Thrombotic thrombocytopenic purpura triggered by influenza A virus subtype H1N1 infection

Koh, Young Rae; Hwang, Sang‐Hyun; Chang, Chulhun L.; Lee, Eun Yup; Son, Hyojoo; Kim, Hyung Hoi

doi:10.1016/j.transci.2011.10.024

Cited by 18 publications

(10 citation statements)

References 25 publications

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“…Only recently have a few cases of HUS associated with influenza B virus infection been published (Table 1 ) [ 22 , 23 ]. Ten patients with HUS were noted during the 2009 influenza A(H1N1) pandemic [ 26 – 35 ], and one during a later wave [ 36 ], constituting 44% of all reported occurrences of influenza-associated thrombotic microangiopathy (iTMA; Tables 1 , 2 ). The distribution of these cases corresponded to the course of the pandemic [ 44 ] and differed from the usual seasonal influenza pattern (Fig.…”

Section: Influenza-associated Thrombotic Microangiopathymentioning

confidence: 99%

“…Influenza A virus, including A(H1N1) has been invoked as a cause of TTP in at least four published reports [ 34 , 35 , 39 , 40 ]. ADAMTS13 activity was depleted in 2 patients; both demonstrated increased anti-ADAMTS13 antibody concentrations [ 39 , 40 ].…”

Section: Influenza and Ttpmentioning

confidence: 99%

“…ADAMTS13 activity was depleted in 2 patients; both demonstrated increased anti-ADAMTS13 antibody concentrations [ 39 , 40 ]. The TTP diagnosis of the remaining 2 patients was clinical, based on the combination of MAHA and neurological manifestations, while ADAMTS13 and complement studies were lacking (Table 3 ) [ 34 , 35 ]. The mechanism leading to the rise of anti-ADAMTS13 and other autoantibodies by influenza and influenza vaccines [ 48 , 49 ] warrants additional research.…”

Section: Influenza and Ttpmentioning

confidence: 99%

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Influenza-associated thrombotic microangiopathies

Bitzan

Zieg

2017

Pediatr Nephrol

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Thrombotic microangiopathy (TMA) refers to phenotypically similar disorders, including hemolytic uremic syndromes (HUS) and thrombotic thrombocytopenic purpura (TTP). This review explores the role of the influenza virus as trigger of HUS or TTP. We conducted a literature survey in PubMed and Google Scholar using HUS, TTP, TMA, and influenza as keywords, and extracted and analyzed reported epidemiological and clinical data. We identified 25 cases of influenza-associated TMA. Five additional cases were linked to influenza vaccination and analyzed separately. Influenza A was found in 83%, 10 out of 25 during the 2009 A(H1N1) pandemic. Two patients had bona fide TTP with ADAMTS13 activity <10%. Median age was 15 years (range 0.5–68 years), two thirds were male. Oligoanuria was documented in 81% and neurological involvement in 40% of patients. Serum C3 was reduced in 5 out of 14 patients (36%); Coombs test was negative in 7 out of 7 and elevated fibrin/fibrinogen degradation products were documented in 6 out of 8 patients. Pathogenic complement gene mutations were found in 7 out of 8 patients tested (C3, MCP, or MCP combined with CFB or clusterin). Twenty out of 24 patients recovered completely, but 3 died (12%). Ten of the surviving patients underwent plasma exchange (PLEX) therapy, 5 plasma infusions. Influenza-mediated HUS or TTP is rare. A sizable proportion of tested patients demonstrated mutations associated with alternative pathway of complement dysregulation that was uncovered by this infection. Further research is warranted targeting the roles of viral neuraminidase, enhanced virus-induced complement activation and/or ADAMTS13 antibodies, and rational treatment approaches.Electronic supplementary materialThe online version of this article (10.1007/s00467-017-3783-4) contains supplementary material, which is available to authorized users

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Section: Influenza-associated Thrombotic Microangiopathymentioning

confidence: 99%

Section: Influenza and Ttpmentioning

confidence: 99%

Section: Influenza and Ttpmentioning

confidence: 99%

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Influenza-associated thrombotic microangiopathies

Bitzan

Zieg

2017

Pediatr Nephrol

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“…Therefore, it assumes a scientific relevance the clinical observation by Kosugi et al [10], that influenza infection triggers TTP by producing anti-ADAMTS13 IgGs. The observation is crucial in light of the fact that the association between influenza infection and TTP is clinically well known [11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29], so making feasible the hypothesis that the anti-influenza immune responses that follow influenza infection may cross-react with ADAMTS13 protein thus generating anti-ADAMTS13 AAbs. To prove or disprove the cross-reactivity hypothesis, the present study analyzed the peptide commonality between influenza virus and ADAMTS13 proteins since, actually, peptide sharing can lead to autoimmunity through cross-reactivity phenomena following pathogen infection.…”

Section: Introductionmentioning

confidence: 99%

From influenza infection to anti-ADAMTS13 autoantibodies via cross-reactivity

Kanduc

2018

Infection International

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Autoantibodies (AAbs) against von Willebrand factor (vWF)-cleaving protease ADAMTS13 causally relate to thrombotic thrombocytopenic purpura (TTP). How anti-ADAMTS13 AAbs are generated is unknown. Starting from reports according to which influenza infection can trigger TTP by the production of ADAMTS13 AAbs, this study explores influenza viruses and ADAMTS13 protein for common peptide sequences that might underlie anti-influenza immune responses able to cross-react with ADAMTS13. Results document that numerous peptides are shared between influenza A and B viruses and ADAMTS13, thus supporting the hypothesis of cross-reactivity as a mechanism driving the generation of anti-ADAMTS13 AAbs.

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“…Review of the literature reveals single casuistic reports of TTP associated with pathogens including Brucella [4], streptococci [5], Mycoplasma pneumoniae [6] and Varicella zoster [7]. During the past 3 decades, only three reports on TTP associated with influenza A infection were published [8][9][10], of which only one caused by the von Willebrand factor (VWF)-cleaving protease a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13) inhibitor and with undetectable ADAMTS13 activity. This patient was treated with daily plasma exchange and high-dose methylprednisolone therapy, but died after 3 days in hospital.…”

Section: Introductionmentioning

confidence: 99%

A 35-year-old woman with influenza A-associated thrombotic thrombocytopenic purpura

Jonsson

Hammenfors²,

Oppegaard³

et al. 2015

Blood Coagulation &Amp; Fibrinolysis

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A previously healthy 35-year-old woman presented with severe thrombotic thrombocytopenic purpura (TTP) affecting several organs and concomitant influenza A infection. On admission to hospital, haemoglobin was 5.4 g/dl, platelet count 6 × 10/l, Schistocyte count in peripheral blood 5%, and throat swab positive for influenza A RNA. The patient was treated with antiviral medication and transfusions of fresh frozen plasma before plasma exchange therapy with excellent response. Plasmaphereses were attenuated after 5 days, resulting in TTP relapse 3 days later. A disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13) protein was very low (<0.04 U/l) and anti-ADAMTS13 elevated (>2 U/l), consistent with acquired TTP. Platelet counts normalized after five additional plasma exchanges and oral corticosteroids. Antinuclear antibodies and subgroup anti-Ro/Sjögren's syndrome A antigen (SSA) were detected in serum and have remained borderline-elevated, although evaluation during TTP, recovery and follow-up have lacked clinical manifestations of connective tissue disease. Influenza A infection induced production of ADAMTS13 inhibitor, which resulted in TTP in a patient with circulating antinuclear antibodies, lacking other manifestations of connective tissue disease.

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Thrombotic thrombocytopenic purpura triggered by influenza A virus subtype H1N1 infection

Cited by 18 publications

References 25 publications

Influenza-associated thrombotic microangiopathies

Influenza-associated thrombotic microangiopathies

From influenza infection to anti-ADAMTS13 autoantibodies via cross-reactivity

A 35-year-old woman with influenza A-associated thrombotic thrombocytopenic purpura

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