AIM: Anti-platelet factor 4/heparin complex antibodies (anti-PF4/heparin Ab) have been found to cause heparin-induced thrombocytopenia (HIT), a clinical syndrome thrombocytopenia and thrombosis. There is still controversy as to whether the presence of anti-PF4/heparin antibodies in hemodialysis patients augments clot formation in access fistula thrombosis, peripheral artery disease (PAD), and coronary heart disease (CHD). METHODS: We enrolled 111 non-diabetic hemodialysis patients without liver cirrhosis and without an ankle-brachial index (ABI) ≥1.3 (arterial calcification). ABI measurements were performed and patients with an ABI ≤0.9 were defined as having PAD and included in the PAD group. ELISA was used for determination of anti-PF4/heparin Ab. Correlation factors include PAD, native arteriovenous fistula (AVF) thrombosis, platelet count, and CHD. RESULTS: Thirty-seven of 111 patients (33.3%) presented with anti-PF4/heparin Ab. Thirty-eight of 111 patients (34%) had PAD; fourteen of these patients (36.8%) and 23/73 of patients without PAD (31.5%) were anti-PF4/heparin Ab-positive (P = 0.57). Fifty-two of 111 patients (46.8%) had AVF thrombosis; twenty-three of these patients (44.2%) and 14/59 of patients without AVF thrombosis (23.7%) were anti-PF4/heparin Ab-positive (P = 0.02). The odds ratio for AVF thrombosis was 2.55 (95% CI 1.14-5.71) for anti-PF4/heparin Ab-positive patients. Thirty-two of 111 patients (28.8%) had thrombocytopenia (platelet count <140 × 10(3)/μL); eleven of these patients (34.3%) and 26/79 patients without thrombocytopenia (32.9%) were anti-PF4/heparin Ab-positive (P = 0.88). Ten of 111 patients (9%) had CHD; two of these patients (20%) and 35/101 patients without CHD (34.6%) were anti-PF4/heparin Ab-positive (P = 0.49). CONCLUSIONS: We found that anti-PF4/heparin Ab may contribute to an increased risk of AVF thrombosis in non-diabetic hemodialysis patients.
AIM: Anti-platelet factor 4/heparin complex antibodies (anti-PF4/heparin Ab) have been found to cause heparin-induced thrombocytopenia (HIT), a clinical syndrome thrombocytopenia and thrombosis. There is still controversy as to whether the presence of anti-PF4/heparin antibodies in hemodialysis patients augments clot formation in access fistula thrombosis, peripheral artery disease (PAD), and coronary heart disease (CHD). METHODS: We enrolled 111 non-diabetic hemodialysispatients without liver cirrhosis and without an ankle-brachial index (ABI) ≥1.3 (arterial calcification). ABI measurements were performed and patients with an ABI ≤0.9 were defined as having PAD and included in the PAD group. ELISA was used for determination of anti-PF4/heparin Ab. Correlation factors include PAD, native arteriovenous fistula (AVF) thrombosis, platelet count, and CHD. RESULTS: Thirty-seven of 111 patients (33.3%) presented with anti-PF4/heparin Ab. Thirty-eight of 111 patients (34%) had PAD; fourteen of these patients (36.8%) and 23/73 of patients without PAD (31.5%) were anti-PF4/heparin Ab-positive (P = 0.57). Fifty-two of 111 patients (46.8%) had AVF thrombosis; twenty-three of these patients (44.2%) and 14/59 of patients without AVF thrombosis (23.7%) were anti-PF4/heparin Ab-positive (P = 0.02). The odds ratio for AVF thrombosis was 2.55 (95% CI 1.14-5.71) for anti-PF4/heparin Ab-positive patients. Thirty-two of 111 patients (28.8%) had thrombocytopenia (platelet count <140 × 10(3)/μL); eleven of these patients (34.3%) and 26/79 patients without thrombocytopenia (32.9%) were anti-PF4/heparin Ab-positive (P = 0.88). Ten of 111 patients (9%) had CHD; two of these patients (20%) and 35/101 patients without CHD (34.6%) were anti-PF4/heparin Ab-positive (P = 0.49). CONCLUSIONS: We found that anti-PF4/heparin Ab may contribute to an increased risk of AVF thrombosis in non-diabetic hemodialysispatients.
Authors: I J Welsby; E F Krakow; J A Heit; E C Williams; G M Arepally; S Bar-Yosef; D F Kong; S Martinelli; I Dhakal; W W Liu; J Krischer; T L Ortel Journal: J Thromb Haemost Date: 2016-11-30 Impact factor: 5.824