971
views
2
recommends
+1 Recommend
2 collections
    6
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Why Is Heparin, Despite Being an Anticoagulant, Rarely Associated with Blood Clotting? A Systematic Review

      Preprint
      In review

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          The paradoxical behaviour of heparin as an effective anticoagulant and a promoter of severe fatal rare blood clots involving autoantibodies needs to be understood for prevention purposes. This review explains the rationale behind this behaviour of heparin in such rare cases of blood clot, which is usually followed by its characteristic thrombocytopenia—a phenomenon known as heparin-induced thrombocytopenia (HIT).

          Methods

          Peer-reviewed scientific literature relating to heparin-induced thrombocytopenia was deconstructed and reconstructed to expose the inductive factors behind the involvement of heparin in severe blood clot and inducement of thrombocytopenia.

          Results

          Studies show that defective B cells of class B-1 cells and marginal zone B are the key players of HIT, as they fail to confer the autoantibodies they express with the needed protein to distinguish between self and non-self. These corrupt autoantibodies bind to the heparin-PF4 complex, which was identified as one of the autoantigens that induces the expression of the IgG autoantibodies. The molar ratio of heparin to PF4 is a determinant of the immunogenicity and avidity of the autoantibody IgG, which desist from binding to them, but the autoantibodies from the defective B cells move towards these autoantigens to initiate HIT. Defective anticoagulant secreting cells and pre-existing risk factors of blood clots, such as birth hormone pills and SARS-Cov-2, may also contribute to HIT in people who develop some of these defective B cells.

          Conclusion

          The moderate formation of heparin-PF4 complex is likely an unrecognized part of the healthy mechanism our body uses to trigger IgG autoantibodies and deploy them as a first line of defence during an inflammation. However, due to anomalies in some B-1 cells and marginal zone B cells, this healthy mechanism could result in the inducement of thrombocytopenia.

          Related collections

          Author and article information

          Journal
          ScienceOpen Preprints
          ScienceOpen
          20 April 2021
          Affiliations
          [1 ] Athlone Institute of Technology
          Article
          10.14293/S2199-1006.1.SOR-.PPVJVZU.v1

          This work has been published open access under Creative Commons Attribution License CC BY 4.0 , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Conditions, terms of use and publishing policy can be found at www.scienceopen.com .

          All data generated or analysed during this study are included in this published article (and its supplementary information files).

          Medicine, Life sciences

          PF4, autoantigens, coagulants, Blood clot, HIT, heparin-induced thrombocytopenia, SARS-Cov-2, thrombocytopenia, heparin-PF4 complex, anticoagulants

          Comments

          Comment on this article