Thursday, January 1, 2026

Thrombotic thrombocytopenic purpura (TTP)

Vignette says a 35 year old female presents with a 3 day history of fatigue, headaches and confusion; She also reports small purple spots on her legs; On examination, she has pallor, petechiae on her legs, and mild jaundice; Vital signs show blood pressure of 130/80 mm of Hg, pulse rate of 98 bpm, respiratory rate of 18 breaths/min, oxygen saturation of 92% in RA and temperature of 99.9 F; Examination shows pale bulbar conjunctiva and palms; Laboratory studies show hemoglobin of 8.0 mg/dL, platelet count of 30K, LDH of 600 U/L (normal range is 135-225 U/L), serum creatinine levels of 1.8 (normal range is 0.7-1.3 mg/dL), indirect bilirubin of 1.8 mg/dL (normal range is 0.2 to 0.8 mg/dL) and low haptoglobin levels; PBS shows schistocytes; Coombs test is negative; ADAMTS13 assay activity is decreased (i.e. <10% of ADAMTS13 activity; Diagnosis?

Diagnosis is Thrombotic thrombocytopenic purpura (TTP)

Thrombotic thrombocytopenic purpura (TTP) is a microangiopathic hemolytic anemia
(MAHA) characterized by the pentad of fever, hemolytic anemia, thrombocytopenia, and
renal and neurologic dysfunction.

Pathophysiology:- Inhibition or deficiency of ADAMTS13 activity (a protease that cleaves von Willebrand factor); It leads to decreased degradation of large vWF multimers; persistence of large vWF multimers on the endothelial surface causes platelet adhesion, aggregation and subsequent thrombus formation.

Clinical features:-
1. MAHA
2. Thrombocytopenia
3. Acute renal failure
4. Altered mental status
5. Fever

Diagnosis:-
1. CBC shows decreased platelet count, decreased hemoglobin, increased reticulocyte count.
2. Coagulation profile shows normal PT and aPTT.
3. PBS analysis shows schistocytes (>2–3/hpf).
4. Increased LDH, increased indirect bilirubin, decreased haptoglobin, Coombs negative
hemolytic anemia.
5. Deranged RFT.
6. ADAMTS13 assay detects auto antibody against ADAMTS13.
7. ADAMTS13 assay activity is decreased (i.e. <10% of ADAMTS13 activity).

Treatment:-
1. Plasmapheresis and high dose steroids are the mainstay of therapy.
2. Rituximab (i.e. Anti-CD20 monoclonal antibody).
3. No platelet transfusions (may cause thrombus formation).
4. Splenectomy if refractory to plasmapheresis & steroids.