Acquired Angioedema Related to Transient C1- Inhibitor Deficiency Triggered by Mycoplasma pneumoniae Infection: A Case Report

<b>Background and Clinical Significance</b>: Acquired angioedema (AAE) is a rare and potentially life-threatening condition characterized by acquired deficiency of C1-inhibitor (C1-INH) resulting in hyperactivation of the classical complement pathway. AAE occurs in association with malignancies or autoimmune diseases. Infectious triggers are rarely encountered, and the underlying mechanisms have yet to be completely clarified. <b>Case Presentation</b>: This case involves a previously healthy 19-year-old male who was admitted with <i>Mycoplasma pneumonia</i> and oral ulcers, subsequently developing unilateral facial angioedema. Laboratory studies demonstrated reduced C4, decreased levels and activity of C1-INH, and reduced C1q, all consistent with acquired C1-INH deficiency. These findings were attributed to the presence of cold agglutinins, which are frequently observed in <i>Mycoplasma pneumoniae</i> infections. Following treatment with icatibant, a bradykinin B2 receptor antagonist, the patient's angioedema resolved rapidly. An exhaustive workup found no evidence of underlying systemic disorders, and the patient did not experience any angioedema attacks following resolution of the infection. <b>Conclusions</b>: The presence of cold agglutinins, commonly associated with <i>Mycoplasma</i> infections, can precipitate a decline in C1-INH levels, resulting in complement pathway dysregulation. This disruption leads to an excess of bradykinin, followed by increased vascular permeability and localized edema.