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Medication-Induced Erythrocytosis: Common Culprits and Possible Consequences
Secondary erythrocytosis, although more common than primary erythrocytosis, has uncertain consequences and management (especially when the condition arises from prescription drug use). In this systematic review of 45 studies, mostly retrospective, Liu et al. evaluated diagnosis, management, and clinical outcomes of drug-induced erythrocytosis. The analysis focused on testosterone (35 studies) and sodium–glucose cotransporter-2 (SGLT-2) inhibitors (5 studies).
For testosterone, the most common indication was hypogonadism, with reported erythrocytosis rates varying from 0% to 66.7% (highest with intramuscular formulations). Thrombotic complications were rare, and management strategies were heterogenous, and included dose reduction, drug discontinuation, phlebotomy, and anticoagulation. For SGLT-2 inhibitors, rates of erythrocytosis were 2.1% to 22.0%; hemoglobin levels plateaued in some patients, while in others, hemoglobin normalized during drug use or after discontinuation. In the two studies that described thromboembolic events, rates of thrombosis ranged from 6.1% to 10.0%.
Comment
Although the pathophysiology of secondary (including drug-induced) erythrocytosis is quite different from that of polycythemia vera, clinicians are often tempted to treat both conditions in the same way. While testosterone and SGLT-2 inhibitors cause erythrocytosis, it's less clear that these drugs are associated with thrombosis. In this systematic review, the retrospective nature of most included studies makes it difficult to address confounding baseline risk factors for thrombosis. I agree with the authors that clinicians should engage in multidisciplinary collaboration to help patients weigh the risks and benefits before stopping culpable medications.
Citation(s)
Author:
Liu J et al.
Title:
Diagnosis, management, and outcomes of drug-induced erythrocytosis: A systematic review.
Source:
Blood Adv
2025
May
13; [e-pub].
(Abstract/FREE Full Text)
Empfohlen von
Brady L. Stein, MD, MHS