2019 Research Forum
Kulraj Grewal MS IV 1 , Mandakini Patel MD R3 1 , Simmer Kaur MD R2 1 , Greti Petersen MD 1 , Bao Quynh Huynh MD 1 1. Department of Medicine - Kern Medical, Bakersfield, CA A Case of Opioid-Induced Systemic Vasculitis
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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 gastrointestinal and cutaneous involvement in which the skin lesions predominantly affect the lower extremities. We report a case of a relapse of drug-induced systemic leukoclastic vasculitis associated with intake of opioids. ➔ 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. ➔ 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 (figure 1) in association with hematuria and bloody bowel movements. ➔ 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 ( figure 2) , which has been noted in entities like dermatitis herpetiform or linear IgA dermatosis. ➔ 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 (figure 3). ➔ 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. Hospital Course
Case Presentation
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. Conclusions ➔ 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. ➔ 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.
References
Acknowledgements
1. Calabrese LH, Duna GF. Drug-induced vasculitis. Current Opinion in Rheumatolgy . 1996;8(1):34.
The authors would like to acknowledge the contributions of the patient care team and research support staff for their roles in bringing awareness of this drug-induced condition for the medical community.
2. Martinez-Taboada VM, Blanco R, Garcia-Fuentes M, Rodriguez-Valverde V. Clinical features and outcome of 95 patients with hypersensitivity vasculitis. Am J Med. 1997;102(2):186.
3. Mullick FG, McAllister HA Jr, Wagner BM, Fenoglio JJ Jr. Drug related vasculitis.Clinicopathologic correlations in 30 patients. Hum Pathol . 1979;10(3):313.
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This case study was conducted after approval from the Institutional Review Board.
4. Parker CW. Allergic reactions in man. Pharmacol Rev . 1982;34(1):85.
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