PNH Cells in Aplastic Anemia (AA) and/or Myelodysplastic Syndromes (MDS) Occur Frequently, with Important Prognostic and Therapeutic Implications1-4

PNH cells (granulocytes) are common in bone marrow disorders1-4

  • Approximately 70% of patients with AA have PNH cells5*
  • As many as 55% of patients with MDS have PNH cells5*
  • PNH is characterized by the continuous destruction of PNH red blood cells; AA and MDS are characterized by the diminished production of RBCs, WBCs, and platelets1,6

Evaluate your AA patients for PNH at diagnosis and annually, as clones may expand rapidly and unpredictably over time.3

Conduct high-sensitivity flow cytometry on peripheral blood in addition to bone marrow aspirate to confirm the presence of PNH cells or clones during evaluation for AA, MDS, or unexplained cytopenias.3

*0.01% PNH cell threshold.




IMPORTANT SAFETY INFORMATION

WARNING: SERIOUS MENINGOCOCCAL INFECTIONS

Soliris increases the risk of meningococcal infections. Meningococcal infection may become rapidly life-threatening or fatal if not recognized and treated early

  • Vaccinate patients with a meningococcal vaccine at least 2 weeks prior to receiving the first dose of Soliris; revaccinate according to current medical guidelines for vaccine use
  • Monitor patients for early signs of meningococcal infections, evaluate immediately if infection is suspected, and treat with antibiotics if necessary

The effect of withdrawal of anticoagulant therapy during Soliris treatment has not been established. Therefore, treatment with Soliris should not alter anticoagulant management.

The most frequent adverse events observed in clinical studies were headache, nasopharyngitis, back pain, nausea, and fatigue.

SEE FULL PRESCRIBING INFORMATION FOR COMPLETE BOXED WARNING INCLUDING WARNINGS, PRECAUTIONS, AND ADVERSE REACTIONS.

References: 1. Dunn DE, Tanawattanacharoen P, Boccuni P, et al. Paroxysmal nocturnal hemoglobinuria cells in patients with bone marrow failure syndromes. Ann Intern Med. 1999;131:401-408. 2. Myelodysplastic syndromes. NCCN Clinical Practice Guidelines in Oncology. Version 1; 2009. National Comprehensive Cancer Network. 3. Parker C, Omine M, Richards S, et al; for International PNH Interest Group. Diagnosis and management of paroxysmal nocturnal hemoglobinuria. Blood. 2005;106:3699-3709. 4. Maciejewski JP, Selleri C. Evolution of clonal cytogenetic abnormalities in aplastic anemia. Leuk Lymphoma. 2004;45:433-440. 5. Galili N, Ravandi F, Palermo G, et al. Prevalence of paroxysmal nocturnal hemoglobinuria (PNH) cells in patients with myelodysplastic syndromes (MDS), aplastic anemia (AA) or other bone marrow failure syndromes (BMF): interim results from the EXPLORE trial [ASCO abstract]. J Clin Oncol. 2009;27(suppl): Abstract 7082. 6. Ishikawa T, Tohyama K, Nakao S, et al. A prospective study of cyclosporine A treatment of patients with low-risk myelodysplastic syndrome: presence of CD55–CD59– blood cells predicts platelet response. Int J Hematol. 2007;86:150-157. 7. Hillmen P, Muus P, Dührsen U, et al. Effect of the complement inhibitor eculizumab on thromboembolism in patients with paroxysmal nocturnal hemoglobinuria. Blood. 2007;110:4123-4128. 8. Rother RP, Rollins SA, Mojcik CF, Brodsky RA, Bell L. Discovery and development of the complement inhibitor eculizumab for the treatment of paroxysmal nocturnal hemoglobinuria. Nat Biotechnol. 2007;25:1256-1264. 9. Richards SJ, Barnett D. The role of flow cytometry in the diagnosis of paroxysmal nocturnal hemoglobinuria in the clinical laboratory. Clin Lab Med. 2007;27:577-590.

This site is intended for US audiences only. © Copyright and Terms of Use 1999 - 2010 Alexion Pharmaceuticals. All rights reserved. Site Map | Privacy Policy | Legal | Glossary
SOLUS03-0157-001