Immune thrombocytopenic purpura in Adult
The pathogenesis of ITP is not completely understood but is generally attributed to the autoimmune production of antibodies against platelet surface antigens, in particular to glycoprotein (GP) IIb/IIIa. Antibody-coated platelets have reduced lifespans due to increased clearance by the reticuloendothelial system.
The trigger for ITP is not well established and seems to have both genetic and environmental contributions. Although usually idiopathic, ITP can be triggered by viral infections (eg, HIV, cytomegalovirus [CMV], hepatitis C virus [HCV], varicella zoster virus [VZV]), systemic autoimmune diseases (eg, systemic lupus erythematosus), and lymphoproliferative disorders. It is important to exclude other causes of thrombocytopenia that have similar clinical presentations as ITP but significantly different management strategies. Secondary thrombocytopenia may be drug-induced, alcohol-related, or caused by chronic liver disease with associated hypersplenism.
ITP may be classified as acute or chronic, based on the duration of disease. The acute form lasts less than 6 months and is generally more common in children, in whom it tends to be a self-limiting disease. The chronic form lasts longer than 6 months, is more commonly seen in adults, and often requires medical treatment. ITP has been estimated to have a prevalence of 8 in 100 000 in children and 12 in 100 000 in adults, due to the often chronic nature of the disease in adults. While ITP has been reported to have a higher incidence in young women, the incidence is the same between men and women later in life. ITP can also be seen in pregnancy with an incidence of 1-3 in 10 000 (a much higher rate than in the general population). ITP in children is clinically distinct from ITP in adults.
D69.3 – Immune thrombocytopenic purpura
2897005 – Immune thrombocytopenia
Differential Diagnosis & Pitfalls
Drug Reaction Data