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.

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.

For myelofibrosis patients with profound splenomegaly but only moderate thrombocytopenia (platelets 50k-100k), fedratinib may be the best frontline option. It is arguably the most potent JAK inhibitor for spleen reduction and is approved for use in patients with platelet counts as low as 50,000.

A critical distinction exists between a clinical adverse event (AE) and its impact on a patient's quality of life (QOL). For example, a drop in platelet count is a reportable AE, but the patient may be asymptomatic and feel fine. This highlights the need to look beyond toxicity tables to understand the true patient experience.

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.

While eradicating H. pylori can improve platelet counts in ITP, its efficacy shows significant geographical variation. The strategy is successful in Europe and Japan but often fails in the United States, a difference attributed to regional variations in H. pylori strains.

Historical data showing high cure rates for splenectomy in ITP is outdated.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.