**5. Conclusion**

Not only heparin but also autoimmune antibodies induce thrombocytopenia. Large antigenic complexes formed between PF4 and either heparin or antibody activate platelets, cause a prothrombotic and result in a variety of thromboembolic and systemic consequences. In autoimmune HIT, aPF4/P Abs activate platelets in the absence of heparin. These antibodies are highly reactive. They can self-cluster PF4-molecules forming antigenic complexes and allow binding of otherwise aPF4/P Abs. The resulting immunocomplexes induce massive platelet activation in the absence of heparin. The source and length of heparins play an important role in inducing thrombocytopenia. Improvement of heparin quality together with discovering new non-heparin drugs should be highly desirable. Patients who are suspected of HIT need to be immediately stopped heparin exposure and switched to an alternative anticoagulant. Regarding patients with antibody-induced thrombocytopenia, the level of complication is much higher than the general heparin-induced thrombocytopenia. To date, these humanderived antibodies are hardly controlled, and therefore, efforts in the field would be appreciated. Clinical tests for detecting HIT antibodies as well as autoimmune HIT antibodies must be improved to achieve an appropriate identification of clinical HIT patients.
