Based on the role of platelets in inflammation and hemostasis it has been assumed that antiplatelet therapy could be beneficial for patients suffering from ulcerative colitis. Platelets present a link between inflammation and coagulation. They have more than 300 active mediators stored in their granules. Upon activation, platelet degranulate and release a lot of microparticles and mediators and interact with other immune and non-immune cells thereby amplifying inflammation. The most important parameters of platelet activation are P-selectin and CD40 ligand expressed on their surface upon activation, and their soluble forms presented in blood. Today, we have potent anti-platelet drugs that can inhibit platelet activation and degranulation, and thereby reduce inflammation. The most important drugs are P2Y12 receptor antagonists such as ticagrelor and clopidogrel and glycoprotein IIbIIIa inhibitors. Ticagrelor is an active drug and besides antiplatelet activity, it has bactericidal activity against Gram-positive strains and Clostridium difficile. Clopidogrel is a prodrug with less anti-inflammatory effect than ticagrelor and no proven bactericidal activity. Glycoprotein IIbIIIa inhibitors are very potent in reducing platelet aggregation but have lower anti-inflammatory potential than ticagrelor and clopidogrel.
Part of the book: Ulcerative Colitis
The number of people suffering from diabetes mellitus, especially Type 2 diabetes mellitus, is increasing every year. Approximately one-third of the patients with diabetes mellitus will develop diabetic nephropathy and chronic kidney disease. Diabetic nephropathy represents the main cause of end-stage renal disease. Vitamin D deficiency is often present in patients with diabetes mellitus and could present a risk factor for a higher incidence of cardiovascular events. Vitamin D supplementation could have a renoprotective effect and the potential to delay occurrence and slow down the progression of diabetic nephropathy. The renoprotective effect is reflected in better glycoregulation, reduction of proteinuria and proinflammatory cytokines, and improved lipid regulation. New research shed the light on the important role of vitamin D in reducing renal fibrosis and stabilization of podocyte function. If we take into consideration the cost of end-stage renal disease treatment and the quality of life of patients on dialysis, any delay in end-stage renal disease is significant.
Part of the book: Vitamin D Deficiency