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Low molecular weight heparin fractions as an alternative therapy in heparin-induced thrombocytopenia
90
THROMBOSIS RESEARCH
Suppl . VI,
1986
178 LOW MOLECULAR WEIGHT HEPARIN THROMBCCYTOPENIA. M. Gouwl+lielI~n, D. Payen, M. Levent. Hi?pltal Henrl
FRACTIONS AS AN ALTERNATIVE THERAPY IN HEPARIN-INDUCED Y. Huet, S. Adnot, G. Contant, F. Bonnet, L. Intrator, Condor - 94010 CRETEIL - FRANCE.
Delayed onset heparln-induced thrombocytopenla (HIT) Is often associated with thrombotlc events wlth maJor morbldlty. These patients requlre lmmedlate dlscontlnuatlon of heparln. Depending on the nature of the underlylng thrombosis other antlthrombotlc therapy may be needed. We report on elght consecutive patlents with HIT, requlrlng Immediate antlcoagulatlon, who have been given low molecular weight heparln (LMWH) fractions as alternative therapy to unfractlonated heparln (UH). Elght patlents (6M, 2F), 33 to 83 year-old, wlth HIT are Included In thls study. These patlents were recelvlng heparln therapy for lower Ilmb phlebltls (4 patients) associated wlth pulmonary embollsm In 1 case, for vascular surgery (3 patients), or as prophylaxls of post-operatl thrcmboembollc compllcatlons (1 patlent). Thrombocytopenla was noted between the tOth and 20 Y6 : pulmoanry day of heparln therapy, and was associated with thrombotlc events In all cases embolism (3 pts), DVT (2 pts), arterlal thrombosls (3 pts). Three patlents received LMWH fraction CY 216 (Choay Laboratorles), flve received LMWH fraction PK 10169 (Pharmuka In vltro platelet aggregatlon studles were performed In the presence of UH and Laboratories). LMWH(s). Monltorlng of LMWH treatment was done according to anti-Xa actlvlty assays by amldolytlc methods. normallzatlon of platelet count was In 6/E patlents (2 recelvlng CY216 and 4 recelvlng PK101691, observed wlthln 3-5 days, with an uneventful recovery (4 patients), recovery after transclent renal failure (1 patlent) and death from sequellae of acute lower Ilmb Ischemla (1 patlent). In LMWH therapy lead to persistent 2/B patients (1 recelvlng CY216 and 1 recelvlng PK10169). thrombocytopenla. In vltro platelet aggregatlon studies, performed a poster1orl on plasma samples collected after cessation of UH therapy and before starting LMWH treatment showed posltlve results In the presence of UH In B/B patlents and posltlve results In the presence of LMWH fractions In the 2 patlents who exhlblted persistent thranbocytopenla with this treatment. These results confirm that LWH therapy may be useful In patients wlth HIT and thromboembollc corn Ilcatlons provldlng that In vltro platelet aggregatlon tests are negative In the presence of e MWH fractfons.
179 PENTOSANE POLYSULFATE LIKE HEPARIN MAY INDUCE SEVERE THROMBOCYTOPENIA A. Le Querrec, A. Derlon, G. Tobelem*, M. Thomas. C.H.U. Caen, 14000 - "INSERM U. 150, Paris, FRANCE. DEPT. Hematology, The analytical characteristics of pentosane polysulfate (PSP. HEMOCLARR) MWru4700 place it among the heparinoyds of low molecular weight (LMWH). Here we report on five patients who presented PSP induced thrombocytopenia. Treatment was PSP (50 mg IM X 2/day). Platelet count (PC) was normal before treatment and decreased within the 5th and 15th day after the induction of PSP therapy. In all cases PC was5 50 OOO/pL. One patient developed an intracerebral hematom associated with venous thrombosis,and two patients both venous and arterial thrombosis. In one case only, arterial thrombosis was observed and in the last patient hemorrhagic disorders were associated with disseminated intravascular coagulation. The presence of a platelet-aggregating factor was evaluated in a mixture of normal platelet rich plasma (three donors) and platelet poor plasma from the five patients. While saline control induced no aggregation, PSP, heparin and LMWH (CY 216, K 2165) induced a platelet aggregation. With heparin (2 cases) or Acenocoumarol treatment (2 cases) both associated with an antiplatelet drug clinical and biological signs resolved and PC increased to normal range by 2 to 6 days. Our five observations suggest that PSP may induce thrombocytopenia associated with venous and arterial thrombosis or bleeding. Further, our results suggest that PSP or heparin induced thrombocytopenia are similar and would be due to an immune mechanism.
THROMBOSIS RESEARCH
Suppl . VI,
1986
178 LOW MOLECULAR WEIGHT HEPARIN THROMBCCYTOPENIA. M. Gouwl+lielI~n, D. Payen, M. Levent. Hi?pltal Henrl
FRACTIONS AS AN ALTERNATIVE THERAPY IN HEPARIN-INDUCED Y. Huet, S. Adnot, G. Contant, F. Bonnet, L. Intrator, Condor - 94010 CRETEIL - FRANCE.
Delayed onset heparln-induced thrombocytopenla (HIT) Is often associated with thrombotlc events wlth maJor morbldlty. These patients requlre lmmedlate dlscontlnuatlon of heparln. Depending on the nature of the underlylng thrombosis other antlthrombotlc therapy may be needed. We report on elght consecutive patlents with HIT, requlrlng Immediate antlcoagulatlon, who have been given low molecular weight heparln (LMWH) fractions as alternative therapy to unfractlonated heparln (UH). Elght patlents (6M, 2F), 33 to 83 year-old, wlth HIT are Included In thls study. These patlents were recelvlng heparln therapy for lower Ilmb phlebltls (4 patients) associated wlth pulmonary embollsm In 1 case, for vascular surgery (3 patients), or as prophylaxls of post-operatl thrcmboembollc compllcatlons (1 patlent). Thrombocytopenla was noted between the tOth and 20 Y6 : pulmoanry day of heparln therapy, and was associated with thrombotlc events In all cases embolism (3 pts), DVT (2 pts), arterlal thrombosls (3 pts). Three patlents received LMWH fraction CY 216 (Choay Laboratorles), flve received LMWH fraction PK 10169 (Pharmuka In vltro platelet aggregatlon studles were performed In the presence of UH and Laboratories). LMWH(s). Monltorlng of LMWH treatment was done according to anti-Xa actlvlty assays by amldolytlc methods. normallzatlon of platelet count was In 6/E patlents (2 recelvlng CY216 and 4 recelvlng PK101691, observed wlthln 3-5 days, with an uneventful recovery (4 patients), recovery after transclent renal failure (1 patlent) and death from sequellae of acute lower Ilmb Ischemla (1 patlent). In LMWH therapy lead to persistent 2/B patients (1 recelvlng CY216 and 1 recelvlng PK10169). thrombocytopenla. In vltro platelet aggregatlon studies, performed a poster1orl on plasma samples collected after cessation of UH therapy and before starting LMWH treatment showed posltlve results In the presence of UH In B/B patlents and posltlve results In the presence of LMWH fractions In the 2 patlents who exhlblted persistent thranbocytopenla with this treatment. These results confirm that LWH therapy may be useful In patients wlth HIT and thromboembollc corn Ilcatlons provldlng that In vltro platelet aggregatlon tests are negative In the presence of e MWH fractfons.
179 PENTOSANE POLYSULFATE LIKE HEPARIN MAY INDUCE SEVERE THROMBOCYTOPENIA A. Le Querrec, A. Derlon, G. Tobelem*, M. Thomas. C.H.U. Caen, 14000 - "INSERM U. 150, Paris, FRANCE. DEPT. Hematology, The analytical characteristics of pentosane polysulfate (PSP. HEMOCLARR) MWru4700 place it among the heparinoyds of low molecular weight (LMWH). Here we report on five patients who presented PSP induced thrombocytopenia. Treatment was PSP (50 mg IM X 2/day). Platelet count (PC) was normal before treatment and decreased within the 5th and 15th day after the induction of PSP therapy. In all cases PC was5 50 OOO/pL. One patient developed an intracerebral hematom associated with venous thrombosis,and two patients both venous and arterial thrombosis. In one case only, arterial thrombosis was observed and in the last patient hemorrhagic disorders were associated with disseminated intravascular coagulation. The presence of a platelet-aggregating factor was evaluated in a mixture of normal platelet rich plasma (three donors) and platelet poor plasma from the five patients. While saline control induced no aggregation, PSP, heparin and LMWH (CY 216, K 2165) induced a platelet aggregation. With heparin (2 cases) or Acenocoumarol treatment (2 cases) both associated with an antiplatelet drug clinical and biological signs resolved and PC increased to normal range by 2 to 6 days. Our five observations suggest that PSP may induce thrombocytopenia associated with venous and arterial thrombosis or bleeding. Further, our results suggest that PSP or heparin induced thrombocytopenia are similar and would be due to an immune mechanism.