Literature DB >> 24249282

Successful treatment of DEAP-HUS with eculizumab.

Damien Noone1, Aoife Waters, Fred G Pluthero, Denis F Geary, Michael Kirschfink, Peter F Zipfel, Christoph Licht.   

Abstract

BACKGROUND: Deficiency of complement factor H-related (CFHR) proteins and CFH autoantibody-positive hemolytic uremic syndrome (DEAP-HUS) represents a unique subgroup of complement-mediated atypical HUS (aHUS). Autoantibodies to the C-terminus of CFH block CFH surface recognition and mimic mutations found in the genetic form of (CFH-mediated) aHUS. CFH autoantibodies are found in 10-15 % of aHUS patients and occur--so far unexplained--almost exclusively in the background of CFHR1 or CFHR3/CFHR1 deletions.
METHODS: As a well-defined role for eculizumab in the treatment of complement-mediated aHUS is becoming established, its role in DEAP-HUS is less conspicuous, where a B-cell-depleting and immunosuppressive treatment strategy is being proposed in the literature.
RESULTS: We here show eculizumab to be safe and effective in maintaining a disease-free state, without recurrence, in a previously plasma-therapy-dependent DEAP-HUS patient, and in another patient in whom, although showing a good clinical response to plasma therapy, the therapy was hampered by allergic reactions to fresh frozen plasma and contend there is a rationale for the use of eculizumab in concert with an immunosuppressive strategy in the treatment of DEAP-HUS. Considering the high rate of early relapse, the possible coexistence and contribution of both known and unknown complement-gene mutations, the probable pathogenic role of CFHR1 as a complement alternative pathway (CAP) regulator, the experimental nature of measuring and using anti-CFH autoantibodies to guide management, and until the positive reports of immunosuppression in addition to plasma therapy are confirmed in prospective studies, we feel that a complement-directed therapy should not be neglected in DEAP-HUS. Serial CFH autoantibody titer testing may become a valuable tool to monitor treatment response, and weaning patients off eculizumab may become an option once CFH autoantibody levels are depleted.
CONCLUSIONS: A prospective study of eculizumab treatment in a larger cohort of DEAP-HUS patients is required to validate the applicability of our positive experience.

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Year:  2013        PMID: 24249282     DOI: 10.1007/s00467-013-2654-x

Source DB:  PubMed          Journal:  Pediatr Nephrol        ISSN: 0931-041X            Impact factor:   3.714


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4.  Terminal complement complex (C5b-9) in children with recurrent hemolytic uremic syndrome.

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Review 7.  DEAP-HUS: deficiency of CFHR plasma proteins and autoantibody-positive form of hemolytic uremic syndrome.

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9.  Anti factor H autoantibodies block C-terminal recognition function of factor H in hemolytic uremic syndrome.

Authors:  Mihály Józsi; Stefanie Strobel; Hans-Martin Dahse; Wei-shih Liu; Peter F Hoyer; Martin Oppermann; Christine Skerka; Peter F Zipfel
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10.  Characterization of complement factor H-related (CFHR) proteins in plasma reveals novel genetic variations of CFHR1 associated with atypical hemolytic uremic syndrome.

Authors:  Cynthia Abarrategui-Garrido; Rubén Martínez-Barricarte; Margarita López-Trascasa; Santiago Rodríguez de Córdoba; Pilar Sánchez-Corral
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Review 4.  Successful discontinuation of eculizumab under immunosuppressive therapy in DEAP-HUS.

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Review 9.  The Immunopathology of Complement Proteins and Innate Immunity in Autoimmune Disease.

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Review 10.  Deficiency of CFHR plasma proteins and autoantibody positive hemolytic uremic syndrome: treatment rationale, outcomes, and monitoring.

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