C49-14 Hepatic Abscess and Septic Shock in a Young Adult Receiving Risankizumab for Psoriasis

Introduction Risankizumab, an IL-23 inhibitor used in psoriasis, is associated with serious infections. However, hepatic abscesses are extremely rare. We report the first known case of hepatic abscess while receiving risankizumab therapy. Case Description A 24-year-old man with chronic plaque psoriasis on risankizumab presented with fever, chills, nausea, vomiting, diarrhea, and right upper quadrant abdominal pain. Laboratory tests showed leukocytosis (WBC 27.5 K/µL), anemia (Hb 10.7 g/dL), thrombocytosis (platelets 444 K/µL), and transaminitis (AST 208 U/L, ALT 203 U/L). Total bilirubin was 4.9 mg/dL and INR was 1.56. Magnetic resonance imaging revealed a 12 cm multiloculated hepatic abscess (Figure 1). Broad-spectrum antibiotics were initiated with IV piperacillin-tazobactam and vancomycin. Patient underwent ultrasound-guided aspiration with catheter drainage. Due to clinical deterioration and a rise in WBC to 60.9 K/µL, antibiotics were escalated to IV meropenem and linezolid. Clinical course was complicated with hemodynamic instability, requiring admission to the ICU. All bacterial, fungal, AFB, and parasitic cultures were negative. Patient recovered with continued antibiotic therapy and was discharged with plans for six weeks of IV antibiotics and outpatient drain management. Discussion Hepatic abscesses are uncommon in healthy, immunocompetent individuals, but immunomodulatory biologics may impair host defenses, increasing susceptibility to deep infections. Risankizumab targets IL-23, a cytokine critical for the function of Th17 cells, which produce IL-17, a key player in mucosal defense and neutrophil activation. Disruption of the IL-23/IL-17 axis has been shown to weaken barrier immunity, especially in the gut and liver, raising the risk of bacterial translocation and systemic infections.While clinical trials like UltIMMa-1 and UltIMMa-2 showed a generally favorable safety profile for risankizumab in psoriasis, they also noted increased rates of serious infections, most commonly pneumonia. Rare events like hepatic abscesses may be underrepresented. The hepatic immune environment depends on innate immunity, including Kupffer cells and neutrophils, to control gut-derived bacteria. IL-23 inhibition may compromise this defense. In our case, the absence of identifiable organisms may suggest sterile inflammation or an undetectable pathogen. Immunocompetent patients on biologics presenting with abdominal symptoms may warrant early imaging and broad-spectrum antibiotics; even in the absence of positive cultures. Conclusions Clinicians should maintain a high index of suspicion for atypical infections in patients receiving IL-23 inhibitors and consider early imaging and empiric antibiotics when warranted. This abstract is funded by: None