Hypercoagulable States

  1. Wendell A. Wilson, MD; and
  2. Azzudin E. Gharavi, MD
  1. Louisiana State University Medical Center; New Orleans, LA 70112-2822

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    TO THE EDITOR:

    We read with interest the review by Thomas and Roberts [1], which mainly discussed genetic defects in coagulation that cause hypercoagulability and thrombosis. We question the authors' summary statement: “No evidence indicates that the measurement of endogenous anticoagulant pathways has a useful role to play in assessing patients at risk for arterial thrombosis.” This generalization is probably relevant to arteriosclerotic thrombosis, but it does not apply to arterial thrombosis in patients suspected of having the antiphospholipid syndrome. As correctly stated by the authors themselves earlier in their review, “… persons with hypercoagulable states include patients with the antiphospholipid syndrome who can develop both arterial and venous thrombosis.”

    Unexplained elevation of the activated partial thromboplastin time is often the first clue to the presence of the antiphospholipid syndrome in patients with arterial (or venous) thrombosis, but the dilute Russel viper venom time and anticardiolipin antibody measurements are more sensitive tests for this syndrome [2, 3]. The syndrome may be secondary to a connective tissue disease, usually systemic lupus erythematosus, or it may be primary, occurring without other autoimmune diseases. Recognition of the syndrome is particularly important because recent retrospective analyses have suggested that patients who have the condition may require long-term warfarin therapy to maintain the prothrombin time (international normalized ratio) at relatively high levels and thus prevent recurrences of thrombosis [4]. However, as is also true for thromboses caused by genetic deficiencies affecting antithrombin III, protein C, and protein S, prospective clinical trials are needed to establish definitive recommendations for treatment of thromboses in the antiphospholipid syndrome [5]. Although the origin and mechanisms of action of antiphospholipid antibodies are not fully understood, both genetic and environmental factors may be important [5].

    Wendell A. Wilson, MD

    Azzudin E. Gharavi, MD

    Louisiana State University Medical Center; New Orleans, LA 70112-2822

    The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:

    •Include no more than 300 words of text, three authors, and five references

    •Type with double-spacing

    •Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.

    Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.

    Annals welcomes electronically submitted letters.

    References

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