Fibrin- and fibrinogen-related antigens in patients with venous disease and venous ulceration

Falanga, Vincent

doi:10.1001/archderm.127.1.75

Cited by 16 publications

(8 citation statements)

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“…Fibrin and fibrinogen have a direct down-regulatory effect on procollagen type I synthesis (7). Our results support the therapeutic relevancy of enhancing fibrinolysis in patients with venous disease (9; 10). Conversely, we have shown that keratinocytes attach and spread well in fibrin that is fully cross-linked (11).…”

Section: Discussionsupporting

confidence: 81%

Evaluation of dermal pericapillary fibrin cuffs in venous ulceration using confocal microscopy

Kobrin

Thompson

Scheur

et al. 2008

Wound Repair Regeneration

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Dermal pericapillary fibrin is a hallmark of venous disease and is thought to play a pathogenic role in the development of ulceration. However, the actual spatial configuration of pericapillary fibrin is unknown, and it remains unclear whether it truly represents a barrier that can impair physiological exchanges between the blood and dermis. Using confocal microscopy on tissue specimens taken from the edges of venous ulcers in six patients, we report a detailed analysis of dermal pericapillary fibrin deposits. Sections were evaluated with an antibody to human fibrinogen/fibrin and viewed, vertically and horizontally, with confocal microscopy. The distribution of fibrin deposition was highly variable and patchy, with areas of great intensity next to others of marginal intensity. Vertical cut sections showed the highest concentration of fluorescent material next to the lumen of dermal capillaries. Horizontal sections showed that maximal fluorescence was distributed at random. Our findings indicate that fibrin deposits in venous ulcers are patchy and discontinuous around dermal vessels. As such, these deposits are unlikely to act as a true and stable anatomic barrier as originally proposed. However, pericapillary fibrin may still act as a physiological barrier under conditions of poor blood flow where even marginal or patchy fibrin deposition might have a greater effect on the exchange of oxygen and other nutrients between blood and dermis.

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Section: Discussionsupporting

confidence: 81%

Evaluation of dermal pericapillary fibrin cuffs in venous ulceration using confocal microscopy

Kobrin

Thompson

Scheur

et al. 2008

Wound Repair Regeneration

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“…The latter was also using oral hormonal contraceptives. Venous insufficiency regardless of accompanying ulceration, mildly enhances D-dimer levels 22, 23 . Moreover, slight elevation of D-dimer levels occurs in patients taking hormonal contraceptives, with mean level increasing from 0.172μg/ml to 0.351μg/ml, which is still within the normal limits (< 0.5μg/ml) 24–26 .…”

Section: Commentsmentioning

confidence: 99%

Elevated D-dimer Level in the Differential Diagnosis of Venous Malformations

Dompmartin¹,

Ballieux²,

Thibon³

et al. 2009

Arch Dermatol

137

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“…The presence of the perivascular ‘fibrin cuff’ (with other components) is a reflection of the inflammatory process and is seen in other chronic inflammatory conditions. In patiens with venous disease, increased plasma D dimer levels have been observed, suggesting enhanced deposition of fibrin [32]. The perturbed state of the endothelium allows the passage of large molecules through the endothelium permitting their perivascular accumulation and explains the presence of the ‘fibrin cuff’.…”

Section: Histological Studiesmentioning

confidence: 99%

Neutrophil Activation and Mediators of Inflammation in Chronic Venous Insufficiency

Smith¹

1999

J Vasc Res

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The effect of venous hypertension on the state of activation of leucocytes has been investigated in patients with venous disease and control subjects. Leucocytes become ‘trapped’ in the circulation of the leg during periods of venous hypertension produced by sitting or standing. This is greater in the limbs of patients with chronic venous disease than controls. Studies of the plasma levels of neutrophil granule enzymes show that these are increased during periods of venous hypertension, suggesting that this causes activation of the neutrophils. Investigation of the leucocyte surface ligand CD11b shows that the more activated neutrophils and monocytes are sequestered during venous hypertension. Measurement of plasma levels of the soluble parts of the vascular (VCAM), intercellular (ICAM) and endothelial leucocyte (ELAM) adhesion molecules show that these are all elevated in patients with chronic venous disease compared to controls. Following 30 min of venous hypertension produced by standing, these levels are further increased. These data suggest that venous hypertension causes neutrophil and monocyte activation, which in turn causes injury to the endothelium. I believe that this may be the mechanism that initiates the pathological processes which lead to venous ulceration. It has recently been shown that the venotonic drug Daflon 500 mg (450 mg diosmin, 50 mg hesperidin, Servier, France) influences these processes. Surface expression of CD62L is reduced in neutrophils and monocytes, and plasma levels of soluble endothelial adhesion molecules are reduced. These observations may explain the anti-inflammatory effects of Daflon 500 mg.

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Fibrin- and fibrinogen-related antigens in patients with venous disease and venous ulceration

Cited by 16 publications

References 0 publications

Evaluation of dermal pericapillary fibrin cuffs in venous ulceration using confocal microscopy

Evaluation of dermal pericapillary fibrin cuffs in venous ulceration using confocal microscopy

Elevated D-dimer Level in the Differential Diagnosis of Venous Malformations

Neutrophil Activation and Mediators of Inflammation in Chronic Venous Insufficiency

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