2019 Research Forum

Applicant: Kulraj Grewal MS IV Principal Investigator & Faculty Sponsor: Greti Petersen MD

A Case of Opioid-Induced Systemic Vasculitis

Kulraj Grewal MS IV, Mandakini Patel MD R3, Simmer Kaur MD R2, Greti Petersen MD, Bao Quynh Huynh MD

INTRODUCTION Leukocytoclastic vasculitis (LCV) is an uncommon autoimmune disease characterized pathologically by fibrinoid necrosis of the blood vessel wall and immune complex deposition. In rare cases, drug- induced leukocytoclastic vasculitis (LCV) will present in the setting of a syndrome such as Henoch-Schönlein Purpura (HSP) with cutaneous and gastrointestinal involvement.

PURPOSE Drug-induced systemic LCV has been noted in literature, however there are no reports of LCV associated with relapsed intake of opioids.

DISCUSSION A 41-year-old man presented with worsening abdominal pain, arthralgia, and palpable purpura on bilateral lower extremities. He denied having any prior history of autoimmune disorders. Blood testing revealed initial serum creatinine levels (1.16 mg/dl), CRP (1.9 mg/dl), ESR (12 mm/hr) with moderate leukocytosis of 17.8 but no thrombocytopenia or hypocomplementemia. Follow up C3, C4, ANA, antiphospholipid antibody, ANCA, and hepatitis panels were found to be negative. On further assessment, a drug panel was positive for opiates. The patient admitted that he had taken Norco to relieve the pain a few days prior to presentation. CT imaging of abdomen/pelvis revealed diffuse thickening of the small bowel and colon, suggesting an inflammatory morphology such as HSP. Biopsies from cutaneous purpura exhibited histologic features best supporting HSP with mild LCV and erythrocyte extravasation; other findings also included subepidermal split with neutrophilic pustules consistent for subepidermal vesiculobullous dermatosis, which has been noted in entities like dermatitis herpetiform or linear IgA dermatosis. Daily therapy with Prednisone was initiated as he continued to complain of worsening pain. The patient was given a single dose of oxycodone overnight for breakthrough pain. Consequently, his purpuric rash began to get worse in association with hematuria and bloody bowel movements. On labs, creatinine elevated to 3.16 mg/dl. Therapy with Solumedrol and Rituximab was begun as all opiates were immediately held and prohibited from further use. Upon completion of treatment, his creatinine began to return to baseline. The gross hematuria and hematochezia resolved. The purpuric rash began to disappear as the abdominal pain also improved. He was discharged with a tapering steroid regimen. CONCLUSION Through evidence provided by objective causality, it was determined that the probable adverse drug reaction from the use of opioids had caused the systemic LCV. Although this event could be considered rare, important advances have been made in providing new insights into the pathogenesis of both drug-induced vasculitis and idiopathic vasculitis. Thus, with increased understanding of the potential etiologies of drug- induced vasculitis, we may be able to accurately recognize it upon initial presentation and provide prompt therapeutic interventions with close monitoring so that further systemic damage could be avoided.

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