1985
DOI: 10.1177/014107688507800505
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Skin Oxygen Tension in Venous Insufficiency of the Lower Leg

Abstract: Summary: Tissue anoxia has for long been invoked as a cause of venous leg ulcers, and recently it has been suggested that pericapillary fibrin prevents the diffusion of oxygen in the skin. In the present study direct measurements of skin oxygen levels on the lower leg were made using a transcutaneous oxygen monitor. In the recumbent position mean oxygen tensions were higher in patients than in controls, thus disproving the existence of any block to oxygen diffusion. In both groups there was a fall in oxygen te… Show more

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Cited by 77 publications
(16 citation statements)
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“…In these wounds, TIMP and other proteinase inhibitors were found to be in decreased levels contrary to the increased MMP levels. [23][24][25] In our study, the MMP levels were elevated in both treatment and control groups. However, the TIMP-1 level was high only in the treatment group.…”
Section: Figuresupporting
confidence: 48%
“…In these wounds, TIMP and other proteinase inhibitors were found to be in decreased levels contrary to the increased MMP levels. [23][24][25] In our study, the MMP levels were elevated in both treatment and control groups. However, the TIMP-1 level was high only in the treatment group.…”
Section: Figuresupporting
confidence: 48%
“…On the contrary, mucin deposition in obesity‐associated lymphoedematous mucinosis seems to be a secondary process. In fact, surface ischaemia with venous insufficiency, often associated with lymphoedema, could overstimulate the production of hyaluronic acid 12 . Alternatively, the simple extravascular accumulation of plasma protein in the interstice could induce mucopolysaccharide synthesis 13,14 …”
Section: Discussionmentioning
confidence: 99%
“…Most cases of pretibial mucinosis without thyroid disease have clinical and histologic features of stasis dermatitis (2, 3). Pretibial mucinosis may be caused by underlying venous stasis dermatitis; the resultant surface ischemia with venous insufficiency might stimulate excess production of hyaluronic acid (4). Another explanation of the pathology is that the extravascular accumulation of plasma proteins might stimulate mucopolysaccharide synthesis in the lymphedema setting (58).…”
Section: To the Editormentioning
confidence: 99%