From the Guidelines
Thrombocytopenia in young adults is most commonly caused by immune thrombocytopenia (ITP), drug-induced thrombocytopenia, viral infections, bone marrow disorders, and systemic diseases, as evidenced by the American Society of Hematology 2019 guidelines for immune thrombocytopenia 1.
Causes of Thrombocytopenia
The causes of thrombocytopenia in young adults can be diverse, including:
- Immune thrombocytopenia (ITP), where the immune system mistakenly attacks platelets
- Drug-induced thrombocytopenia from medications like heparin, quinine, sulfonamides, and certain antibiotics
- Viral infections such as HIV, hepatitis C, and Epstein-Barr virus
- Bone marrow disorders including leukemia and aplastic anemia
- Systemic diseases like lupus and antiphospholipid syndrome
- Other potential causes are alcohol abuse, vitamin deficiencies, hereditary conditions, pregnancy-related conditions, and hypersplenism
Diagnosis and Treatment
Diagnosis typically involves a complete blood count, peripheral blood smear, and potentially bone marrow examination. Treatment depends on identifying and addressing the underlying cause, ranging from discontinuing offending medications to immunosuppressive therapy for autoimmune causes, or platelet transfusions for severe cases with bleeding, as recommended by the American Society of Hematology 2011 evidence-based practice guideline for immune thrombocytopenia 1.
Importance of Prompt Evaluation
Prompt evaluation is essential as thrombocytopenia can lead to serious bleeding complications if left untreated, highlighting the need for timely and accurate diagnosis and management, as emphasized in the international consensus report on the investigation and management of primary immune thrombocytopenia 1.
From the FDA Drug Label
The FDA drug label does not answer the question.
From the Research
Causes of Thrombocytopenia in Young Adults
- Immune thrombocytopenia (ITP) is a rare hematological disorder characterized by an autoimmune-mediated reduction of platelets in peripheral blood 2.
- The pathophysiology of ITP involves antiplatelet autoantibodies and antigen-specific T cells that destroy platelets peripherally in the spleen or impair platelet production in the bone marrow 3.
- ITP is predominately a T cell disorder, which leads to a breakdown in self-tolerance mechanisms and allows for the generation of anti-platelet autoantibodies and T cells 3.
- The destruction of platelets in ITP is mediated by multiple mechanisms, including:
- Platelet phagocytosis by splenic macrophages through interactions with Fc gamma receptors (FcγRs) and complement receptors 4.
- Activation of the classical complement pathway, which participates in platelet opsonization and destruction by complement-dependent cytotoxicity 4.
- A FcγR-independent pathway, involving platelet desialylation that favors their binding to the Ashwell-Morell receptor and their clearance in the liver 4.
- Cytotoxic T cells, which contribute to ITP pathogenesis by mediating cytotoxicity against megakaryocytes and peripheral platelets 4.
- In adolescents and young adults, ITP does not neatly fit into either the pediatric or adult ITP group, and a deeper understanding of its natural history, risk factors for chronicity, and outcomes is needed to develop tailored treatment algorithms 5.