Tumor necrosis factor antagonists for paradoxical inflammatory reactions in the central nervous system tuberculosis

Santín, Miguel; Escrich, Cristina; Majós, Carles; Llaberia, Mariona; Grijota, María D.; Grau, Imma

doi:10.1097/md.0000000000022626

Cited by 18 publications

(7 citation statements)

References 34 publications

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“…When PR is identified, anti-TB therapy should be continued and corticosteroid therapy should be either increased or re-initiated. TNF-α plays an important role in promoting the inflammatory response to TB and TNF-α antagonists have been proposed as a treatment for refractory PR [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

Pelvic and central nervous system tuberculosis complicated by a paradoxical response manifesting as a spinal tuberculoma: a case report

et al. 2022

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Background The post-partum period is a risk factor for tuberculosis (TB), possibly including the period after miscarriage as illustrated here. This case demonstrates how non-specific symptoms can hide widely disseminated TB. Case presentation A healthy 26-year-old female with a history of recent miscarriage presented to the emergency department with non-specific symptoms of headache, abdominal pain, and sub-acute fevers. She had immigrated to the United States from the Marshall Islands 9 years prior. Two months prior to presentation she had a miscarriage at 18 weeks of pregnancy. On admission, transvaginal ultrasound revealed retained products of conception and abdominal computed tomography revealed findings consistent with tubo-ovarian abscesses and peritonitis. The obstetrics and gynecology service performed dilation and curettage (D&C) to remove retained products of conception. Acid-fast bacilli cultures from cerebrospinal fluid as well as specimens from D&C and intra-abdominal abscesses subsequently all grew TB. She was diagnosed with TB meningitis, peritonitis, endometritis, and tubo-ovarian abscesses. Her treatment course was complicated by a paradoxical response resulting in a spinal tuberculoma causing lower extremity weakness. The tuberculoma was treated with surgical decompression as well as continuation of treatment with anti-tubercular chemotherapy and steroids. Conclusion Disseminated and extrapulmonary TB can present with non-specific symptoms. Recognition of risk factors for TB is critical for prompt diagnostic evaluation and treatment of this deadly disease. A paradoxical reaction needs to be taken into consideration when any new neurological symptoms occur during TB treatment.

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Section: Discussionmentioning

confidence: 99%

Pelvic and central nervous system tuberculosis complicated by a paradoxical response manifesting as a spinal tuberculoma: a case report

et al. 2022

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“…For patients with steroid-refractory TB-IRIS, the use of TNF-α inhibitors for adjunctive therapy has been reported. The largest body of evidence exists for patients who had not previously been treated with TNF-α inhibition [ 9 , 10 ]. A review of the literature by Santin et al found 43 patients (13 adults and 30 children) with steroid-refractory CNS TB-IRIS who were treated with infliximab (6 patients), adalimumab (2 patients), or thalidomide.…”

Section: Discussionmentioning

confidence: 99%

“…Nine patients had concurrent HIV infection as a risk factor for IRIS, and 16 patients were not immunocompromised; the other patients were immunocompromised due to an underlying autoimmune condition, a hematologic malignancy, or malnutrition. There was an overall survival rate of 83.5%, with approximately half of surviving patients experiencing full recovery without neurologic sequelae [ 9 ].…”

Section: Discussionmentioning

confidence: 99%

CNS TB-IRIS Following Cessation of Adalimumab in an Adolescent With Crohn’s Disease

Christian

Johnston

2022

Open Forum Infectious Diseases

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Immune reconstitution inflammatory syndrome to tuberculosis (TB-IRIS) is an inflammatory response to M. tuberculosis infection that arises following restoration of the immune system and is increasingly recognized as a risk in patients treated with TNF-α inhibitors who develop active tuberculosis infection. We present the case of a 19 year old man treated with adalimumab for Crohn’s disease, who presented with disseminated miliary tuberculosis. His treatment course was complicated by central nervous system (CNS) TB-IRIS following cessation of his immunosuppression. We review the presentation and differential diagnosis of TB-IRIS, as well as risk factors for developing IRIS and the treatment of IRIS in this population.

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“…The proportion of HIV-negative patients with TBM who develop PR ranges from 31.2% to 56% [ 82 - 84 ]. After receiving standard ATT with adequate corticosteroids, patients usually experience worsening basal cistern exudates and hydrocephalus, frequently involving the cranial nerves [ 81 , 85 , 86 ]. Corticosteroid usage alone is insufficient in those PR cases, and whether corticosteroids reduce the morbidity of PR remains controversial [ 87 ].…”

Section: Corticosteroidsmentioning

confidence: 99%

Potential of Neuroinflammation-Modulating Strategies in Tuberculous Meningitis: Targeting Microglia

Lu¹,

Guo²,

Wei³

2023

Aging and disease

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Tuberculous meningitis (TBM) is the most severe complication of tuberculosis (TB) and is associated with high rates of disability and mortality. Mycobacterium tuberculosis (M. tb), the infectious agent of TB, disseminates from the respiratory epithelium, breaks through the blood-brain barrier, and establishes a primary infection in the meninges. Microglia are the core of the immune network in the central nervous system (CNS) and interact with glial cells and neurons to fight against harmful pathogens and maintain homeostasis in the brain through pleiotropic functions. However, M. tb directly infects microglia and resides in them as the primary host for bacillus infections. Largely, microglial activation slows disease progression. The non-productive inflammatory response that initiates the secretion of pro-inflammatory cytokines and chemokines may be neurotoxic and aggravate tissue injuries based on damages caused by M. tb. Host-directed therapy (HDT) is an emerging strategy for modulating host immune responses against diverse diseases. Recent studies have shown that HDT can control neuroinflammation in TBM and act as an adjunct therapy to antibiotic treatment. In this review, we discuss the diverse roles of microglia in TBM and potential host-directed TB therapies that target microglia to treat TBM. We also discuss the limitations of applying each HDT and suggest a course of action for the near future.

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Tumor necrosis factor antagonists for paradoxical inflammatory reactions in the central nervous system tuberculosis

Cited by 18 publications

References 34 publications

Pelvic and central nervous system tuberculosis complicated by a paradoxical response manifesting as a spinal tuberculoma: a case report

Pelvic and central nervous system tuberculosis complicated by a paradoxical response manifesting as a spinal tuberculoma: a case report

CNS TB-IRIS Following Cessation of Adalimumab in an Adolescent With Crohn’s Disease

Potential of Neuroinflammation-Modulating Strategies in Tuberculous Meningitis: Targeting Microglia

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