What is the most likely mechanism of thrombocytopenia (low platelet count) in an 18-year-old woman with a history of recent upper respiratory infection (uri) and presentation of purpura (rash) and ear bruising?

From the Guidelines

The most likely mechanism of thrombocytopenia in this patient is the production of platelet autoantibodies, leading to immune thrombocytopenic purpura (ITP). This patient is presenting with symptoms consistent with ITP, including:

• Sudden onset of purpura (rash) and ear bruising
• Recent upper respiratory infection (URI), which can trigger ITP
• Low platelet count, which is a hallmark of ITP In ITP, the immune system mistakenly produces antibodies against platelets, leading to their destruction and removal from circulation, resulting in a significantly decreased platelet count and causing easy bruising and petechiae 1. The recent URI likely triggered this autoimmune response, as ITP often occurs 1-3 weeks after a viral infection, which fits the timeline in this case. Treatment typically involves corticosteroids (e.g., prednisone) as first-line therapy to suppress the immune response, and in severe cases or if steroids are ineffective, other treatments like intravenous immunoglobulin (IVIG) or rituximab may be considered 1. Some key points to consider in the management of ITP include:
• The decision to treat is highly complex and varies based on comorbidities, medications, and age, which all impact the risk of bleeding 1
• The choice of therapy varies greatly among practitioners, and few randomized studies have compared the outcomes of different approaches 1
• The patient should be monitored closely, avoid activities with high risk of injury, and seek immediate medical attention for any signs of severe bleeding 1
• ITP has a significant impact on health-related quality of life (HRQoL), particularly in the first year after diagnosis, related to restrictions on activities, anxiety due to the risk of bleeding, and the burden of treatment and monitoring 1

From the Research

Mechanism of Thrombocytopenia

The most likely mechanism of thrombocytopenia in an 18-year-old woman with a history of recent upper respiratory infection (URI) and presentation of purpura (rash) and ear bruising is:

• Immune-mediated platelet destruction, where autoantibodies against platelet glycoproteins (such as GPIIb-IIIa and GPIb-IX) lead to accelerated platelet destruction by the reticuloendothelial cells in the spleen and liver 2, 3, 4, 5, 6
• Suppressed platelet production, where autoantibodies bind to megakaryocytes, resulting in decreased thrombopoiesis 3, 5, 6

Evidence for Platelet Destruction

Evidence for platelet destruction in immune thrombocytopenic purpura (ITP) includes:

• Infusion of ITP blood or plasma into normal recipients may result in thrombocytopenia 3
• Decreased intravascular survival of radiolabeled platelets in most ITP patients 3
• Morphologic and in vitro evidence of platelet phagocytosis can be demonstrated 3
• Cytotoxic T cells can induce lysis of autologous platelets 3, 6

Evidence for Suppressed Platelet Production

Evidence for suppressed platelet production in ITP includes:

• Morphologic studies show megakaryocyte damage in most ITP patients 3, 5
• Normal or decreased platelet turnover in the majority of patients 3, 5
• In vitro studies show antibody-induced inhibition of megakaryocyte production and maturation 3, 5
• An increase in the platelet count occurs in many ITP patients receiving treatment with thrombopoietin mimetics 3, 5