PNH Is a Progressive and Life-Threatening Disease That Warrants Early Diagnosis and Intervention1-3

Evaluate high-risk patient populations for PNH

The PNH Diagnostic Pathway can help you identify patients at high risk for PNH, including those with aplastic anemia, myelodysplastic syndromes, and unexplained thromboses.

*Adapted from Parker, et al, Blood, 2005.

The life-threatening and destructive consequences of hemolysis (as measured by LDH) warrant early identification in these high-risk subpopulations

Chronic hemolysis is the underlying cause of progressive morbidities and mortality in PNH 6; therefore, reducing chronic hemolysis is the primary goal of PNH treatment.4,7 Early identification of PNH in high-risk populations is optimal for long-term disease management.

Early diagnosis drives effective PNH management4

If any of these conditions are evident in your patients, they should be tested for PNH4†

  • Evaluate your patients with myelodysplastic syndromes (MDS) at diagnosis and your patients with aplastic anemia (AA) at diagnosis and annually4
    • Many patients with AA or MDS go on to develop PNH
    • The presence of even a very small number of PNH cells in patients with AA or MDS may be predictive of response to immunosuppressive therapy8,9
  • Unexplained arterial (eg, transient ischemic attack [TIA]) or venous thromboses in typical (eg, DVT) or atypical sites4,10
  • Coombs-negative hemolytic anemia4,10
  • Hemolysis in the presence of anemia, fatigue, smooth muscle dystonia (dysphagia, abdominal pain, dyspnea, erectile dysfunction), unexplained visceral pain, or hemoglobinuria4,10
  • End organ damage with hemolysis4,7
    • Renal insufficiency
    • Liver disease

Adapted from Parker, et al, Blood, 2005.

Click on the following links for more information regarding diagnosis in populations at high risk for PNH:





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. Hillmen P, Lewis SM, Bessler M, Luzzatto L, Dacie JV. Natural history of paroxysmal nocturnal hemoglobinuria. N Engl J Med. 1995;333:1253-1258. 2. Socié G, Mary J-Y, de Gramont A, et al; for French Society of Haematology. Paroxysmal nocturnal haemoglobinuria: long-term follow-up and prognostic factors. Lancet. 1996;348:573-577. 3. Nishimura J-I, Kanakura Y, Ware RE, et al. Clinical course and flow cytometric analysis of paroxysmal nocturnal hemoglobinuria in the United States and Japan. Medicine. 2004;83:193-207. 4. 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. 5. Sugimori C, Chuhjo T, Feng X, et al. Minor population of CD55–CD59– blood cells predicts response to immunosuppressive therapy and prognosis in patients with aplastic anemia. Blood. 2006;107:1308-1314. 6. Brodsky RA. Advances in the diagnosis and therapy of paroxysmal nocturnal hemoglobinuria. Blood Rev. 2008;22:65-74. 7. Rother RP, Bell L, Hillmen P, Gladwin MT. The clinical sequelae of intravascular hemolysis and extracellular plasma hemoglobin: a novel mechanism of human disease. JAMA. 2005;293:1653-1662. 8. 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. 9. 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. 10. Brodsky RA. How I treat paroxysmal nocturnal hemoglobinuria. Blood. 2009;113:6522-6527. 11. 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. 12. 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.