Disseminated CNS tuberculosis in SLE without anti-TNF exposure: implications for LTBI screening in endemic settings—case report

Patients with systemic lupus erythematosus (SLE) are vulnerable to tuberculosis (TB) because of disease-related immune dysfunction, immunosuppressive therapy, and background exposure in TB-endemic settings. Although latent TB infection (LTBI) screening is routinely recommended before biologic and targeted synthetic disease-modifying antirheumatic drugs (DMARDs), guidance for glucocorticoids, conventional DMARDs, and other immunosuppressive therapies is less prescriptive. We report 2 HIV-negative Kenyan women with established SLE who developed disseminated extrapulmonary TB after approximately 12 and 20 months of mycophenolate mofetil therapy, respectively, while also receiving maintenance prednisolone 10 mg daily. The second patient had also received rituximab 7 months before TB diagnosis. In case 1, cerebrospinal fluid (CSF) GeneXpert Mycobacterium tuberculosis (MTB)/rifampicin and gluteal-abscess culture-confirmed disseminated central nervous system (CNS) TB with bilateral gluteal involvement. In case 2, lymph-node histology and culture-confirmed TB in the setting of widespread lymphadenopathy and splenic microabscesses; despite negative CSF investigations, neuroimaging demonstrated a cerebral lesion radiologically consistent with tuberculoma. Both patients received anti-TB therapy with adjunctive corticosteroids for CNS disease. Both patients demonstrated eventual clinical and radiological improvement. These cases demonstrate that severe disseminated TB, including CNS involvement, may occur in patients with SLE receiving nontumour necrosis factor (TNF) immunosuppressive regimens in TB-endemic settings. Although causal effects of individual immunosuppressive agents cannot be established, the cases support structured TB-risk assessment and a low threshold for LTBI testing before prolonged corticosteroid exposure or combination immunosuppression. Risk-stratified national guidance specifying therapy-related triggers for LTBI assessment may improve implementation and reduce preventable TB morbidity in high-burden settings.

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Journal
EULAR Rheumatology Open
Published
2026-10-26
DOI
https://doi.org/10.1016/j.ero.2026.100264
Primary Topic
Tuberculosis Research and Epidemiology
Type
article
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article

Disseminated CNS tuberculosis in SLE without anti-TNF exposure: implications for LTBI screening in endemic settings—case report

Mark P. Hawken, Shah Reena, Fredrick C. F. Otieno, Effie Kamadi
EULAR Rheumatology Open
Tuberculosis Research and Epidemiology
article

Disseminated CNS tuberculosis in SLE without anti-TNF exposure: implications for LTBI screening in endemic settings—case report

Mark P. Hawken, Shah Reena, Fredrick C. F. Otieno, Effie Kamadi
article en

Abstract

Patients with systemic lupus erythematosus (SLE) are vulnerable to tuberculosis (TB) because of disease-related immune dysfunction, immunosuppressive therapy, and background exposure in TB-endemic settings. Although latent TB infection (LTBI) screening is routinely recommended before biologic and targeted synthetic disease-modifying antirheumatic drugs (DMARDs), guidance for glucocorticoids, conventional DMARDs, and other immunosuppressive therapies is less prescriptive. We report 2 HIV-negative Kenyan women with established SLE who developed disseminated extrapulmonary TB after approximately 12 and 20 months of mycophenolate mofetil therapy, respectively, while also receiving maintenance prednisolone 10 mg daily. The second patient had also received rituximab 7 months before TB diagnosis. In case 1, cerebrospinal fluid (CSF) GeneXpert Mycobacterium tuberculosis (MTB)/rifampicin and gluteal-abscess culture-confirmed disseminated central nervous system (CNS) TB with bilateral gluteal involvement. In case 2, lymph-node histology and culture-confirmed TB in the setting of widespread lymphadenopathy and splenic microabscesses; despite negative CSF investigations, neuroimaging demonstrated a cerebral lesion radiologically consistent with tuberculoma. Both patients received anti-TB therapy with adjunctive corticosteroids for CNS disease. Both patients demonstrated eventual clinical and radiological improvement. These cases demonstrate that severe disseminated TB, including CNS involvement, may occur in patients with SLE receiving nontumour necrosis factor (TNF) immunosuppressive regimens in TB-endemic settings. Although causal effects of individual immunosuppressive agents cannot be established, the cases support structured TB-risk assessment and a low threshold for LTBI testing before prolonged corticosteroid exposure or combination immunosuppression. Risk-stratified national guidance specifying therapy-related triggers for LTBI assessment may improve implementation and reduce preventable TB morbidity in high-burden settings.

EULAR Rheumatology OpenVol. 2(4)
Aga Khan University Hospital Nairobi (KE), Aga Khan University Nairobi (KE)
Openalex Percentile: Top 12%
Tuberculosis Research and Epidemiology
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