A70-40 Do We Need Tuberculosis Screening Before Omalizumab? A Case Highlighting a Potential Gap in Practice

Abstract Introduction Omalizumab is a recombinant humanized monoclonal antibody that binds IgE, preventing its interaction with the high-affinity IgE receptor (FcεRI) on mast cells and basophils [1]. These cells trigger allergic inflammation through the release of vasoactive substances, mainly histamine [2]. This process recruits inflammatory mediators and leukocytes, resulting in symptoms ranging from urticaria to anaphylaxis [3]. Omalizumab suppresses this pathway and is used to treat IgE-mediated disorders such as chronic spontaneous urticaria (CSU). However, excessive mast cell suppression may predispose to infection. We describe a case of reactivated tuberculosis (TB) following Omalizumab therapy. Case Presentation A 40-year-old woman with CSU recently started on Omalizumab presented with a 3-month history of cough and dyspnea, followed by fever, chills, weight loss, night sweats, and hemoptysis. She was repeatedly treated for presumed community-acquired pneumonia without improvement. Her history included remote TB exposure over 10 years ago with prior negative testing. On presentation, she was febrile (99.3 °F), tachycardic (HR 114), and anemic (Hgb 7.8 g/dL). Chest CT revealed a thick-walled cavitary lesion in the apical and posterior segments of the right upper lobe (Figure 1). HIV testing was negative. Acid-fast bacilli smear confirmed pulmonary TB. Antitubercular therapy with RIPE and pyridoxine was initiated, with clinical improvement. Discussion Omalizumab inhibits the IgE-mediated allergic cascade by reducing eosinophil levels and mast cell and basophil activation [4], the latter particularly relevant in CSU [5]. No established link exists between Omalizumab and pulmonary disease, nor are there guidelines recommending TB screening before therapy [6]. A single report described a 32-year-old Filipino woman diagnosed with pulmonary and extrapulmonary TB after starting Omalizumab for CSU [7]. Mast cells play a paradoxical role in TB, contributing to both defense and chronic infection through T-helper type 1 cells and interferon-gamma pathways that modulate macrophage activation [8]. Patients with atopy may have an imbalanced immune response, and further mast cell suppression by Omalizumab may promote TB reactivation. [9]. Conclusion This case highlights the need for clinician awareness of potential infectious complications during Omalizumab therapy. Although TB screening is not currently recommended, identifying latent TB before treatment could guide risk-benefit discussions. Further research should clarify immunologic mechanisms linking Omalizumab to TB reactivation, particularly in immunocompetent patients. This abstract is funded by: None