Update on chronic-venous-insufficiency-induced inflammatory processes - PubMed (original) (raw)
Review
Update on chronic-venous-insufficiency-induced inflammatory processes
P D Smith. Angiology. 2001 Aug.
Abstract
The causes of venous ulceration remain unclear. Twentieth-century hypotheses concentrated on the possibility that this problem was caused by failure of oxygen delivery to the skin. However, it has been difficult to substantiate these predictions in practice. Although the presence of tissue hypoxia has been suggested by studies in which transcutaneous oxygen tension has been assessed with transducers heated to unphysiological temperatures, when oxygen measurements are made at room temperature there is little evidence of tissue hypoxia. This has led to the assessment of alternative mechanisms of ulcer development. There has been considerable interest in recent years in the inflammatory processes that surround venous ulceration. A complex sequence of events appears to surround the development of leg ulceration. Increased leukocyte activation has been shown in patients with venous disease as well as increased expression of soluble endothelial adhesion molecules. Histologic studies of the skin in patients with chronic venous disease show a perivascular infiltration of the capillaries of the papillary plexus (the most superficial part of the dermis) with monocytes, macrophages, and connective tissue proteins including fibrin. Fibrosis of the skin and subcutaneous tissues may be initiated by increased gene expression and production of transforming growth factor-beta1. Vascular endothelial growth factor may be involved in the capillary proliferation that has been reported in the skin by a number of authors. Increased expression of several tissue metalloproteinases has been reported both in liposclerotic skin and periulcer skin. The tissue inhibitors of metalloproteinases are also increased and the net result is unclear. Treatment of venous disease using micronized purified flavonoid fraction moderates some of the inflammatory markers, including leukocyte ligand expression and endothelial adhesion molecule shedding. These compounds have also been shown to reduce leukocyte-endothelial adhesion in animal models of ischemia-reperfusion injury. Many inflammatory processes have now been shown to be involved in the development of the skin changes in patients with chronic venous disease. However, the precise sequence of events that leads to leg ulceration is still unclear. Pharmacologic treatments aimed at moderating some of these inflammatory processes are now under investigation as potential ways of treating patients with the more advanced stages of venous disease.
Similar articles
- Pathomechanism of chronic venous insufficiency and leg ulcer.
Sándor T. Sándor T. Acta Physiol Hung. 2004;91(2):131-45. doi: 10.1556/APhysiol.91.2004.2.5. Acta Physiol Hung. 2004. PMID: 15484713 Review. - Therapeutic approach to chronic venous insufficiency and its complications: place of Daflon 500 mg.
Bergan JJ, Schmid-Schönbein GW, Takase S. Bergan JJ, et al. Angiology. 2001 Aug;52 Suppl 1:S43-7. doi: 10.1177/0003319701052001S06. Angiology. 2001. PMID: 11510596 Review. - Deleterious effects of white cells in the course of skin damage in CVI.
Coleridge Smith PD. Coleridge Smith PD. Int Angiol. 2002 Jun;21(2 Suppl 1):26-32. Int Angiol. 2002. PMID: 12515977 Review. - The causes of skin damage and leg ulceration in chronic venous disease.
Smith PC. Smith PC. Int J Low Extrem Wounds. 2006 Sep;5(3):160-8. doi: 10.1177/1534734606292429. Int J Low Extrem Wounds. 2006. PMID: 16928672 Review. - Microcirculatory dysfunction in chronic venous insufficiency (CVI).
Jünger M, Steins A, Hahn M, Häfner HM. Jünger M, et al. Microcirculation. 2000;7(6 Pt 2):S3-12. Microcirculation. 2000. PMID: 11151969 Review.
Cited by
- Application of Menstrual Blood Derived Stromal (stem) Cells Exert Greater Regenerative Potency Than Fibroblasts/Keratinocytes in Chronic Wounds of Diabetic Mice.
Mirzadegan E, Golshahi H, Saffarian Z, Edalatkhah H, Darzi M, Khorasani S, Saliminejad K, Kazemnejad S. Mirzadegan E, et al. Avicenna J Med Biotechnol. 2023 Jul-Sep;15(3):139-156. doi: 10.18502/ajmb.v15i3.12923. Avicenna J Med Biotechnol. 2023. PMID: 37538236 Free PMC article. - Th17-Gene Expression Profile in Patients with Chronic Venous Disease and Venous Ulcers: Genetic Modulations and Preliminary Clinical Evidence.
Amato R, Dattilo V, Brescia C, D'Antona L, Iuliano R, Trapasso F, Perrotti N, Costa D, Ielapi N, Aiello F, Provenzano M, Bracale UM, Andreucci M, Serra R. Amato R, et al. Biomolecules. 2022 Jun 28;12(7):902. doi: 10.3390/biom12070902. Biomolecules. 2022. PMID: 35883458 Free PMC article. - Arginase Signalling as a Key Player in Chronic Wound Pathophysiology and Healing.
Szondi DC, Wong JK, Vardy LA, Cruickshank SM. Szondi DC, et al. Front Mol Biosci. 2021 Oct 29;8:773866. doi: 10.3389/fmolb.2021.773866. eCollection 2021. Front Mol Biosci. 2021. PMID: 34778380 Free PMC article. Review. - Understanding Chronic Venous Disease: A Critical Overview of Its Pathophysiology and Medical Management.
Ortega MA, Fraile-Martínez O, García-Montero C, Álvarez-Mon MA, Chaowen C, Ruiz-Grande F, Pekarek L, Monserrat J, Asúnsolo A, García-Honduvilla N, Álvarez-Mon M, Bujan J. Ortega MA, et al. J Clin Med. 2021 Jul 22;10(15):3239. doi: 10.3390/jcm10153239. J Clin Med. 2021. PMID: 34362022 Free PMC article. Review. - Chemokines as Therapeutic Targets to Improve Healing Efficiency of Chronic Wounds.
Satish L. Satish L. Adv Wound Care (New Rochelle). 2015 Nov 1;4(11):651-659. doi: 10.1089/wound.2014.0602. Adv Wound Care (New Rochelle). 2015. PMID: 26543679 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources