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Blood, 1 November 2005, Vol. 106, No. 9, pp. 3264-3267. Prepublished online as a Blood First Edition Paper on June 28, 2005; DOI 10.1182/blood-2005-04-1594. This Article Full Text (PDF) All Versions of this Article: 2005-04-1594v1 106/9/3264    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Nolan, V. G Articles by Steinberg, M. H Search for Related Content PubMed PubMed Citation Articles by Nolan, V. G Articles by Steinberg, M. H Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted April 20, 2005 Accepted June 22, 2005 Hemolysis associated priapism in sickle cell disease Vikki G Nolan, Diego F Wyszynski, Lindsay A Farrer, and Martin H Steinberg* Department of Medicine, Boston University School of Medicine, Boston, MA, USA Department of Medicine, Boston University School of Medicine, Boston, MA, USA; Boston University School of Public Health, Boston, MA, USA * Corresponding author; email: mhsteinb{at}bu.edu. Priapism, though uncommon in the general population, is one of the many serious complications associated with sickle cell disease (SCD). Few studies have described the clinical and hematological characteristics of individuals with priapism and SCD. Using data from the Cooperative Study for Sickle Cell Disease, we assembled 273 cases with priapism and 979 controls. Cases, compared with controls, had significantly lower levels of hemoglobin, higher levels of lactate dehydrogenase, bilirubin, and aspartate aminotransferase, and higher reticulocyte, white blood cell and platelet counts. These findings suggest an association of priapism with increased hemolysis. Hemolysis decreases the availability of circulating nitric oxide which plays an important role in erectile function. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Unraveling the hemolytic subphenotype of sickle cell disease Mark T. Gladwin Blood 2005 106: 2925-2926. [Full Text] [PDF] This article has been cited by other articles: M. T. Gladwin and E. Vichinsky Pulmonary Complications of Sickle Cell Disease N. Engl. J. Med., November 20, 2008; 359(21): 2254 - 2265. [Full Text] [PDF] P. C. Minneci, K. J. Deans, S. Shiva, H. Zhi, S. M. Banks, S. Kern, C. Natanson, S. B. Solomon, and M. T. Gladwin Nitrite reductase activity of hemoglobin as a systemic nitric oxide generator mechanism to detoxify plasma hemoglobin produced during hemolysis Am J Physiol Heart Circ Physiol, August 1, 2008; 295(2): H743 - H754. [Abstract] [Full Text] [PDF] M. L. Krajewski, L. L. Hsu, and M. T. Gladwin The proverbial chicken or the egg? Dissection of the role of cell-free hemoglobin versus reactive oxygen species in sickle cell pathophysiology Am J Physiol Heart Circ Physiol, July 1, 2008; 295(1): H4 - H7. [Full Text] [PDF] M. T. Gladwin and G. J. Kato Hemolysis-associated hypercoagulability in sickle cell disease: the plot (and blood) thickens! Haematologica, January 1, 2008; 93(1): 1 - 3. [Full Text] [PDF] C. R. Morris Mechanisms of Vasculopathy in Sickle Cell Disease and Thalassemia Hematology, January 1, 2008; 2008(1): 177 - 185. [Abstract] [Full Text] [PDF] C. R. Morris, J. H. Suh, W. Hagar, S. Larkin, D. A. Bland, M. H. Steinberg, E. P. Vichinsky, M. Shigenaga, B. Ames, F. A. Kuypers, et al. Erythrocyte glutamine depletion, altered redox environment, and pulmonary hypertension in sickle cell disease Blood, January 1, 2008; 111(1): 402 - 410. [Abstract] [Full Text] [PDF] R. I. Liem, L. T. Young, and A. A. Thompson Tricuspid regurgitant jet velocity is associated with hemolysis in children and young adults with sickle cell disease evaluated for pulmonary hypertension Haematologica, November 1, 2007; 92(11): 1549 - 1552. [Abstract] [Full Text] [PDF] P. Sebastiani, V. G. Nolan, C. T. Baldwin, M. M. Abad-Grau, L. Wang, A. H. Adewoye, L. C. McMahon, L. A. Farrer, J. G. Taylor IV, G. J. Kato, et al. A network model to predict the risk of death in sickle cell disease Blood, October 1, 2007; 110(7): 2727 - 2735. [Abstract] [Full Text] [PDF] L. L. Hsu, H. C. Champion, S. A. Campbell-Lee, T. J. Bivalacqua, E. A. Manci, B. A. Diwan, D. M. Schimel, A. E. Cochard, X. Wang, A. N. Schechter, et al. Hemolysis in sickle cell mice causes pulmonary hypertension due to global impairment in nitric oxide bioavailability Blood, April 1, 2007; 109(7): 3088 - 3098. [Abstract] [Full Text] [PDF] R. F. Machado, A. Anthi, M. H. Steinberg, D. Bonds, V. Sachdev, G. J. Kato, A. M. Taveira-DaSilva, S. K. Ballas, W. Blackwelder, X. Xu, et al. N-terminal pro-brain natriuretic peptide levels and risk of death in sickle cell disease. JAMA, July 19, 2006; 296(3): 310 - 318. [Abstract] [Full Text] [PDF] D. B. Kim-Shapiro, A. N. Schechter, and M. T. Gladwin Unraveling the Reactions of Nitric Oxide, Nitrite, and Hemoglobin in Physiology and Therapeutics Arterioscler Thromb Vasc Biol, April 1, 2006; 26(4): 697 - 705. [Abstract] [Full Text] [PDF] G. J. Kato, V. McGowan, R. F. Machado, J. A. Little, J. Taylor VI, C. R. Morris, J. S. Nichols, X. Wang, M. Poljakovic, S. M. Morris Jr, et al. Lactate dehydrogenase as a biomarker of hemolysis-associated nitric oxide resistance, priapism, leg ulceration, pulmonary hypertension, and death in patients with sickle cell disease Blood, March 15, 2006; 107(6): 2279 - 2285. [Abstract] [Full Text] [PDF]

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