Feature	Immune Thrombocytopenia (ITP)	Thrombotic Thrombocytopenic Purpura (TTP)
Pathophysiology	Autoantibody-mediated destruction of platelets	Deficiency of ADAMTS13 enzyme leading to excessive platelet aggregation
Platelet Count	Usually moderately low (20,000-70,000/μL)	Severely low (<20,000/μL)
Coagulation Tests	Normal PT, PTT	Normal PT, PTT
Organ Involvement	Limited systemic involvement	Widespread (brain, kidneys, heart)
Neurological Symptoms	Rare	Common (confusion, headache, seizures, stroke)
Renal Involvement	Rare	Common (acute kidney injury)
Microangiopathic Hemolytic Anemia	Absent	Present (schistocytes on blood smear)
Fever	Uncommon	Common
Primary Treatment	Corticosteroids, IVIG, anti-D	Plasma exchange, rituximab
Mortality without Treatment	Low	High (>90%)
Age Distribution	Bimodal (young adults and elderly)	Adults (more common in women)
Associated Conditions	Autoimmune disorders	Pregnancy, medications, infections, cancers

Etiology

• Primary ITP: idiopathic (most common)
• Secondary ITP associated with:
  • Autoimmune disorders: SLE, Antiphospholipid syndrome
  • Malignancy: lymphoma, leukemia (particularly CLL)
  • Infection: HIV, HCV
  • Drugs: e.g., quinine, beta-lactam antibiotics, carbamazepine, heparin, vaccines, linezolid, sulfonamides, vancomycin, TMP-SMX, antiepileptics

The acute form is typically seen in children after a viral disease.

Pathophysiology

Antiplatelet antibodies (mostly IgG directed against, e.g., GpIIb/IIIa, GpIb/IX) bind to surface proteins on platelets → sequestration by spleen and liver → ↓ platelet count → bone marrow megakaryocytes and platelet production increase in response (in most cases).

Clinical features

• Mostly asymptomatic. Splenomegaly is very unusual in ITP and makes other diagnoses more likely!
  • Although platelets can undergo splenic sequestration in ITP, the primary mechanism responsible for the thrombocytopenia is immune destruction.