Heparin-induced thrombocytopenia (HIT) is caused by the formation of abnormal antibodies that activate platelets. Heparin occurs naturally in the human body, but the development of HIT antibodies suggests heparin sulfate may act as a hapten, and thus be targeted by the immune system. In HIT, the immune system forms antibodies against heparin when it is bound to a protein called platelet factor 4 (PF4). These antibodies are usually of the IgG class and their development usually takes about five days. However, those who have been exposed to heparin in the last few months may still have circulating IgG, as IgG-type antibodies generally continue to be produced even when their precipitant has been removed. This is similar to immunity against certain microorganisms, with the difference that the HIT antibody does not persist more than three months. HIT antibodies have been found in individuals with thrombocytopenia and thrombosis who had no prior exposure to heparin sulfate, but the majority are found in people who are receiving heparin. The IgG antibodies form a complex with heparin and PF4 in the bloodstream. The tail of the antibody then binds to the FcγIIa receptor, a protein on the surface of the platelet. This results in platelet activation and the formation of platelet microparticles, which initiate the formation of blood clots; the platelet count falls as a result, leading to thrombocytopenia. (Wikipedia)
The cause of the serum aminotransferase elevations during heparin therapy is not known, but it is likely due to a direct hepatotoxic effect on the liver (L2102).
Heparin-induced hyperkalemia is the result of heparin-induced aldosterone suppression (Wikipedia). The most important, but probably not the only mechanism of aldosterone inhibition appears to involve reduction in both the number and affinity of the angiotensin-II receptors in the zona glomerulosa (A15335).
Alopecia connected to chronic heparin use may be due to the antimitotic effect of heparin on the epithelial cells (A15336).
Heparin causes bone loss by decreasing bone formation. The few studies of the mechanism of bone loss have revealed decreased bone formation, increasing bone resorption, or both (L2103).