The Prevalence of Factor V Leiden Mutation in Patients With Leg Ulcers and Venous Insufficiency

Maessen-Visch, M. B.; Hamulyák, Karly; Tazelaar, D.J.; Crombag, N.H.C.M.N.; Neumann, H. A. Martino

doi:10.1001/archderm.135.1.41

Cited by 40 publications

(34 citation statements)

References 26 publications

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“…In this Erythema score after Tx Ulceration score before Tx Ulceration score after Tx Pain score before Tx Pain score after Tx Total clinical score before Tx Total clinical score after Tx 1 3 1 2 1 3 0 8 2 2 3 2 2 0 2 0 7 2 3 3 1 2 1 3 1 8 3 4 2 1 1 0 2 0 5 1 5 3 1 1 1 1 0 5 2 6 2 1 1 0 2 0 5 1 7 2 0 3 0 2 0 7 0 8 context, concomitant protein C deficiency, factor V Leiden mutation, and prothrombin G20210A gene mutation have been reported. [12][13][14][15] However, there was no evidence of abnormal coagulation in our patients. Interestingly, all patients in this trial were longterm cigarette smokers before initiating of IVIg.…”

Section: Discussioncontrasting

confidence: 59%

Pulsed intravenous immunoglobulin therapy in livedoid vasculitis: An open trial evaluating 9 consecutive patients

Kreuter¹,

Gambichler²,

Breuckmann³

et al. 2004

Journal of the American Academy of Dermatology

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Section: Discussioncontrasting

confidence: 59%

Pulsed intravenous immunoglobulin therapy in livedoid vasculitis: An open trial evaluating 9 consecutive patients

Kreuter¹,

Gambichler²,

Breuckmann³

et al. 2004

Journal of the American Academy of Dermatology

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“…Although the mutant allele is found at a frequency of approximately 5% in Caucasian populations, the prevalence of this SNP in patients with recognized venous thrombosis is as high as 30% (11), whereas in the group of CVU-suffering individuals it ranges between 8 and 36%, depending on the estimated population size (11,17). Heterozygotes present a 8-fold increased risk of DVT.…”

Section: Factor V Leiden Polymorphismmentioning

confidence: 99%

“…Heterozygotes present a 8-fold increased risk of DVT. However, homozygous patients (approximately 1% of patients with the factor V Leiden variant) display a 100-fold higher risk of developing DVT and present a more severe clinical condition than those carrying the wild-type factor V gene (17)(18)(19).…”

Section: Factor V Leiden Polymorphismmentioning

confidence: 99%

Genetic risk factors of chronic venous leg ulceration: Can molecular screening aid in the prevention of chronic venous insufficiency complications?

Grzela¹

2010

Mol Med Rep

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Abstract. Venous leg ulceration is a severe complication of chronic venous insufficiency. Despite numerous studies, understanding of the possible mechanisms involved in venous ulceration development remains incomplete. It is assumed that, in addition to well-documented behavioral and/or environmental conditions, as yet poorly defined genetic risk factors may play important roles in chronic wound progression or healing. It is difficult to overestimate the clinical usefulness of genetic screening in the determination of the risk of wound development and/or its healing course. From a pharmacogenomic perspective, genetic screening may aid in the planning of individualized treatment. In addition, the detection of venous ulcer-promoting gene variants may facilitate the decision to introduce prophylaxis or, if necessary, appropriate treatment for venous insufficiency, long before a leg ulcer develops. In addition to significant economic benefits, this approach would reduce the risk of health-and life-threatening conditions. In this review, we focus on several gene mutations/polymorphisms with previously documented significance in leg ulceration pathophysiology, and briefly speculate about possible candidates for further study.

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“…(3,14 ) (See table 1) Exercise programs, the use of compression stockings, smoking cessation and avoidance of estrogen therapies can greatly reduce risks of recurrent DVT. Long term anticoagulation may be necessary in these patients.…”

Section: Investigating Leg Ulcers Non-invasive Investigations Venous mentioning

confidence: 99%

Diagnosis Of Leg Ulcers

2002

IJD

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In the United States, leg ulcers present a significant clinical problem, occurring at a rate of approximately 600,000 new cases per year. (1) The most common types are venous, arterial, and neuropathic ulcers. Venous hypertension is the primary culprit in venous ulcerations. Peripheral vascular disease due to atherosclerosis with microvascular or macrovascular changes leads to ischemic ulcers. Sensory impairment with loss of protective sensation in the foot and repetitive trauma lead to neuropathic ulcers. Unusual causes of leg ulcers must be considered in the differential diagnosis. To arrive at the diagnosis, the clinician must perform a thorough history and physical examination, and order relevant investigative studies. Good management of chronic leg ulcers depends on correction of identified underlying conditions, long-term multidisciplinary care effort, and integrating traditional and new wound-healing technologies. Most patients with chronic leg ulcers benefit from the use of compression bandaging at a level appropriate to their vascular status. Venous ulcers must be managed with an arsenal of strategies to control venous insufficiency, heal the wound, and prevent recurrence. Surgery with revascularization remains the treatment of choice for chronic ischemic leg ulcers. In the absence of vascular compromise, up to 90 percent of neuropathic ulcers will heal with proper ulcer debridement, treatment of infection, saline wet-to-dry dressings, and relief of weight from the ulcerated area. The available armamentarium for wound care includes over 2000 wound dressing products and elastic compression wraps. Chronic leg ulcer treatment options have been expanded by alternatives available to treating these wounds. These alternatives include hyperbaric oxygen therapy, bioengineered skin substitutes, recombinant platelet-derived growth factors and vacuum assisted wound closure. Patients with large leg ulcers may benefit from skin grafting. Other patients may benefit from ligation and stripping of superficial veins or subfascial interruption of perforating veins.

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The Prevalence of Factor V Leiden Mutation in Patients With Leg Ulcers and Venous Insufficiency

Cited by 40 publications

References 26 publications

Pulsed intravenous immunoglobulin therapy in livedoid vasculitis: An open trial evaluating 9 consecutive patients

Pulsed intravenous immunoglobulin therapy in livedoid vasculitis: An open trial evaluating 9 consecutive patients

Genetic risk factors of chronic venous leg ulceration: Can molecular screening aid in the prevention of chronic venous insufficiency complications?

Diagnosis Of Leg Ulcers

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