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"immune thrombocytopenia" ITP

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Immune Thrombocytopenia (ITP)

Definition

ITP (Immune Thrombocytopenia) is an acquired autoimmune disorder characterized by isolated thrombocytopenia (platelet count < 100 × 10⁹/L) in the absence of other identifiable causes. It was previously called idiopathic thrombocytopenic purpura or autoimmune thrombocytopenic purpura. Antiplatelet autoantibodies cause both:
  • Premature platelet destruction (via reticuloendothelial system clearance)
  • Suppression of megakaryopoiesis (reduced platelet production)
  • Washington Manual of Medical Therapeutics, p. 757

Classification

TypeDescription
Primary ITPNo identifiable trigger or associated condition
Secondary ITPDue to underlying disease (SLE, HIV, HCV, lymphoma, etc.)
Drug-Induced (DITP)Drug-dependent platelet antibodies
By duration:
  • Newly diagnosed: within 3 months of diagnosis
  • Persistent: 3-12 months from diagnosis
  • Chronic: lasting more than 12 months
  • Severe: bleeding symptoms requiring treatment or dose escalation
  • Henry's Clinical Diagnosis and Management by Laboratory Methods, p. 968

Epidemiology

  • Adult primary ITP incidence: ~3.3 cases per 100,000 persons
  • Acute (pediatric) form: most common in children aged 2-6 years; often follows a viral prodrome (within 3 weeks); platelet count usually drops below 20,000/mm³; >90% rate of spontaneous remission
  • Chronic form: primarily an adult disease, found 3 times more often in women; insidious onset without prodrome
  • Rosen's Emergency Medicine, p. 111

Pathophysiology

  • Autoantibodies (primarily IgG) bind to platelet surface glycoproteins (especially GPIIb/IIIa)
  • Antibody-coated platelets are phagocytosed by splenic macrophages
  • T cell-mediated platelet destruction also plays a role
  • Megakaryopoiesis is also suppressed, impairing platelet production

Etiology of Secondary ITP

  • Autoimmune: SLE, rheumatoid arthritis, antiphospholipid antibody syndrome (APS)
  • Infections: HIV, Hepatitis C (HCV), Hepatitis B (HBV), EBV, CMV, H. pylori, rubella, varicella
  • Malignancy: Lymphoproliferative disorders (CLL, lymphoma)
  • Drugs: quinidine/quinine, abciximab, eptifibatide, linezolid, rifampin, sulfonamides, vancomycin, phenytoin, valproic acid, cimetidine, heparin (in hospitalized patients)

Clinical Presentation

  • Mild/Moderate: petechiae, purpura, easy bruising, prolonged menses, mucosal bleeding (gingival, epistaxis)
  • Severe: major bleeding (GI, intracranial - rare but life-threatening)
  • Risk of bleeding is highest when platelet count is < 30 × 10⁹/L
  • Severe ITP is defined by platelet count < 20,000/mm³
  • Hepatosplenomegaly is typically absent (differentiates from other causes of thrombocytopenia)

Diagnosis

ITP is a diagnosis of exclusion - there are no confirmatory tests. The workup aims to rule out secondary causes:
Basic Evaluation:
  • Complete blood count + reticulocyte count
  • Peripheral blood smear (confirm platelet count, exclude clumping, assess morphology)
  • HIV, HCV testing
  • H. pylori testing
  • Direct antiglobulin test (Coombs)
  • Blood group (Rh typing)
  • Quantitative immunoglobulin levels
Note: Serologic antiplatelet antibody tests have poor sensitivity and low negative predictive value - they generally do not help diagnose ITP. Bone marrow examination is not routinely required but may be done in selected patients (atypical presentation, older age, treatment failure).

Treatment

Adults

Platelet CountIntervention
< 30,000/mm³ (asymptomatic or minor bleeding)Corticosteroids (dexamethasone 40 mg PO/IV × 4 days preferred)
< 10,000/mm³ or significant bleedingIVIG (1 g/kg single dose) + corticosteroids
Life-threatening bleeding / refractoryTPO receptor agonist (eltrombopag, romiplostim)
Refractory chronic ITPSplenectomy (last resort)

Children (Acute ITP)

  • Mostly supportive - >90% achieve spontaneous remission
  • IVIG or corticosteroids for significant bleeding
  • Observation is appropriate for mild cases

Other Considerations

  • Rituximab (anti-CD20) for refractory cases
  • Plasmapheresis and recombinant factor VIIa are no longer recommended
  • Splenectomy: removes the primary site of platelet destruction and antibody production; considered after failure of medical therapy
  • For drug-induced ITP: discontinue the offending drug
  • Rosen's Emergency Medicine, p. 111; Washington Manual of Medical Therapeutics, p. 757

Recent Evidence (2025)

Recent systematic reviews highlight evolving treatment approaches:

Key Points Summary

  1. ITP = autoimmune thrombocytopenia from anti-platelet antibodies + impaired production
  2. Diagnosis of exclusion - peripheral smear + targeted labs to exclude secondary causes
  3. Children: usually acute, self-limited, post-viral; adults: often chronic, more common in women
  4. Treatment threshold is typically platelet count < 30,000 or active bleeding
  5. Corticosteroids are first-line; IVIG for rapid response; TPO agonists/splenectomy for refractory disease
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