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New hypothesis of venous ulceration
New hypothesis of venous ulceration
* tinyurl . com /ys3eo2
Based on these findings a new hypothesis of venous ulceration is
postulated.
Chronic venous insufficiency in the lower leg causes leakage of
erythrocytes from cutaneous blood vessels into the interstitial
tissue. Inflammatory cells initially phagocytose these, however with
continued extravasation these cells become overloaded and excess iron
is then taken up by dermal fibroblasts. Accumulation of low levels of
iron in dermalfibroblasts in skin subjected to chronic venous
insufficiency leads to the production of lipid peroxidation by-
products and the development of fibrotic skin changes. However, the
build-up of iron to high levels in dermalfibroblasts results in cell
death and eventual ulcer formation. These events are likely to be
through the production of free radicals and enhanced by ischaemia/
reperfusion. The presence of iron-loaded LDS skin around a venous
ulcer will perpetuate the fibrotic process so preventing ulcer healing
and may lead to more extensive tissue damage and an increase ulcer
size.
Treatment of this problem has for many years relied on established
principles of compression and limb elevation and no drug treatment has
been shown to be more effective. Yet there is clearly a role for drugs
in the management of venous disease either alone or in combination
with compression therapy. It is likely to be beneficial to intervene
in the initial processes that cause thelipodermatosclerotic skin
changes leading to ulceration rather than to modify the repair
processes when an ulcer has formed. The same processes that caused the
ulcer are likely to contribute to its perpetuation and delayed
healing. The free radical scavengers, topical allopurinol or dimethyl
sulfoxide, were given to 88 ulcer patients, on a 3 months, double
blind controlled study and showed a significant increase in
healing(Salim A. S. The role of oxygen derived free radicals in the
management of venous(varicose) ulceration : a new approach. World J.
Surg. 15,264-269 (1991) ).
We have found that there is little evidence of haemosiderin in ulcer
base tissue, although others have found raised iron levels in chronic
wound fluid suggesting that much of the iron leaks out of the wound.
Therefore, it is logical to address the problem of iron overload by
applying ironchelators topically to pre-ulcerated skin.
--------------------------------------------------------------------------------
Data supplied from the esp@cenet database - Worldwide
Who loves ya.
Tom
Jesus Was A Vegetarian!
* jesuswasavegetarian.7h . com
Man Is A Herbivore!
* tinyurl . com /a3cc3
DEAD PEOPLE WALKING
* tinyurl . com /zk9fk
* tinyurl . com /ys3eo2
Based on these findings a new hypothesis of venous ulceration is
postulated.
Chronic venous insufficiency in the lower leg causes leakage of
erythrocytes from cutaneous blood vessels into the interstitial
tissue. Inflammatory cells initially phagocytose these, however with
continued extravasation these cells become overloaded and excess iron
is then taken up by dermal fibroblasts. Accumulation of low levels of
iron in dermalfibroblasts in skin subjected to chronic venous
insufficiency leads to the production of lipid peroxidation by-
products and the development of fibrotic skin changes. However, the
build-up of iron to high levels in dermalfibroblasts results in cell
death and eventual ulcer formation. These events are likely to be
through the production of free radicals and enhanced by ischaemia/
reperfusion. The presence of iron-loaded LDS skin around a venous
ulcer will perpetuate the fibrotic process so preventing ulcer healing
and may lead to more extensive tissue damage and an increase ulcer
size.
Treatment of this problem has for many years relied on established
principles of compression and limb elevation and no drug treatment has
been shown to be more effective. Yet there is clearly a role for drugs
in the management of venous disease either alone or in combination
with compression therapy. It is likely to be beneficial to intervene
in the initial processes that cause thelipodermatosclerotic skin
changes leading to ulceration rather than to modify the repair
processes when an ulcer has formed. The same processes that caused the
ulcer are likely to contribute to its perpetuation and delayed
healing. The free radical scavengers, topical allopurinol or dimethyl
sulfoxide, were given to 88 ulcer patients, on a 3 months, double
blind controlled study and showed a significant increase in
healing(Salim A. S. The role of oxygen derived free radicals in the
management of venous(varicose) ulceration : a new approach. World J.
Surg. 15,264-269 (1991) ).
We have found that there is little evidence of haemosiderin in ulcer
base tissue, although others have found raised iron levels in chronic
wound fluid suggesting that much of the iron leaks out of the wound.
Therefore, it is logical to address the problem of iron overload by
applying ironchelators topically to pre-ulcerated skin.
--------------------------------------------------------------------------------
Data supplied from the esp@cenet database - Worldwide
Who loves ya.
Tom
Jesus Was A Vegetarian!
* jesuswasavegetarian.7h . com
Man Is A Herbivore!
* tinyurl . com /a3cc3
DEAD PEOPLE WALKING
* tinyurl . com /zk9fk
