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High prevalence of infectious events in thrombotic thrombocytopenic purpura and genetic relationship with toll-like receptor 9 polymorphisms: experience of the French Thrombotic Microangiopathies Reference Center.

Morgand, Marjolaine; Buffet, Marc; Busson, Marc; Loiseau, Pascale; Malot, Sandrine; Amokrane, Kahina; Fortier, Catherine; London, Jonathan; Bonmarchand, Guy; Wynckel, Alain; Provôt, François; Poullin, Pascale; Vanhille, Philippe; Presne, Claire; Bordessoule, Dominique; Girault, Stéphane; Delmas, Yahsou; Hamidou, Mohamed; Mousson, Christiane; Vigneau, Cécile; Lautrette, Alexandre; Pourrat, Jacques; Galicier, Lionel; Azoulay, Elie; Pène, Frédéric; Mira, Jean-Paul; Rondeau, Eric; Ojeda-Uribe, Mario; Charron, Dominique; Maury, Eric; Guidet, Bertrand; Veyradier, Agnès; Tamouza, Ryad; Coppo, Paul.
Transfusion; 54(2): 389-97, 2014 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-23711330

BACKGROUND:

Infectious events have been reported as major environmental triggers of thrombotic thrombocytopenic purpura (TTP). We detail here the potential association between infections and TTP.

STUDY DESIGN AND METHODS:

We recruited randomly and prospectively a cohort of 280 consecutive TTP patients during a 9-year period. Features of infection were systematically recorded.

RESULTS:

Features consistent with an infectious event were observed in 114 patients (41%) at time of TTP diagnosis. Infectious agents were documented in 34 cases and were mainly Gram-negative bacilli. At time of diagnosis infected patients more frequently had fever (p < 0.001). Infections at diagnosis did not impact prognosis and outcome. Thirty-six percent of patients experienced an infectious event during hospitalization, which resulted in more exacerbation of TTP (p = 0.02). Infections were not overrepresented during treatment in patients who received steroids and/or rituximab. Further genetic analysis of toll-like receptor (TLR)-9 functionally relevant polymorphisms revealed that TLR-9 +2848 G and TLR-9 +1174 A genotypes were more frequent in TTP patients than in controls (p = 0.04 and p = 0.026, respectively) and more particularly in patients negative for the Class II human leukocyte antigen system susceptibility allele DRB1*11 (p = 0.001 and p = 0.002, respectively). Haplotypes estimation showed that 1174A-2848G haplotype was significantly more frequent in TTP (p = 0.004), suggesting a primary role for this haplotype variation in conferring a predisposition for acquired TTP.

CONCLUSION:

Infections should be considered as an aggravating factor during the course of TTP. Particular polymorphisms in TLR-9 gene may represent risk factors for TTP.
Selo DaSilva