Pleural Effusion and Neuropsychiatric Involvement in a Patient with SLE: A Report from a Resource-Limited, Tuberculosis-Endemic Country

Introduction

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by multisystem involvement resulting from immune dysregulation and autoantibody formation.

Serositis, including pleural effusion, is a recognized manifestation of SLE and is associated with increased disease activity.¹ In tuberculosis-endemic regions, pleural effusion is frequently attributed to pulmonary tuberculosis (TB), often leading to empirical anti-TB therapy and delayed recognition of underlying autoimmune disease.^2,3 This diagnostic overlap represents a significant challenge where access to advanced immunological testing is limited. Neuropsychiatric systemic lupus erythematosus (NPSLE) represents a severe manifestation including seizures, psychosis, and behavioral disturbances.^4,5 These manifestations frequently mimic infectious or primary psychiatric conditions, increasing the risk of delayed diagnosis in resource-limited settings.⁶ We report a case of SLE presenting with neuropsychiatric manifestations and pleural effusion initially misdiagnosed as TB.

Case Presentation

A 19-year-old Somali female student with no prior medical history presented with a three-month progression of symptoms. The illness began in July with symmetrical joint pain in the small joints of the hands (MCP and PIP joints), accompanied by morning stiffness and fatigue. Three weeks later, she developed a malar rash and dark scaly lesions on her ears (Figure 1).

Figure 1 An erythematous flat, non-scarring malar rash, was present symmetrically across the cheeks and the bridge of the nose sparing nasolabial folds.

She subsequently developed a dry cough, pleuritic chest pain, and shortness of breath. A chest radiograph (Figure 2) showed bilateral pleural effusion and left lower zone consolidation. Despite a negative sputum GeneXpert test, empirical anti-TB therapy (HRZE) was started based on regional epidemiology. One month later, she developed vomiting and abdominal pain, leading to treatment interruption. She was later re-started on anti-TB therapy in Ethiopia, but her condition deteriorated.

Figure 2 Posteroanterior chest radiograph revealed bilateral pleural effusion, predominantly on the right side, with associated consolidation in the left lower lung zone.

The patient developed new neuropsychiatric symptoms: persistent headache, visual and auditory hallucinations, delusions, agitation, and a one-minute generalized tonic-clonic seizure. Upon transfer to Hargeisa Group Hospital, physical examination revealed an anxious, restless patient with a well-defined malar rash and discoid plaques (Figures 3 and 1). Respiratory exam showed bilateral fine crackles and decreased air entry.

Figure 3 Scaly discoid plaques were observed involving the outer ear and ear lobes with well-defined margins and adherent scaling.

Laboratory investigations (Summarized in the Table 1) were notable for anemia of chronic disease, elevated ESR, and positive autoimmune serology (ANA 400 U/mL, positive anti-dsDNA, and SS-A/Ro 60 kD). Complement levels were unavailable due to resource limitations.

Table 1 Summary of Laboratory Investigations

Imaging Studies

Chest radiography: demonstrated consolidation in the left lower lung zone with bilateral pleural effusion, more prominent on the left side. These findings were initially interpreted as suggestive of pulmonary tuberculosis but were later considered compatible with lupus-related pleuritis.

Echocardiography: revealed normal cardiac chamber size and ventricular function, with no evidence of pericardial effusion.

Abdominopelvic ultrasonography revealed no hepatosplenomegaly, ascites, or structural renal abnormalities.

Therapeutic Intervention

The diagnosis was confirmed as SLE with NPSLE and lupus pleuritis. Management included intravenous methylprednisolone (1g daily for 5 days), followed by oral prednisolone (40mg tapering), mycophenolate mofetil (titrated to 2g daily), and hydroxychloroquine (200mg twice daily). Risperidone (2mg daily) was used briefly for psychosis and completed by the outer ear discoid manifestation after the treatment (Figure 4).

Figure 4 The outer ear discoid manifestations completely resolution after treatment.

Follow-Up and Outcomes

The patient showed marked improvement for the malar rash by the completely resolved the treatment as (Figure 5). At six months, all neuropsychiatric and joint symptoms had resolved. At 16 months, she returned to school and remained stable Follow-up ANA levels decreased to 135.6 U/mL, and anti-ds DNA normalized. (Figures 1 and 2) (panels B) show the complete resolution of cutaneous lesions.

Figure 5 The malar rash completely resolved following treatment.

Discussion

Systemic lupus erythematosus often mimics infectious conditions, particularly in TB endemic regions.² In such settings, pleural effusion is frequently attributed to TB, leading to empirical therapy even when microbiological confirmation is lacking,⁷ (Table 2) compares the overlapping and distinguishing features of SLE and TB to aid clinical differentiation.

Table 2 Clinical Comparison: Systemic Lupus Erythematosus (SLE) vs. Tuberculosis

Neuropsychiatric SLE includes a wide range of symptoms, including seizures and psychosis.⁴ In this case, these symptoms contributed to diagnostic confusion, especially without advanced neuroimaging.⁸ Early recognition is essential, as delayed treatment may result in irreversible neurological damage.⁹

Serositis is a well-recognized manifestation of SLE.¹ Lupus pleuritis can mimic infectious pleural disease, and in TB-endemic areas, it is commonly misinterpreted as tuberculosis pleurisies due to overlapping clinical and radiologic features.² Persistent or unexplained pleural effusion should prompt reconsideration of alternative diagnoses when TB therapy fails.³

Similar cases in the literature emphasize the risk of misdiagnosis in resource-limited settings.^2,3

Management of severe SLE requires prompt initiation of high-dose corticosteroids and immune suppressants.¹⁰ Despite limited diagnostic resources, targeted serologic testing enabled a favorable outcome in this patient. This case underscores several lessons: First, failure to improve on empirical TB therapy should prompt immediate reconsideration of autoimmune disease.² Second, neuropsychiatric symptoms in patients with systemic inflammation are a red flag for NPSLE.⁴ Third, clinicians in endemic areas must maintain high suspicion for SLE in patients with unexplained multisystem involvement.

Conclusion

The main take-home messages are:

1) SLE is a great mimicker of TB in resource-limited settings;

2) Empirical TB therapy should be re-evaluated if no response is seen within weeks; and

3) Early use of targeted autoimmune serology is cost-effective in preventing irreversible organ damage and unnecessary TB treatment.