Connective tissue growth factor reacts as an IL - World Journal of ...

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A B Figure 3 Contrast-enhanced computed tomography scan in arterial phase at the time of diagnosis of initial splenic infarction (A) and 2 mo later (B). A: When splenic infarction was diagnosed, an approximately 4 cm x 4 cm sized hepatocellular carcinoma (HCC) (arrow) was shown in S6; B: Two months later, the size of HCC was enlarged to 5 cm × 5 cm (arrow) and an intrahepatic metastatic nodule was also seen (arrowhead) beside main mass. prostacyclin, and inhibits proliferation of vascular smooth muscle cells. Reduction in NO and prostacyclin, after inhibition of VEGF signaling, may predispose to thromboembolic events [7] . Moreover, VEGF inhibition may also increase the risk of thrombosis by increasing the hematocrit and blood viscosity via overproduction of erythropoietin [8] . Other concurrent pathological findings in a patient might also play a central role. There are some reports of anti-VEGF agent-related thromboembolic events such as myocardial infarction and cerebrovascular accidents. To date, thrombotic risks with intravenous bevacizumab have been studied extensively, in contrast to oral VEGFR TKIs where data on arterial events have not yet been evaluated. Recently, Choueiri et al [9] reported the relative risk of arterial thrombotic events with bevacizumab and a VEGFR TKI (sorafenib or sunitinib); a two-fold and three-fold increase was reported, respectively. This risk did not depend on the type of malignancy. In a meta-analysis of bevacizumab-treated patients, the major underlying risk factors of arterial thrombotic events were advanced age, hypertension, diabetes, and a prior history of thrombotic events. The treatment duration for the incidence of thrombotic events was within the first 3 mo of therapy; however, the data regarding the occurrence of the events, during the course of the trial, were frequently not reported [10] . In the case reported here, the patient was of advanced age but had no predisposing factors. The WJG|www.wjgnet.com Kim SO et al . Sorafenib-induced spontaneous splenic infarction thromboembolic event was a splenic infarction with the clinical symptom of LUQ pain. The symptoms developed 2 mo after administration of sorafenib. Most prior reports of TKI-associated arterial thrombotic events have shown myocardial infarctions and/or cerebrovascular accidents; a splenic artery infarction has not been previously reported. Possible causes of splenic infarction were investigated. The physical examination, laboratory findings, imaging studies and other drug history did not suggest any other possible causes except for the sorafenib administration. Although the patient had a history of other therapeutic procedures such as PEIT, TACE, and HAI chemotherapy, the last TACE was administered 16 mo previously and the HAI chemotherapy was continued without LUQ pain. The HAI catheter was inserted at the correct hepatic arterial level, and the distal end was connected to the port at the right femoral artery. Anatomically this should not contribute to occlusion of the splenic artery. Furthermore, the patient tolerated HAI chemotherapy without the sorafenib. The time interval from the initial administration of sorafenib to onset of LUQ pain, and the fact that discontinuing sorafenib was associated with resolution of symptoms, suggested that the sorafenib was the cause of the acute splenic infarction. Two months later, the follow up CT scan showed improvement of the splenic lesion; however, the HCC had progressed. In this case, discontinuing sorafenib resolved the splenic infarction, however, at the expense of the HCC. Perhaps if the sorafenib had been continued with other pain medications and anticoagulants, the outcome would have been better. The use of low-dose aspirin for the prophylaxis of arterial thromboembolic events in high-risk patients is supported by an extensive body of literature [11] and is recommended as the standard of care [12] . Therefore, if a patient has a good response to sorafenib, it might be better to continue the sorafenib with the addition of lowdose aspirin to prevent events such as a splenic infarction, which is not life threatening. REFERENCES 1 Vaklavas C, Lenihan D, Kurzrock R, Tsimberidou AM. Antivascular endothelial growth factor therapies and cardiovascular toxicity: what are the important clinical markers to target? Oncologist 2010; 15: 130-141 2 Dvorak HF, Brown LF, Detmar M, Dvorak AM. Vascular permeability factor/vascular endothelial growth factor, microvascular hyperpermeability, and angiogenesis. Am J Pathol 1995; 146: 1029-1039 3 Llovet JM, Ricci S, Mazzaferro V, Hilgard P, Gane E, Blanc JF, de Oliveira AC, Santoro A, Raoul JL, Forner A, Schwartz M, Porta C, Zeuzem S, Bolondi L, Greten TF, Galle PR, Seitz JF, Borbath I, Häussinger D, Giannaris T, Shan M, Moscovici M, Voliotis D, Bruix J. Sorafenib in advanced hepatocellular carcinoma. N Engl J Med 2008; 359: 378-390 4 Kamba T, McDonald DM. Mechanisms of adverse effects of anti-VEGF therapy for cancer. Br J Cancer 2007; 96: 1788-1795 5 Zangari M, Fink LM, Elice F, Zhan F, Adcock DM, Tricot GJ. Thrombotic events in patients with cancer receiving antiangiogenesis agents. J Clin Oncol 2009; 27: 4865-4873 6 Kilickap S, Abali H, Celik I. Bevacizumab, bleeding, thrombosis, and warfarin. J Clin Oncol 2003; 21: 3542; author reply 269 January 14, 2011|Volume 17|Issue 2|
Kim SO et al . Sorafenib-induced spontaneous splenic infarction 3543 7 Zachary I. Signaling mechanisms mediating vascular protective actions of vascular endothelial growth factor. Am J Physiol Cell Physiol 2001; 280: C1375-C1386 8 Spivak JL. Polycythemia vera: myths, mechanisms, and management. Blood 2002; 100: 4272-4290 9 Choueiri TK, Schutz FA, Je Y, Rosenberg JE, Bellmunt J. Risk of arterial thromboembolic events with sunitinib and sorafenib: a systematic review and meta-analysis of clinical trials. J Clin Oncol 2010; 28: 2280-2285 10 Scappaticci FA, Skillings JR, Holden SN, Gerber HP, Miller WJG|www.wjgnet.com K, Kabbinavar F, Bergsland E, Ngai J, Holmgren E, Wang J, Hurwitz H. Arterial thromboembolic events in patients with metastatic carcinoma treated with chemotherapy and bevacizumab. J Natl Cancer Inst 2007; 99: 1232-1239 11 Patrono C, Coller B, FitzGerald GA, Hirsh J, Roth G. Plateletactive drugs: the relationships among dose, effectiveness, and side effects: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 2004; 126: 234S-264S 12 Tran H, Anand SS. Oral antiplatelet therapy in cerebrovascular disease, coronary artery disease, and peripheral arterial disease. JAMA 2004; 292: 1867-1874 S- Editor Sun H L- Editor Logan S E- Editor Zheng XM 270 January 14, 2011|Volume 17|Issue 2|
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World Journal of Gastroenterology W
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Robert JL Fraser, Daw Park Jacob Ge
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Italy Donato F Altomare, Bari Piero
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Fernando Azpiroz, Barcelona Ramon B
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S Contents EDITORIAL TOPIC HIGHLIGH
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Contents APPENDIX FLYLEAF EDITORS F
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Ouyang D et al . Pancreatic endocri
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Online Submissions: http://www.wjgn
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Diamantis G et al . Quality of life
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Gressner OA et al . CTGF is a negat
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A B CTGF luciferase activity (lcps)
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A B IL-6 (35 μg/L) - - + + + + - s
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F mt distal mt proximal wt 9 8 7 6
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+ CTGF TGF-β IL-6 + - + an acute p
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2007; 46: 295-303 21 Karger A, Fitz
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2011; 17(2): 164-173 Available from
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A B C -80 mV E Relative expression
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A C Park KS et al . Serotonergic si
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19 Li T, Weng SG, Leng XS, Peng JR,
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Recurrent GB cancer has been report
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Table 2 Surgical procedures for muc
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esection of the common bile duct sh
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NaF, 1% Triton X-100, and 0.5 mmol/
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A Oxaliplatin LY294002 C Oxaliplati
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A Tumor volume (mm 3 ) C 5000 4000
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2 Hundahl SA, Phillips JL, Menck HR
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the typical MII pattern of GOR. Thi
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emptying, that arises from the anch
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medical treatment, age at diagnosis
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Table 3 Odds ratio for the studied
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Table 6 Published associations betw
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anti-CBir1 and ASCA, and show reduc
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Faria GR et al . Acute diverticulit
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Changes in flow vs T0 (%) Changes i
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