Livedoid Vasculopathy Treatment & Management
- Author: Noah S Scheinfeld, MD, JD, FAAD; Chief Editor: William D James, MD more...
Medical Care
While ruling out the various disease states that have been associated with livedoid vasculopathy, physicians can offer a number of therapies that have been very helpful in reducing pain and ulceration. Instituting treatment as soon as possible is best. Note the following:
- Pentoxifylline (Trental) (400 mg 3 times/d) may be effective. Pentoxifylline is believed to enhance the blood flow in the capillaries. The blood flow enhancement is attributed to making red blood cells more flexible and thereby reducing viscosity.[26]
- In 2003, Hairston et al[27] described treatment of livedoid vasculopathy with low molecular weight heparin (LMWH).
- As reported by Yang et al[28] in 2003, intractable livedoid vasculopathy was successfully treated with hyperbaric oxygen therapy. Additionally, Juan et al[29] reported a study of 12 subjects with active livedoid vasculopathy. Subjects received hyperbaric oxygen therapy 5 times/wk. Eight completed the study. Resumption of ambulation and reduction of analgesics were achieved after an average of 4.9 hyperbaric oxygen therapy sessions. Leg ulcers healed completely in these 8 subjects at a mean of 3.4 weeks (range, 2-5 wk). Six patients had relapses of ulceration and responded to additional hyperbaric oxygen therapy. No patients had adverse effects.
- Also in 2003, Marzano et al[19] noted a good clinical response was obtained using intravenous methylprednisolone combined with pentoxifylline for wide spread livedoid vasculopathy.
- Dipyridamole (Persantine) (75 mg 4 times/d) with up to 325 mg of aspirin per day is reported to reduce pain after 3-6 weeks of therapy. Similar results have been reported using 50 mg of dipyridamole 3 times a day and 325 mg of aspirin once a day.[30] Note that aspirin is not to be administered in conjunction with coumarin anticoagulants. Dipyridamole is not considered safe in children or breastfeeding mothers.
- Nifedipine (Procardia) (20 mg 3 times/d) is reported to maintain perfusion in the superficial vessels; therefore, the deposition of fibrin in the vessel walls is impeded.[31]
- Deng et al[7] noted that livedoid vasculopathy associated with plasminogen activator inhibitor-1 (PAI-1) promoter homozygosity (4G/4G) was effectively abated with tissue-type plasminogen activator (tPA). Antunes et al also reported on livedoid vasculopathy associated with PAI-1 promoter homozygosity (4G/4G) and prothrombin G20210A heterozygosity that responded to tPA treatment.[32]
- Some reports have noted that intravenous immunoglobulin can be useful in treating atrophie blanche and livedoid vasculopathy, but this remains an experimental treatment.[33]
- The combination of phenformin and ethylestrenol, which enhances endogenous blood fibrinolytic activity by increasing plasminogen activating enzymes, has been suggested as a treatment.
- Browning and Callen[34] reported that warfarin is a useful and effective treatment for livedoid vasculopathy associated with cryofibrinogenemia and hyperhomocysteinemia. Kavala et al reported successful warfarin therapy in livedoid vasculopathy associated with factor V Leiden mutation.[35] Additionally, Davis and Wysokinski reported that livedoid vasculopathy associated with a prothrombotic state responded to warfarin.[36]
- Some reports have noted the use of heparin,[37] LMWH, psoralen plus ultraviolet A (PUVA), and low molecular weight dextran.
- If ulcers are superinfected, they should be treated with oral antibiotics.
- Meiss et al[8] noted that hyperhomocysteinemia can be another cause of hypercoagulability and livedoid vasculopathy and that the combination of folic acid, vitamin B-12, and vitamin B-6 (cofactors of homocysteine metabolism) is an effective treatment for hyperhomocysteinemia, hypercoagulability, and livedoid vasculopathy.
Consultations
To fully evaluate for the comorbid conditions of livedoid vasculopathy, consult a hematologist (to evaluate for factors that lead to hypercoagulable states) and vascular surgeons (to evaluate and treat underlying defects of coagulation).
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