Incidence, risk factors and treatment of central nervous system immune reconstitution inflammatory syndrome in non-HIV patients with tuberculous meningitis: a multicentre observational study.

central nervous system immune reconstitution inflammatory syndrome risk factors tuberculous meningitis

Journal

Internal medicine journal
ISSN: 1445-5994
Titre abrégé: Intern Med J
Pays: Australia
ID NLM: 101092952

Informations de publication

Date de publication:
08 Dec 2023
Historique:
received: 28 05 2023
accepted: 15 10 2023
medline: 8 12 2023
pubmed: 8 12 2023
entrez: 8 12 2023
Statut: aheadofprint

Résumé

Immune reconstitution inflammatory syndrome (IRIS) affecting the central nervous system (CNS) is associated with poor outcomes. To report on risk factors for CNS-IRIS following tuberculous meningitis (TBM) in HIV-negative patients. In this retrospective multicentre study, all HIV-negative adult patients admitted between 2003 and 2021 with microbiologically proven TBM were included. The primary outcome measure was IRIS onset over follow-up. Characteristics of patients who developed IRIS were described. Factors associated with IRIS were identified using a multivariable logistic regression procedure. Fifty-six patients (33.0 (27.0-44.3) years, 39 (69.6%) men) with microbiologically proven TBM were studied. All patients received antituberculosis treatment and 48 (n = 48/56; 85.7%) steroids at TBM diagnosis. During a median follow-up of 18.0 (12.0-27.3) months, IRIS occurred in 28 (n = 28/56, 50.0%) patients, at a median time of 2.0 (1.0-3.0) months after antituberculosis treatment was started. IRIS involved the CNS in all but one case. Imaging revealed new (n = 23/28, 82.1%) and/or worsening (n = 21/28; 75.0%) of previously recognised lesions. Multivariable analysis showed that meningeal enhancement on brain magnetic resonance imaging (MRI) (odds ratio (OR): 15.3; 95% confidence interval (CI): (1.19-1193.5)) at TBM diagnosis and high blood albumin level (OR: 1.21; 95% CI: (1.02-1.60)) were associated with the occurrence of CNS-IRIS during follow-up. CNS-IRIS following TBM in non-HIV patients appears frequent and severe. Meningeal enhancement on brain MRI at tuberculosis diagnosis is a risk factor for CNS-IRIS.

Sections du résumé

BACKGROUND BACKGROUND
Immune reconstitution inflammatory syndrome (IRIS) affecting the central nervous system (CNS) is associated with poor outcomes.
AIMS OBJECTIVE
To report on risk factors for CNS-IRIS following tuberculous meningitis (TBM) in HIV-negative patients.
METHODS METHODS
In this retrospective multicentre study, all HIV-negative adult patients admitted between 2003 and 2021 with microbiologically proven TBM were included. The primary outcome measure was IRIS onset over follow-up. Characteristics of patients who developed IRIS were described. Factors associated with IRIS were identified using a multivariable logistic regression procedure.
RESULTS RESULTS
Fifty-six patients (33.0 (27.0-44.3) years, 39 (69.6%) men) with microbiologically proven TBM were studied. All patients received antituberculosis treatment and 48 (n = 48/56; 85.7%) steroids at TBM diagnosis. During a median follow-up of 18.0 (12.0-27.3) months, IRIS occurred in 28 (n = 28/56, 50.0%) patients, at a median time of 2.0 (1.0-3.0) months after antituberculosis treatment was started. IRIS involved the CNS in all but one case. Imaging revealed new (n = 23/28, 82.1%) and/or worsening (n = 21/28; 75.0%) of previously recognised lesions. Multivariable analysis showed that meningeal enhancement on brain magnetic resonance imaging (MRI) (odds ratio (OR): 15.3; 95% confidence interval (CI): (1.19-1193.5)) at TBM diagnosis and high blood albumin level (OR: 1.21; 95% CI: (1.02-1.60)) were associated with the occurrence of CNS-IRIS during follow-up.
CONCLUSION CONCLUSIONS
CNS-IRIS following TBM in non-HIV patients appears frequent and severe. Meningeal enhancement on brain MRI at tuberculosis diagnosis is a risk factor for CNS-IRIS.

Identifiants

pubmed: 38064539
doi: 10.1111/imj.16295
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Assistance Publique - Hôpitaux de Paris
Organisme : Université de Paris
Organisme : Ecole de l'Inserm Liliane Bettencourt Programme

Informations de copyright

© 2023 The Authors. Internal Medicine Journal published by John Wiley & Sons Australia, Ltd on behalf of Royal Australasian College of Physicians.

Références

Müller M, Wandel S, Colebunders R, Attia S, Furrer H, Egger M. Immune reconstitution inflammatory syndrome in patients starting antiretroviral therapy for HIV infection: a systematic review and meta-analysis. Lancet Infect Dis 2010; 10: 251-261.
Cheng VC, Yam WC, Woo PC, Lau SK, Hung IF, Wong SP et al. Risk factors for development of paradoxical response during antituberculosis therapy in HIV-negative patients. Eur J Clin Microbiol Infect Dis 2003; 22: 597-602.
Rivoisy C, Amrouche L, Carcelain G, Sereni D, Bourgarit A. Paradoxical exacerbation of tuberculosis after TNFalpha antagonist discontinuation: beware of immune reconstitution inflammatory syndrome. Joint Bone Spine 2011; 78: 312-315.
Rivoisy C, Tubach F, Roy C, Nicolas N, Mariette X, Salmon D et al. Paradoxical anti-TNF-associated TB worsening: frequency and factors associated with IRIS. Joint Bone Spine 2016; 83: 173-178.
Goulenok T, Gaudemer A, Rouzaud D, Chauveheid MP, Alexandra JF, Sacre K et al. Infliximab to treat severe paradoxical reaction in HIV-negative tuberculous meningoencephalitis. Neurology 2022; 98: 118-119.
Eshagh D, Benali K, Dossier A, Chauveheid MP, Rouzaud D, Goulenok T et al. Infliximab use for corticosteroid-resistant tuberculosis immune reconstitution inflammatory syndrome (TB-IRIS) in an immunocompetent patient. Infection 2020; 48: 799-802.
Cheng VC, Ho PL, Lee RA, Chan KS, Chan KK, Woo PC et al. Clinical spectrum of paradoxical deterioration during antituberculosis therapy in non-HIV-infected patients. Eur J Clin Microbiol Infect Dis 2002; 21: 803-809.
Marais S, Thwaites G, Schoeman JF, Torok ME, Misra UK, Prasad K et al. Tuberculous meningitis: a uniform case definition for use in clinical research. Lancet Infect Dis 2010; 10: 803-812.
Marais S, Meintjes G, Pepper DJ, Dodd LE, Schutz C, Ismail Z et al. Frequency, severity, and prediction of tuberculous meningitis immune reconstitution inflammatory syndrome. Clin Infect Dis 2013; 56: 450-460.
Wendel KA, Alwood KS, Gachuhi R, Chaisson RE, Bishai WR, Sterling TR. Paradoxical worsening of tuberculosis in HIV-infected persons. Chest 2001; 120: 193-197.
Breton G, Duval X, Estellat C, Poaletti X, Bonnet D, Mvondo Mvondo D et al. Determinants of immune reconstitution inflammatory syndrome in HIV type 1-infected patients with tuberculosis after initiation of antiretroviral therapy. Clin Infect Dis 2004; 39: 1709-1712.
Jung JW, Shin JW, Kim JY, Park IW, Choi BW, Seo JS et al. Risk factors for development of paradoxical response during anti-tuberculosis treatment in HIV-negative patients with pleural tuberculosis. Tohoku J Exp Med 2011; 223: 199-204.
Thwaites GE, Nguyen DB, Nguyen HD, Hoang TQ, Do TT, Nguyen TC et al. Dexamethasone for the treatment of tuberculous meningitis in adolescents and adults. N Engl J Med 2004; 351: 1741-1751.
Meintjes G, Wilkinson RJ, Morroni C, Pepper DJ, Rebe K, Rangaka MX et al. Randomized placebo-controlled trial of prednisone for paradoxical tuberculosis-associated immune reconstitution inflammatory syndrome. AIDS 2010; 24: 2381-2390.
Meintjes G, Stek C, Blumenthal L, Thienemann F, Schutz C, Buyze J et al. Prednisone for the prevention of paradoxical tuberculosis-associated IRIS. N Engl J Med 2018; 379: 1915-1925.
Blackmore TK, Manning L, Taylor WJ, Wallis RS. Therapeutic use of infliximab in tuberculosis to control severe paradoxical reaction of the brain and lymph nodes. Clin Infect Dis 2008; 47: e83-e85.

Auteurs

Marie Robert (M)

Service de Médecine Interne, Hôpital Bichat, Assistance Publique - Hôpitaux de Paris (AP-HP), Paris, France.

Arthur Mageau (A)

Service de Médecine Interne, Hôpital Bichat, Assistance Publique - Hôpitaux de Paris (AP-HP), Paris, France.

Augustin Gaudemer (A)

Service de Radiologie, Hôpital Bichat, Assistance Publique - Hôpitaux de Paris (AP-HP), Paris, France.

Michael Thy (M)

Service de Maladies infectieuses, Hôpital Bichat, Assistance Publique - Hôpitaux de Paris (AP-HP), Paris, France.

Nathan Peiffer Smadja (N)

Service de Maladies infectieuses, Hôpital Bichat, Assistance Publique - Hôpitaux de Paris (AP-HP), Paris, France.

Victoire de Lastours (V)

Service de Médecine Interne, Hôpital Bichat, Assistance Publique - Hôpitaux de Paris (AP-HP), Paris, France.

Thomas De Broucker (T)

Service de Neurologie, Hôpital Delafontaine, Saint-Denis, France.

Thomas Papo (T)

Service de Médecine Interne, Hôpital Bichat, Assistance Publique - Hôpitaux de Paris (AP-HP), Paris, France.
Centre de Recherche sur l'Inflammation, INSERM UMR1149, CNRS ERL8252, Faculté de Médecine site Bichat, Laboratoire d'Excellence, Inflamex, Université de Paris, Paris, France.

Tiphaine Goulenok (T)

Service de Médecine Interne, Hôpital Bichat, Assistance Publique - Hôpitaux de Paris (AP-HP), Paris, France.

Karim Sacré (K)

Service de Médecine Interne, Hôpital Bichat, Assistance Publique - Hôpitaux de Paris (AP-HP), Paris, France.
Centre de Recherche sur l'Inflammation, INSERM UMR1149, CNRS ERL8252, Faculté de Médecine site Bichat, Laboratoire d'Excellence, Inflamex, Université de Paris, Paris, France.

Classifications MeSH