Treatment Of Livedoid Vasculopathy Research Articles

Rivaroxaban in the treatment of livedoid vasculopathy: A long-term retrospective study

Rivaroxaban in the treatment of livedoid vasculopathy: A long-term retrospective study

A comprehensive review on pathogenesis, associations, clinical findings, and treatment of livedoid vasculopathy.

Livedoid vasculopathy (LV) is a thrombo-occlusive vasculopathy that involves the dermal vessels. Clinically, it is characterized by the presence of painful purpuric ulcers on the lower extremities. Histopathologically, it shows intraluminal fibrin deposition and thrombosis, segmental hyalinization, and endothelial proliferation. It is important to notice that the term "atrophie blanche" is descriptive and it includes not only patients with LV but also patients with a combination of vasculitis and vasculopathy, that is, LV and medium-sized vasculitis such as cutaneous polyarteritis nodosa (PANc). Diagnosis is based on a proper clinicopathological correlation, excluding the main differential diagnosis and considering vasculitis as a mimicker or concomitant diagnosis. Coagulation disorders must also be studied although they are not found in all LV. Its frequency is reviewed as well. Treatment of LV is challenging, and different therapies have been attempted. Among them, pain management, wound care, control of cardiovascular risk factors, and both antiplatelets and anticoagulants, mostly rivaroxaban, are the main therapies used. These different therapies as well as their degree of evidence are reviewed.

Comparative Efficacy of Rivaroxaban and Immunoglobulin Therapy in the Treatment of Livedoid Vasculopathy: A Systematic Review.

Livedoid vasculopathy (LV) is an uncommon chronic coagulation disorder whose underlying etiology is not yet fully understood. It predominantly affects females, especially those in late adolescence. There is currently limited research on treatment options for those with this diagnosis. The present systematic review aims to compare the efficacy of rivaroxaban and intravenous immunoglobulin (IVIG) therapy in the treatment of livedoid vasculopathy. A detailed search was conducted from April 20, 2022, to May 1, 2022, using four databases: Elsevier, Medline Complete, Medline Ovid, and PubMed. Out of these, 20 relevant articles were used, and the data was extracted and analyzed. Both rivaroxaban and IVIG were shown to be effective treatment options with similar treatment response times. However, future large-scale clinical trials are needed to determine an established treatment regimen for these patients.

Livedoid Vasculopathy Secondary to Protein C Deficiency: A Case Successfully Treated With Rivaroxaban

Introduction: Livedoid vasculopathy is a chronic noninflammatory skin disease secondary to hypercoagulable states. No therapeutic guideline has yet been established for livedoid vasculopathy. We herein report a case of livedoid vasculopathy secondary to protein C deficiency that was successfully treated with rivaroxaban. Case presentation: A 31-year-old Thai woman who had been diagnosed with livedoid vasculopathy 10 years previously presented with a 2-month history of worsening leg ulcers and failure to respond to aspirin, colchicine, and pentoxifylline. Further investigations confirmed protein C deficiency. Rivaroxaban was initiated, and clinical improvement was achieved in 8 weeks. Discussion: When livedoid vasculopathy is confirmed by skin biopsy, additional investigations for hypercoagulable states should be performed to exclude secondary causes. Identification of the causes of livedoid vasculopathy can direct physicians to therapeutic options based on previously reported cases of successful treatment. Our patient, whose livedoid vasculopathy was caused by protein C deficiency, responded well to rivaroxaban. Conclusion: Protein C deficiency results in a hypercoagulable state, and affected patients can present with livedoid vasculopathy. The anticoagulant rivaroxaban has been beneficial in the treatment of livedoid vasculopathy.

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

Novel oral anticoagulant (NOAC) medications have revolutionized hematology and cardiology. Recently, NOACs have demonstrated additional promise in dermatology. Specifically, rivaroxaban, a direct factor Xa inhibitor NOAC, has been shown to be successful in the treatment of livedoid vasculopathy. Herein, we describe a patient with systemic lupus erythematosus who presented with painful cutaneous vasculopathy, demonstrated on biopsy with occlusive microvascular fibrin thrombi without evidence of concurrent vasculitis. Interestingly, imaging and laboratory studies did not show evidence of hypercoagulability, arterial disease, or embolic disease. The patient’s vasculopathy and pain progressed despite antiplatelet therapy, often considered first-line in cases of microvascular occlusive disease. However, with rivaroxaban therapy, the patient experienced complete regression of her painful lesions, thereby supporting a further role for NOACs in cutaneous vasculopathy treatment. J Drugs Dermatol. 2020;19(5) doi:10.36849/JDD.2020.4684.

Treatment of livedoid vasculopathy with alprostadil (PGE‐1): case report and review of published literature

Treatment of livedoid vasculopathy with alprostadil (PGE‐1): case report and review of published literature

Treatment of Livedoid Vasculopathy with Short-cycle Intravenous Immunoglobulins

Sir, Livedoid vasculopathy manifests in the form of painful, recurrent ulcers on the lower limbs. The condition is mainly found in young and middle-aged women (1). Histologically, the disorder is characterized by the presence of hyaline thrombi in the cutaneous microcirculation. The underlying pathogenesis is not known, although local or systemic alterations in coagulation control appear to be involved, leading to fibrin thrombus formation in the blood vessels of the superficial dermis. Although sometimes considered synonymous, it is advisable to avoid the terms livedoid vasculitis and segmental hyalinizing vasculitis, as there is no histological evidence of vasculitis (2). The term atrophie blanche should also be avoided, as it is merely descriptive – referring to the formation of whitish scars with telangiectatic margins, although without considering the aetiology or physiology of the lesions. The term livedoid vasculopathy should be reserved for the primary idiopathic presentations of the disease. No controlled comparative studies have been made of the different treatment modalities used. We report here a case of livedoid vasculopathy treated with intravenous immunoglobulins (IVIg).