Thanks to D Kwon for presenting an interesting management dilemma of a patient with ITP who also is on warfarin for a-fib stroke risk, presenting w/ scant hemoptysis. We spent a lot of time talking about ITP so I thought I’d highlight some key learning points here.
#What is it? immune thrombocytopenic purpura occurs as a result of increased platelet destruction through autoantibodies to platelet membrane antigens. There is also an effect on marrow megakaryocytes which prevents adequate new production for the increased destruction. Most of the antibodies act against the GP IIb/IIIa antigen.
#Who gets it? Classically a disease of young women, about 70% of patients diagnosed in early childhood are women, a proporition persisting until about age 40. Classical evidence of platelet-induced bleeding: gingival bleeding, epistaxis, purpura are most common. ITP in children is different in that most kids will have complete remission whereas adults end up on lifelong therapy.
#Diagnosis? No pathognomic features but isolated thrombocytopenia is a good start. ITP can present w/ platelet counts in the single digits, as opposed to HIT or TTP which usually don’t get that low. Always look for HIT and TTP first, ITP is usually diagnosed after drug-induced and other more common causes are ruled out.
#Treatment? Flares are usually treated with prednisone (1mg/kg) until the platelet count gets up to 50000 or higher. IT’s okay to transfuse when treating a flare, the “fuel for the fire” argument is dated and probably wrong in ITP. Long term, a RCT in 2007 demonstrated better durable response rates of platelets > 50K in patients on eltrombopag (TPO receptor agonist) than without. Splenectomy is rarely done now in refractory cases.