PURPOSE: To determine whether low molecular weight heparin (LMWH) can be an alternative to unfractionated heparin (UH) for patients with heparin-induced thrombocytopenia syndrome (HIT). METHODS: The diagnosis of HIT was established in 126 patients by platelet aggregometry with UH (1 U/ml). These plasma samples were also tested for the ability to aggregate platelets in the presence of the LMWH enoxaparin (1 U/ml). Two patients with the HIT syndrome, after negative platelet aggregometry testing with enoxaparin, were anticoagulated with enoxaparin. RESULTS: Fifteen plasma samples that tested negative to UH also tested negative to enoxaparin. Forty-three of 126 (34%) UH-positive plasma samples aggregated platelets in the presence of enoxaparin. Twenty-two of 102 (22%) plasma samples with limited positive aggregation responses (minimal or no change in optical density) aggregated platelets in the presence of enoxaparin. However, 21 of 24 (88%) strongly positive plasma samples (30% to 60% change in optical density at 3 to 27 minutes) also aggregated platelets in the presence of enoxaparin. Two patients with HIT who received enoxaparin after aggregation testing demonstrated no cross-reactivity to enoxaparin achieved adequate anticoagulation and did not develop HIT. CONCLUSIONS: Thirty-four percent of plasma samples from patients with HIT (88% of those strongly positive) aggregated platelets in the presence of enoxaparin. Patients with HIT may safely receive enoxaparin if their plasma does not aggregate platelets in the presence of enoxaparin.
PURPOSE: To determine whether low molecular weight heparin (LMWH) can be an alternative to unfractionated heparin (UH) for patients with heparin-induced thrombocytopenia syndrome (HIT). METHODS: The diagnosis of HIT was established in 126 patients by platelet aggregometry with UH (1 U/ml). These plasma samples were also tested for the ability to aggregate platelets in the presence of the LMWH enoxaparin (1 U/ml). Two patients with the HIT syndrome, after negative platelet aggregometry testing with enoxaparin, were anticoagulated with enoxaparin. RESULTS: Fifteen plasma samples that tested negative to UH also tested negative to enoxaparin. Forty-three of 126 (34%) UH-positive plasma samples aggregated platelets in the presence of enoxaparin. Twenty-two of 102 (22%) plasma samples with limited positive aggregation responses (minimal or no change in optical density) aggregated platelets in the presence of enoxaparin. However, 21 of 24 (88%) strongly positive plasma samples (30% to 60% change in optical density at 3 to 27 minutes) also aggregated platelets in the presence of enoxaparin. Two patients with HIT who received enoxaparin after aggregation testing demonstrated no cross-reactivity to enoxaparin achieved adequate anticoagulation and did not develop HIT. CONCLUSIONS: Thirty-four percent of plasma samples from patients with HIT (88% of those strongly positive) aggregated platelets in the presence of enoxaparin. Patients with HIT may safely receive enoxaparin if their plasma does not aggregate platelets in the presence of enoxaparin.
Authors: Asheley B Wathen; Daniel D Myers; Paul Zajkowski; Graham Flory; F Claire Hankenson Journal: J Am Assoc Lab Anim Sci Date: 2009-09 Impact factor: 1.232