2010, Number 2
<< Back Next >>
Med Int Mex 2010; 26 (2)
Therapeutics with biological agents and risk of opportunistic infections
Martínez BMM, Sánchez RPA, Mora ATT, Rodríguez WFL
Language: Spanish
References: 42
Page: 140-147
PDF size: 344.73 Kb.
ABSTRACT
In recent years, the role of the immune system in the physiopathology of disease processes has gained greater recognition, giving way to new biotechnologies such as monoclonal antibody based biological agents. These antibodies limit immunopathological processes by targeting T and B lymphocyte receptors. The four basic mechanisms are receptor to ligand blocking, complement mediated cellular lysis, antibody mediated cellular lysis and through vehicles. Their effectiveness in a variety of diseases has been demonstrated, especially for patients resistant to conventional therapy, and represents one of the most innovative areas of clinical research. The most frequent complications are related to constitutional symptoms with intravenous administration such as fever, hypotension, arthralgias and myalgias, and a local inflammatory response with subcutaneous administration. However, because infection by opportunistic microorganisms is the most severe complication, all patients require appropriate scrutiny and prevention measures before treatment is started.
REFERENCES
Delves PJ, Roitt IM. The immune System: first of two parts. The New England Journal of Medicine 2000;343(1): 37-49.
Delves PJ, Roitt IM. The immune System: second of two parts. The New England Journal of Medicine, 2000;343(2):108- 117.
Machado NP. Monoclonal antibodies: physical development and therapeutic perspectives. Infectio 2006;10(3):186-197.
Lutterotti A, Roland M. Getting specific: monoclonal antibodies in multiple sclerosis. Lancet Neurology 2008;7:538- 547.
Kappos L, Bates D, Hans-Peter H. Natalizumab treatment for multiple sclerosis: recommendations for patient selection and monitoring. Lancet Neurology 2007:6;431-441.
Department of Dermatology, Mount Sinai Medical Center. Potential complications associated with the use of Biologic Agents for Psoriasis. Dermatol Clin 2007;(25):207-213.
Kozuch PL, Hanauer SB. General Principles and Pharmacology of Biologics in Inflammatory Bowel Disease. Gastroenterol Clin N Am 2006;35:757-773.
Gea-Banacloche JC, Geoffrey AW. Monoclonal Antibody Therapeutics and Risk for Infection. The Pediatric Infectious Disease Journal 2007(26).
Hernandez C, Cetner AS. Tuberculosis in the age of biologic therapy. J Am Acad Dermatol 2008;59:363-380.
Mohan AK, Cote TR, Block JA, et al. Tuberculosis following the use of etanercept, a tumor necrosis factor inhibitor. Clin Infect Dis 2004;39:295-299.
Wallis RS. Infections associated with anti-tumor necrosis factor therapy. UpToDate April 2008.
Wolfe F, Michaud K, Anderson J, Urbansky K. Tuberculosis infection in patients with rheumatoid arthritis and the effect of infliximab therapy. Arthritis Rhuem 2005;50:372-379.
Paraskevi IV, et al. Infliximab therapy in established rheumatoid arthritis: An observational study. Am J Med 2005(118): 515-520.
Jagadeshwar G, et al. Safety of Infliximab and other biologic agents in the inflamatory bowel diseases. Gastroenterology Clinics of North America 2006;(35):837-855.
Lesley AS, Espinoza LR. Impact of biologic agents on infectious diseases. Infect Dis Clin N Am 2006;20:931-961.
De Furst, Breedveld FC, Kalden JR. Updated consensus statement on biological agents for the treatment of rheumatic diseases. Ann Rheum Dis 2007;66.
Kader El Tal A, Posner MR, Spigelman Z. Rituximab: A monoclonal antibody to CD20 used in the treatment of pemphigus vularis. J Am Acad Dermatol 2006;55:449-459.
Fassi D. B Lymphocyte depletion with the monoclonal antibody rituximab in Graves´Disease: A controlled pilot study. J Clin Endocr Met 2007; 92(5):1769-1772.
Cacoub P, Delluc A. Anti-CD20 monoclonal antibody (rituximab) treatment for cryoglobulinemic vasculitis: where do we stand? Ann Rhum Dis 2008;67:283-287.
Leveque D, Wisniewski S. Pharmacokinetics of therapeutic monoclonal antibodies used in oncology. N Cancer Research 2005;25:2327-2344.
Graves J, et al. Off-label uses of biologics in dermatology: Rituximab, omalizumab, infliximab, etanercept, adalimumab, efalizumab and alefacept. J Am Dermatol 2007;56:55-79.
Selvasekar, et al. Effect of Infliximab on short-term complications in patients undergoing operation for chronic ulcerative colitis. J Am Coll Surg 2007;204, 5 May.
Popa C, Netea MG, Radstake T. Influence of anti-tumour necrosis factor therapy on cardiovascular risk factors in patients with active rheumatoid arthritis. Ann Rheum Dis 2005;64:303-305.
El-Hallak M, Binstadt BA, Leichtner AM. Clinical effects and safety of rituximab for treatment of refractory pediatric autoimmune diseases. Journal Pediatric 2007;150:376-382.
Welch B. Adalimumab (Humira) for the treatment of rheumatoid arthritis. Steps New Drug Reviews 2008.
Frampton JE, Wagstaff AJ. Alefacept. Am J Dermatol 2003;4(4):277-286.
Brunasso A, Cesare M. Thrombocytopenia associated with the use of anti-tumor necrosis factor-α agent for psoriasis. J Am Acad Dermatol 2009;60:781-785.
Zaja F, Battista ML. Lower dose rituximab is active in adults patients with idiopathic thrombocytopenic purpura. Haematologica 2008;93(6):930-934
Legat FJ, Hfer A, Wackernagel A. Narrowband UV-B phototherapy, Alefacept, and clearance of psoriasis. Arch Dermatol 2007;143(8):1016-1022.
Saketkoo LA, Espinoza LR. Impact of biologic agents on infectious diseases. Infectious Disease Clinics of North America 2006;20:931-961.
Askling J, Michael C, Brandt I, et al. Time-dependent increase in risk of hospitalization with infection among Swedish RA patients treated with TNF antagonists. Ann Rheum Dis 2007;66:1339-1344.
Salvana EMT, Salata RA. Infectious complications associated with monoclonal antibodies and related small molecules. Clinical Microbiology Reviews 2009; 274-290.
Ravindran V, Scott DL. A systematic review and meta-analysis of efficacy and toxicity of disease modifying anti-rheumatic drugs and biological agents for psoriatic artrhritis. Ann Rheum Dis 2008;67:855-859.
Salliot C, Dougados M, Gossec L. Risk of serious infections during rituximab, abatacept and anakinra treatments for rheumatoid arthritis: meta-analyses of randmised placebocontrolled trials. Ann Rheum Dis 2009;68:25-32.
Zhou Xuhui, Hu Weiguo, Qin Xuebin. The role of complement in the mechanism of action of Rituximab for B-Cell lymphoma: implications for therapy. The Oncologist 2008;13:954-966.
Saini R, Weinberg TW. Advences in therapy for psoriasis: an overview of Infliximab, Etarnercept, Efalizumab, alefacept, Adalimumab, Tazarotene and Pimecrolimus. Current Pharmaceutical Design 2005;11:273-280.
Tsiodoras Sotirios, Samonis G, Boumpas D, Kontoyiannis D. Fungal infections complicating tumor necrosis factor α blockade therapy. Mayo Clinic Proc 2008;83(2):181-194.
Reynolds J, Toescu V, Yee C, et al. Effects of rituximab on resistant SLE disease including lung involvement. Lupus 2009;18:67-73.
Joshi A, Bauer R, Kuebler P, et al. An overview of the phramacokinetics and phermacodynamics of Efalizumab: a monoclonal antibody approved for use in psoriasis. J Cli Pharmacol 2006;46:10
Wallis RS. Tumor necrosis factor antagonists: structure, function, and tuberculosis risks. Lancet Infect Dis 2008;8:601- 611.
Atzeni F, et al. Potencial target of infliximab in autoimmune and inflammatory diseases. Autoimmunity Reviews 2007;6:529- 536.
Fortun J. Principal infections in the oncology patient: practical treatment. Ann Sist Sanit Naver 2004;27:17-31.