RECURRENT ANGIOEDEMA IN SLE PATIENT

TOPIC: Allergy and Airway TYPE: Medical Student/Resident Case Reports INTRODUCTION: The pathophysiology of angioedema is broad. It may be hereditary, idiopathic, or a reaction to range medications allergens; there have been few case reports describing recurrent in patients with autoimmune conditions such as systemic lupus erythematosus (SLE). We present the patient SLE who suffered from face, including lips, tongue, throat, without urticaria, normal C1-Inhibitor levels. CASE PRESENTATION: A 69-year-old female history presented progressive swelling eyes, tongue for one week. She did not consume angiotensin-converting enzyme inhibitors reported no medication changes exposure unknown substances. Physical examination revealed facial, periorbital, edema respiratory distress. Initial lab work was unremarkable. Histamine blockers steroids were immediately administered, she intubated due compromise. Racemic epinephrine also initiated, tracheostomy performed definitive airway management. Workup infection unrevealing. C1-Inhibitor, CH50, C4 levels deficit. Once her status stabilized, discharged long-term care facility. DISCUSSION: Angioedema, defined localized subcutaneous submucosal extravasation fluid into interstitial tissues, maybe mast cell-mediated kinin-mediated. former often associated urticaria triggered by an allergic medications. At same time, latter occurs absence specific trigger hereditary deficiency dysfunction. Our had C1 esterase inhibitor levels, rendering diagnosis less likely. Furthermore, taking known cause exposed any new allergens before presentation. Literature states that characteristically exhibit reduced components classical complement pathway. defect can either originate lymphoproliferative disease catabolizes circulating antibodies inactivate C1-Inhibitor. However, our fulfill above-mentioned criteria. Even though similar cases literature, occurrence still scarce. CONCLUSIONS: has rarely angioedema. unclear. patient's late age presentation lack family favored independent risk factor Cl-inhibitor dysfunction heterogeneous distinct acquired Hence, more needs done early recognition prompt prevention. REFERENCE #1: Dunckley H, Gatenby PA, Hawkins B, Naito S, Serjeantson SW. Deficiency C4A genetic determinant three ethnic groups. J Immunogenet. 1987 Aug-Oct;14(4-5):209-18. doi: 10.1111/j.1744-313x.1987.tb00383.x. PMID: 3502648. #2: Alsenz J, Bork K, Loos M. Autoantibody-mediated inhibitor. N Engl Med. May 28;316(22):1360-6. 10.1056/NEJM198705283162202. 3494945. #3: Thong BY, Thumboo Howe HS, Feng PH. Life-threatening erythematosus. Lupus. 2001;10(4):304-308. doi:10.1191/096120301680417011 DISCLOSURES: No relevant relationships Asim Amjad, source=Web Response Zamara Hamid, Dan Kazmierski, Si Li, Pius Ochieng, NISHANT SHARMA,