Related Experiment Video
Updated: May 23, 2025

Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Anagrelide in the management of essential thrombocythemia: a systemic review and meta-analysis
Barbara Abreu Lopez1, Joanne Arvelaez Pascucci2, Safiya Mohamed Ramzy3
1Universidad De Carabobo, Naguanagua, Venezuela.
Background:
Essential thrombocythemia (ET) is a myeloproliferative neoplasm commonly treated with hydroxyurea, while anagrelide is a second-line option. Although anagrelide has thrombocyte-specific action, its comparative efficacy remains debated. This systematic review and meta-analysis aimed to measure platelet reduction, thromboembolic events, and adverse events.
Methods:
A systematic search of PubMed, Cochrane, Web of Science, Scopus, EMBASE, and CINAHL databases up to October 6, 2024, was conducted following the PRISMA guidelines. Randomized controlled trials and cohort studies comparing anagrelide and hydroxyurea were included.
Results:
Six studies with 1555 participants met the inclusion criteria. Anagrelide was associated with significantly lower platelet counts than hydroxyurea (MD - 65.22; 95% CI - 80.78 to - 49.66; p < 0.01; I2 = 0%), but no significant difference in thrombohemorrhagic events (RR 1.34; 95% CI 1.10 to 1.62; p < 0.01; I2 = 12.5%). In single-arm analysis, JAK-positive patients showed a higher incidence of thrombotic events (0.23; 95% CI 0.14-0.35) than JAK-negative patients (0.10; 95% CI 0.08-0.13). Adverse event rates varied (RR 1.37; 95% CI 0.37-5.12; I2 = 94.9%).
Conclusion:
Although comparative analyses against hydroxyurea have demonstrated the efficacy of anagrelide for platelet reduction in ET, its higher bleeding risk requires caution, especially in patients with risk factors. Further studies are needed to confirm long-term safety and refine dosing.
Related Concept Videos
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Anticoagulant Drugs: Low-Molecular-Weight Heparins
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
Antianginal Drugs: Calcium Channel Blockers and Ranolazine
CCBs, a diverse class that includes dihydropyridines (nifedipine) and diphenylalkylamines (verapamil and diltiazem), exert their effect by blocking calcium channels in cardiac and smooth muscle cells. This...
Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
Antianginal Drugs: Nitrates and β-Blockers
Organic nitrates, such as nitroglycerin, play a pivotal role. Once metabolized, they liberate nitric oxide, a molecular marvel. Nitric oxide triggers guanylyl cyclase and augments cGMP production. This biochemical cascade orchestrates the relaxation of vascular smooth muscles, ushering in vasodilation and enhancing coronary blood flow....

