Disseminated CNS tuberculosis in SLE without anti-TNF exposure: implications for LTBI screening in endemic settings—case report
- 1Department of Medicine, Aga Khan University Medical College of East Africa, Nairobi, Kenya
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.
Related
- Missed Early Signs of Tuberculosis in Pregnancy: Insights From a Case Series of Disseminated Life-Threatening Maternal Disease and Adverse Fetal Outcomes.
- The Placenta as a Diagnostic Specimen in Disseminated Tuberculosis of Pregnancy presenting as Acute Respiratory Distress Syndrome – A case report
- Severe Inflammatory Response and Moderate Acute Respiratory Distress Syndrome (ARDS) in an Immunocompetent Patient With Disseminated Tuberculosis: A Case Report.
- Disseminated Tuberculosis With Ocular Involvement After 12 Years of Anti-TNF-α Therapy.
- Whole genome sequencing and tuberculosis surveillance and control: a critical view from resources limited settings
BibTeX
@article{kamadi2026disseminated,
title = {{Disseminated CNS tuberculosis in SLE without anti-TNF exposure: implications for LTBI screening in endemic settings—case report}},
author = {Effie Kamadi and Mark Hawken and Reena Shah and Fredrick Otieno},
journal = {EULAR rheumatology open},
year = {2026},
month = oct,
doi = {10.1016/j.ero.2026.100264},
url = {https://europepmc.org/article/PMC/PMC13722078},
note = {CC BY},
}
RIS
TY - JOUR
TI - Disseminated CNS tuberculosis in SLE without anti-TNF exposure: implications for LTBI screening in endemic settings—case report
AU - Effie Kamadi
AU - Mark Hawken
AU - Reena Shah
AU - Fredrick Otieno
PY - 2026
DA - 2026/10/26
JO - EULAR rheumatology open
DO - 10.1016/j.ero.2026.100264
UR - https://europepmc.org/article/PMC/PMC13722078
AB - 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.
SN - 3050-7081
ER -