A Case Report of Serum Sickness Following Administration of Equine Anti-Thymocyte Globulin in a Patient with Severe Aplastic Anemia.

Serum sickness is an immune complex-mediated hypersensitivity reaction, classically manifested by the triad of fever, rash, and arthralgias. It results from the formation and deposition of antigen–antibody complexes, leading to complement activation and small-vessel inflammation. Agents that commonly provoke serum sickness are heterologous proteins such as animal serums, antivenoms, and certain vaccines. The reaction typically occurs 7–21 days after antigen exposure, with resolution of symptoms within 2–3 weeks. Primary management is the discontinuation of the offending agent. Moderate reactions may be treated with steroids, while rare but severe reactions may necessitate hospitalization and/or plasmapheresis. Herein, we present a 61-year-old male patient from Colombia with no previous medical history, who was diagnosed with severe aplastic anemia while undergoing a pancytopenia workup. He was admitted for initial therapy with equine anti-thymocyte globulin (ATG), cyclosporine, and eltrombopag. Post-discharge, he followed up in clinic with wrist pain and adenopathy and was prescribed Augmentin, only to be admitted the following day for neutropenic fever, rash, and worsening polyarthralgia. Symptoms resolved rapidly with supportive care alone. Following a thorough infectious workup and dermatology evaluation, the patient was discharged on a prolonged oral steroid taper with a diagnosis of serum sickness secondary to ATG therapy. Serum sickness presents with nonspecific symptoms, and while objective data can be used to support a diagnosis, no standardized diagnostic criteria exist. Additionally, susceptible patient populations often harbor immuno-compromising comorbidities. Therefore, the initial differential should be broad, including infectious, autoimmune, and other drug-related etiologies, including serum sickness-like reaction (SSLR) and Stevens-Johnson syndrome (SJS). In this case, the timing of symptoms following ATG exposure and the absence of alternative infectious or autoimmune causes supported the diagnosis. Given the often self-limiting nature of the disease process, suppression of the immune system with steroids should only be initiated in the setting of sufficient infectious rule out and high clinical suspicion. Furthermore, offending agents should be permanently discontinued given the risk of life-threatening reactions like anaphylaxis upon re-exposure.