Nonhealing ulcer secondary to factor V Leiden mutation and cryofibrinogenemia

Barrio, Victoria R.; Sanfilippo, Angela M; Malone, Janine C.; Callen, Jeffrey P.

doi:10.1016/j.jaad.2004.04.043

Cited by 14 publications

(5 citation statements)

References 13 publications

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“…Chronic ulcerations can develop into malignancies 57 . When ulcers are resistant to any therapy, the cause may be pyoderma gangrenosum 63 or a mutation of factor V Leiden (one of the coagulation factors in human blood) and cryofibrinogenaemia (cryofibrinogen is a precipitate formed in plasma of fibrin, fibrinogen and fibronectin by in vivo occlusion of small blood vessels) 64 …”

Section: Resultsmentioning

confidence: 99%

Skin problems in lower limb amputees: an overview by case reports

Meulenbelt

Geertzen

Dijkstra

et al. 2006

Acad Dermatol Venereol

101

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The stump in lower limb amputees is prone to skin problems because it is exposed to several unnatural conditions (shear and stress forces and increased humidity) when a prosthesis is used. This study reviews the literature on case reports of lower limb amputees with skin problems on the stump. In total, 56 reports comprising 76 cases were identified in the literature. The main disorders are acroangiodermatitis, allergic contact dermatitis, bullous diseases, epidermal hyperplasia, hyperhidrosis, infections, malignancies and ulcerations.

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Section: Resultsmentioning

confidence: 99%

Skin problems in lower limb amputees: an overview by case reports

Meulenbelt

Geertzen

Dijkstra

et al. 2006

Acad Dermatol Venereol

101

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“…Anabolic steroids, perhaps due to their being used by athletes, are probably underutilized as therapeutic agents. Other promising uses of this class of agents in challenging conditions include livedoid vasculitis, 27 cryofibrinogenemia associated with factor V Leiden mutation, 28 and skin popping of illicit drugs in HIV patients. 29…”

Section: Discussionmentioning

confidence: 99%

Liver Enzymes and Lipid Levels in Patients With Lipodermatosclerosis and Venous Ulcers Treated With a Prototypic Anabolic Steroid (Stanozolol)

Carson

Hong

Otero-Viñas

et al. 2015

The International Journal of Lower Extremity Wounds

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Anabolic steroids have been used to treat lower extremity ulcerations, including venous and cryofibrinogenemic ulcers and lipodermatosclerosis (LDS). Yet there have been no studies to determine the severity and reversibility of side effects of anabolic steroids on liver enzymes and lipid profiles in elderly patients. We therefore evaluated, in a prospective, randomized, double-blinded, placebo-controlled trial, the extent and reversibility of abnormal liver enzymes and lipid profiles in patients with LDS and venous leg ulcers treated with stanozolol at 2 mg twice daily for up to 6 months. Follow-up laboratory testing was done for 2 months after cessation of treatment. A total of 44 patients with LDS and venous ulcers were enrolled and treated with either leg compression alone (placebo) or leg compression plus oral stanozolol 2 mg twice daily (active). Baseline and follow-up laboratory testing of liver enzymes and lipid profiles were obtained. A total of 21 active and 23 placebo patients were treated and evaluated. We measured liver enzymes (aspartate aminotransferase [AST/SGOT], alanine aminotransferase [ALT/SGPT], γ-glutamyl transferase [GGT]) and lipid profile components (high-density lipoprotein [HDL], low-density lipoprotein [LDL], total cholesterol) before, during, and after the treatment period. We found that AST/SGOT and ALT/SGPT became significantly elevated in 29% (P = .0415 at 2 months) and 33% (P = .0182 at 1 month) of patients treated with stanozolol or placebo, respectively, with return to baseline in the posttreatment period. Unexpectedly, 91% of patients on stanozolol developed a significant (P < .0001) decrease in HDL levels, by as much as 37 U/L. All patients remained asymptomatic and levels returned to baseline after discontinuation of the drug. We conclude that low-dose stanozolol, 2 mg twice daily, produces asymptomatic and temporary elevation of liver transaminases and depression of the HDL level in a significant proportion of patients.

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“…Histopathology analyses reveal damage to the microvasculature with fibrin thrombi in the post-capillary venules and small veins and diffuse but non-specific necrosis of the dermis and subcutaneous tissues [36,[52][53][54][55][56][57].…”

Section: Warfarin-induced Cutaneous Necrosismentioning

confidence: 99%

Thrombophilia: the dermatological clinical spectrum

Criado¹,

Duarte²,

Magalhães³

et al. 2016

Glob Dermatol

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The aim of this article is to review the hypercoagulable states (thrombophilia) most commonly encountered by dermatologists, as well as their cutaneous signs, including livedo racemosa, cutaneous necrosis, digital ischemia and ulcerations, reticulated purpura, leg ulcers, and other skin conditions. Recognizing these cutaneous signs is the first step to proper treatment. Our aim is to describe which tests are indicated, and when, in these clinical settings.

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Nonhealing ulcer secondary to factor V Leiden mutation and cryofibrinogenemia

Cited by 14 publications

References 13 publications

Skin problems in lower limb amputees: an overview by case reports

Skin problems in lower limb amputees: an overview by case reports

Liver Enzymes and Lipid Levels in Patients With Lipodermatosclerosis and Venous Ulcers Treated With a Prototypic Anabolic Steroid (Stanozolol)

Thrombophilia: the dermatological clinical spectrum

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