{"title":"An experience of oseltamivir phosphate (tamiflu™) in a pediatric patient with chronic idiopathic thrombocytopenic purpura: a case report.","authors":"Bulent Alioglu, Aysin Tasar, Cinar Ozen, Beray Selver, Yildiz Dallar","doi":"10.1159/000321379","DOIUrl":"https://doi.org/10.1159/000321379","url":null,"abstract":"<p><p>We report a pediatric patient with chronic idiopathic thrombocytopenic purpura who suffered from an influenza A (H1N1) virus infection. A 13-year-old girl presented with fever, coughing, and generalized petechiae. The influenza A antigen was positive in her pharyngeal aspirate. She was successfully treated with neuraminidase inhibitor oseltamivir phosphate. Her platelet counts progressively increased with oseltamivir phosphate without another blood product or agent. We suggest that oseltamivir phosphate can be used in patients with immune thrombocytopenic purpura who present with influenza virus A infection. We also suggest that oseltamivir phosphate can be effective in patients with immune thrombocytopenic purpura. Large study groups are needed to confirm the relationship between idiopathic thrombocytopenic purpura and neurominidase inhibitors.</p>","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"37 2-4","pages":"55-8"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000321379","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29457209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Title Page / Table of Contents","authors":"","doi":"10.1159/000198248","DOIUrl":"https://doi.org/10.1159/000198248","url":null,"abstract":"","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 1","pages":"109 - 111"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000198248","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65353690","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Author Index Vol. 36, No. 3–4, 2007–08","authors":"","doi":"10.1159/000198177","DOIUrl":"https://doi.org/10.1159/000198177","url":null,"abstract":"","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 1","pages":"215 - 215"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000198177","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65352883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Subject Index Vol. 36, No. 3–4, 2007–08","authors":"","doi":"10.1159/000198240","DOIUrl":"https://doi.org/10.1159/000198240","url":null,"abstract":"","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 1","pages":"216 - 216"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000198240","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65353234","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
R. Dijkgraaf, H. Föllmer, H. Lenstra, Manin, Y. Meyer, C. Simó, M. Vigneras, O. Viro, A. Wiles
{"title":"Plenary Lectures","authors":"R. Dijkgraaf, H. Föllmer, H. Lenstra, Manin, Y. Meyer, C. Simó, M. Vigneras, O. Viro, A. Wiles","doi":"10.1159/000142053","DOIUrl":"https://doi.org/10.1159/000142053","url":null,"abstract":"Andrew J. Wiles The mathematics of M-theory Probabilistic aspects of financial risk Flags and lattice basis reduction Moduli, motives, mirrors The role of oscillations in non-linear problems New families of solutions in N-body problems Local Langlands correspondence for GL(ra, Qp) modulo I ^ p Dequantization of real algebraic geometry on a logarithmic paper Galois representations and automorphic forms","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 1","pages":"1 - 6"},"PeriodicalIF":0.0,"publicationDate":"2008-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000142053","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64771615","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
J. Bellos, M. Moschou, E. Avgerinos, A. Kostakis, K. Mahmoodi, Joost Brouwer, N. Veeger, J. Meer, T. Severinsen, S. Kristensen, S. Johnsen, C. Dethlefsen, A. Tjønneland, K. Overvad, J. Saour, A. Sheereen, M. Shoukri, T. Saou’r, L. Mammo
{"title":"Oral Presentations","authors":"J. Bellos, M. Moschou, E. Avgerinos, A. Kostakis, K. Mahmoodi, Joost Brouwer, N. Veeger, J. Meer, T. Severinsen, S. Kristensen, S. Johnsen, C. Dethlefsen, A. Tjønneland, K. Overvad, J. Saour, A. Sheereen, M. Shoukri, T. Saou’r, L. Mammo","doi":"10.1159/000142056","DOIUrl":"https://doi.org/10.1159/000142056","url":null,"abstract":"","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 1","pages":"136 - 156"},"PeriodicalIF":0.0,"publicationDate":"2008-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000142056","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64771879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effects of alteplase, a thrombolytic agent, in a rat photothrombotic middle cerebral artery occlusion model.","authors":"Kazuo Umemura, Katsuya Higo, Takeshi Sakata, Satoshi Yuki, Koji Iwata, Kazumasa Yamaguchi","doi":"10.1159/000252820","DOIUrl":"https://doi.org/10.1159/000252820","url":null,"abstract":"<p><p>In this study, we examined the effects of alteplase, a recombinant tissue-type plasminogen activator (t-PA), in a simple and reproducible rat middle cerebral artery (MCA) occlusion model induced by photoillumination with 12 mg/kg of rose bengal. A clinically equivalent dose of alteplase (3 mg/kg), which was administered just after thrombotic occlusion of the MCA, significantly reopened the thrombotic MCA occlusion in 16 of 23 animals (69.6%) when compared with vehicle-treated animals (8 of 22 animals, 36.4%). In addition, alteplase significantly reduced cerebral damage and improved neurological deficits. Although it has been reported that t-PA possesses neurotoxicity, the present findings suggest that alteplase was effective in a rat acute stroke model due to reopening of thrombotic MCA occlusion. This new model is very useful for investigating the efficacy of thrombolytic agents in stroke research, providing a condition similar to the clinical setting.</p>","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 5","pages":"245-50"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000252820","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28582576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Granulocyte colony-stimulating factor increases the platelet volume in peripheral stem cell apheresis donors.","authors":"Akihiro Ihara, Keiko Matsui, Ryouta Minami, Shuzou Uchida, Shuji Ueda, Tetsuo Nishiura","doi":"10.1159/000252823","DOIUrl":"https://doi.org/10.1159/000252823","url":null,"abstract":"<p><p>We investigated the short-term influence of granulocyte colony-stimulating factor (G-CSF) administration on platelet counts and platelet indices in 12 donors (8 males and 4 females; median age 34 years, range 16-49) for peripheral stem cell transplantation using an automated blood cell analyzer. On day 3 (D3) compared with D0, 11 donors with normal laboratory and physical findings showed increases in platelet indices (chi(2) = 12.0, p = 0.0025). Furthermore, mean platelet volume (MPV) was significantly increased (p = 0.04). Also, platelet count decreased, and platelet distribution width and platelet-large cell ratio were increased, but these were not significant. On the contrary, 1 donor with abnormal laboratory findings who had large platelets (MPV 11.4 fl) before G-CSF administration showed decreases in platelet indices (MPV 10.3 fl) on D3, although platelet count (18.2 x 10(4)/microl) decreased after G-CSF administration. G-CSF administration induces an inflammatory process with endothelial cell activation. This is probably the reason why platelet volume increases after G-CSF use. This is the first report showing that G-CSF administration immediately induces increases in large platelets in peripheral stem cell transplant donors before harvest.</p>","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 5","pages":"266-70"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000252823","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28582579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Leukocytosis, JAK2V617F mutation, and hemostasis in myeloproliferative disorders.","authors":"Marina Marchetti, Anna Falanga","doi":"10.1159/000175153","DOIUrl":"https://doi.org/10.1159/000175153","url":null,"abstract":"<p><p>Thrombosis is a leading cause of morbidity and mortality in patients with essential thrombocythemia (ET) and polycythemia vera (PV). Several mechanisms have been proposed to cause or to contribute to the acquired thrombophilic state of these patients, including platelet and red blood cell abnormalities. The increase in white blood cell count, found in most subjects with these disorders, raises the possibility that circulating leukocytes may represent another prothrombotic factor, as demonstrated for other conditions, including sickle cell, coronary heart, and peripheral arterial diseases. Published data demonstrate that neutrophil activation occurs in ET and PV patients in parallel with the appearance of laboratory signs of hemostatic system activation, suggesting an involvement of these cells in the pathogenesis of the thrombotic predisposition of these subjects. In 2005, an acquired point mutation in the pseudokinase domain of Janus kinase 2 (JAK2(V617F)) has been described in these disorders, and has attracted an enormous interest both as a diagnostic and prognostic tool, and as a potential therapeutic target. Retrospective data have identified JAK2(V617F) as a risk factor for thrombosis in ET, and have also shown a close association with abdominal vein thrombosis. JAK2(V617F) is variably associated with thrombosis and, more consistently, with elevations in blood cell counts. A clear link appears to exist between leukocytosis, JAK2(V617F), and the hemostatic system activation in patients with Bcl-negative myeloproliferative disorders.</p>","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 3-4","pages":"148-59"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000175153","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27952324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Stephen J Kling, Cambria A Judd, Keith B Warner, George M Rodgers
{"title":"Regulation of ADAMTS13 expression in proliferating human umbilical vein endothelial cells.","authors":"Stephen J Kling, Cambria A Judd, Keith B Warner, George M Rodgers","doi":"10.1159/000252818","DOIUrl":"https://doi.org/10.1159/000252818","url":null,"abstract":"<p><p>ADAMTS13, the von Willebrand factor-cleaving protease, is constitutively produced by endothelial cells. The aim was to quantify ADAMTS13 production in proliferating and nonproliferating human umbilical vein endothelial cells (HUVECs) and to determine if such production was regulated. HUVECs were plated at 50,000 cells/cm(2) or 10,000 cells/cm(2), densities yielding confluence or subconfluence, respectively. Subconfluent HUVEC supernatants and cell lysates contained at least 2-fold more ADAMTS13 antigen than those of confluent HUVECs (p < 0.05). Immunohistochemistry supported this increase and indicated no dramatic shifts in subcellular localization of HUVEC ADAMTS13 by HUVEC proliferation. The activity of the ADAMTS13 produced by subconfluent HUVECs was increased about 2-fold also. HUVECs rapidly increased ADAMTS13 mRNA in response to subconfluent conditions. This change in regulation, in turn, leads to increased ADAMTS13 protein production and activity by these proliferating cells.</p>","PeriodicalId":19817,"journal":{"name":"Pathophysiology of Haemostasis and Thrombosis","volume":"36 5","pages":"233-40"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000252818","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28582574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}