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Peer-reviewedCC BY 4.0Case Reports in Rheumatology

A Case of SLE Flare With Class IV Lupus Nephritis and Tuberculous Meningitis Presenting as Neuropsychiatric Symptoms: A Diagnostic Dilemma

  1. 1Institute of Medicine Maharajgunj Medical Campus Kathmandu Nepal
  2. 2Department of Internal Medicine Tribhuvan University Teaching Hospital Kathmandu Nepal teachinghospital.org.np

Abstract

Background: Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease with potential neuropsychiatric involvement (NPSLE) and increased susceptibility to opportunistic infections like tuberculosis (TB), particularly in endemic regions such as Nepal where the estimated incidence is 229 per 100,000 population. Differentiating NPSLE from tuberculous meningitis (TBM) is diagnostically challenging due to overlapping clinical and cerebrospinal fluid (CSF) findings.

Case Presentation: A 25‐year‐old male with a 1‐year history of SLE presented with facial puffiness, oral ulcers, polyarthritis, lower limb edema, and a 6‐week history of renal symptoms. Laboratory investigations revealed microcytic anemia (Hb 7.4 g/dL), nephrotic‐range proteinuria (urine protein‐to‐creatinine ratio 4.8 g/g), strongly positive anti‐dsDNA, and low complement levels. ENA panel was positive for anti‐Ro/SSA but negative for antiribosomal P and antiphospholipid antibodies. Renal biopsy confirmed class IV lupus nephritis (Activity Index 11/24 and Chronicity Index 3/12). Following intravenous methylprednisolone pulse therapy (500 mg/day for 3 days), he developed generalized tonic‐clonic seizures and altered sensorium. EEG revealed epileptiform discharges. CSF analysis showed lymphocytic pleocytosis (500 cells/μL and 80% lymphocytes), elevated protein (578 mg/dL), low glucose (1.4 mmol/L), and elevated ADA (10.9 U/L), suggestive of TBM despite negative GeneXpert MTB/RIF, viral PCR, and cryptococcal antigen assays. MRI brain showed cerebral atrophy, calcified granulomas in the right temporal lobe, and a nonspecific demyelinating white matter lesion. Based on clinical, CSF, and imaging findings, empirical antitubercular therapy (ATT) was initiated alongside tailored immunosuppression. The patient’s neurological and renal status markedly improved with complete resolution of seizures.

Discussion: Distinguishing NPSLE from CNS infections requires careful evaluation of serial CSF parameters, biomarkers, and MRI findings. In endemic regions, empirical ATT should be initiated early when clinical and laboratory features suggest TBM, even when molecular or culture tests are negative.

Conclusion: In SLE patients with neuropsychiatric symptoms in TB‐endemic areas, clinicians must consider TBM even when definitive microbiological tests are negative. Early empirical treatment can significantly improve patient survival and long‐term outcomes.

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BibTeX
@article{bhandari2026case,
  title = {{A Case of SLE Flare With Class IV Lupus Nephritis and Tuberculous Meningitis Presenting as Neuropsychiatric Symptoms: A Diagnostic Dilemma}},
  author = {Govinda Bhandari and Anupam Katuwal Chhetri and Rajan Gyawali and Binay Chapagain and Anush Acharya},
  journal = {Case Reports in Rheumatology},
  year = {2026},
  month = nov,
  doi = {10.1155/crrh/8150858},
  url = {https://doi.org/10.1155/crrh/8150858},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - A Case of SLE Flare With Class IV Lupus Nephritis and Tuberculous Meningitis Presenting as Neuropsychiatric Symptoms: A Diagnostic Dilemma
AU  - Govinda Bhandari
AU  - Anupam Katuwal Chhetri
AU  - Rajan Gyawali
AU  - Binay Chapagain
AU  - Anush Acharya
PY  - 2026
DA  - 2026/11/02
JO  - Case Reports in Rheumatology
DO  - 10.1155/crrh/8150858
UR  - https://doi.org/10.1155/crrh/8150858
AB  - Background: Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease with potential neuropsychiatric involvement (NPSLE) and increased susceptibility to opportunistic infections like tuberculosis (TB), particularly in endemic regions such as Nepal where the estimated incidence is 229 per 100,000 population. Differentiating NPSLE from tuberculous meningitis (TBM) is diagnostically challenging due to overlapping clinical and cerebrospinal fluid (CSF) findings.  Case Presentation: A 25‐year‐old male with a 1‐year history of SLE presented with facial puffiness, oral ulcers, polyarthritis, lower limb edema, and a 6‐week history of renal symptoms. Laboratory investigations revealed microcytic anemia (Hb 7.4 g/dL), nephrotic‐range proteinuria (urine protein‐to‐creatinine ratio 4.8 g/g), strongly positive anti‐dsDNA, and low complement levels. ENA panel was positive for anti‐Ro/SSA but negative for antiribosomal P and antiphospholipid antibodies. Renal biopsy confirmed class IV lupus nephritis (Activity Index 11/24 and Chronicity Index 3/12). Following intravenous methylprednisolone pulse therapy (500 mg/day for 3 days), he developed generalized tonic‐clonic seizures and altered sensorium. EEG revealed epileptiform discharges. CSF analysis showed lymphocytic pleocytosis (500 cells/μL and 80% lymphocytes), elevated protein (578 mg/dL), low glucose (1.4 mmol/L), and elevated ADA (10.9 U/L), suggestive of TBM despite negative GeneXpert MTB/RIF, viral PCR, and cryptococcal antigen assays. MRI brain showed cerebral atrophy, calcified granulomas in the right temporal lobe, and a nonspecific demyelinating white matter lesion. Based on clinical, CSF, and imaging findings, empirical antitubercular therapy (ATT) was initiated alongside tailored immunosuppression. The patient’s neurological and renal status markedly improved with complete resolution of seizures.  Discussion: Distinguishing NPSLE from CNS infections requires careful evaluation of serial CSF parameters, biomarkers, and MRI findings. In endemic regions, empirical ATT should be initiated early when clinical and laboratory features suggest TBM, even when molecular or culture tests are negative.  Conclusion: In SLE patients with neuropsychiatric symptoms in TB‐endemic areas, clinicians must consider TBM even when definitive microbiological tests are negative. Early empirical treatment can significantly improve patient survival and long‐term outcomes.
SN  - 2090-6889
SN  - 2090-6897
ER  -