What is the main treatment for TTP/HUS?

• A. Platelet transfusion
• B. Desmopressin
• C. Antibiotics
• D. Plasma exchange

Answer: (D)

Treating TTP/HUS hinges on plasma exchange because it tackles the underlying driver of disease: a severe disruption of ADAMTS13 activity that allows ultra-large vWF multimers to cause widespread platelet microthrombi. Therapeutic plasma exchange both removes the circulating autoantibodies that inhibit ADAMTS13 and replenishes functional ADAMTS13, while also clearing the ultra-large vWF multimers. This directly reduces ongoing platelet consumption, limits microvascular occlusions, and improves organ perfusion—dramatically lowering mortality when started promptly.

Other options don’t address the root problem. Transfusing platelets can fuel the very thrombosis you’re trying to stop, so it’s avoided unless there’s life-threatening bleeding. Desmopressin helps other bleeding disorders but doesn’t fix ADAMTS13 deficiency. Antibiotics aren’t the treatment for TTP/HUS and would be directed only if a separate infection is present. For typical HUS from Shiga toxin, management is mainly supportive care; plasma exchange is not the standard therapy unless it’s an atypical form where complement dysregulation is involved. In practice, plasma exchange remains the cornerstone therapy for TTP and suspected TTP-HUS to rapidly correct the pathogenic process.