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Vol. 2. Núm. 6.
Páginas 302-312 (Noviembre - Diciembre 2006)
Vol. 2. Núm. 6.
Páginas 302-312 (Noviembre - Diciembre 2006)
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Terapia biológica e infecciones
Biologic therapy and infections
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Francisco Medina Rodríguez
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fmedina99@gmail.com

Correspondencia: Dr. F. Medina Rodríguez. Unidad de Investigación en Enfermedades Autoinmunes. Departamento de Reumatología. Hospital de Especialidades Bernardo Sepúlveda. Centro Médico Nacional Siglo XXI. Instituto Mexicano del Seguro Social. Avda. Cuauhtémoc, 330. 06720 México D.F. México.
Unidad de Investigación en Enfermedades Autoinmunes. Centro Médico Nacional Siglo XXI. Instituto Mexicano del Seguro Social. México DF. México
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La terapia biológica es una adición importante en el arsenal terapeútico de las enfermedades reumáticas. Los fármacos anti-TNF afectan las defensas contra infecciones, ya que el TNF modula inflamación e inmunidad celular. Se han observado casos de tuberculosis en pacientes tratados con anti-TNF, principalmente por la presencia de infección tuberculosa latente o “dormida” (LTB1). Otros microorganismos asociados a infecciones con terapia biológica son patógenos intracelulares que pueden evadir el sistema inmune y condicionar estado de latencia, persistiendo por grandes períodos sin causar daño: Mycobacterium sp., Listeria monocytogenes, Legionella sp., Brucella sp., toxoplasmosis y micosis profundas. El diagnóstico puede requerir elevado índice de sospecha clínica y obtener muestras y/o tejidos para análisis microscópico y cultivos. Los pacientes que desarrollan infecciones al estar en terapia biológica deben ser moniterados estrechamente. La administración de anti-TNF debe descontinuarse si en presencia de infección severa o sepsis. La relación entre inhibición de TNF y riesgo de infección debe esclarecerse mejor, ya que muchas de las infecciones severas se han observado en pacientes con terapia inmunosuporesora concomitante, que adicionado a enfermedades reumatológicas agresivas puede predisponer a infecciones, y la mayoría de los reportes publicados tienen un bajo nivel de evidencia. Sin embargo, un diagnóstico temprano y tratamiento oportuno es necesario para prevenir mortalidad secundaria a infecciones.

Palabras clave:
Terapia biológica
Fármacos anti-TNF
Infecciones

Biologic therapy is an important therapeutic arsenal in rheumatic diseases. Anti-TNF therapies affect host defenses against infections, since TNF mediates inflammation and modulates cellular immune responses. Cases of tuberculosis have been observed in patients treated with TNF antagonists, mainly due to the presence of latent or “dormant” tuberculosis infection (LTB1). Other microorganisms responsible for the infectious complications associated with biologic therapy are generally intracellular pathogens or pathogens that commonly exist in a chronic latent state: Mycobacterium sp., Listeria monocytogenes, Legionella sp., Brucella sp., toxoplasmosis and deep mycoses, that are normally held in control by cell-mediated immunity. Diagnosis may require a high index of suspicion and prompt acquisition of appropriate tissue samples for microscopic examination and microbiologic culture. Patients who develop a new infection while undergoing treatment with biologic therapy should be monitored closely. Administration of anti-TNF should be discontinued if a patient develops a serious infection or sepsis. The relationship between TNF-inhibition and infection risk remains unclear, many of the serious infections have occurred in patients on concomitant immunosuppressive therapy that, in addition to severe rheumatic diseases, could predispose them to infections, and most reports present low level of evidence. Nevertheless, prompt diagnosis and empiric therapy infections is necessary to prevent mortality.

Key words:
Biologic therapy
Anti-TNF therapies
Infections
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Bibliografía
[1.]
C.H.M. Van Jaarsveld, J.W.G. Jacobs, M.J. Van der Veen, et al.
Aggressive treatment in early rheumatoid arthritis: a randomized controlled trial.
Ann Rheum Dis, 59 (2000), pp. 468-477
[2.]
T. Mottenen, P. Hannonen, M. Korpela, et al.
Delay in institution of therapy of remission using single-drug or combination-disease-modifying antirheumatic drug therapy in early rheumatoid arthritis.
Arthritis Rheum, 46 (2002), pp. 894-898
[3.]
M. Feldmann, R.N. Maini.
Anti-TNF alpha therapy of rheumatoid arthritis: what have we learned?.
Annu Rev Immunol, 19 (2001), pp. 163-196
[4.]
A.K. Mohan, T.R. Coté, J.N. Siegel, M.M. Braun.
Infectious complications of biologic treatments of rheumatoid arthritis.
Curr Op Rheumatol, 15 (2003), pp. 179-184
[5.]
M.E. Weinblatt, J.M. Kremer, A.D. Bankhurst, K.J. Bulpitt, R.M. Fleichsmann, R.I. Fox, et al.
A trial of etanercept, a recombinant tumor necrosis factor receptor:Fc fusion protein, in patients with rheumatoid arthritis receiving MTX.
N Engl J Med, 340 (1999), pp. 253-259
[6.]
P.E. Lipsky, D.M. Van der Heijde, E.W. St Clair, et al.
Infliximab and methotrexate in the treatment of rheumatoid arthritis. Anti-Tumor Necrosis Factor Trial in Rheumatoid Arthritis with Concomitant Therapy Study Group.
N Engl J Med, 343 (2000), pp. 1594-1602
[7.]
M.E. Weinblatt, E.C. Keystone, D.E. Furst, et al.
Adalimumab, a fully Human anti-tumor necrosis factor monoclonal antibody for the treatment of rheumatoid arthritis in patients taking concomitant methotrexate. The ARMADA trial.
Arthritis Rheum, 48 (2003), pp. 35-45
[8.]
W.J. Shergy, R.M. Phillips, R.E. Hunt, J. Hernández.
Safety and efficacy of Infliximab therapy after etanercept failure: a case series.
Arthritis Rheum, 44 (2001), pp. S81
[9.]
R.F. Vollenhoven, E. Gullstrom, S. Brannemark, L. Klareskog.
Dose escalation of Infliximab in clinical practice: data from the Stockholm TNF-a registry.
Arthritis Rheum, 44 (2001), pp. S 82
[10.]
U. S. Food and Drug Administration. Arthritis Drugs Advisory Committee: Safety update on TNF-a antagonists: infliximab and etanercept (consultado 2 febrero 2005). Disponible en: http://www.fda.gov/ohrms/dockets/ac/01/briefing/3779b2.htm
[11.]
M.D. Rawlins.
Pharmacovigilance: paradise lost, regained or postponed.
J R Coll Physicians Lond, 29 (1995), pp. 41-49
[12.]
R.M. Martin, K.V. Kapoor, L.V. Wilton, et al.
Underreporting of suspected adverse drug reactions to newly marketed (“black triangle”) drugs in general practice: observational study.
BMJ, 317 (1998), pp. 119-120
[13.]
E. Heeley, J. Riley, D. Layton, et al.
Prescription event monitoring and reporting of adverse drug reactions.
Lancet, 358 (2001), pp. 1872-1873
[14.]
J.L. Flynn, M.M. Goldstein, J. Chan, K.J. Triebold, K. Pfeffer, C.J. Lowenstein, et al.
Tumor necrosis factor-alpha is required in the protective immune response against Mycobacterium tuberculosis in mice.
Immunity, 2 (1995), pp. 561-572
[15.]
L.G. Bekker, S. Freeman, P.J. Murray, B. Ryffel, G. Kaplan.
TNF-alpha controls intracellular mycobacterial growth by both inducible nitric oxide synthase-dependent and inducible nitric oxide synthase-independent pathways.
J Immunol, 166 (2001), pp. 6728-6734
[16.]
J. Keane, H.G. Remold, H. Kornfeld.
Virulent Mycobacterium tuberculosis strains evade apoptosis of infected alveolar macrophages.
J Immunol, 164 (2000), pp. 2016-2020
[17.]
H. Wajant, K. Pfizenmaier, P. Scheurich.
Tumor necrosis factor signaling.
Cell Death Differ, 10 (2003), pp. 45-65
[18.]
I. Mellman, R.M. Steinman.
Dendritic cells: specialized and regulated antigen processing machines.
Cell, 106 (2001), pp. 255-258
[19.]
D.R. Roach, A.G. Bean, C. Demangel, M.P. France, H. Briscoe, W.J. Britton.
TNF regulates chemokine induction essential for cell recruitment, granuloma formation, and clearance of mycobacterial infection.
J Immunol, 168 (2002), pp. 4620-4627
[20.]
J.M. Tufariello, J. Chan, J.L. Flynn.
Latent tuberculosis: mechanisms of host and bacillus that contribute to persistent infection.
Lancet Inf Dis, 3 (2003), pp. 578-590
[21.]
M. Desjardins, L.A. Huber, R.G. Parton, G. Griffiths.
Biogenesis of phagolysosomes proceeds through a sequential series of interactions with the endocytic apparatus.
J Cell Biol, 124 (1994), pp. 677-688
[22.]
B. Springer, S. Master, P. Sander, et al.
Silencing of oxidative stress response in Mycobacterium tuberculosis: expression patterns of ahpC in virulent and avirulent strains and effect of ahpC inactivation.
Infect Immun, 69 (2001), pp. 5967-5973
[23.]
S.S. Master, B. Springer, P. Sander, E.C. Boettger, V. Deretic, G.S. Timmins.
Oxidative stress response genes in Mycobacterium tuberculosis: role of ahpC in resistance to peroxynitrite and stage-specific survival in macrophages.
Microbiology, 148 (2002), pp. 3139-3144
[24.]
Y. Nozaki, Y. Hasegawa, S. Ichiyama, I. Nakashima, K. Shimokata.
Mechanism of nitric oxide-dependent killing of Mycobacterium bovis BCG in human alveolar macrophages.
Infect Immun, 65 (1997), pp. 3644-3647
[25.]
T.R. Mikuls, L.W. Moreland.
TNF blockade in the treatment of rheumatoid arthritis: infliximab versus etanercept.
Expert Opin Pharmacother, 2 (2001), pp. 75-84
[26.]
M.A. Gardam, E.C. Keystone, R. Menzies, et al.
Anti-tumour necrosis factor agents and tuberculosis risk: mechanisms of action and clinical management.
Lancet Inf Dis, 3 (2003), pp. 148-155
[27.]
S. Ehlers.
Role of tumour necrosis factor (TNF) in host defence against tuberculosis: implications for immunotherapies targeting TNF.
Ann Rheum Dis, 62 (2003), pp. ii37-42
[28.]
S. Ehlers, J. Benini, S. Kutsch, R. Endres, E.T. Rietschel, K. Pfeffer.
Fatal granuloma necrosis without exacerbated mycobacterial growth in tumor necrosis factor receptor p55 gene-deficient mice intravenously infected with Mycobacterium avium.
Infect Immun, 67 (1999), pp. 3571-3579
[29.]
J. Benini, E.M. Ehlers, S. Ehlers.
Different types of pulmonary granuloma necrosis in immunocompetent vs. TNFRp55-gene-deficient mice aerogenically infected with highly virulent Mycobacterium avium.
[30.]
S. Ehlers, S. Kutsch, E.M. Ehlers, J. Benini, K. Pfeffer.
Lethal granuloma disintegration in mycobacteria-infected TNFRp55-/- mice is dependent on T cells and IL-12.
J Immunol, 165 (2000), pp. 483-492
[31.]
T. Ten Hove, C. Van Montfrans, M.P. Peppelenbosch, et al.
Infliximab treatment induces apoptosis of lamina propria T lymphocytes in Crohn's disease.
Gut, 50 (2002), pp. 206-211
[32.]
A. Lugering, M. Schmidt, N. Lugering, et al.
Infliximab induces apoptosis in monocytes from patients with Crohn's disease by using a caspase-dependent pathway.
Gastroenterology, 121 (2001), pp. 1145-1157
[33.]
J.MHV. Van den Brande, H. Braat, G.R. Van den Brink, et al.
Infliximab but not etanercept induces apoptosis in lamina propria T-lymphocytes from patients with Crohn's disease.
Gastroenterology, 124 (2003), pp. 1774-1785
[34.]
E.C. Keystone.
Safety of biologic therapies –an update.
J Rheumatol, 32 (2005), pp. 8-12
[35.]
S. Ehlers.
Why does tumor necrosis factor targeted therapy reactivate tuberculosis?.
J Rheumatol, 32 (2005), pp. 35-39
[36.]
A.L. Hersh, A.N. Tosteson, C.F. Von Reyn.
Dual skin testing for latent tuberculosis infection. A decision analysis.
Am J Prev Med, 24 (2003), pp. 254-259
[37.]
J. Keane, S. Gershon, R.P. Wise, E. Mirabil-Levens, J. Kasznica, W.D. Schwiterman, et al.
Tuberculosis associated with infliximab, a tumor necrosis factor alpha-neutralizing agent.
N Engl J Med, 345 (2001), pp. 1098-1104
[38.]
L. Mayordomo, J.L. Marenco, J. Gómez-Mateos, et al.
Pulmonary miliary tuberculosis in a patient with anti-TNF-alpha treatment.
Scand J Rheumatol, 31 (2002), pp. 44-45
[39.]
E.N. Liberopoulos, A.A. Drosos, M.S. Elisaf.
Exacerbation of tuberculosis enteritis after treatment with infliximab.
Am J Med, 113 (2002), pp. 615
[40.]
S. Roth, E. Delmont, P. Heudier, et al.
Anti-TNF alpha monoclonal antibodies (infliximab) and tuberculosis: apropos of 3 cases.
Rev Med Interne, 23 (2002), pp. 312-316
[41.]
P. Rovere Querini, M. Vecellio, M.G. Sabbadini, et al.
Miliary tuberculosis after biologic therapy for rheumatoid arthritis.
Rheumatology, 41 (2002), pp. 231
[42.]
O. Núñez Martínez, C. Ripoll Noiseux, J.A. Carneros Martín, et al.
Reactivation tuberculosis in a patient with anti-TNF-alpha treatment.
Am J Gastroenterol, 96 (2001), pp. 1665-1666
[43.]
W.S. Lim, R.J. Powell, I.D. Johnston.
Tuberculosis and treatment with infliximab.
N Engl J Med, 346 (2002), pp. 623-626
[44.]
J. Keane, S. Gershon, M.M. Braun.
Tuberculosis and treatment with infliximab.
N Engl J Med, 346 (2002), pp. 625-626
[45.]
A. Myers, J. Clark, H. Foster.
Tuberculosis and treatment with infliximab.
N Engl J Med, 346 (2002), pp. 623-626
[46.]
J.J. Gómez-Reino, L. Carmona, V. Rodríguez-Valverde, et al.
An active surveillance of rheumatoid arthritis patients treated with tumor necrosis factor inhibitors indicates significant tuberculosis risk increase.
Arthritis Rheum, 48 (2003), pp. 2122-2127
[47.]
F. Wolfe, K. Michaud, J. Anderson, et al.
Tuberculosis infection in patients with rheumatoid arthritis and the effect of infliximab therapy.
Arthritis Rheum, 50 (2004), pp. 372-379
[48.]
J.D. Kent, A.L. Pangan, S.B. Fitzpatrick.
Análisis de la seguridad postmarketing de adalimumab en pacientes con artritis reumatoide durante los primeros 18 meses posteriores a su lanzamiento en el mercado norteamericano.
Abbott, archivo interno, (2005),
[49.]
C.D. Hamilton.
Infectious complications of treatment with biologic agents.
Curr Op Rheumatol, 18 (2004), pp. 393-398
[50.]
C.D. Hamilton.
Tuberculosis in the cytokine era: what rheumatologists need to know.
Arthritis Rheum, 48 (2003), pp. 2085-2091
[51.]
Grupo de trabajo sobre tuberculosis.
Ministerio de Sanidad y Consumo. Conferencia nacional para el control de la tuberculosis en España.
Med Clin (Barc), 98 (1992), pp. 24-31
[52.]
Joint Statement of the American Thoracic Society, the Centers for Disease Control and the Council of the Infectious Disease Society of America.
Targeted tuberculin testing and treatment of latent tuberculosis infection.
MMWR, 49 (2000), pp. 1-51
[53.]
Grupo de Trabajo sobre Tuberculosis.
Consenso nacional para el control de la tuberculosis en España.
Med Clin (Barc), 98 (1992), pp. 24-31
[54.]
Grupo de Trabajo del área TIR de SEPAR.
Recomendaciones SEPAR. Normativa sobre la prevención de la tuberculosis.
Arch Bronconeumol, 38 (2002), pp. 441-451
[55.]
E. Nuermberger, W.R. Bishai, J.H. Grosset.
Latent tuberculosis infection.
Sem Resp Crit Care Med, 25 (2004), pp. 317-336
[56.]
L.G. Wayne, C.D. Sohaskey.
Nonreplicating persistence of Mycobacterium tuberculosis.
Annu Rev Microbiol, 55 (2001), pp. 139-193
[57.]
Centers for Disease Control and Prevention.
The role of BCG vaccine in the prevention and control of tuberculosis in the United States: a joint statement by the Advisory Council for the Elimination of Tuberculosis and the Advisory Committee on Immunization Practices.
MMWR, 45 (1996), pp. 8-9
[58.]
F. Medina, V. Rivera, J. Fuentes, L. Sánchez, M. Portela, J. Moreno.
Is there a role for PPD and chest radiography in identification of asymptomatic tuberculosis in rheumatic diseases?.
Arthritis Rheum, 48 (2004), pp. S197
[59.]
V. Rivera, N. Chávez, I. Carranza, I. Fuentes, M. Portela, J. Moreno, et al.
Prevalence of skin Reactivity to tuberculin in patients with Rheumatoid Arthritis (RA) and Systemic Lupus Erythematosus (SLE).
Arthritis Rheum, 48 (2004), pp. S185
[60.]
T.E. Wagner, E.S. Huseby, J.S. Huseby.
Exacerbation of Mycobacterium tuberculosis enteritis masquerading as Crohn's disease after treatment with a tumor necrosis factor-alpha inhibitor.
Am J Med, 112 (2002), pp. 67-69
[61.]
Centers for Disease Control and Prevention.
Prevention and treatment of tuberculosis among patients infected with human immunodeficiency virus: principles of therapy and revised recommendations.
MMWR, 47 (1998), pp. 1-58
[62.]
American Thoracic Society.
Targeted tuberculin testing and treatment of latent tuberculosis infection.
Am J Respir Crit Care Med, 161 (2000), pp. S221-S247
[63.]
Comité Científico de BIOBADASER.
BIOBADASER: informe de situación semestral.
Rev Esp Reumatol, 30 (2003), pp. 554-564
[64.]
F. Gómez-Rodríguez, J.A. Bernal-Bermúdez, A. García-Egido.
Evaluación y tratamiento de la tuberculosis latente en el adulto.
Med Clin (Barc), 117 (2001), pp. 111-114
[65.]
X. Mariette, D. Salmon.
French guidelines for diagnosis and treating latent and active tuberculosis in patients with RA treated with TNF blockers.
Ann Rheum Dis, 62 (2003), pp. 791
[66.]
Grupo de Trabajo TIR.
Quimioprofilaxis antituberculosa. Recomendaciones SEPAR.
Arch Bronconeumol, 28 (1992), pp. 270-278
[67.]
D. Maher.
The internationally recommended tuberculosis control strategy. World Health Organization.
Trop Doct, 29 (1999), pp. 185-186
[68.]
F.M. Gordin, R.E. Chaison, J.P. Matts, C. Miller, M. De Lourdes García, R. Hafner, et al.
An international, randomized trial of rifampin and pyrazinamide versus isoniazid for prevention of tuberculosis in HIV-infected persons.
JAMA, 283 (2000), pp. 1445-1450
[69.]
Update: fatal and severe liver injuries associated with rifampin and pyrazinamide treatment for latent tuberculosis infection, and revisions in American Thoracic Society/CDC recommendations: United States, 2001. MMWR. 2001;50:733-5.
[70.]
J. Caminero.
¿Es la quimioprofilaxis una buena estrategia para el control de la tuberculosis?.
Med Clin (Barc), 116 (2001), pp. 223-229
[71.]
K.G. Castro, J.A. Jereb, V.R. Koppaka, et al.
Fatal liver injury associated with rifampin-pyrazinamide treatment of latent tuberculosis infection.
Chest, 123 (2003), pp. 967
[72.]
L. McNeill, M. Allen, C. Estrada, et al.
Pyrazinamide and rifampin vs isoniazid for the treatment of latent tuberculosis-improved completion rates but more hepatotoxicity.
Chest, 123 (2003), pp. 102-106
[73.]
J.E. Stout, J.J. Engemann, A.C. Cheng, et al.
Safety of 2 months of rifampin and pyrazinamide for treatment of latent tuberculosis.
Am J Respir Crit Care Med, 167 (2003), pp. 824-827
[74.]
Joint Tuberculosis Committee of the British Thoracic Society.
Control and prevention of tuberculosis in the United Kingdom: Code of Practice 2000.
Thorax, 55 (2000), pp. 887-901
[75.]
M. Lizasoain-Hernández, J.M. Aguado-García.
Protocolo de detección y tratamiento de la tuberculosis latente.
Medicine, 8 (2002), pp. 3607-3610
[76.]
B. Mehrad, R.M. Strieter, T.J. Standiford.
Role of TNF-alpha in pulmonary host defense in murine invasive aspergillosis.
J Immunol, 162 (1999), pp. 1633-1640
[77.]
E. Roilides, A. Dimitriadou-Georgiadou, T. Sein, et al.
Tumor necrosis factor alpha enhances antifungal activities of polymorphonuclear and mononuclear phagocytes against Aspergillus fumigatus.
Infect Immun, 66 (1998), pp. 5999-6003
[78.]
A. Warris, A. Bjorneklett, P. Gaustad.
Invasive pulmonary aspergillosis associated with infliximab therapy.
N Eng J Med, 344 (2001), pp. 1099-1100
[79.]
W.J. Steinbach, D.A. Stevens.
Review of newer antifungal and immunomodulatory strategies for invasive aspergillosis.
Clin Infect Dis, 37 (2003), pp. 157-187
[80.]
G.F. Keenan, T.F. Schaible, J.A. Boascia.
Invasive pulmonary aspergillosis associated with infliximab therapy.
N Engl J Med, 344 (2001), pp. 1100
[81.]
L. Bergstrom, D.E. Yocum, N.M. Ampel, et al.
Increased risk of coccidioidomycosis in patients treated with tumor necrosis factor alpha antagonists.
Arthritis Rheum, 50 (2004), pp. 1959-1966
[82.]
C.A. Hage, K.L. Wood, H.T. Winer-Muram, et al.
Pulmonary cryptococcosis after initiation of anti-tumor necrosis factor-alpha therapy.
Chest, 124 (2003), pp. 2395-2397
[83.]
P. Zhou, G. Miller, R.A. Seder.
Factors involved in regulating primary and secondary immunity to infection with Histoplasma capsulatum: TNF-alpha plays a critical role in maintaining secondary immunity in the absence of IFN-gamma.
J Immunol, 160 (1998), pp. 1359-1368
[84.]
L.J. Wheat, T.G. Slama, M.L. Zeckel.
Histoplasmosis in the acquired immune deficiency syndrome.
Am J Med, 78 (1985), pp. 203-210
[85.]
Wheat LJ, Smith EJ, Sathapatayavongs B, et al. Histoplasmosis in renal allograft recipients. Two large urban outbreaks. Arch Intern Med. 19893;143:703-7.
[86.]
J.H. Lee, N.R. Slifman, S.K. Gershon, et al.
Life-threatening histoplasmosis complicating immunotherapy with tumor necrosis factor alpha antagonists infliximab and etanercept.
Arthritis Rheum, 46 (2002), pp. 2565-2570
[87.]
K.L. Wood, C.A. Hage, K.S. Knox, et al.
Histoplasmosis after treatment with anti-tumor necrosis factor-alpha therapy.
Am J Respir Crit Care Med, 167 (2003), pp. 1279-1282
[88.]
S. Singh, N. Rau, H. Harris, et al.
Cutaneous nocardiosis complicating Crohn's disease management with infliximab.
Am J Gastroenterol, 96 (2001), pp. S308
[89.]
P. Ocón, J.M. Reguera, P. Morata, C. Juárez, A. Alonso, J.D. Colmenero, et al.
Phagocyte cell function in active brucellosis.
Infect Immun, 62 (1994), pp. 910-914
[90.]
A. Gross, A. Terraza, S. Ouahrani-Bettache, J.P. Liautard, J. Dornand.
In vitro Brucella suis infection prevents the programmed cell death of human monocytic cells.
Infect Immun, 68 (2000), pp. 342-351
[91.]
M.J. Corbel.
Recent advances in brucellosis.
J Med Microbiol, 46 (1997), pp. 101-103
[92.]
Y. Zhan, Z. Liu, C. Cheers.
Tumor necrosis factor alpha and interleukin- 12 contribute to resistance to the intracellular bacterium Brucella abortus by different mechanism.
Infect Immun, 64 (1996), pp. 2782-2786
[93.]
F.G. Jiménez, M.V. Colmenero, M.V. Irigoyen.
Reactivation of brucellosis after treatment with infliximab in a patient with rheumatoid arthritis.
J Infect, 50 (2005), pp. 370-371
[94.]
R. Van Furth, T.L. Van Zwet, A.M. Buisman, et al.
Anti-tumor necrosis factor antibodies inhibit the influx of granulocytes and monocytes into an inflammatory exudate and enhance the growth of Listeria monocytogenes in various organs.
J Infect Dis, 170 (1994), pp. 234-237
[95.]
J. Rothe, W. Lesslauer, H. Lotscher, et al.
Mice lacking the tumour necrosis factor receptor 1 are resistant to TNF-mediated toxicity but highly susceptible to infection by Listeria monocytogenes.
Nature, 364 (1993), pp. 798-802
[96.]
K. Pfeffer, T. Matsuyama, T.M. Kundig, et al.
Mice deficient for the 55 kd tumor necrosis factor receptor are resistant to endotoxic shock, yet succumb to L. monocytogenes infection.
Cell, 73 (1993), pp. 457-467
[97.]
T. Gluck, H.J. Linde, J. Scholmerich, et al.
Anti-tumor necrosis factor therapy and Listeria monocytogenes infection: report of two cases.
Arthritis Rheum, 46 (2002), pp. 2255-2257
[98.]
B.M. Kamath, P. Mamula, R.N. Baldassano, et al.
Listeria meningitis after treatment with infliximab.
J Pediatr Gastroenterol Nutr, 34 (2002), pp. 410-412
[99.]
N.R. Slifman, S.K. Gershon, H. Lee J-, et al.
Listeria monocytogenes infection as a complication of treatment with anti tumor necrosis factor aneutralizing agents.
Arthritis Rheum, 48 (2003), pp. 319-324
[100.]
A.G. Aparicio, S. Muñoz-Fernández, G. Bonilla, et al.
Report of an additional case of anti-tumor necrosis factor therapy and Listeria monocytogenes infection: comment on the letter by Gluck, et al.
Arthritis Rheum, 48 (2003), pp. 1764-1765
[101.]
J.T. Santamauro, R.N. Aurora, D.E. Stover.
Pneumocystis carinii pneumonia in patients with and without HIV infection.
Compr Ther, 28 (2002), pp. 96-108
[102.]
T.L. Tai, K.P. O’Rourke, M. McWeeney, et al.
Pneumocystis carinii pneumonia following a second infusion of infliximab.
Rheumatology, 41 (2002), pp. 951-952
[103.]
S. Centeno-Lima, H. Silveira, C. Casimiro, et al.
Kinetics of cytokine expression in mice with invasive aspergillosis: lethal infection and protection.
Immunol Med Microbiol, 14 (2002), pp. 167-173
[104.]
B. Killingley, V. Carpenter, K. Flanagan, G. Pasvol.
Pneumococcal meningitis and etanercept-chance or association?.
J Infect Dis, 51 (2005), pp. E49-51
[105.]
P.P. Kaur, T.D. Chris, M. Chatterji, R.J. Dehoratius.
Septic arthritis caused by Actinobacillus uraeae in a patient with rheumatoid arthritis receiving anti-tumor necrosis factor-α therapy.
J Rheumatol, 31 (2004), pp. 1663-1665
[106.]
M.A. Ritz, R. Jost.
Severe pneumococcal pneumonia following treatment with infliximab for Crohn's disease.
Inflamm Bowel Dis, 7 (2001), pp. 327
[107.]
K. Phillips, M.E. Husni, E.W. Karlson, et al.
Experience with etanercept in an academic medical center: are infection rates increased?.
Arthritis Rheum, 47 (2002), pp. 17-21
[108.]
P. Reichardt, I. Dahnert, G. Tiller, et al.
Possible activation of an intramyocardial inflammatory process (Staphylococcus aureus) after treatment with infliximab in a boy with Crohn disease.
Eur J Pediatr, 161 (2002), pp. 281-283
[109.]
A.T. Chan, V. Cleeve, T.J. Daymond.
Necrotising fasciitis in a patient receiving infliximab for rheumatoid arthritis.
Postgrad Med J, 78 (2002), pp. 47-48
[110.]
A. Kirchgatterer, T. Weber, M. Hinterreiter, et al.
Hemorrhagic colitis due to Escherichia coli O103:H2 associated with infliximab therapy in a patient with rheumatoid arthritis.
Rheumatology, 41 (2002), pp. 355-356
[111.]
M. Michel, Hezode C. Duvoux, D. Cherqui.
Fulminant hepatitis after infliximab in a patient with hepatitis B virus treated for an adult onset still's disease.
J Rheumatol, 30 (2003), pp. 1624-1625
[112.]
V.V. Menghini, A.S. Arora.
Infliximab-associated reversible cholestatic liver disease.
Mayo Clin Proc, 76 (2001), pp. 84-86
[113.]
G. Saleem, S.C. Li, B.R. MacPherson, S.M. Cooper.
Hepatitis with interface inflammation and IgG, IgM, and IgA anti-double stranded DNA antibodies following infliximab therapy [letter].
[114.]
I. Dervite, D. Hober, P. Morel.
Acute hepatitis B in a patient with antibodies to hepatitis B surface antigen who was receiving rituximab.
N Engl J Med, 344 (2001), pp. 68-69
[115.]
L.H. Calabrese, N. Zein, D. Vassilopoulos.
Safety of antitumour necrosis factor (anti-TNF) therapy in patients with chronic viral infections: hepatitis C, hepatitis B, and HIV infection.
Ann Rheum Dis, 63 (2004), pp. ii18-24
[116.]
J.R. Peterson, F.C. Hsu, P.A. Simkin, M.H. Wener.
Effect of tumor necrosis factor alfa antagonists on serum transaminases and viraemia in patients with rheumatoid arthritis and chronic hepatitis C infection.
Ann Rheum Dis, 62 (2003), pp. 1078-1082
[117.]
S.L. Goldberg, A.L. Pecora, R.S. Alter, et al.
Unusual viral infections (progressive multifocal leukoencephalopathy and cytomegalovirus disease) after high-dose chemotherapy with autologous blood stem cell rescue and peritransplantation rituximab.
Blood, 99 (2002), pp. 1486-1488
[118.]
G. Damaj, A. Charbonnier, R. Bouabdallah, et al.
Monoclonal antibodies and cytomegalovirus infections.
Eur J Haematol, 73 (2004), pp. 73-74
[119.]
P. Matteucci, M. Magni, M. Di Nicola, et al.
Leukoencephalopathy and papovavirus infection after treatment with chemotherapy and anti-CD20 monoclonal antibody.
Blood, 100 (2002), pp. 1104-1105
[120.]
T. Ellerin, R.H. Rubin, M.E. Weinblatt.
Infections and anti-tumor necrosis factor a therapy.
Artritis Rheum, 48 (2003), pp. 3013-3022
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