fibrin has been researched along with Leg-Ulcer* in 19 studies
3 review(s) available for fibrin and Leg-Ulcer
Article | Year |
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Understanding the aetiology of leg ulcers.
Topics: Fibrin; Humans; Leg Ulcer; Risk Factors; Urokinase-Type Plasminogen Activator | 1996 |
Etiology of venous ulceration.
The etiology of venous ulceration is far more complex than Homans' theory of stagnation and hypo-oxygenation. Indeed, studies have shown that flow in lipodermatosclerotic limbs is actually faster than normal. We suggest, therefore, that the terms "stasis dermatitis" and "stasis ulcer" be dropped from medical parlance. The term "lipodermatosclerosis with ulceration" as used by the British, or simply "venous ulcer," would seem more appropriate. Venous hypertension, produced by incompetence of deep and communicating vein valves and thrombosis of segments of the deep system, is closely correlated with the development of venous ulcers. Precisely how this venous hypertension translates into ulceration is unclear. Burnand et al showed that fibrin cuffs are deposited around the capillaries in lipodermatosclerotic limbs. These cuffs may serve as barriers to the diffusion of oxygen, leading to local ischemia and epidermal necrosis. Others suggest that trapped leukocytes in the microcirculation alter capillary permeability by releasing various inflammatory mediators that hasten the flow of fibrinogen across the capillary membrane and promote the formation of fibrin cuffs. Proof of this hypothesis is still lacking, but may eventually come from using radioactive WBC tagging procedures. A synthesis of these two theories may in fact explain the etiology of venous ulceration. Topics: Capillary Permeability; Cell Hypoxia; Chronic Disease; Fibrin; Fibrinogen; Humans; Hypertension; Leg Ulcer; Leukocytes; Microcirculation; Necrosis; Terminology as Topic; Thrombosis; Venous Insufficiency; Venous Pressure | 1993 |
Dowling oration 1975. Fibrinolysis and vasculitis.
Topics: Administration, Topical; Adolescent; Adult; Aged; Anabolic Agents; Animals; Child; Child, Preschool; Chronic Disease; Endothelium; Ethylestrenol; Female; Fibrin; Fibrinolysin; Fibrinolysis; Follow-Up Studies; Histocytochemistry; Humans; Inflammation; Leg Ulcer; Male; Middle Aged; Phenformin; Purpura; Rats; Skin Diseases; Thrombophlebitis; Vascular Diseases; Wound Healing | 1976 |
16 other study(ies) available for fibrin and Leg-Ulcer
Article | Year |
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Locomotion of human skin keratinocytes on polystyrene, fibrin, and collagen substrata and its modification by cell-to-cell contacts.
Epithelial wound repair assures the recovery of the epithelial barrier after wounding. During wound healing epithelial cells migrate to cover the wound surface. The presented experiments were carried out to compare the migration of human keratinocytes from primary and secondary culture on polystyrene, collagen, and fibrin glue used in clinical techniques. The images of migrating keratinocytes were recorded and analyzed using computer-aided methods. The results show that the character of the substrate strongly affects the speed and turning behavior of keratinocytes locomoting over it. The highest motile activity of human skin keratinocytes was found on fibrin glue substratum. It was found that locomotion of freely moving isolated cells was much faster than that of cell sheets. The autologous keratinocytes cultured in vitro were applied with fibrin glue to cover trophic wounds. The transplantation of human autologous keratinocyte suspension in fibrin glue upon long-lasting trophic wounds appeared to induce rapid and permanent wound healing. Topics: Cell Communication; Cell Movement; Cells, Cultured; Collagen; Fibrin; Fibrin Tissue Adhesive; Humans; Keratinocytes; Kinetics; Leg Ulcer; Polystyrenes; Skin; Wound Healing | 2001 |
Venous ulceration.
Topics: Fibrin; Fibrinogen; Growth Substances; Humans; Leg Ulcer; Macromolecular Substances; Transforming Growth Factor beta | 1993 |
The occurrence of pericapillary fibrin in venous hypertension and ischaemic leg ulcers: a histopathological study.
The presence of pericapillary fibrin and complement C3c in the ulcers of 19 patients with venous hypertension and 14 patients with ischaemic leg ulcers was investigated using histochemical and immunohistochemical techniques. There was deposition of fibrin around the capillaries in the central part of the ischaemic ulcers, and the venous hypertension ulcers, and in the non-ulcerated skin around one of the venous hypertension ulcers and two of the ischaemic leg ulcers. The deposition of fibrin is a secondary phenomenon that occurs in the area of ulcerated skin and does not play a major causal role in the formation of chronic leg ulcers. Topics: Aged; Aged, 80 and over; Capillaries; Complement System Proteins; Female; Fibrin; Humans; Ischemia; Leg; Leg Ulcer; Male; Middle Aged; Venous Pressure | 1992 |
Factor XIII-deficiency in the blood of venous leg ulcer patients.
Pericapillary fibrin cuffs are probably involved in the pathogenesis of venous leg ulcers. Factor XIII (Fibrin stabilizing factor) is of importance in wound healing. Its activity, which may affect ulceration, was found to be significantly reduced in the blood of venous leg ulcer patients and in post-phlebitic patients, compared with healthy controls. Topics: Chronic Disease; Factor XIII; Factor XIII Deficiency; Fibrin; Humans; Leg Ulcer; Postphlebitic Syndrome; Varicose Ulcer; Wound Healing | 1991 |
Pericapillary fibrin cuff: a histological sign of venous leg ulceration.
The incidence of pericapillary fibrin cuffs was investigated in 49 biopsies of venous leg ulcers and 67 biopsies of leg ulcers of non-venous etiology. Pericapillary fibrin cuffs were seen in 28 biopsies (57.1%) of venous leg ulcers, but only in 11 biopsies (16.4%) of non-venous leg ulcers. In the venous leg ulcers pericapillary fibrin cuffs occurred predominantly near the ulcer surface and around dilated capillaries. Dilation of the capillaries and inflammation probably contribute more to the pathogenesis of pericapillary fibrin cuffs than venous hypertension. Topics: Capillaries; Fibrin; Humans; Leg Ulcer; Skin; Thrombophlebitis; Varicose Ulcer | 1990 |
Biochemical and biological profile of a new enzyme preparation from Antarctic krill (E. superba) suitable for debridement of ulcerative lesions.
A protease extract from Antarctic krill (E. superba) intended as a new enzymatic debrider for necrotic ulcers has been characterized by sodium dodecyl sulphate polyacrylamide gradient gel electrophoresis and fast protein liquid chromatography. The predominant enzymes in the preparation represent trypsin-like activity associated with three serine proteinases. In addition two carboxypeptidases A and B are present as cooperative enzymes for a more complete breakdown of complex proteinaceous substrates. Biological studies on a well-defined substrate (fibrin) originating from leg ulcers, demonstrated more effective degradation by krill enzymes than bovine trypsin, a common component in marketed enzymatic debriders. These findings support previously in vitro/in vivo studies in an animal model (rat) using excised rat skin as "necrotic" tissue. Topics: Animals; Carboxypeptidase B; Carboxypeptidases; Carboxypeptidases A; Chromatography, High Pressure Liquid; Crustacea; Electrophoresis, Polyacrylamide Gel; Enzyme Therapy; Enzymes; Fibrin; Humans; Leg Ulcer; Trypsin | 1989 |
Investigations on the pathogenesis of venous leg ulcers.
Based on a prospective study of 92 patients with DVT initiated in 1979, including a follow-up every year, the following investigations were performed: phlebography, Doppler-ultrasound, plethysmography (strain gauge and PPG) and foot-volumetry. In ulcer-patients skin blood flow was measured by Laser-Doppler and local oxygen supply by measurement of transcutaneous oxygen. Transcapillary protein-leakage was assessed by isotopic methods, local lymph-drainage by isotopic lymphography and indirect x-ray lymphography. From the results of these investigations the following course of events, which may be of importance for the development of venous ulceration, can be outlined: 1. Venous refluxes penetrating into the venules of the skin. 2. Chronic venous ambulatory hypertension (lack of pressure-fall during walking), waves of high pressure in the capillaries. 3. Protein-rich oedema. 4. Failure of fibrin clearance from the pericapillary space due to inadequate (exhausted?) fibrinolysis and deficient local lymph drainage. 5. Resulting changes in the ground substance, proliferation of fibres. 6. Local hypoxia due to a diffusion block by the impermeable pericapillary cuffs, partially due to a reduction of capillaries in the superficial layers. Topics: Blood Proteins; Capillary Permeability; Fibrin; Follow-Up Studies; Humans; Leg; Leg Ulcer; Lymph; Oxygen; Phlebography; Plethysmography; Postphlebitic Syndrome; Prospective Studies; Skin; Ultrasonography; Venous Insufficiency; Venous Pressure | 1988 |
The aetiology of venous ulceration.
Topics: Arteriovenous Fistula; Capillary Permeability; Fibrin; Fibrinogen; Fibrinolysis; Humans; Leg Ulcer; Oxygen; Postphlebitic Syndrome; Venous Insufficiency; Venous Pressure | 1988 |
Familial atrophie blanche-like lesions with subcutaneous fibrinoid vasculitis. The Georgian ulcers.
Atrophie blanche is an uncommon condition characterized by the development of white atrophic patches of skin on the lower extremities, which form as a result of fibrinoid vasculitis of superficial and mid-dermal vessels followed by necrosis and ulceration of the epidermis. We report four cases in which similar lesions developed on the legs and ankles of young Jewish Russian immigrants to Israel. Although the lesions share many features with atrophie blanche, they differ in their early age of onset, the male predilection, and the extension of the fibrinoid vasculitic process into the subcutaneous tissue. Additionally, the peculiar population clustering (Georgia, U.S.S.R.), common ethnic background, and a family history of similar lesions in close relatives seem to point to a familial or genetic predisposition underlying the development of the disease. Topics: Adolescent; Adult; Atrophy; Biopsy; Capillaries; Female; Fibrin; Humans; Leg Ulcer; Male; Necrosis; Skin; Skin Ulcer; Vasculitis | 1986 |
Stellate fibrin-fibronectin microclot formation from keratinocytes and fibroblasts stimulated by plasma from patients with psoriasis.
Plasma from patients with active psoriasis has been shown to induce the formation of stellate fibrin-fibronectin microclots in vitro around cultured keratinocytes and fibroblasts. Such a stellate radiation of fibronectin and fibrin was also demonstrated around monocytes from patients with psoriasis. The phenomenon was not observed in healthy subjects but has been found in various disorders. Topics: Adolescent; Adult; Aged; Cells, Cultured; Eczema; Epidermal Cells; Fibrin; Fibroblasts; Fibronectins; Fluorescent Antibody Technique; Humans; Leg Ulcer; Middle Aged; Psoriasis | 1985 |
Venous hypertension, fibrin and leg ulcers.
Topics: Adult; Animals; Child; Dogs; Fibrin; Fibrinolytic Agents; Humans; Hypertension; Leg Ulcer; Oxygen Consumption; Stanozolol; Thrombophlebitis; Venous Pressure | 1983 |
Pericapillary fibrin in the ulcer-bearing skin of the leg: the cause of lipodermatosclerosis and venous ulceration.
Forty-one biopsy specimens, taken from the ulcer-bearing skin of 41 legs of 21 patients attending the varicose vein clinic, were selectively stained for fibrin with phosphotungstic acid haemotoxylin before being blindly assessed,. Layers of fibrin were found surrounding the dermal capillaries in all 26 legs with lipodermatosclerosis. None of the specimens from the 15 legs with clinically normal skin contained fibrin. There was also an increased number of dermal capillaries cut in cross section per high powered field in 24 of the 26 legs with lipodermatosclerosis compared with two of the 15 legs with normal skin (p less than 0.001). The mean reduction in foot vein pressure during exercise was significantly less in the 26 limbs with pericapillary fibrin than in the other 15 limbs (p less than 10(-6). Lipodermatosclerosis is synonymous with pericapillary fibrin deposition and is associated with, and probably secondary to, both a persistently raised venous pressure and an increase in the size of the dermal capillary bed. This extravascular deposition of fibrin probably stimulates tissue fibrosis and blocks the diffusion of oxygen to the overlying epidermis, producing cellular death and venous ulceration. Topics: Capillaries; Female; Fibrin; Humans; Leg Ulcer; Male; Scleroderma, Localized; Skin; Varicose Ulcer | 1982 |
Why do skin grafts fail?
Fibrin is shown to be the agent responsible for the adherence of biological dressings and of autografts to wounds. Its presence is associated with graft success, and its absence with graft failure. The results suggest that the deposition of fibrin provides the basis for the anti-bacterial actions of biological dressings and for the sterilization of the wound under adherent autografts. The total number of bacteria per gram of tissue in the wound, though important, is not critical to the result of skin grafting. The mechanism by which different organisms cause grafts to fail is by the production of plasmin and proteolytic enzymes which dissolve the important fibrin scaffold--thus ensuring their own survival. Thus, it is the levels of these (and the numbers of organisms efficient in producing them) which cause success or failure of applied skin grafts. Topics: Aged; Biological Dressings; Burns; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Graft Rejection; Humans; Leg Ulcer; Male; Middle Aged; Peptide Hydrolases; Skin Transplantation; Transplantation, Autologous; Transplantation, Heterologous; Wound Healing; Wound Infection | 1979 |
Wound healing and fibrinolytic activity.
Topics: Fibrin; Fibrinolysis; Humans; Leg Ulcer; Plasminogen; Streptokinase; Wound Healing | 1973 |
[On local fibrinolysis in leg ulcer].
Topics: Antifibrinolytic Agents; Benzoates; Fibrin; Fibrinolysis; Hot Temperature; Humans; Leg Ulcer; Peptide Hydrolases | 1968 |
[Treatment of chronic pyococcal leg ulcers with the use of perforated fibrin film].
Topics: Fibrin; Humans; Leg Ulcer; Staphylococcal Infections | 1965 |