Treatment of Livedoid Vasculopathy with Short-cycle Intravenous Immunoglobulins

Pitarch, Gerard; Rodríguez‐Serna, Mercedes; Torrijos, Arantxa; Oliver, V.; Fortea, José M.

doi:10.1080/00015550510027865

Cited by 9 publications

(19 citation statements)

References 7 publications

(6 reference statements)

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“…Clinical improvement were also reported using novel treatments, including tissue plasminogen activator [13,22], intravenous immunoglobulin [23], and the prostacyclin analogue, iloprost [24]. Our patient was refractory to the initial dapsone and hydroxychloroquine treatment, and prednisone inclusion did not show any improvement.…”

Section: Discussionsupporting

confidence: 53%

Livedoid vasculopathy associated with combined prothrombin G20210A and factor V (Leiden) heterozygosity and MTHFR C677T homozygosity

Irani-Hakime

Stephan

Kreidy

et al. 2008

J Thromb Thrombolysis

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Livedoid vasculopathy (LV) is an occlusive thrombotic disease of lower extremities. A 34-year-old woman presented with 4-year history of recurrent necrotic and painful lesions with violaceous and purpuric border on both legs. Initial treatment with hydroxychloroquine, dapsone and prednisone were unsuccessful. Skin biopsy showed inflammatory infiltrate with epidermal necrosis. Prothrombin G20210A and factor V-Leiden heterozygosity, and MTHFR C677T homozygosity with hyperhomocysteinemia were confirmed. LV diagnosis was made; acetylsalicylic acid, folic acid, vitamin B12, and prednisone treatement resulted in complete healing. This is the first report on coexistence of prothrombin G20210A, factor V-Leiden, and homozygous MTHFR C677T with hyperhomocysteinemia in LV.

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Section: Discussionsupporting

confidence: 53%

Livedoid vasculopathy associated with combined prothrombin G20210A and factor V (Leiden) heterozygosity and MTHFR C677T homozygosity

Irani-Hakime

Stephan

Kreidy

et al. 2008

J Thromb Thrombolysis

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“…steroid has little or no effect in LV . Many therapeutic strategies have been employed, including drugs stimulating endogenous fibrinolytic activity (danazol), antiplatelet agents (aspirin, dipyridamole, cilostazol, clopidogrel, ticlopidine hydrochloride), vasodilators (nifedipine, cilostazol, nicotinic acid), hemorheologicals (pentoxifylline), anticoagulants (warfarin, enoxaparin), modulation of lymphocyte response (phototherapy UVA, cyclosporine A, methotrexate, azathioprine, colchicine, sulfasalazine), prostanoids (alprostadil, beraprost, iloprost), oral factor‐X inhibitor (rivaroxaban), hyperbaric oxygen, and IVIg .…”

Section: Discussionmentioning

confidence: 99%

Pulsed intravenous immunoglobulin therapy in refractory ulcerated livedoid vasculopathy: seven cases and a literature review

Kim

Yoon

Park

et al. 2015

Dermatologic Therapy

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Livedoid vasculopathy (LV) is a thrombotic vasculopathy of the skin of unknown origin. No treatment has been validated in this indication, but case reports demonstrated successful use of intravenous immunoglobulins (IVIg) in LV. We assessed the efficacy and tolerability of 2 g/kg IVIg therapy every month for 2∼3 cycles in patients with refractory LV. We analyzed the efficacy, side effects and recurrence after long-term follow-up (51.9 ± 14.0 months) in seven patients with LV treated with 2 g/kg of IVIg. Mean clinical score of sum of erythema, ulceration and pain index (each: 0-3) was 5.7 ± 0.9 before the therapy and significantly lower after therapy (1.1 ± 0.5) (p = 0.001). Even after just one cycle of IVIg, the score decreased significantly from 5.7 ± 0.9 to 3.7 ± 0.9 (p = 0.002), especially the pain score. In one patient, LV has not recurred for over 7 years; six patients experienced recurrence after a mean of 12.7 ± 2.8 months. Out of the six patients, two patients were re-administered IVIg whereas the others were well controlled by conventional therapy. We propose that IVIg is a rapid, effective, and safe therapeutic option in LV refractory to other treatment modalities.

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“…Proposed mechanisms of actions of IVIG include: (i) the modulation of Fc receptor expression; (ii) the elimination of circulating immune complexes and autoantibodies; (iii) the inhibition of complement‐mediated damage; (iv) the modulation of cytokine production and release; (v) the blockade of Fas ligand; and (vi) the reduction of thromboxane A2 and endothelin (prothrombotic and vasoconstrictor) synthesis accompanied by an increase in prostacyclin secretion . Some authors have reported the successful use of IVIG in LV . Seventeen cases of ulcerated LV treated with IVIG have been described to date (Table ).…”

Section: Discussionmentioning

confidence: 99%

“…Therapeutic strategies include the use of antithrombotic, anti‐inflammatory, or immunosuppressive agents, which have varying degrees of efficacy. Encouraging case reports about the successful use of intravenous immunoglobulins (IVIG) in LV have been published . We report five patients who received IVIG for treatment‐resistant ulcerated LV.…”

Section: Introductionmentioning

confidence: 99%

Intravenous immunoglobulins in difficult‐to‐treat ulcerated livedoid vasculopathy: five cases and a literature review

et al. 2013

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Treatment of Livedoid Vasculopathy with Short-cycle Intravenous Immunoglobulins

Cited by 9 publications

References 7 publications

Livedoid vasculopathy associated with combined prothrombin G20210A and factor V (Leiden) heterozygosity and MTHFR C677T homozygosity

Livedoid vasculopathy associated with combined prothrombin G20210A and factor V (Leiden) heterozygosity and MTHFR C677T homozygosity

Pulsed intravenous immunoglobulin therapy in refractory ulcerated livedoid vasculopathy: seven cases and a literature review

Intravenous immunoglobulins in difficult‐to‐treat ulcerated livedoid vasculopathy: five cases and a literature review

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