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Oxidative Stress Is Predominant in Female but Not in Male Patients with Autoimmune Thrombocytopenia

DOI: 10.1155/2014/720347

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Abstract:

As the involvement of oxidative stress (OS) in autoimmune thrombocytopenia (AITP) has been reported, a fast and rapid test for the reliable measurement of OS and antioxidant capacities (AOCs) might be a useful tool in extending current diagnostic possibilities. The free oxygen radical test (FORT) and free oxygen radical defence (FORD) assay (Callegari, Italy) are easy to perform and reliable, with results available within 15 minutes. Thirty-seven AITP patients and 37 matched healthy individuals were included in this study. All participants responded to a standard questionnaire provided by these assays. Female patients with AITP were observed to demonstrate significantly higher OS in comparison to female controls ( ) and male AITP patients ( ). The AOCs were not reduced in patients with AITP ( ). Correlation of OS with platelet count identified a weak positive correlation ( , Spearman ). The questionnaire revealed that ITP patients in comparison to healthy controls are more stressed, feel exhausted and fatigued, and eat a healthier diet. In conclusion, OS is predominant in female but not in male patients with AITP suggesting gender-specific differences in the pathomechanisms of AITP. Identification of patients with high levels of OS might be beneficial in the management of AITP. 1. Introduction Primary autoimmune thrombocytopenia (AITP) is an acquired autoimmune disorder defined by isolated thrombocytopenia and exclusion of other causes [1, 2]. The triggering event for AITP remains unknown [3]. The dominant clinical symptoms are petechia and bleeding, which generally correlate with the severity of thrombocytopenia [4]. A normal platelet count in a healthy individual is between 150 and 450 × 109?platelets/L. Most AITP patients are asymptomatic in the presence of platelet counts above 50 × 109?platelets/L [5]. The clinical manifestation of AITP is extremely variable [4] and, to date, there are no AITPspecific diagnostic markers or disease-specific therapeutic treatments available [6]. AITP embodies a prototype of a B-cell mediated autoimmune lymphoproliferative disease. Antiplatelet autoantibodies are detectable in 50–60% of patients and are thus of diagnostic relevance [7]. Autoreactive T-cells also play a significant role in the cross talk between antigen presenting cells and autoantibody producing B-cells [8]. Oxidative stress (OS) is termed as an imbalance between the systemic manifestation of reactive oxygen and nitrogen species (ROS and RNS, resp.) and an individual’s ability to detoxify these highly reactive species to prevent and/or repair damaged

References

[1]  J. N. George, S. H. Woolf, G. E. Raskob et al., “Idiopathic thrombocytopenic purpura: a practice guideline developed by explicit methods for the American Society of Hematology,” Blood, vol. 88, no. 1, pp. 3–40, 1996.
[2]  F. Rodeghiero, R. Stasi, T. Gernsheimer et al., “Standardization of terminology, definitions and outcome criteria in immune thrombocytopenic purpura of adults and children: report from an international working group,” Blood, vol. 113, no. 11, pp. 2386–2393, 2009.
[3]  M. D. Coopamah, M. B. Garvey, J. Freedman, and J. W. Semple, “Cellular immune mechanisms in autoimmune thrombocytopenic purpura: an update,” Transfusion Medicine Reviews, vol. 17, no. 1, pp. 69–80, 2003.
[4]  D. B. Cines, J. B. Bussel, H. A. Liebman, and E. T. Luning Prak, “The ITP syndrome: pathogenic and clinical diversity,” Blood, vol. 113, no. 26, pp. 6511–6521, 2009.
[5]  R. Stasi, M. L. Evangelista, E. Stipa, F. Buccisano, A. Venditti, and S. Amadori, “Idiopathic thrombocytopenic purpura: current concepts in pathophysiology and management,” Thrombosis and Haemostasis, vol. 99, no. 1, pp. 4–13, 2008.
[6]  A. Salama, “Current treatment options for primary immune thrombocytopenia,” Expert Review of Hematology, vol. 4, no. 1, pp. 107–118, 2011.
[7]  R. McMillan, “Autoantibodies and autoantigens in chronic immune thrombocytopenic purpura,” Seminars in Hematology, vol. 37, no. 3, pp. 239–248, 2000.
[8]  M. Kuwana and Y. Ikeda, “The role of autoreactive T-cells in the pathogenesis of idiopathic thrombocytopenic purpura,” International Journal of Hematology, vol. 81, no. 2, pp. 106–112, 2005.
[9]  G. Bartosz, “Peroxynitrite: mediator of the toxic action of nitric oxide,” Acta Biochimica Polonica, vol. 43, no. 4, pp. 645–659, 1996.
[10]  H. Ischiropoulos, “Biological selectivity and functional aspects of protein tyrosine nitration,” Biochemical and Biophysical Research Communications, vol. 305, no. 3, pp. 776–783, 2003.
[11]  H. Ischiropoulos and A. Gow, “Pathophysiological functions of nitric oxide-mediated protein modifications,” Toxicology, vol. 208, no. 2, pp. 299–303, 2005.
[12]  R. P. Patel, J. McAndrew, H. Sellak et al., “Biological aspects of reactive nitrogen species,” Biochimica et Biophysica Acta, vol. 1411, no. 2-3, pp. 385–400, 1999.
[13]  S. Kannan, “Free radical theory of autoimmunity,” Theoretical Biology and Medical Modelling, vol. 3, article 22, 2006.
[14]  B. T. Kurien, K. Hensley, M. Bachmann, and R. H. Scofield, “Oxidatively modified autoantigens in autoimmune diseases,” Free Radical Biology and Medicine, vol. 41, no. 4, pp. 549–556, 2006.
[15]  B. T. Kurien and R. H. Scofield, “Autoimmunity and oxidatively modified autoantigens,” Autoimmunity Reviews, vol. 7, no. 7, pp. 567–573, 2008.
[16]  M.-Y. Chou, L. Fogelstrand, K. Hartvigsen et al., “Oxidation-specific epitopes are dominant targets of innate natural antibodies in mice and humans,” Journal of Clinical Investigation, vol. 119, no. 5, pp. 1335–1349, 2009.
[17]  Y. Ohno, T. Kanoh, and H. Uchino, “Idiopathic thrombocytopenic purpura with defective oxidative metabolism of neutrophils,” Acta Haematologica Japonica, vol. 47, no. 6, pp. 1257–1264, 1984.
[18]  A. G. Brox, K. Howson-Jan, and A. A. Fauser, “Treatment of idiopathic thrombocytopenic purpura with ascorbate,” British Journal of Haematology, vol. 70, no. 3, pp. 341–344, 1988.
[19]  S. J. Jubelirer, “Pilot study of ascorbic acid for the treatment of refractory immune thrombocytopenic purpura,” American Journal of Hematology, vol. 43, no. 1, pp. 44–46, 1993.
[20]  A. Karduss Urueta, M. R. Morales Polanco, J. Pizzuto Chávez, and L. A. Meillón García, “Results of the treatment of chronic idiopathic thrombocytopenic purpura with ascorbic acid,” Gaceta Medica de Mexico, vol. 129, no. 1, pp. 23–25, 1993.
[21]  N. Vianelli, L. Gugliotta, L. Gianni, M. M. Belmonte, L. Catani, and S. Tura, “Ascorbic acid for the treatment of chronic refractory idiopathic thrombocytopenic purpura (ITP),” Haematologica, vol. 77, no. 1, pp. 92–93, 1992.
[22]  S. Akbayram, M. Dogan, C. Akgün et al., “The association of oxidant status and antioxidant capacity in children with acute and chronic ITP,” Journal of Pediatric Hematology/Oncology, vol. 32, no. 4, pp. 277–281, 2010.
[23]  B. Zhang, C. Lo, L. Shen et al., “The role of vanin-1 and oxidative stress-related pathways in distinguishing acute and chronic pediatric ITP,” Blood, vol. 117, no. 17, pp. 4569–4579, 2011.
[24]  G. Polat, L. Tamer, K. Tanriverdi, E. Gürkan, F. Baslamisli, and U. Atik, “Levels of malondialdehyde, glutathione and ascorbic acid in idiopathic thrombocytopaenic purpura,” East African Medical Journal, vol. 79, no. 8, pp. 446–449, 2002.
[25]  C. Q. Jin, H. X. Dong, P. P. Cheng, J. W. Zhou, B. Y. Zheng, and F. Liu, “Antioxidant status and oxidative stress in patients with chronic ITP,” Scandinavian Journal of Immunology, vol. 77, pp. 482–487, 2013.
[26]  J. Kamhieh-Milz, G. Bal, V. Sterzer, S. Kamhieh-Milz, O. Arbach, and A. Salama, “Reduced antioxidant capacities in platelets from patients with autoimmune thrombocytopenia purpura (ITP),” Platelets, vol. 23, no. 3, pp. 184–194, 2012.
[27]  C. Neunert, W. Lim, M. Crowther, A. Cohen, L. Solberg Jr., and M. A. Crowther, “The American Society of Hematology 2011 evidence-based practice guideline for immune thrombocytopenia,” Blood, vol. 117, no. 16, pp. 4190–4207, 2011.
[28]  H. Frederiksen and K. Schmidt, “The incidence of idiopathic thrombocytopenic purpura in adults increases with age,” Blood, vol. 94, no. 3, pp. 909–913, 1999.
[29]  W. M. Schoonen, G. Kucera, J. Coalson et al., “Epidemiology of immune thrombocytopenic purpura in the General Practice Research Database,” British Journal of Haematology, vol. 145, pp. 235–244, 2009.
[30]  J. B. Segal and N. R. Powe, “Prevalence of immune thrombocytopenia: analyses of administrative data,” Journal of Thrombosis and Haemostasis, vol. 4, no. 11, pp. 2377–2383, 2006.
[31]  C. Vassalle, S. Maffei, C. Boni, and G. C. Zucchelli, “Gender-related differences in oxidative stress levels among elderly patients with coronary artery disease,” Fertility and Sterility, vol. 89, no. 3, pp. 608–613, 2008.
[32]  A. Kikuchi, A. Takeda, H. Onodera et al., “Systemic increase of oxidative nucleic acid damage in Parkinson's disease and multiple system atrophy,” Neurobiology of Disease, vol. 9, no. 2, pp. 244–248, 2002.
[33]  K. Schuessel, S. Leutner, N. J. Cairns, W. E. Müller, and A. Eckert, “Impact of gender on upregulation of antioxidant defence mechanisms in Alzheimer's disease brain,” Journal of Neural Transmission, vol. 111, no. 9, pp. 1167–1182, 2004.
[34]  L. Dreyer, E. Prescott, and F. Gyntelberg, “Association between atherosclerosis and female lung cancer—a Danish cohort study,” Lung Cancer, vol. 42, no. 3, pp. 247–254, 2003.
[35]  E. Ortona, P. Margutti, P. Matarrese, F. Franconi, and W. Malorni, “Redox state, cell death and autoimmune diseases: a gender perspective,” Autoimmunity Reviews, vol. 7, no. 7, pp. 579–584, 2008.
[36]  U. Nussinovitch and Y. Shoenfeld, “The role of gender and organ specific autoimmunity,” Autoimmunity Reviews, vol. 11, no. 6-7, pp. A377–A385, 2012.
[37]  P. Invernizzi, S. Pasini, C. Selmi, M. E. Gershwin, and M. Podda, “Female predominance and X chromosome defects in autoimmune diseases,” Journal of Autoimmunity, vol. 33, no. 1, pp. 12–16, 2009.
[38]  G. Di Comite, M. Grazia Sabbadini, A. Corti, P. Rovere-Querini, and A. A. Manfredi, “Conversation galante: how the immune and the neuroendocrine systems talk to each other,” Autoimmunity Reviews, vol. 7, no. 1, pp. 23–29, 2007.
[39]  A. Lleo, P. M. Battezzati, C. Selmi, M. E. Gershwin, and M. Podda, “Is autoimmunity a matter of sex?” Autoimmunity Reviews, vol. 7, no. 8, pp. 626–630, 2008.
[40]  A. V. Rubtsov, K. Rubtsova, J. W. Kappler, and P. Marrack, “Genetic and hormonal factors in female-biased autoimmunity,” Autoimmunity Reviews, vol. 9, no. 7, pp. 494–498, 2010.
[41]  D. Fairweather and N. R. Rose, “Women and autoimmune diseases,” Emerging Infectious Diseases, vol. 10, no. 11, pp. 2005–2011, 2004.
[42]  B. Poljsak, “Strategies for reducing or preventing the generation of oxidative stress,” Oxidative Medicine and Cellular Longevity, vol. 2011, Article ID 194586, 15 pages, 2011.
[43]  J. L. Newton, J. A. Reese, S. I. Watson et al., “Fatigue in adult patients with primary immune thrombocytopenia,” European Journal of Haematology, vol. 86, no. 5, pp. 420–429, 2011.
[44]  S. Tomic, S. Brkic, D. Maric, and A. N. Mikic, “Lipid and protein oxidation in female patients with chronic fatigue syndrome,” Archives of Medical Science, vol. 8, pp. 886–891, 2012.
[45]  M. Meyer, R. Schreck, and P. A. Baeuerle, “H2O2 and antioxidants have opposite effects on activation of NF-χB and AP-1 in intact cells: AP-1 as secondary antioxidant-responsive factor,” EMBO Journal, vol. 12, no. 5, pp. 2005–2015, 1993.
[46]  R. Schreck, P. Rieber, and P. A. Baeuerle, “Reactive oxygen intermediates as apparently widely used messengers in the activation of the NF-κB transcription factor and HIV-1,” EMBO Journal, vol. 10, no. 8, pp. 2247–2258, 1991.
[47]  S. J. Kim, P. Angel, R. Lafyatis et al., “Autoinduction of transforming growth factor β1 is mediated by the AP-1 complex,” Molecular and Cellular Biology, vol. 10, no. 4, pp. 1492–1497, 1990.
[48]  A. Voigt, A. Rahnefeld, P. M. Kloetzel, and E. Kruger, “Cytokine-induced oxidative stress in cardiac inflammation and heart failure-how the ubiquitin proteasome system targets this vicious cycle,” Frontiers in Physiology, vol. 4, article 42, 2013.
[49]  B. He, A. Chadburn, E. Jou, E. J. Schattner, D. M. Knowles, and A. Cerutti, “Lymphoma B cells evade apoptosis through the TNF family members BAFF/BLyS and APRIL,” Journal of Immunology, vol. 172, pp. 3268–3279, 2004.
[50]  J.-O. Pers, C. Daridon, V. Devauchelle et al., “BAFF overexpression is associated with autoantibody production in autoimmune diseases,” Annals of the New York Academy of Sciences, vol. 1050, pp. 34–39, 2005.
[51]  E.-Y. Moon, J.-H. Lee, S.-Y. Oh et al., “Reactive oxygen species augment B-cell-activating factor expression,” Free Radical Biology and Medicine, vol. 40, no. 12, pp. 2103–2111, 2006.
[52]  F. Tada, M. Abe, K. Kawasaki et al., “B cell activating factor in obesity is regulated by oxidative stress in adipocytes,” Journal of Clinical Biochemistry and Nutrition, vol. 52, pp. 120–127, 2013.
[53]  F. Emmerich, G. Bal, A. Barakat et al., “High-level serum B-cell activating factor and promoter polymorphisms in patients with idiopathic thrombocytopenic purpura,” British Journal of Haematology, vol. 136, no. 2, pp. 309–314, 2007.
[54]  C. Cerella, S. Coppola, V. Maresca, M. De Nicola, F. Radogna, and L. Ghibelli, “Multiple mechanisms for hydrogen peroxide-induced apoptosis,” Annals of the New York Academy of Sciences, vol. 1171, pp. 559–563, 2009.
[55]  N. Rukoyatkina, U. Walter, and S. Gambaryan, “NO inhibits platelet apoptosis by cGMP-dependent and-independent pathways,” BMC Pharmacology, vol. 9, article P60, 2009.
[56]  J. Thachil, “Nitric oxide in immune thrombocytopenic purpura,” Hematology, vol. 14, no. 1, pp. 59–62, 2009.
[57]  K. D. Mason, M. R. Carpinelli, J. I. Fletcher et al., “Programmed anuclear cell death delimits platelet life span,” Cell, vol. 128, no. 6, pp. 1173–1186, 2007.
[58]  B. Qi and J. M. Hardwick, “A Bcl-xL timer sets platelet life span,” Cell, vol. 128, no. 6, pp. 1035–1036, 2007.

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