Heparin/platelet factor 4 (H:PF4) antibodies are the causative agent in heparin-induced thrombocytopenia (HIT). The antibodies are frequently formed after exposure to heparin, most commonly without any signs of clinical HIT. Heparin-induced thrombocytopenia antibodies have been detected by enzyme-linked immunosorbent assay (ELISA) in individuals who have not been exposed to heparin. It is possible that the antibodies could be elicited by PF4 associated with endogenous, heparin-like glycosaminoglycans (GAGs). This risk would be higher in individuals with endothelial dysfunction and chronic platelet activation. In the setting of an outpatient endocrinology clinic, both diabetic and nondiabetic patients were studied and compared with healthy volunteers. Heparin/platelet factor 4 antibody titers were measured by ELISA and analyzed to determine the frequency of clinically seropositive responses, and median and interquartile ranges of baseline antibody titers. The study found no increase in frequency of ELISA-positive patients among diabetic patients. Moreover, the diabetic population had lower overall level of H:PF4 antibody titer, especially the subgroups treated with thiazolidinedione drugs or angiotensin receptor blockers. Further studies are needed to determine whether subthreshold titers of HIT antibody may be reflective of the physiological state of platelet/endothelial balance.
Heparin (H) anticoagulation in populations characterized by elevated platelet factor 4
(PF4) frequently elicits PF4/H antibodies, presenting a risk of heparin-induced
thrombocytopenia. Recent studies have shown that anti-PF4/H enzyme-linked immunosorbent
assays (ELISAs) detect antibodies in individuals never exposed to heparin. Platelet factor
4/H cross-reactive antibodies may result from PF4-mediated defense responses to injury or
infection. This study questioned whether patients with diabetes are more likely to develop
the endogenous cross-reactive antibodies. A comparison of healthy volunteers versus
hospitalized patients with or without diabetes showed no significant differences in the
prevalence of PF4/H ELISA-positive results. However, the group of patients who had both
diabetes and an infectious condition had higher median antibody titer compared to other
patients with or without diabetes regardless of reason for hospitalization. Higher PF4/H
titers were also associated with patients with diabetes who were not on any medical
therapy. In the future, determining whether PF4/H cross-reactive antibodies sensitize
patients to respond adversely to heparin anticoagulation or predispose patients to other
complications may be relevant to diabetes care.
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