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Increased thromboinflammatory load in hereditary angioedema.

Olav Rogde Gramstad1, Camilla Schjalm2,3, Tom Eirik Mollnes2,3,4

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Clinical and Experimental Immunology
|August 10, 2023
PubMed
Summary

C1 inhibitor deficiency in hereditary angioedema patients is linked to higher levels of inflammatory markers and blood clotting factors, suggesting a heightened baseline thromboinflammatory state. This indicates patients may experience subclinical attacks even without visible swelling.

Keywords:
C1 inhibitorbradykinincomplementcytokineshereditary angioedema

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Area of Science:

  • Immunology and Hematology
  • Thromboinflammation
  • Complement System

Background:

  • C1 inhibitor (C1Inh) regulates key inflammatory and hemostatic systems, including the kallikrein-kinin, complement, coagulation, and fibrinolytic pathways.
  • C1Inh deficiency, characteristic of hereditary angioedema (HAE), is known to cause plasma leakage but may also impact thrombosis and inflammation.
  • Understanding the baseline thromboinflammatory status in HAE patients is crucial for managing potential long-term complications.

Purpose of the Study:

  • To investigate the thromboinflammatory load in patients with C1 inhibitor deficiency (HAE types 1 and 2) during clinical remission.
  • To compare cytokine profiles, complement activation markers, and hemostatic markers between HAE patients and healthy controls.

Main Methods:

  • Multiplex technology was used to measure 27 cytokines, including interleukins, chemokines, and growth factors.
  • Enzyme immunoassays were employed to quantify complement activation markers (C4d, C3bc, sC5b-C9/TCC) and hemostatic markers (TAT, F1+2, β-TG, PAI-1).
  • Plasma and serum samples from 20 HAE patients in remission and 20 age- and sex-matched healthy controls were analyzed.

Main Results:

  • HAE patients exhibited significantly elevated levels of numerous pro-inflammatory cytokines (e.g., TNF, IL-1β, IL-6, IL-17A) and chemokines (e.g., CXCL8, CCL3, CCL4) compared to controls.
  • Increased levels of thrombin-antithrombin complexes (TAT) and prothrombin fragment 1+2 (F1+2), indicative of heightened coagulation activity, were observed in HAE patients.
  • While some markers like G-CSF, β-TG, and PAI-1 were higher in HAE patients, these did not reach statistical significance after multiple testing correction.

Conclusions:

  • C1 inhibitor deficiency is associated with a significantly increased baseline thromboinflammatory load in HAE patients.
  • Elevated inflammatory and pro-coagulant markers suggest HAE patients may exist in a subclinical inflammatory state, even between overt attacks.
  • These findings highlight the systemic impact of C1Inh deficiency beyond acute edema, potentially contributing to thrombotic risk.