C50-08 Colchicine Toxicity as a Trigger for Hemophagocytic Lymphohistiocytosis

Abstract Introduction Colchicine, a medication commonly used for gout and other clinical indications, is classically described as having a narrow therapeutic index. Though most cases of colchicine toxicity are self-limiting, a subset of patients can develop severe and life-threatening complications. We describe a patient who initially presented with non-specific gastrointestinal symptoms who developed rapid and progressive multiorgan failure ultimately found to have hemophagocytic lymphohistiocytosis (HLH) from colchicine toxicity. Case A 78-year-old female with a history of type 2 diabetes mellitus, severe peripheral artery disease, hypertension, complete heart block requiring pacemaker placement, chronic kidney disease, and gout presented to the hospital with nausea, vomiting, and diarrhea with new onset pancytopenia that coincided with initiation of colchicine therapy for gout treatment. Within 3 days of admission, the patient developed progressive renal failure, liver failure, cardiac dysfunction, and encephalopathy requiring intubation. With ongoing pancytopenia, multiorgan failure, and diagnostic uncertainty, a bone marrow biopsy was performed, which was negative for malignancy but showed hemophagocytosis. Corroborative HLH blood work revealed marked elevations in ferritin, triglycerides, and soluble interleukin-2 receptor. Given timing of symptoms with colchicine initiation, a colchicine level was obtained on day 5 of admission and resulted at 3.7 ng/ml, despite the medication being held since admission. As other etiologies for HLH including infection, malignancy, and autoimmune conditions were excluded, the final diagnosis was secondary HLH from colchicine toxicity. With treatment, she demonstrated improvements in pancytopenia, liver injury, and coagulopathy. Mental status also improved allowing extubation, however did not return to prior baseline. Ultimately, she was unable to tolerate intermittent hemodialysis and was transitioned to comfort care. Discussion The clinical manifestations of colchicine toxicity are well described in literature; however, this case describes the associated development of secondary HLH in the setting of colchicine toxicity. A literature review revealed two cases of colchicine-associated HLH, both requiring treatment in the intensive care setting; one in a pediatric patient receiving colchicine treatment for Familial Mediterranean Fever, and one describing a pediatric patient who ingested colchicine in an overdose attempt. To our knowledge, there are no prior reports linking these two entities in an adult patient. As demonstrated in this case, the widespread multi-organ failure caused by colchicine toxicity may lead to an inappropriate immunologic response triggering secondary HLH. Intensivists should be aware of this rare complication of a commonly administered drug, particularly in patients with pre-existing renal dysfunction. This abstract is funded by: None