A33-26 Rapid Onset of Kaposi’s Sarcoma IRIS in a Newly Diagnosed HIV Patient: Clinical Course and Management Challenges

Abstract Introduction First described in 1872 by Moritz Kaposi, Kaposi’s sarcoma (KS) is an endothelial neoplasm linked to human herpesvirus 8 (HHV-8). KS has four subtypes: classic/Mediterranean, endemic/African, HIV-associated/epidemic, and iatrogenic/transplant-related. We present a case of visceral KS in an HIV-positive patient, likely representing Immune Reconstitution Inflammatory Syndrome-Kaposi’s sarcoma (IRIS-KS). Visceral KS primarily affects lymph nodes, lungs, and the gastrointestinal tract. Antiretroviral therapy (ART) typically leads to KS improvement; however, IRIS can trigger new onset (unmasking KS-IRIS) or rapid progression of existing KS (paradoxical KS-IRIS), even in mildly immunocompromised patients. Case A 24-year-old male was newly diagnosed with HIV and syphilis, with a viral load of 677,000 and CD4 count of 138. He was initially started on DOVATO, later switched to Biktarvy, and placed on Bactrim for PJP prophylaxis. Two weeks later, he presented with nausea, vomiting, diarrhea, and a maculopapular rash on his torso, tongue, hard palate, and pharynx. Skin biopsy confirmed Kaposi’s sarcoma. His gastrointestinal symptoms were attributed to norovirus. Imaging showed cervical lymphadenopathy, innumerable pulmonary nodules, ground-glass opacities, mediastinal and supraclavicular lymphadenopathy, hepatomegaly, and borderline splenomegaly. Bronchoscopy revealed violaceous lesions on the distal trachea and mainstem bronchi. A lymph node biopsy confirmed Kaposi’s sarcoma (HHV-8). After antibiotic treatment, outpatient chemotherapy with doxorubicin was planned. However, days later, he presented with epiglottitis secondary to candidal infection and HSV stomatitis. He was treated with Decadron, fluconazole, valacyclovir, and Augmentin. Despite treatment, his condition worsened. Increasing throat swelling prompted laryngoscopy, revealing adenoid/lymphoid hypertrophy with purple changes consistent with KS. CT neck confirmed epiglottitis and lymphadenopathy. He developed respiratory distress, requiring emergent cricothyroidotomy. Bedside echocardiography revealed cardiac tamponade, necessitating pericardiocentesis. Despite all efforts, he ultimately succumbed to his death. Conclusion KS incidence has declined since ART’s advent; however, flares may occur post-ART initiation. Risk factors for KS-IRIS include advanced tumor stage (T1), HIV viral load 5 log10 copies/mL, and ART initiation without concurrent chemotherapy. Liposomal anthracyclines remain the gold standard. Close monitoring is essential when starting or modifying ART, as IRIS-KS can emerge within three weeks. This abstract is funded by: None