Contrary to initial concerns, long-term safety data for thrombopoietin receptor agonists has allayed fears of malignant transformation and irreversible bone marrow fibrosis. The increased reticulin fibrosis observed is reversible upon drug discontinuation, offering significant reassurance for long-term prescribing.

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The target platelet count for ITP patients should be tailored to their lifestyle, bleeding history, and quality of life goals. A normal platelet count is not necessary, and different thresholds are appropriate for different patients (e.g., someone planning a ski trip versus a sedentary individual).

Clinicians can reassure myelofibrosis patients that the drop in hemoglobin often seen when starting ruxolitinib does not carry the same negative prognostic weight as anemia caused by the disease itself. This distinction is crucial for managing patient expectations and continuing effective therapy despite initial side effects.

ITP caused by immune checkpoint inhibitors (ICIs) is rare (0.25% incidence) but generally has a good prognosis. Most patients respond to standard first-line ITP therapies, and approximately 70% of those re-challenged with the ICI can continue treatment without a recurrence of ITP.

Beyond raising platelet counts, the newly approved BTK inhibitor rilzabrutinib provides dramatic improvements in the fatigue associated with ITP. This unique benefit, likely due to its anti-inflammatory properties, makes it a strong consideration for patients where fatigue is a primary quality of life issue.

The treatment paradigm for ITP is shifting towards early combination therapy. Recent clinical trials are investigating augmented first- and second-line regimens, such as combining dexamethasone with rituximab or romiplostim, to achieve more durable, treatment-free responses than monotherapy.

To combat the significant myelosuppression from the standard 28-day venetoclax cycle in AML, many clinicians are adopting a strategy of performing a bone marrow biopsy around day 21 and pausing the drug if blast clearance is achieved to allow for hematologic recovery.

While these drugs can cause neutropenia, it rarely leads to infections. Patients often feel clinically well despite low neutrophil counts. This 'paper problem' can usually be managed with G-CSF without needing to dose-reduce the primary CLL therapy.

Patients with ITP who fail or are intolerant to one TPO receptor agonist (e.g., eltrombopag) should not be considered a class failure. Switching to another TPO agent is a viable strategy that can induce a response in nearly half of these cases, particularly for intolerance.

Historical data showing high cure rates for splenectomy in ITP is outdated. Recent data indicates that if a patient has already failed both a TPORA and rituximab, the chance of a successful splenectomy is less than 50%, repositioning it as a later-line salvage option.

In cases of severe ITP unresponsive to standard therapies, the anti-CD38 monoclonal antibody daratumumab can be highly effective. It works by eliminating the long-lived plasma cells responsible for secreting platelet autoantibodies, a mechanism distinct from other ITP treatments.

Long-Term TPO Agonist Use in ITP Does Not Cause Leukemic Transformation or Irreversible Bone Marrow Fibrosis | RiffOn