Immune Thrombocytopenic Purpura: Between Infections and Vaccinations

Immune thrombocytopenic purpura (ITP) is an autoimmune condition characterized by low platelet count and mucocutaneous bleeding. Antibody-coated platelets undergo reticuloendothelial phagocytosis, resulting in reduced platelet survival. Furthermore, CD8+ and CD4+ T cell-mediated responses are both implicated in the pathogenesis of autoimmune thrombocytopenia. The onset can be primary or secondary following infections including, among others, Helicobacter pylori, hepatitis C virus, and human immunodeficiency virus. A number of vaccines have been associated with the development of ITP, including measles, mumps, and rubella (MMR), influenza, hepatitis B, and diphtheria-tetanus-pertussis vaccines. Several immune-mediated mechanisms have been hypothesized to be involved in ITP pathogenesis, including molecular mimicry and bystander and polyclonal activation. Given that the course and outcome of ITP can be very serious, even fatal, it is fundamental to recognize its underlying causes.