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2006, Number 2

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Rev Med Hosp Gen Mex 2006; 69 (2)

Pathogen inactivation of blood products

Rojo J, Picker SM, García GJJ, Gathof BS

Language: Spanish
References: 41
Page: 99-107
PDF size: 217.79 Kb.


ABSTRACT

Improvements of blood donor selection, blood processing, histocompatibility, immunohematology, serologic screening for infectious markers, and more recently, the introduction of nucleic acid testing (NAT-tests) for different virus genoms increased the safety of blood transfusion. To date, the transfusion-associated risk of HIV, HBV or HCV (human immunodeficiency virus, hepatitis B or hepatitis C- virus) infection has become negligible in Western communities. However, blood transfusion is not without risk. Transfusion-transmitted infections based on emerging viruses, parasites or mainly bacterial contamination still exist and can lead to severe morbidity and death of the recipient. Techniques with the potential to directly target the possible pathogen, are expected to diminish this residual risk of blood transfusion. Only recently, procedures for pathogen inactivation (PI) of cellular blood components targeting a broad variety of enveloped and non-enveloped viruses, bacteria, parasites as well as leucocytes by targeting nucleic acids have been developed. The mechanism is based on activation of a so-called photosensitizer with defined light sources. The most intensively studied dyes with photodynamic properties are phenothiazines, porphyrins, cyanins, and riboflavin (vitamin B2). Psoralens like S-59 (amotosalen-HCl) have photochemical properties. Other compounds interfere with nucleic acids without an external energy sources (ethylene imine PEN 110) or upon pH-shift (S-303). Because of the possibility to use visible or UV light for treatment, studies on PI of platelet concentrates and plasma are more advanced than with red blood cell concentrates strongly absorbing light of this energy. Other drawbacks of PI procedures for red blood cell concentrates are cellular damage increasing during prolonged storage in case of porphyrins (partly prevented by the addition of oxygen scavengers) and cyanins, the necessity of an integrated, time consuming washing step in addition to unresolved toxicologic questions in case of PEN 110, and antibody formation in case of S-303. PI techniques may become available for blood services and clinicians in the near future. Before implementation, open questions on safety profile of rest substances, cost effectiveness, and the real extent to which PI procedures affect cell function should be answered.


REFERENCES

  1. Brown P. B lymphocytes and neuroinvasion. Nature 1997; 390: 662-663.

  2. Seyfried E, Roth WK. Optimal blood donation screening. Br J Haematol 2000; 109: 694-698.

  3. Allain JP. Will genome detection replace serology in blood screening for microbial agents? Baill Clin Haematol 2000; 13: 615-629.

  4. Bush MP, Kleinman SH. Nucleic acid amplificaction testing of blood donors for transfusion-transmitted infectious diseases. Transfusion 2000; 40: 143-159.

  5. Dodd RY. The safety of the blood supply: Current concepts. In: Blood supply monography. Hiller CD (ed). Atlanta, Georgia: Fenwal-Baxter, 1999; 1-17.

  6. Stramer SL. Pathogeninaktivierung. Pathogenreduktion. Curr Op Hematol 2000; 7: 387-391.

  7. Pillonel J, Saura C, Couroucé AM. Dépistage des marqueurs d’une infection par le VIH et les virus des hépatites B et C chez les donneurs de sang en France et risque résiduel de transmissión de ces virus par transfusión sanguine. Eurosurveillance 1998; 3: 76-79.

  8. Williams AE et al, Estimates of infectious disease risk factors in U.S in blood donors. JAMA 1997; 277: 967-972.

  9. Chamberland ME, Alter HJ, Busch MP. Emerging infectious disease issues in blood safety. Emerg Infect Dis 2001; 7: 552-553.

  10. Perez P, Salmi LR, Follea G. Determinants of transfusionassociated bacterial contamination: Results of the French BACTHEM case-control-study. Transfusion 2001; 41: 862-872.

  11. Hernández BA, García RP, Cruz EA, Rojo J. Seroprevalencia de brucelosis en disponentes de sangre del Hospital General de México. Rev Med Hosp Gen Mex 1999; 62 (2): 107-112.

  12. Blajchman MA. Incidence and significance of the bacterial contamination of blood components. Dev Biol Basel Karger 2002; 108; 59-67.

  13. Jacobs MR, Palavecino E, Yomtovian R. Don’t bug me: The problem of bacterial contamination of blood components – challenges and solutions. Transfusion 2001; 41: 1331-1334.

  14. Love EM, Jones H, Williamson LM et al. On behalf of the SHOT steering group. Serious hazards of transfusion annual report 1999-2000 (March, 2001).

  15. Ballou GA, Boyer PD, Luck JM. Chemical, clinical, and immunological studies on the production of human plasma fractionation. J Clin Invest 1994; 23: 454-457.

  16. Council of Europe expert committee in blood transfusion study group on pathogen inactivation of labile blood components. Pathogen inactivation of labile blood products. Transf Med 2001; 11: 149-175

  17. Lin L, Alfonso R, Behrman B, Corten L, Damonte PB, DiKeman R, Dupuis M et al. Photochemical treatment of platelet concentrates with a novel Psoralen an UVA to enhance the safety of platelet transfusion. Inf Ther Trans Med 1998; 25: 39-48.

  18. Cook D, Stassinopoulos A, Merritt J, Lin C, Reames A, Liu W, Schott M et al. Inactivation of pathogens in packed red blood cell (PRBC) concentrates using S-303. (Presented at the 39th Annual Meeting of the American Society of Hematology). Blood 1997; 90: 10 (S1): 409a.

  19. Iudicone P, Andreoni M, Lavorino C. Photodynamic treatment of fresh frozen plasma by methylene blue: effect on HIV, HCV and parvovirus B19. Infus Ther Transfus Med 1999; 26: 262-266.

  20. Wagner SJ, Skripchenko A, Robinette D. Preservation of red cell properties after virucidal phototreatment with dimethylene blue. Transfusion 1998; 38: 729-737.

  21. Stevenick van J, Trannoy LL, Besselink GA. Selective protection of red blood cells against photodynamic damage by band 3 ligand dipyridamole. Transfusion 2000; 40: 1330-1336.

  22. Mohr H, Knuever-Hopf J, Lambrecht B. Platelet functions are maintained after pathogen inactivation by photodynamic treatment with UV-B irradiation. Infus Ther Transfus Med 2001; 28: 66.

  23. Chapman J. Progress in improving the pathogen safety of red cell concentrates. Vox Sang 2000; 78: 203-204.

  24. Lazo A, Tassello J, Aytay S. Inactivation of non-enveloped viruses in red cell concentrates using the INACTINETM compound PEN110. Blood 2001; 98: 540.

  25. Lazo A, Tassello J, Jayarama V, Ohagen A, Gibaja V, Kramer E. Broad spectrum virus reduction in red cell concentrates using INACTINE PEN110 chemistry. Vox Sang 2002; 83: 313-323.

  26. AuBuchon JP, Pickard CA, Herschel LH. Production of pathogen-inactivated RBC concentrates using PEN110 chemistry: a phase I clinical study. Transfusion 2002; 42: 146-152.

  27. Purma A, Valeri CR, Dzik W. Process for the preparation of pathogen-inactivated RBC concentrates by using PEN110 chemistry: Preclinical study. Transfusion 2002; 42: 139-145.

  28. Snyder, Mintz P, Burks S. Pathogen inactivated red blood cell using INACTINETM technology demonstrate 24-hour post transfusion recovery equal to untreated red cells after 42 days of storage. Blood 2001; 98: 709.

  29. Janssens M. The use of riboflavin for pathogen inactivation in platelets, plasma and red blood cells. Infus Ther Transfus Med 2001; 28: 1-70.

  30. Corbin F. Pathogen inactivation of blood components: Current status and introduction of an approach using riboflavin as a photosensitizer. Int J Hematol 2002; 76: 253-257.

  31. Piper JT, Hansen ET, Woolum MD. Evaluation of genotoxicity and acute toxicity risks associated with a riboflavin based pathogen inactivation process. Blood 2001; 98: 108b.

  32. Goodrich RP, Woolum A, Hansen E. Recovery and survival of radiolabelled platelets following treatment with a riboflavin based pathogen inactivation procedure. Blood 2001; 98: 541.

  33. Ali L, Naseem I. Hemolysis of human red blood cells by combination of riboflavin and aminophylline. Life Sci 2002; 15: 2013-2022.

  34. Cook D, Stassinopoulos A, Merrit J. Inactivation of pathogens in packed red blood cell (PRBC) concentrates using S-303. Blood 1997; 90: 409a.

  35. Ciaravino V. Preclinical safety of a nucleic acid-targeted Helinx compound. A clinical perspective. Semin Hematol 2001; 38: 12-19.

  36. Greenwalt TJ, Hambleton J, Wages D. Viability of red blood cells treated with a novel pathogen inactivation system. Transfusion 1999; 39: 109S.

  37. Wages D, Hambleton J, Viele M. RBCs trated with HelinxTM pathogen inactivation show comparable recovery and survival to standard RBCs in a randomized crossover trial. Blood 2001; 98: 449a.

  38. Rhenen van DJ, Vermeij J, Mayaudon V, Hind C, Lin L, Corash L. Functional characteristics of S-59 photochemically treated platelet concentrates derived from buffycoats. Vox Sang 2000; 79: 206-214.

  39. Janetzko K, Klinger M, Mayaudon V, Lin L, Eichler H, Klüter H. Storage characteristics of split double-dose platelet concentrates derived from apheresis and treated with amotosalen-HCl and UVA light for pathogen inactivation. Infus Ther Transfus Med 2002; 29: 193-198.

  40. Slichter S. Intercept platelets provide effective hemostasis increments: Comparison to conventional platelets in two phase clinical trials. Poster presented at the 7th Annual Congress of the European Hematology Association, Florence, Italy, June 2003.

  41. Picker SM, Speer R, Gathof BS. Functional characteristic of platelets photochemically-treated with amotosalen-HCl for inactivation. Transfusion 2003; 44 (3): 320-329.




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