Partial depletion of peripheral autoreactive NOD CD4 T cells is needed to achieve full reversal of isletitis by mixed chimerism induction from a protective donor strain, but it is not required for induction of specific tolerance to donor alloantigens. Thus, the requirements for tolerizing alloreactive and autoreactive NOD CD4 cells are distinct.
Transplantation 01/2010; 89(1):23-32. · 4.00 Impact Factor
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ABSTRACT: In recent years, research advancement in stem cell therapy has been rapid. Accordingly, general clinical, scientific, and public attention to the application of stem cell therapy has been substantial. Promises are great, most notably with regard to the application of stem cell therapy for diseases that are currently difficult to treat or incurable such as Parkinson disease or diabetes mellitus. It is in the best interest of patient care for diagnostic and interventional radiologists to be actively involved in the development of these therapies, both at the bench and at the bedside in clinical studies. Specifically, the diagnostic radiologist can become an expert in imaging, tracking, and monitoring of stem cells and in the assessment of engraftment efficiency, whereas the interventionalist is a natural expert in targeted stem cell delivery by means of different routes (percutaneous, selective intravenous, or intraarterial). In addition, there is a potential role for the interventionalist to create engraftment territory and increase engraftment bed fertility with controlled intentional tissue destruction (eg, by means of thermal ablation) that might precede stem cell administration.
Journal of vascular and interventional radiology: JVIR 09/2009; 20(8):999-1012. · 1.81 Impact Factor
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ABSTRACT: To determine whether radiofrequency (RF) ablation causes increased hepatic embryonic stem cell trafficking in the rat liver model.
Right hepatic lobe RF ablation was performed in rats for 5 minutes at 15 minutes (n = 2) and 48 hours (n = 2) before administration of rat hepatic embryonic stem cells (rhESCs). Green fluorescent protein-labeled rhESCs were injected intravenously, and all rats were killed 5 days after rhESC injection. Tissue was removed from RF ablation areas and untreated liver, the latter of which served as control. Slides were evaluated with fluorescent microscopy, and software fluorescence count was performed for evaluation of rhESC distribution. Regions of rhESC destination were divided into inner coagulation (zone A), periablational (zone B), and peripheral (zone C) zones. Fluorescence comparison was additionally performed between RF ablation areas and corresponding control tissues of the left hepatic lobe (segment II). Kruskal-Wallis testing was used for evaluations.
Fluorescent pixel count was significantly higher in RF ablation areas than in respective controls: mean at 15 minutes, 10,471 +/- 3,830 (SD) versus 1,889 +/- 1,427 (P < .05); mean at 48 hours, 15,177 +/- 7,091 versus 2,868 +/- 1,714 (P < .05). High-power field samples showed significant distribution differences across zones: zone B, mean, 1,015.4 +/- 311; zone A, mean, 17.8 +/- 11; and zone C, mean, 141.2 +/- 51.4 (P < .05).
RhESCs administered after RF ablation are trafficked to the periablational margin in significantly greater numbers than the remaining liver.
Journal of vascular and interventional radiology: JVIR 06/2009; 20(5):640-7; quiz 571. · 1.81 Impact Factor
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Boris Nikolic
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ABSTRACT: End-stage renal disease is one of the main epidemiologic health problems and dialysis access continues to be the Achilles' heel of its treatment. Consequently, hemodialysis fistula maintenance is of great importance which can best be accomplished by close collaboration between primary care, nephrology, surgery and interventional radiology services, routine access monitoring as well as early intervention in cases of impending access failure. Also, knowledge and application of specific interventional techniques that are additionally described in this article may increase intervention efficiency, decrease the incidence of complications and overcome technical challenges thus improving procedural outcome and maximizing access patency rates.
Techniques in vascular and interventional radiology 10/2008; 11(3):167-74.
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Changli Wei,
Clemens C Möller,
Mehmet M Altintas,
Jing Li,
Karin Schwarz,
Serena Zacchigna,
Liang Xie,
Anna Henger,
Holger Schmid,
Maria P Rastaldi,
Peter Cowan,
Matthias Kretzler,
Roberto Parrilla,
Moïse Bendayan,
Vineet Gupta, Boris Nikolic,
Raghu Kalluri,
Peter Carmeliet,
Peter Mundel,
Jochen Reiser
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ABSTRACT: Podocyte dysfunction, represented by foot process effacement and proteinuria, is often the starting point for progressive kidney disease. Therapies aimed at the cellular level of the disease are currently not available. Here we show that induction of urokinase receptor (uPAR) signaling in podocytes leads to foot process effacement and urinary protein loss via a mechanism that includes lipid-dependent activation of alphavbeta3 integrin. Mice lacking uPAR (Plaur-/-) are protected from lipopolysaccharide (LPS)-mediated proteinuria but develop disease after expression of a constitutively active beta3 integrin. Gene transfer studies reveal a prerequisite for uPAR expression in podocytes, but not in endothelial cells, for the development of LPS-mediated proteinuria. Mechanistically, uPAR is required to activate alphavbeta3 integrin in podocytes, promoting cell motility and activation of the small GTPases Cdc42 and Rac1. Blockade of alphavbeta3 integrin reduces podocyte motility in vitro and lowers proteinuria in mice. Our findings show a physiological role for uPAR signaling in the regulation of kidney permeability.
Nature medicine 02/2008; 14(1):55-63. · 27.14 Impact Factor
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ABSTRACT: Human immunodeficiency virus type 1 (HIV-1) infection depletes thymocytes and destroys thymic structure. Functional, tolerant human T cells develop in vivo in immunodeficient mice receiving porcine thymus and human fetal liver fragments under the kidney capsule. In this model, we evaluated the potential of porcine thymus to protect human thymocytes from the effects of HIV-1. Compared with that observed in control mice with human thymic grafts, porcine thymus attenuated human thymocyte depletion by the CCR5-tropic isolate JR-CSF without preventing thymocyte infection. Porcine thymus protected human thymocytes from infection and depletion by a CXCR4-tropic HIV-1 isolate without reducing peripheral blood viral loads or T cell infection. Human thymocytes from human but not porcine grafts showed decreased Bcl-2 expression and increased apoptosis after NL4.3 infection. Thus, porcine thymus protects human thymocytes from the cytopathic effect of HIV-1, suggesting a possible approach to achieving immune restoration in patients with acquired immunodeficiency syndrome who have incomplete responses to antiretroviral therapy. The model allows analysis of the mechanisms of HIV-mediated thymic dysfunction.
The Journal of Infectious Diseases 10/2007; 196(6):900-10. · 6.41 Impact Factor
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Sanja Sever,
Mehmet M Altintas,
Sharif R Nankoe,
Clemens C Möller,
David Ko,
Changli Wei,
Joel Henderson,
Elizabetta C del Re,
Lianne Hsing,
Ann Erickson,
Clemens D Cohen,
Matthias Kretzler,
Dontscho Kerjaschki,
Alexander Rudensky, Boris Nikolic,
Jochen Reiser
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ABSTRACT: Kidney podocytes and their foot processes maintain the ultrafiltration barrier and prevent urinary protein loss (proteinuria). Here we show that the GTPase dynamin is essential for podocyte function. During proteinuric kidney disease, induction of cytoplasmic cathepsin L leads to cleavage of dynamin at an evolutionary conserved site, resulting in reorganization of the podocyte actin cytoskeleton and proteinuria. Dynamin mutants that lack the cathepsin L site, or render the cathepsin L site inaccessible through dynamin self-assembly, are resistant to cathepsin L cleavage. When delivered into mice, these mutants restored podocyte function and resolve proteinuria. Our study identifies dynamin as a critical regulator of renal permselectivity that is specifically targeted by proteolysis under pathological conditions.
Journal of Clinical Investigation 09/2007; 117(8):2095-104. · 15.39 Impact Factor
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ABSTRACT: The objective of our study was to evaluate the frequency and extent of residual uterine perfusion via the ovarian arteries after bilateral uterine artery embolization (UAE) for the treatment of symptomatic uterine leiomyomas.
One hundred forty-five consecutive patients who underwent UAE were retrospectively evaluated for blood supply to the uterus via the ovarian arteries after UAE. After completion of UAE, uterine supply from the ovarian arteries was assessed by performing abdominal aortography in all patients. Selective ovarian arteriography, in addition, was performed in some patients. The criteria used to characterize ovarian artery perfusion as seen on the aortograms were vessel size compared with a 5-French catheter and visualization and extent of flow. When the ovarian arteries visibly supplied uterine tissue, a quantification system was applied as follows: the uterus was divided in 24 segments on the basis of a clock model that was superimposed over the uterine territory in the anteroposterior projection. Depending on its distance from the midpoint of the clock, perfusion segments were labeled as central, middle, distal, or peripheral for each hour of the clock resulting in a total of 24 (12 x 2) potential segments of residually perfused uterine tissue via the ovarian arteries.
Two hundred ninety ovarian arteries were evaluated on aortography; of these, 202 (70%) were not seen during aortography. Of the visualized ovarian arteries (n = 88), 52% (46/88) were smaller than, 25% (22/88) were equal to, and 23% (20/88) were larger than the diameter of a 5-French catheter. The aortogram revealed that 61% (54/88) of the ovarian arteries extended into the pelvis, whereas 38% (33/88 [one missing data point]) did not. Selective injections were performed in 54 ovarian arteries. Of these, 69% (37/54) of the ovarian arteries had residual fibroid perfusion from the ovarian arteries after UAE (10 left-sided, 15 right-sided, six bilateral = 37 ovarian arteries). Residual fibroid perfusion was more likely in large ovarian arteries, particularly those with rapid flow visualized extending into the pelvis. The perfusion scores ranged from one to 18 segments (< 6 segments, n = 21 ovarian arteries; 6-12 segments, n = 12; > 12 segments, n = 4). Direct communication with the uterine arteries was seen in 20 ovarian arteries, 40% (8/20) of which did not show any uterine or fibroid perfusion, suggesting that fibroid flow had been occluded by UAE.
Based on aortography, the presence of residual fibroid perfusion is more likely if the ovarian arteries are large, have rapid flow, or have flow that extends into the pelvis. Selective ovarian artery evaluation may be indicated in these cases to determine the extent of residual fibroid perfusion.
American Journal of Roentgenology 06/2007; 188(6):1558-63. · 2.78 Impact Factor
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Keiji Ikawa,
Takashi Nishioka,
Zhiqian Yu,
Yumiko Sugawara,
Junichi Kawagoe,
Toshiaki Takizawa,
Valeria Primo, Boris Nikolic,
Toshinobu Kuroishi,
Takashi Sasano,
Hidetoshi Shimauchi,
Haruhiko Takada,
Yasuo Endo,
Shunji Sugawara
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ABSTRACT: Activated neutrophils produce serine proteases, which activate cells through protease-activated receptor 2 (PAR2). As proteinase 3 (PR3) induces the secretion of interleukin (IL)-18 from epithelial cells in combination with lipopolysaccharide (LPS) in vitro, we examined whether neutrophils, serine proteases, and PAR2 are involved in the induction of serum IL-18 and IL-18-dependent liver injury in mice treated with heat-killed Propionibacterium acnes and LPS. LPS-induced serum IL-18 levels in P. acnes-primed mice were reduced significantly by anti-Gr-1 injection (depletion of neutrophils and macrophages) but not by a macrophage "suicide" technique, using liposomes encapsulating clodronate. The IL-18 induction was decreased significantly by coadministration of a serine protease inhibitor [Nafamostat mesilate (FUT-175)] with LPS. Serum levels of tumor necrosis factor alpha and liver enzymes induced by P. acnes and LPS were abolished by anti-Gr-1 treatment, and concomitantly, liver injury (necrotic change and granuloma formation) and Gr-1(+) cell infiltration into the liver were prevented by the treatment. A deficiency of PAR2 in mice significantly impaired IL-18 induction by treatment with P. acnes and LPS, and only slight pathological changes in hepatic tissues occurred in the PAR2-deficient mice treated with P. acnes and LPS. Furthermore, coadministration of exogenous murine PR3 or a synthetic PAR2 agonist (ASKH95) with LPS in the anti-Gr-1-treated mice restored the serum IL-18 levels to those in control mice treated with P. acnes and LPS. These results indicate that neutrophil recruitment and PAR2 activation by neutrophil serine proteases are critically involved in the induction of IL-18 and IL-18-dependent liver injury in vivo.
Journal of Leukocyte Biology 12/2005; 78(5):1118-26. · 4.99 Impact Factor
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ABSTRACT: Transplantation of haematopoietic stem cells--cells capable of self renewing and reconstituting all types of blood cell--can treat numerous lethal diseases, including leukaemias and lymphomas. It may now be applicable for the treatment of severe autoimmune diseases, such as therapy-resistant rheumatoid arthritis and multiple sclerosis. Studies in animal models show that the transfer of haematopoietic stem cells can reverse autoimmunity, and several mechanistic pathways may explain this phenomenon. The outcome of ongoing clinical trials, as well as of studies in patients and animal models, will help to determine the role that stem-cell transplantation can play in the treatment of autoimmune diseases.
Nature 07/2005; 435(7042):620-7. · 36.28 Impact Factor
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ABSTRACT: Lipoxin A(4) (LXA(4)) and aspirin-triggered 15-epi-LXA(4) are potent endogenous lipid mediators thought to define the inflammatory set-point. We used single prophylactic administrations of a synthetic aspirin-triggered lipoxin A(4) signal mimetic, ATLa, to probe dynamics of early host-donor interactions in a mouse model for the inflammation-associated multifactorial disease of allogeneic bone marrow transplant (BMT) -induced graft-vs.-host disease (GvHD). We first demonstrated that both host and donor are responsive to the ATLa signals. The simple and restricted regimen of a single prophylactic administration of ATLa [100 ng/mL to donor cells or 1 microg (approximately 50 microg/kg) i.v. to host] was sufficient to delay death. Clinical indicators of weight, skin lesions, diarrhea and eye inflammation were monitored. Histological analyses on day 45 post-BMT showed that the degree of cellular trafficking, particularly neutrophil infiltrate, and protection of end-organ target pathology are different, depending on whether the host or donor was treated with ATLa. Taken together, these results chart some ATLa protective effects on GvHD cellular dynamics over time and identify a previously unrecognized effect of host neutrophils in the early phase post-BMT as important determinants in the dynamics of GvHD onset and progression.-Devchand, P. R., Schmidt, B. A., Primo, V. C., Zhang, Q.-y., Arnaout, M. A., Serhan, C. N., Nikolic, B. A synthetic eicosanoid LX-mimetic unravels host-donor interactions in allogeneic BMT-induced GvHD to reveal an early protective role for host neutrophils.
The FASEB Journal 03/2005; 19(2):203-10. · 5.71 Impact Factor
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ABSTRACT: The authors describe a case of the development of a pyosalpinx from a preexisting hydrosalpinx after uterine artery embolization (UAE) for leiomyomata. The hydrosalpinx preexisted the UAE procedure and did not cause the patient any symptoms or signs of infection. UAE was performed with standard technique and was technically as well as initially clinically successful. However, the patient presented 8 weeks post-UAE with a pyosalpinx and superinfection of the previously simple fluid collection, requiring treatment with hysterectomy and oophorectomy. A mechanism for the occurrence of this superinfection is proposed, and potential strategies to avoid this serious complication in the future are discussed.
Journal of Vascular and Interventional Radiology 04/2004; 15(3):297-301. · 2.08 Impact Factor
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ABSTRACT: Bone marrow transplantation from diabetes-resistant strains with complete replacement of the recipient immune system by the allogeneic donor has led to tolerance to donor islets and cure of diabetes in a mouse model of type 1 diabetes. However, the ability to tolerize host T-cells of diabetic NOD mice is unknown. We demonstrate that nonmyeloablative conditioning achieves mixed hematopoietic chimerism across major histocompatibility complex (MHC) barriers in spontaneously diabetic NOD mice. This conditioning preserves alloreactive and autoreactive diabetogenic host NOD T-cells, but when mixed chimerism was established, diabetic NOD mice accepted donor-type allogeneic islet grafts and were cured of diabetes, despite a significant recipient T-cell contribution. Furthermore, induction of mixed chimerism permitted acceptance of NOD islet grafts, demonstrating reversal of autoimmunity. Allogeneic bone marrow transplantation was critical for tolerization of diabetogenic and alloreactive host T-cells. Thus, mixed hematopoietic chimerism induces tolerance to donor islets and reverses established autoimmunity in diabetic NOD mice.
Diabetes 03/2004; 53(2):376-83. · 8.29 Impact Factor
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ABSTRACT: To determine whether a transient hypercoagulable state is induced by the uterine artery embolization (UAE) procedure.
Serial periprocedure blood samples were obtained from 27 patients undergoing the UAE procedure. Five blood samples were obtained from each patient at set time intervals: before the procedure (for baseline determination), immediately before and after embolization of the uterine arteries, 90 minutes after conclusion of the procedure, and between 18 and 24 hours later. Each blood sample was analyzed for the peripheral levels of the following parameters: thrombin-antithrombin complex (TAT), prothrombin fragment 1.2 (F1.2), platelet factor 4 (PF4), D-dimer, and plasmin-alpha(2)-antiplasmin complex (PAP). For each parameter, the baseline values were statistically compared with the pre- and postembolization values for each individual to detect change over time. Overall and global occasion effects for continuous variables were assessed with the Friedman statistic and individual comparisons between occasions with the Wilcoxon signed-rank test.
No evidence was found for a difference in coagulability among the five occasions for D-dimer (P =.7645) or PF4 (P =.09). All three of the remaining measures were found to have statistically significant differences (P <.0001 for F1.2, P =.0026 for PAP, and P =.0006 for TAT). No evidence was found for a difference between preprocedure and preembolization levels for these three latter parameters (P =.595 for F1.2, P =.128 for PAP, P =.9705 for TAT). Hypercoagulability potential as measured by prothrombinase and F1.2 generation increased between preembolization samples and each of the successive postprocedure samples (P <.0001, P <.0001, P =.0082), whereas PAP increased at 90 minutes (P =.0023) and TAT increased immediately after embolization (P <.0001). No clinically apparent thrombotic complications occurred among any of the patients studied.
Surrogate markers of hypercoagulability increase as a result of UAE, suggesting that a prothrombotic state may result after the procedure.
Journal of Vascular and Interventional Radiology 09/2003; 14(9 Pt 1):1147-53. · 2.08 Impact Factor
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American Journal of Roentgenology 02/2003; 180(1):78-80. · 2.78 Impact Factor
