Administration of Eculizumab, a C5 Inhibitor, for the Treatment of Shiga-Toxin-Producing Escherichia coli Infection: A Case Report
American Journal of Clinical and Experimental Medicine
Volume 6, Issue 1, January 2018, Pages: 27-32
Received: Jan. 12, 2018; Accepted: Feb. 1, 2018; Published: Mar. 8, 2018
Views 1449      Downloads 30
Authors
Takahiro Yukawa, Department of Trauma and Critical Care Center, Tokyo Metropolitan Bokutoh Hospital, Tokyo, Japan
Takuto Ishida, Department of Trauma and Critical Care Center, Tokyo Metropolitan Bokutoh Hospital, Tokyo, Japan
Toshinobu Yamagishi, Department of Trauma and Critical Care Center, Tokyo Metropolitan Bokutoh Hospital, Tokyo, Japan
Kazuhiro Sugiyama, Department of Trauma and Critical Care Center, Tokyo Metropolitan Bokutoh Hospital, Tokyo, Japan
Yuichi Hamabe, Department of Trauma and Critical Care Center, Tokyo Metropolitan Bokutoh Hospital, Tokyo, Japan
Article Tools
Follow on us
Abstract
Hemolytic-uremic syndrome (HUS), which is characterized by microvascular hemolytic anemia, consumption thrombocytopenia, and acute renal failure, is a complication of the Shiga-toxin-producing Escherichia coli (STEC) infection. We describe the case of a patient who, despite undergoing plasma exchange and renal replacement therapy for STEC-induced HUS, experienced poor improvement in platelet count, serum creatinine level, and serum lactate dehydrogenase level. The patient developed acute encephalopathy but recovered without permanent organ damage after eculizumab therapy. For severe HUS cases involving the central nervous system, early administration of eculizumab, which inhibits the abnormal activation of the complement activation pathway, may be effective.
Keywords
Hemolytic-Uremic Syndrome, Shiga-Toxin-Producing Escherichia coli Infection, Acute Encephalopathy, Eculizumab
To cite this article
Takahiro Yukawa, Takuto Ishida, Toshinobu Yamagishi, Kazuhiro Sugiyama, Yuichi Hamabe, Administration of Eculizumab, a C5 Inhibitor, for the Treatment of Shiga-Toxin-Producing Escherichia coli Infection: A Case Report, American Journal of Clinical and Experimental Medicine. Vol. 6, No. 1, 2018, pp. 27-32. doi: 10.11648/j.ajcem.20180601.15
Copyright
Copyright © 2018 Authors retain the copyright of this article.
This article is an open access article distributed under the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
References
[1]
O’Brien, A. O., T. A. Lively TA, M. E. Chen, S. W. Rothman, and S. B. Formal. (1983) Escherichia coli O157:H7 strains associated with haemorrhagic colitis in the United States produce a Shigella dysenteriae 1 (SHIGA) like cytotoxin. The Lancet 1, 702.
[2]
Frank, C., D. Werber, J. P. Cramer, M. Askar, M. Faber, M. an der Heiden, et al. (2011) Epidemic profile of Shiga-toxin-producing Escherichia coli O104:H4 outbreak in Germany. The New England Journal of Medicine 365, 1763.
[3]
Tarr, P. I., C. A. Gordon, and W. L. Chandler. (2005) Shiga-toxin-producing Escherichia coli and haemolytic uraemic syndrome. The Lancet 365, 1073-1086.
[4]
Legendre, C. M., C. Licht, P, Muus, L. A. Greenbaum, S. Babu, et al. (2013) Terminal complement inhibitor eculizumab in atypical hemolytic-uremic syndrome. The New England Journal of Medicine 368, 2169-2181.
[5]
Lapeyraque, A. L., M. Malina, V. Fremeaux-Bacchi, T. Boppel, M. Kirschfink, et al. (2011) Eculizumab in severe Shiga-toxin-associated HUS. The New England Journal of Medicine 364, 2561-2563.
[6]
Slutsker, L., A. A. Ries, K. D. Greene, J. G. Wells, L. Hutwagner, et al. (1997) Escherichia coli O157:H7 diarrhea in the United States: clinical and epidemiologic features. Annals of Internal Medicine 126, 505-513.
[7]
Boyce, T. G., D. L. Swerdlow, and P. M. Griffin. (1995) Escherichia coli O157:H7 and the hemolytic-uremic syndrome. The New England Journal of Medicine 333, 364-368.
[8]
Su, C., and L. J. Brandt. (1995) Escherichia coli O157:H7 infection in humans. Annals of Internal Medicine 123, 698-714.
[9]
Siegler, R. L., M. K. Milligan, T. H. Burningham, R. D. Christofferson, S. Y. Chang, et al. (1991) Long-term outcome and prognostic indicators in the hemolytic-uremic syndrome. Journal of Pediatrics 118, 195-200.
[10]
Rosales, A., J. Hofer, L. B. Zimmerhackl, T. C. Jungraithmayr, M. Riedl, et al. (2012) Need for long-term follow-up in enterohemorrhagic Escherichia coli-associated hemolytic uremic syndrome due to late-emerging sequelae. Clinical Infectious Diseases 54, 1413-1421.
[11]
Freedman, S. B., J. Xie, M. S. Neufeld, W. L. Hamilton, L. Hartling, et al. (2016) Shiga toxin-producing Escherichia coli infection, antibiotics, and risk of developing hemolytic uremic syndrome: A meta-analysis. Clinical Infectious Diseases 62, 1251-1258.
[12]
Nathanson, S., T. Kwon, M. Elmaleh, M. Charbit, E. A. Launay, et al. (2011) Acute neurological involvement in diarrhea-associated hemolytic uremic syndrome. Clinical Journal of the American Society of Nephrology 5, 1218-1228.
[13]
Fujii J, Y. Kinoshita, A. Matsukawa, S. Y. Villanueva, T. Yutsudo, et al. (2009) Successful steroid pulse therapy for brain lesion caused by Shiga toxin 2 in rabbits. Microbial Pathogenesis 46, 179-184.
[14]
Roumenina, L. T., R. Roquigny, C. Blanc, N. Poulain, S. Ngo, et al. (2014) Functional evaluation of factor H genetic and acquired abnormalities: application for atypical hemolytic uremic syndrome (aHUS). Methods in Molecular Biology 1100, 237-247.
[15]
Noris, M., J. Caprioli, E. Bresin, C. Mossali, G. Pianetti, et al. (2010) Relative role of genetic complement abnormalities in sporadic and familial aHUS and their impact on clinical phenotype. Clinical Journal of the American Society of Nephrology 5, 1844-1859.
[16]
Ito, N., H. Hataya, K. Saida, Y. Amano, Y. Hidaka, et al. (2016) Efficacy and safety of eculizumab in childhood atypical hemolytic uremic syndrome in Japan. Clinical and Experimental Nephrology 20, 265-272.
[17]
Mizuguchi, M., S. Tanaka, I. Fujii, H. Tanizawa, Y. Suzuki, et al. (1996) Neuronal and vascular pathology produced by verocytotoxin 2 in the rabbit central nervous system. Acta Neuropathologica 91, 254-262.
[18]
Fujii, J., T. Kita, S. Yoshida, T. Takeda, H. Hobayashi, et al. (1994) Direct evidence of neuron impairment by oral infection with verotoxin-producing Escherichia coli O157: H-in mitomycin-treated mice. Infection and Immunity 62, 3447-3453.
[19]
Fitzpatrik, M. M., V. Shah, R. S. Trompeter, M. J. Dillon, T. M. Barratt. (1992) Interleukin-8 and polymorphoneutrophil leucocyte activation in hemolytic uremic syndrome of childhood. Kidney International 142, 951-956.
[20]
Thurman, J. M., R. Marians, W. Emlen, S. Wood, C. Smith, et al. (2009) Alternative pathway of complement in children with diarrhea-associated hemolytic uremic syndrome. Clinical Journal of the American Society of Nephrology 4, 1920-1924.
[21]
Fang, C. J., V. Frémeaux-Bacchi, M. K. Liszewski, G. Pianetti, M. Noris, et al. (2008) Membrane cofactor protein mutations in atypical hemolytic uremic syndrome (aHUS), fatal Stx-HUS, C3 glomerulonephritis, and the HELLP syndrome. Blood 111, 624-632.
ADDRESS
Science Publishing Group
548 FASHION AVENUE
NEW YORK, NY 10018
U.S.A.
Tel: (001)347-688-8931