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Vincent Falanga - One of the best experts on this subject based on the ideXlab platform.
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liver enzymes and lipid levels in patients with Lipodermatosclerosis and venous ulcers treated with a prototypic anabolic steroid stanozolol a prospective randomized double blinded placebo controlled trial
The International Journal of Lower Extremity Wounds, 2015Co-Authors: Polly Carson, Christine J Hong, Marta Oterovinas, Emily Arsenault, Vincent FalangaAbstract: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...
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acute Lipodermatosclerosis is associated with venous insufficiency
Journal of The American Academy of Dermatology, 1996Co-Authors: Adam S Greenberg, Vincent Falanga, Anthony Hasan, B M Montalvo, Anne FalabellaAbstract:Abstract Background: Acute Lipodermatosclerosis is characterized by pain and tenderness in the medial aspect of the leg. It is thought to be the result of venous insufficiency and to be the acute counterpart of chronic Lipodermatosclerosis, a hallmark of venous disease. However, there is no direct evidence linking acute Lipodermatosclerosis to venous disease. Objective: Our purpose was to determine whether acute Lipodermatosclerosis is associated with venous insufficiency. Methods: With air plethysmography, we determined the venous filling index, the ejection fraction, and the residual volume fraction in 15 sequential patients with acute Lipodermatosclerosis. Results: Ten of the 15 patients (67%) had at least one abnormal result, eight (53%) had two, and two (13%) had three. In four patients (27%), abnormalities of both reflux and ejection were noted. Duplex venous ultrasonography, in two of the patients with normal results from air plethysmography, showed incompetent perforators at sites of Lipodermatosclerosis. Conclusion: Acute Lipodermatosclerosis is associated with objective findings of venous insufficiency in a high percentage of patients. It is likely that this condition is the result of venous disease.
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use of a durometer to measure the degree of skin induration in Lipodermatosclerosis
Journal of The American Academy of Dermatology, 1995Co-Authors: Marco Romanelli, Vincent FalangaAbstract:Abstract Background: Chronic Lipodermatosclerosis is characterized by indurated skin on the medial aspect of the leg and is common around venous ulcers. The severity of induration of Lipodermatosclerosis has been associated with poor ulcer healing. Clinical assessment of Lipodermatosclerosis presently relies on a clinical skin severity score adapted from studies of patientswith systemic sclerosis. Objective: It would be desirable for prognostic reasons to develop an objective method for measuring skin hardness in Lipodermatosclerosis. Methods: The degree of skin induration at the midpoint between the upper and lower margin of Lipodermatosclerosis in 30 sequential nonselected patients with Lipodermatosclerosis was assessed by a blinded observer's clinical score and by quadruplicate determinations with a hand-held type O durometer. Skin induration on the medial aspect of the leg was similarly measured in five normal volunteers. Transcutaneous oxygen pressure was measured at the same sites. Results: A direct linear relation ( r = 0.962) was found between skin severity scores and durometer readings ( p p = 0.0016) and, similarly, higher durometer readings were found in skin score of 3 compared with score 2 skin ( p = 0.0093). Transcutaneous oxygen pressure was uniformly reduced in Lipodermatosclerosis ( p Conclusion: The durometer is a reliable instrument for measuring skin hardness in patients with Lipodermatosclerosis. It may be used to test the prognostic value of Lipodermatosclerosis on ulcer healing.
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the clinical spectrum of Lipodermatosclerosis
Journal of The American Academy of Dermatology, 1993Co-Authors: Robert S Kirsner, Jeffrey B Pardes, William H Eaglstein, Vincent FalangaAbstract:Lipodermatosclerosis refers to the skin induration and hyperpigmentation of the legs that often occurs in patients who have venous insufficiency. Lipodermatosclerosis has also been termed hypodermitis sclewdermiformis and appears to be similar if not-identical to the recently described sclerosing panniculitis of the leg. There has been much confusion about the nature, clinical course, and treatment of Lipodermatosclerosis. We believe that Lipodermatosclerosis has an acute, inflammatory phase and a chronic, fibrotic stage, although a spectrum exists. Direct immunofluorescence studies of early and late lesions are helpful in that they show dermal pericapillary fibrin deposits without other immunoreactants, Treatment of Lipodermatosclerosis consists of compression therapy with either graded stockings or elastic bandages. We and others have found that the anabolic steroid stanozolol improves this condition rapidly and consistently.
Johannes Norgauer - One of the best experts on this subject based on the ideXlab platform.
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inhibition of angiogenesis in Lipodermatosclerosis implication for venous ulcer formation
International Journal of Molecular Medicine, 2009Co-Authors: Yared Herouy, Marco Idzko, Sebastian Kreis, Tobias Mueller, Thorsten Duerk, Georg Martinybaron, Petra Reusch, Florian May, Johannes NorgauerAbstract:Abstract Lipodermatosclerosis refers to skin induration of the lower extremities characterized by tortuous, hyperpermeable vessels preceding venous leg ulcerations. Protein ligands and receptor tyrosine kinases that specifically regulate endothelial cell function are mainly involved in physiological as well as in disease-related angiogenesis. These ligand/receptor systems include the vascular endothelial growth factor (VEGF) and the angiopoietin (Ang) families and their receptor the tyrosine kinase with immunoglobulin-like domains (Tie-2) as well as the VEGF receptor family (VEGF-R1 and VEGF-R2). In the present study, the contribution of these endothelium-specific ligand/receptor systems in tissue samples of Lipodermatosclerosis was evaluated. Our results provide evidence, that the mRNA-transcripts of VEGF (p<0.01), Ang-1 (p<0.1), Ang-2 (p<0.1) and VEGF-R1 (p<0.01) were significantly upregulated in all samples of Lipodermatosclerosis in comparison with healthy skin by using reverse transcriptase-polymerase chain reaction. On protein level VEGF (p<0.01), Ang-1 (p<0.1), Ang-2 (p<0.1) and VEGF-R1 (p<0.01) were significantly elevated as well. Solely for Tie-2 and for VEGF-R2 no statistical difference could be detected on mRNA and protein level in patients with Lipodermatosclerosis in comparison with healthy skin. By immunohistochemistry we confirmed upregulated protein expression for VEGF, Ang-1, Ang-2 and VEGF-R1 compared with healthy skin. Our findings strongly suggest that an imbalance between these ligand/receptor systems might contribute to the pathophysiology of advanced stages of chronic venous insufficiency. Inhibition of angiogenesis could significantly impact the tissue breakdown in Lipodermatosclerosis and could hereby enable the formation of venous leg ulcerations.
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the role of the urokinase type plasminogen activator upa and its receptor cd87 in Lipodermatosclerosis
Journal of Cutaneous Pathology, 2001Co-Authors: Yared Herouy, Jon Aizpurua, Christoph Stetter, Stefan Dichmann, Marco Idzko, Clemens Hofmann, G Gitsch, W Vanscheidt, E Schopf, Johannes NorgauerAbstract:Background: Lipodermatosclerosis refers to a sclerosing panniculitis and dermopathy of the lower extremities sometimes seen in association with venous ulceration. Matrix metalloproteinases are implicated in the pathogenesis of venous leg ulcers and the in vitro activation of recombinant MMP-2 is controlled by the plasminogen activation system. To better understand the role of plasminogen activation in the pathogenesis of venous leg ulcers we investigated fibrinolytic factors and their inhibitors in tissue samples of lipodermatolsclerosis. Methods: The expression and the functional state of the urokinase-type plasminogen activator (uPA), the tissue-type plasminogen activator (tPA), the urokinase receptor (CD87), the plasminogen activator inhibitors-1 and -2 (PAI-1 and PAI-2) were assayed using reverse transcription polymerase chain reaction, Western blot, fibrin zymography and immunohistochemistry analyses in tissue samples of Lipodermatosclerosis. Results: Our results provide direct evidence of elevated expression of uPA (p<0.01) and CD87 (p<0.01) mRNA and protein level in Lipodermatosclerosis in comparison with healthy skin. By immunohistochemistry, elevated expression of uPA and CD87 could be detected. Fibrin zymography showed significantly elevated endogenous uPA activity (p<0.01) in liposclerotic lesions compared to healthy controls. Conclusion: Our findings indicate that elevated plasminogen activation in lipodermatosclerotic tissue may play a crucial role in the pathogenesis of venous leg ulceration.
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Lipodermatosclerosis and the significance of proteolytic remodeling in the pathogenesis of venous ulceration review
International Journal of Molecular Medicine, 1999Co-Authors: Yared Herouy, P Nockowski, E Schopf, Johannes NorgauerAbstract:The preceding stage of venous ulceration represents a scleroderma-like hardening of the skin called Lipodermatosclerosis. Clinical stages such as Lipodermatosclerosis and venous ulceration, which succeed one another are highly associated to chronic venous insufficiency. Lipodermatosclerosis is characterized by fibrous scar tissue of the reticular dermis built up of collagen bundles and loss of cellular components, whereas venous ulceration is characterized by total loss of epidermis and partially of matrix structures in the upper dermis. There is a growing recognition that an excessive proteolytic activity by proteases, in particular that of matrix metalloproteinases and fibrinolytic factors of the plasminogen activation system may be a key feature in the pathophysiological understanding of venous leg ulcer formation. Lipodermatosclerosis displays an intense ongoing proteolytic process by elevated matrix metalloproteinase activity, as recently shown on different molecular and biological levels. Elevated expression on mRNA and protein level of matrix metalloproteinases and fibrinolytic factors of the plasminogen activation system have been detected in liposclerotic skin lesions. In addition, matrix metalloproteinases were proteolytically activated confirmed by zymography experiments and collagen degradation assays. Therefore it is well conceivable, that proteolytic enzymes of matrix metalloproteinases could initiate an elevated turnover of the extracellular matrix with subsequent breakdown of the matrix scaffold finally resulting in venous ulceration.
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Lipodermatosclerosis is characterized by elevated expression and activation of matrix metalloproteinases implications for venous ulcer formation
Journal of Investigative Dermatology, 1998Co-Authors: Yared Herouy, Christoph Stetter, E Schopf, Johannes Norgauer, Andreas E May, Gudula Pornschlegel, Harald Grenz, K T Preissner, W VanscheidtAbstract:Lipodermatosclerosis refers to skin induration of the lower extremities and is associated with patients preceding venous ulcerations. To better understand the pathogenesis of ulcer formation we investigated the expression of matrix metalloproteinases (MMP) and tissue inhibitors of metalloproteinases (TIMP) in Lipodermatosclerosis. By preparing biopsies from healthy skin and liposclerotic lesions, MMP-1, MMP-2, MMP-9, TIMP-1, and TIMP-2 were analyzed by using reverse transcriptase-polymerase chain reaction, western blot, zymography, hydrolysis of [ 3 H]labeled collagens, and immunohistochemistry. Our investigations provide evidence that mRNA and protein expression of MMP-1, MMP-2, and TIMP-1 were significantly increased in Lipodermatosclerosis, whereas the total amount of MMP-9 and TIMP-2 mRNA and protein was not altered. Western blot of liposclerotic lesions revealed an inactive proMMP-1-TIMP-1 complex, whereas MMP-2 was prominent as an active 66 kDa band. Increased proteolytic activity of MMP-2 could be proven in lesional in comparison with healthy skin by zymography and [ 3 H]collagen degradation. Increased diffuse staining was found for MMP-1 in the epidermis and dermis in comparison with controls. In Lipodermatosclerosis, MMP-2 was predominantly localized in the basal and suprabasal layers of the epidermis, in perivascular regions, and in the reticular part of the dermis. Furthermore, MMP-2 was imbalanced by locally reduced expression of TIMP-2 in the basement membrane zone of lesional skin. Our findings indicate Lipodermatosclerosis to be characterized by elevated matrix turnover.
W Schmeller - One of the best experts on this subject based on the ideXlab platform.
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surgical removal of ulcer and Lipodermatosclerosis followed by split skin grafting shave therapy yields good long term results in non healing venous leg ulcers
Acta Dermato-venereologica, 2000Co-Authors: W Schmeller, Yvonne GaberAbstract:The purpose of this study was to evaluate the long-term effects of shave therapy in non-healing venous leg ulcers. Forty-one patients with 75 recalcitrant leg ulcers caused by primary deep vein incompetence or post-thrombotic syndrome were operated by shave therapy (removal of ulcer and surrounding Lipodermatosclerosis with a Schink skin-grafting knife and covering of the wounds with meshed split-thickness skin grafts). After an average follow-up period of 2 years and 5 months all patients were evaluated for long-term results. The healing rate of ulcers classified as non-healing was 67% (50 of 75 ulcers). The healing rate was 76% for ulcers associated with primary deep vein incompetence and 58% for ulcers associated with postthrombotic syndrome (p~0.08). Even in cases with recurrence (33%) these ulcers were strikingly reduced by 80 ‐ 90% of their original size. Hypaesthesia was noticed in 38% of the transplanted areas. In ‘‘non-healing’’ venous leg ulcers due to deep venous insufficiency shave therapy yields favourable longterm results. Because it is only a symptomatic treatment which does not reduce the pathological refluxes, continuous compression of the lower leg is important. Key words: shave therapy; non-healing venous ulcers.
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shave therapy is a simple effective treatment of persistent venous leg ulcers
Journal of The American Academy of Dermatology, 1998Co-Authors: W Schmeller, Yvonne Gaber, Hansbjorn GehlAbstract:Abstract Background: Leg ulcers in deep venous insufficiency, especially the postthrombotic type, are often resistant to therapy. Objective: The purpose of this study was to evaluate short-term and long-term effects of shave therapy in persistent or recurrent venous ulcers. Methods: From January 1994 to October 1997, 80 patients with 105 chronic leg ulcers were treated by shave therapy. This method involved removing ulcers together with the surrounding Lipodermatosclerosis and covering the wounds with meshed split-skin graft. Fifty-nine patients with 76 ulcers were examined after 3 months for assessment of short-term results. The first 18 patients with 26 ulcers from the years 1994 and 1995 were evaluated for long-term results. Results: The short-term healing rate after 3 months in 59 patients was 79%. Of 8 patients from 1995 (follow-up period, 1 year and 8 months), 7 patients had complete healing and 1 patient had a small ulcer. Of 10 patients from 1994 (average follow-up period, 2 years and 8 months), 8 patients had complete healing and 2 patients showed small superficial ulcerations within the transplanted areas. From these results, a long-term healing rate of 88% was calculated in 18 patients. Two of the 3 patients with recurrences had stopped compression therapy after good short-term results. Conclusion: For patients with recalcitrant leg ulcers in deep venous insufficiency and/or postthrombosis, shave therapy is a simple, quick, and effective surgical method with favorable short-term and long-term results. (J Am Acad Dermatol 1998;39:232-8.)
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altered x ray diffraction pattern is accompanied by a change in the mode of cross link formation in Lipodermatosclerosis
Journal of Investigative Dermatology, 1996Co-Authors: Jurgen Brinckmann, W Schmeller, Michael Tronnier, Holger Notbohm, P K Muller, Yahya Acil, Boris Batge, Michel H J Koch, Helmut H WolffAbstract:We studied the molecular packing of collagen fibrils by x-ray diffraction in skin specimens of patients with Lipodermatosclerosis and in controls. A difference in the tilt angles of the collagen molecules relative to the fiber axis is suggested by a D-stagger that is 1nm larger in sclerotic skin than in normal skin, In parallel, the collagen cross-links in the skin specimens were analyzed, and a marked increase of both hydroxylysylpyridinoline and lysylpyridinoline, the trivalent mature cross-links characteristic of skeletal tissues, was found. The content of hydroxylysylpyridinoline and lysylpyridinoline was higher in the deep layer of the affected dermis than in the superficial dermis. This increase was always accompanied by an increase in the hydroxylysylpyridinoline/lysylpyridinoline ratio, suggesting that hydroxylysylpyridinoline is a sclerosis-associated cross-links. In addition, lysyl hydroxylation was increased in affected skin, and this increase was apparently restricted to the collagen telopeptides, which are crucial anchoring structures for lysyl dependent cross-links.
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a 20 mhz ultrasound examination of Lipodermatosclerosis
1995Co-Authors: Julia Welzel, W Schmeller, Andreas PlettenbergAbstract:Lipodermatosclerosis (LDS) is a common finding in patients with chronic venous insufficiency (CVI). Clinically the skin of the lower legs is thickened and indurated. Computed tomography, nuclear magnetic resonance tomography, laser Doppler flux and transcutaneous oxygen measurement show pronounced changes in morphological and functional parameters [4–8]. We used high-resolution ultrasound to determine the degree of LDS and to study the acoustic behavior of skin and subcutaneous fat.
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20 mhz ultrasound examination in Lipodermatosclerosis
1994Co-Authors: Julia Welzel, W Schmeller, Andreas PlettenbergAbstract:The degree of Lipodermatosclerosis in chronic venous insufficiency was determined by high-resolution 20 MHz ultrasound. For comparison, skin biopsies were taken and examined by light microscopy. With increasingly extensive sclerosis, ultrasound showed increasing thickness of the dermis with a poorly defined border from the subcutaneous fat. In addition, an echolucent band appeared in the upper dermis, corresponding to regions of glomerular capillaries in histology. In our experience, high-resolution ultrasound examination allows rapid and objective quantification of Lipodermatosclerosis.
Yared Herouy - One of the best experts on this subject based on the ideXlab platform.
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inhibition of angiogenesis in Lipodermatosclerosis implication for venous ulcer formation
International Journal of Molecular Medicine, 2009Co-Authors: Yared Herouy, Marco Idzko, Sebastian Kreis, Tobias Mueller, Thorsten Duerk, Georg Martinybaron, Petra Reusch, Florian May, Johannes NorgauerAbstract:Abstract Lipodermatosclerosis refers to skin induration of the lower extremities characterized by tortuous, hyperpermeable vessels preceding venous leg ulcerations. Protein ligands and receptor tyrosine kinases that specifically regulate endothelial cell function are mainly involved in physiological as well as in disease-related angiogenesis. These ligand/receptor systems include the vascular endothelial growth factor (VEGF) and the angiopoietin (Ang) families and their receptor the tyrosine kinase with immunoglobulin-like domains (Tie-2) as well as the VEGF receptor family (VEGF-R1 and VEGF-R2). In the present study, the contribution of these endothelium-specific ligand/receptor systems in tissue samples of Lipodermatosclerosis was evaluated. Our results provide evidence, that the mRNA-transcripts of VEGF (p<0.01), Ang-1 (p<0.1), Ang-2 (p<0.1) and VEGF-R1 (p<0.01) were significantly upregulated in all samples of Lipodermatosclerosis in comparison with healthy skin by using reverse transcriptase-polymerase chain reaction. On protein level VEGF (p<0.01), Ang-1 (p<0.1), Ang-2 (p<0.1) and VEGF-R1 (p<0.01) were significantly elevated as well. Solely for Tie-2 and for VEGF-R2 no statistical difference could be detected on mRNA and protein level in patients with Lipodermatosclerosis in comparison with healthy skin. By immunohistochemistry we confirmed upregulated protein expression for VEGF, Ang-1, Ang-2 and VEGF-R1 compared with healthy skin. Our findings strongly suggest that an imbalance between these ligand/receptor systems might contribute to the pathophysiology of advanced stages of chronic venous insufficiency. Inhibition of angiogenesis could significantly impact the tissue breakdown in Lipodermatosclerosis and could hereby enable the formation of venous leg ulcerations.
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the role of the urokinase type plasminogen activator upa and its receptor cd87 in Lipodermatosclerosis
Journal of Cutaneous Pathology, 2001Co-Authors: Yared Herouy, Jon Aizpurua, Christoph Stetter, Stefan Dichmann, Marco Idzko, Clemens Hofmann, G Gitsch, W Vanscheidt, E Schopf, Johannes NorgauerAbstract:Background: Lipodermatosclerosis refers to a sclerosing panniculitis and dermopathy of the lower extremities sometimes seen in association with venous ulceration. Matrix metalloproteinases are implicated in the pathogenesis of venous leg ulcers and the in vitro activation of recombinant MMP-2 is controlled by the plasminogen activation system. To better understand the role of plasminogen activation in the pathogenesis of venous leg ulcers we investigated fibrinolytic factors and their inhibitors in tissue samples of lipodermatolsclerosis. Methods: The expression and the functional state of the urokinase-type plasminogen activator (uPA), the tissue-type plasminogen activator (tPA), the urokinase receptor (CD87), the plasminogen activator inhibitors-1 and -2 (PAI-1 and PAI-2) were assayed using reverse transcription polymerase chain reaction, Western blot, fibrin zymography and immunohistochemistry analyses in tissue samples of Lipodermatosclerosis. Results: Our results provide direct evidence of elevated expression of uPA (p<0.01) and CD87 (p<0.01) mRNA and protein level in Lipodermatosclerosis in comparison with healthy skin. By immunohistochemistry, elevated expression of uPA and CD87 could be detected. Fibrin zymography showed significantly elevated endogenous uPA activity (p<0.01) in liposclerotic lesions compared to healthy controls. Conclusion: Our findings indicate that elevated plasminogen activation in lipodermatosclerotic tissue may play a crucial role in the pathogenesis of venous leg ulceration.
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Lipodermatosclerosis and the significance of proteolytic remodeling in the pathogenesis of venous ulceration review
International Journal of Molecular Medicine, 1999Co-Authors: Yared Herouy, P Nockowski, E Schopf, Johannes NorgauerAbstract:The preceding stage of venous ulceration represents a scleroderma-like hardening of the skin called Lipodermatosclerosis. Clinical stages such as Lipodermatosclerosis and venous ulceration, which succeed one another are highly associated to chronic venous insufficiency. Lipodermatosclerosis is characterized by fibrous scar tissue of the reticular dermis built up of collagen bundles and loss of cellular components, whereas venous ulceration is characterized by total loss of epidermis and partially of matrix structures in the upper dermis. There is a growing recognition that an excessive proteolytic activity by proteases, in particular that of matrix metalloproteinases and fibrinolytic factors of the plasminogen activation system may be a key feature in the pathophysiological understanding of venous leg ulcer formation. Lipodermatosclerosis displays an intense ongoing proteolytic process by elevated matrix metalloproteinase activity, as recently shown on different molecular and biological levels. Elevated expression on mRNA and protein level of matrix metalloproteinases and fibrinolytic factors of the plasminogen activation system have been detected in liposclerotic skin lesions. In addition, matrix metalloproteinases were proteolytically activated confirmed by zymography experiments and collagen degradation assays. Therefore it is well conceivable, that proteolytic enzymes of matrix metalloproteinases could initiate an elevated turnover of the extracellular matrix with subsequent breakdown of the matrix scaffold finally resulting in venous ulceration.
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Lipodermatosclerosis is characterized by elevated expression and activation of matrix metalloproteinases implications for venous ulcer formation
Journal of Investigative Dermatology, 1998Co-Authors: Yared Herouy, Christoph Stetter, E Schopf, Johannes Norgauer, Andreas E May, Gudula Pornschlegel, Harald Grenz, K T Preissner, W VanscheidtAbstract:Lipodermatosclerosis refers to skin induration of the lower extremities and is associated with patients preceding venous ulcerations. To better understand the pathogenesis of ulcer formation we investigated the expression of matrix metalloproteinases (MMP) and tissue inhibitors of metalloproteinases (TIMP) in Lipodermatosclerosis. By preparing biopsies from healthy skin and liposclerotic lesions, MMP-1, MMP-2, MMP-9, TIMP-1, and TIMP-2 were analyzed by using reverse transcriptase-polymerase chain reaction, western blot, zymography, hydrolysis of [ 3 H]labeled collagens, and immunohistochemistry. Our investigations provide evidence that mRNA and protein expression of MMP-1, MMP-2, and TIMP-1 were significantly increased in Lipodermatosclerosis, whereas the total amount of MMP-9 and TIMP-2 mRNA and protein was not altered. Western blot of liposclerotic lesions revealed an inactive proMMP-1-TIMP-1 complex, whereas MMP-2 was prominent as an active 66 kDa band. Increased proteolytic activity of MMP-2 could be proven in lesional in comparison with healthy skin by zymography and [ 3 H]collagen degradation. Increased diffuse staining was found for MMP-1 in the epidermis and dermis in comparison with controls. In Lipodermatosclerosis, MMP-2 was predominantly localized in the basal and suprabasal layers of the epidermis, in perivascular regions, and in the reticular part of the dermis. Furthermore, MMP-2 was imbalanced by locally reduced expression of TIMP-2 in the basement membrane zone of lesional skin. Our findings indicate Lipodermatosclerosis to be characterized by elevated matrix turnover.
Yvonne Gaber - One of the best experts on this subject based on the ideXlab platform.
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surgical removal of ulcer and Lipodermatosclerosis followed by split skin grafting shave therapy yields good long term results in non healing venous leg ulcers
Acta Dermato-venereologica, 2000Co-Authors: W Schmeller, Yvonne GaberAbstract:The purpose of this study was to evaluate the long-term effects of shave therapy in non-healing venous leg ulcers. Forty-one patients with 75 recalcitrant leg ulcers caused by primary deep vein incompetence or post-thrombotic syndrome were operated by shave therapy (removal of ulcer and surrounding Lipodermatosclerosis with a Schink skin-grafting knife and covering of the wounds with meshed split-thickness skin grafts). After an average follow-up period of 2 years and 5 months all patients were evaluated for long-term results. The healing rate of ulcers classified as non-healing was 67% (50 of 75 ulcers). The healing rate was 76% for ulcers associated with primary deep vein incompetence and 58% for ulcers associated with postthrombotic syndrome (p~0.08). Even in cases with recurrence (33%) these ulcers were strikingly reduced by 80 ‐ 90% of their original size. Hypaesthesia was noticed in 38% of the transplanted areas. In ‘‘non-healing’’ venous leg ulcers due to deep venous insufficiency shave therapy yields favourable longterm results. Because it is only a symptomatic treatment which does not reduce the pathological refluxes, continuous compression of the lower leg is important. Key words: shave therapy; non-healing venous ulcers.
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shave therapy is a simple effective treatment of persistent venous leg ulcers
Journal of The American Academy of Dermatology, 1998Co-Authors: W Schmeller, Yvonne Gaber, Hansbjorn GehlAbstract:Abstract Background: Leg ulcers in deep venous insufficiency, especially the postthrombotic type, are often resistant to therapy. Objective: The purpose of this study was to evaluate short-term and long-term effects of shave therapy in persistent or recurrent venous ulcers. Methods: From January 1994 to October 1997, 80 patients with 105 chronic leg ulcers were treated by shave therapy. This method involved removing ulcers together with the surrounding Lipodermatosclerosis and covering the wounds with meshed split-skin graft. Fifty-nine patients with 76 ulcers were examined after 3 months for assessment of short-term results. The first 18 patients with 26 ulcers from the years 1994 and 1995 were evaluated for long-term results. Results: The short-term healing rate after 3 months in 59 patients was 79%. Of 8 patients from 1995 (follow-up period, 1 year and 8 months), 7 patients had complete healing and 1 patient had a small ulcer. Of 10 patients from 1994 (average follow-up period, 2 years and 8 months), 8 patients had complete healing and 2 patients showed small superficial ulcerations within the transplanted areas. From these results, a long-term healing rate of 88% was calculated in 18 patients. Two of the 3 patients with recurrences had stopped compression therapy after good short-term results. Conclusion: For patients with recalcitrant leg ulcers in deep venous insufficiency and/or postthrombosis, shave therapy is a simple, quick, and effective surgical method with favorable short-term and long-term results. (J Am Acad Dermatol 1998;39:232-8.)