2008
DOI: 10.1002/ajh.21273
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Delayed‐onset HIT caused by low‐molecular‐weight heparin manifesting during fondaparinux prophylaxis

Abstract: Heparin-induced thrombocytopenia (HIT) is a prothrombotic condition caused by platelet-activating antibodies that react with platelet factor 4 (PF4)/heparin complexes. Delayed-onset HIT occurs after heparin is stopped. Fondaparinux, a synthetic pentasaccharide, is thought to be a safe alternative anticoagulant in HIT. We describe a patient with delayed-onset HIT triggered by low-molecular-weight heparin (LMWH) which occurred during fondaparinux prophylaxis and which was complicated by microangiopathic hemolyti… Show more

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Cited by 40 publications
(32 citation statements)
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“…One of our patients who received a repeat exposure to intraoperative UFH to permit urgent cardiac surgery-patient 17 ( Figure 1)-developed a clinical picture strongly indicative of HIT, and one that essentially recapitulated his prior episode of HIT 11 years earlier. This patient's serum strongly activated platelets even in the absence of heparin (heparin-independent platelet activation 21 ), a serological feature consistent with the antibodies identified in patients with "delayedonset HIT" [28][29][30][31] as well as delayed recovery of thrombocytopenia after stopping heparin, 32 and that plausibly explains why this patient developed HIT 1 week after cardiac surgery, even though no postoperative heparin was being given. A practical consequence of this clinical observation is that patients with previous HIT who undergo heparin rechallenge should undergo platelet count monitoring, perhaps for as long as 10 days, even if they do not receive any postoperative heparin.…”
Section: Discussionsupporting
confidence: 70%
“…One of our patients who received a repeat exposure to intraoperative UFH to permit urgent cardiac surgery-patient 17 ( Figure 1)-developed a clinical picture strongly indicative of HIT, and one that essentially recapitulated his prior episode of HIT 11 years earlier. This patient's serum strongly activated platelets even in the absence of heparin (heparin-independent platelet activation 21 ), a serological feature consistent with the antibodies identified in patients with "delayedonset HIT" [28][29][30][31] as well as delayed recovery of thrombocytopenia after stopping heparin, 32 and that plausibly explains why this patient developed HIT 1 week after cardiac surgery, even though no postoperative heparin was being given. A practical consequence of this clinical observation is that patients with previous HIT who undergo heparin rechallenge should undergo platelet count monitoring, perhaps for as long as 10 days, even if they do not receive any postoperative heparin.…”
Section: Discussionsupporting
confidence: 70%
“…106 Although the quality of the evidence for fondaparinux-induced HIT is of low quality and experts dispute its existence, the quality of the evidence in favor of fondaparinux as a treatment of HIT is also very low quality. The use of argatroban, lepirudin, and danaparoid to treat patients with HITT is supported by studies with less risk of bias.…”
Section: Normal Renal Functionmentioning
confidence: 99%
“…Based on the mechanism of fondaparinux's action, one could postulate that this agent should not induce HIT. However, emerging case reports raise the probability of fondaparinux inducing HIT [7][8][9][10]. With this limited data, the direct relationship between fondaparinux and HIT is still unclear.…”
Section: Discussionmentioning
confidence: 99%