Successful Treatment of Painful Cutaneous Vasculopathy With Rivaroxaban in a Patient With Systemic Lupus Erythematosus

May 2020 | Volume 19 | Issue 5 | Features | 544 | Copyright © May 2020

Published online April 10, 2020

Nathan H. Leisenring , Jennifer L. Rogers , Stacy Telloni , Parisa Mansoori , Rami N. Al-Rohil , Anne L. Marano

aDuke University School of Medicine, Durham, NC bDepartment of Medicine, Duke University Medical Center, Durham, NC cDepartment of Pathology, Duke University Medical Center, Durham, NC dDepartment of Dermatology, Duke University Medical Center, Durham, NC

30-50ml/min, while use is contraindicated in patients with creatinine clearance <30ml/min.3 Rivaroxaban is metabolized by cytochrome P450 3A4 and is a substrate for the p-glycoprotein transporter, which are both inhibited by systemic azole antifungals.2 Dermatologists should be aware of rivaroxaban in terms of its drug interactions, but also as a potential dermatologic therapy.

In dermatology, rivaroxaban has recently been shown to be effective in the treatment of livedoid vasculopathy (LV), with its success suggesting a role for NOACs in the treatment of nonvasculitic cutaneous vasculopathy in general. Prior to the advent of NOACs, a 2012 review of LV treatment amongst dermatologists indicated that most case series utilized antiplatelet agents as first-line therapy.4 However, recently, multiple case reports have demonstrated successful treatment of LV with rivaroxaban, dosed at 10mg or 20mg once daily or 10mg bid.5-10 In many cases, these patients had failed initial treatment with alternative immunosuppressive, antiplatelet, or anticoagulant therapies.5-7,10

In the case presented herein, an unremarkable laboratory and imaging work-up coupled with a biopsy demonstrating dermal fibrin thrombi without evidence of vasculitis was concerning for cutaneous vasculopathy. It is unknown if over time her lesions would have progressed to become more chronic and ulcerative, as is commonly seen in the “atrophie blanche” lesions of LV. Regardless, we observed a rapid, complete response to rivaroxaban, demonstrating its potential utility in patients with idiopathic cutaneous vasculopathy. Furthermore, this case indicates that rivaroxaban therapy remains useful in cutaneous vasculopathy even in the absence of laboratory evidence of hypercoagulability. Most importantly, this case suggests that early intervention with a NOAC in cutaneous vasculopathy can eliminate the need for significant pain medication as well as prevent progression to ulceration and atrophy. Dermatologists should be aware of the potential therapeutic use of NOACs in patients with cutaneous vasculopathy.


The authors have no conflicts of interest to disclose.


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