HEMOPERFUSION AS ADJUNCTIVE THERAPY IN SEPSIS IN AN IMMUNOCOMPROMISED HOST WITH SYSTEMIC LUPUS ERYTHEMATOSUS: A CASE REPORT

Systemic lupus erythematosus (SLE) is an autoimmune disease marked by immune dysregulation that predisposes affected individuals to life-threatening infections. Sepsis is a major cause of morbidity and mortality in SLE due to impaired pathogen clearance, immune exhaustion, and cytokine overproduction. In the setting of overwhelming inflammation, conventional management with antibiotics, corticosteroids, and supportive care may be insufficient to prevent deterioration. Hemoperfusion (HP) is an extracorporeal blood purification therapy that adsorbs circulating cytokines and endotoxins, thereby mitigating hyperinflammatory states associated with septic shock. Growing evidence suggests a role for HP as adjunct therapy in critically ill or immunocompromised patients, though literature in SLE-related sepsis remains limited. This case illustrates the successful application of HP in a young female with severe SLE complicated by hospital-acquired pneumonia, evolving sepsis, and acute kidney injury.

This is a case report conducted at a tertiary government hospital. The patient was a 36-year-old female with active SLE presenting with mucocutaneous lesions, nephritis, and pancytopenia. She was initiated on corticosteroids, subsequently receiving pulse methylprednisolone and later cyclophosphamide for persistent disease activity. Despite broad-spectrum antibiotics and diuretics, she developed progressive hypoxemia, pulmonary congestion, and worsening renal function consistent with evolving sepsis. After multidisciplinary evaluation, she underwent three consecutive sessions of combined hemodialysis and hemoperfusion using a cytokine-adsorbing cartridge. Clinical status, oxygen requirements, renal parameters, and inflammatory markers were recorded before and after intervention.

Before initiation of HP, the patient exhibited rising inflammatory biomarkers (procalcitonin 20.7 ng/mL, CRP 50 mg/L, ESR 96 mm/hr), deteriorating renal function (creatinine 2.0 mg/dL), and progressive respiratory failure requiring high-flow oxygen support. After three HP sessions, she demonstrated marked clinical improvement. Oxygenation normalized and dyspnea resolved, enabling de-escalation of respiratory support. Serum creatinine improved to 0.9 mg/dL with recovery of urine output. Pro-inflammatory markers declined in parallel with radiographic improvement in pulmonary congestion. White blood cell count normalized with reduced neutrophilic predominance. No treatment-related adverse effects were observed. The temporal association between HP initiation and clinical recovery suggests a beneficial immunomodulatory effect in attenuating the cytokine-driven inflammatory response.

This case highlights the potential utility of hemoperfusion as adjunctive therapy in sepsis complicating active SLE, particularly when conventional management fails to control hyperinflammation. By reducing circulating cytokines, HP may help stabilize organ function and accelerate recovery in immunocompromised patients. Although evidence remains emerging, this case supports expanding consideration of HP in selected high-risk septic patients—especially those exhibiting cytokine storm physiology or developing multiorgan dysfunction despite appropriate antimicrobial therapy. Larger prospective studies are warranted to define timing, duration, and patient selection criteria for optimal benefit in autoimmune-associated sepsis.