Patient prognosis is optimal when a prompt diagnosis is made and treatment is started as soon as possible. Neurological or cardiac involvement at presentation, need for intubation and older age are poor prognostic signs.[1]Scully M, Cataland S, Coppo P, et al. Consensus on the standardization of terminology in thrombotic thrombocytopenic purpura and related thrombotic microangiopathies. J Thromb Haemost. 2017 Feb;15(2):312-22.
https://www.doi.org/10.1111/jth.13571
http://www.ncbi.nlm.nih.gov/pubmed/27868334?tool=bestpractice.com
Race also impacts prognosis, non-white people have an increased risk of exacerbation or relapse, but lower mortality.[1]Scully M, Cataland S, Coppo P, et al. Consensus on the standardization of terminology in thrombotic thrombocytopenic purpura and related thrombotic microangiopathies. J Thromb Haemost. 2017 Feb;15(2):312-22.
https://www.doi.org/10.1111/jth.13571
http://www.ncbi.nlm.nih.gov/pubmed/27868334?tool=bestpractice.com
With the use of plasma exchange, mortality has fallen from >90% to between 10% and 30%. Approximately 90% of patients will respond to plasma exchange within 3 weeks, with most responding within 10 days. Although who will respond cannot be predicted, it appears that those without a severe von Willebrand factor cleaving enzyme (ADAMTS-13) deficiency and without evidence of inhibitors to ADAMTS-13 are more likely to have transient or incomplete responses to therapy.[76]Mori Y, Wada H, Gabazza EC, et al. Predicting response to plasma exchange in patients with thrombotic thrombocytopenic purpura with measurement of vWF-cleaving protease activity. Transfusion. 2002;42:572-580.
http://www.ncbi.nlm.nih.gov/pubmed/12084165?tool=bestpractice.com
Other laboratory tests (e.g., platelet count) are not in themselves predictive, however refractory disease is associated with a worse prognosis.[1]Scully M, Cataland S, Coppo P, et al. Consensus on the standardization of terminology in thrombotic thrombocytopenic purpura and related thrombotic microangiopathies. J Thromb Haemost. 2017 Feb;15(2):312-22.
https://www.doi.org/10.1111/jth.13571
http://www.ncbi.nlm.nih.gov/pubmed/27868334?tool=bestpractice.com
Those with a severe ADAMTS-13 deficiency are more likely to have a relapsing course.[1]Scully M, Cataland S, Coppo P, et al. Consensus on the standardization of terminology in thrombotic thrombocytopenic purpura and related thrombotic microangiopathies. J Thromb Haemost. 2017 Feb;15(2):312-22.
https://www.doi.org/10.1111/jth.13571
http://www.ncbi.nlm.nih.gov/pubmed/27868334?tool=bestpractice.com
[77]Zheng XL, Kaufman RM, Goodnough LT, et al. Effect of plasma exchange on plasma ADAMTS13 metalloprotease activity, inhibitor level, and clinical outcome in patients with idiopathic and nonidiopathic thrombotic thrombocytopenic purpura. Blood. 2004;103:4043-4049.
http://bloodjournal.hematologylibrary.org/content/103/11/4043.full
http://www.ncbi.nlm.nih.gov/pubmed/14982878?tool=bestpractice.com
[78]Coppo P, Wolf M, Veyradier A, et al. Prognostic value of inhibitory anti-ADAMTS13 antibodies in adult-acquired thrombotic thrombocytopenic purpura. Br J Haematol. 2006;132:66.
http://www.ncbi.nlm.nih.gov/pubmed/16371021?tool=bestpractice.com