Table 1. Recent advances in understanding and management of thrombocytopenia.

Disease entity	Recent updates
ITP	1.   Absence of platelet-bound antibodies may predict non-response to rituximab.        2.   Patients with lower platelet counts and increased platelet reactivity have lower risk of bleeding.        3.   Multiple cycles of pulsed dexamethasone may result in higher long-term remission rates.        4.   Rituximab combined with high-dose dexamethasone in the first-line setting could result in higher response rates.        5.   Patients who are refractory to one of the TPO-RAs may respond to the other.        6.   Combining TPO-RA might be an option in refractory ITP.        7.   Recombinant thrombopoietin was safe and efficacious in pregnant patients.
HIT	1.   Prerequisites for an immunogenic HIT antigen have been better understood.        2.   The atomic structure of the PF4-heparin complex has been defined.        3.   PF4 released from platelets during a bacterial infection can bind to the bacterial cell wall, resulting in a priming step for HIT.        4.   PF4-heparin complexes can activate, complement, and bind to the complement receptor 2 (CD21) on B cells to enhance antibody production.        5.   Spontaneous HIT developments in the absence of heparin exposure can occur after orthopedic procedures.        6.   Dynamic mechanical thromboprophylaxis may increase the incidence of HIT antibody formation.        7.   Low-molecular-weight heparin use instead of heparin results in significant cost savings due to the reduced incidence of HIT.        8.   Fondaparinux is safe and effective in the treatment of acute HIT.        9.   Accumulating evidence suggests safety and efficacy of direct oral anticoagulants in HIT.        10.   Refractory HIT with prolonged thrombocytopenia may benefit from intravenous immunoglobulin.
TTP	1.   Hyperbilirubinemia and plasma-free hemoglobin can falsely decrease ADAMTS13 activity in fluorescence resonance energy transfer (FRET) assay.        2.   Persistent ADAMTS13 activity of less than 10% within seven days of daily PLEX could be associated with worse outcomes.        3.   Upfront use of rituximab reduces exacerbation, refractoriness, number of PLEX sessions, and possibly hospital stay.        4.   Bortezomib is very promising in rituximab-refractory/relapsed TTP.        5.   Caplacizumab reverses pathophysiology instantly with a potential to reduce early mortality.        6.   ADAMTS13 activity of less than 10% alone is not sufficient for TTP relapse and requires another trigger.        7.   Cardiac and mesenteric ischemia is common.        8.   Delayed neurocognitive defects occur in some patients.
aHUS	1.   Only about 60% of the patients have an identifiable genetic mutation.        2.   A modified Ham test can distinguish aHUS from TTP.        3.   The duration of eculizumab therapy is not clearly defined at the present time.

ADAMTS13, a disintegrin and metalloproteinase with thrombospondin type 1 motif, member 13; aHUS, atypical hemolytic uremic syndrome; HIT, heparin induced thrombocytopenia; ITP, immune thrombocytopenia; PF4, platelet factor 4; PLEX, plasma exchange; TPO-RA, thrombopoietin receptor agonist; TTP, thrombotic thrombocytopenic purpura.