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Wound healing in chronically

Kopera D, Kokol R, Berger C, Haas J (2005) Does the use of low-level laser influence wound healing in chronic venous leg ulcers J Wound Care 4(8) 391-394... [Pg.275]

Gohel MS, Windhaber RAJ, Tarlon JF, Whyman MR, Poskitt KR (2008) The relationship between cytokine concentrations and wound healing in chronic venous ulceration. J Vase Surg 48(5) 1272-1277... [Pg.276]

It is concluded that chronic leg ulcer patients probably lack the mechanisms that normalise their levels of antioxidant enzymes, which normally decrease at early stages of wound healing in order to allow blood granulocytes and tissue macrophages to perform their function in cleansing the wounded area. Consequently re-epitheUalisation and matrix remodeling processes are delayed. LLLT stimulates... [Pg.273]

Hepatic fibrosis is seen with chronic exposure to hepatoxicants that cause increasing damage to hepatocytes and is part of the wound healing response. Chronic fibrosis leads to severe disruption of the liver architecture by the deposition of extracellular matrix (ECM). Advanced fibrosis disrupts the proper blood flow and results in scarring of the liver that can lead to irreversible liver damage known as cirrhosis. Chronic exposure to the hepatoxins CCI4, monocrotaline, and alcohol are examples of compounds that cause excessive fibrosis. [Pg.678]

Gelenkerkrankungen met D-penicillamin und Wundheilungsstdrungen bei rheumaorthopadischen Eingriffen. [Basic therapy of chronic inflammatory joint diseases with D-penicillamine and disorders of wound healing in rheumatoid orthopedic interventions.] Z Rheumatol 1988 47(Suppl l) 41-3. [Pg.2753]

The prolonged severe stress and chronic hypermetabolism present in all patients with severe thermal injuries makes provision of adequate nutrition of paramount importance. The calories required to maintain nutritional balance and to allow wound healing in the burn patient greatly exceed basal metabolic requirements. [Pg.239]

Collagen can be used in acute wounds—where damage of the tissue is usually completely healed within 8-12 weeks and this type of wound leaves a bit of a scar [102] —like burns [103] and medical surgery wounds, or in chronic wounds—which are hard to heal, may recur and the healing duration is more than 12 weeks—like ulcers [ 104] and tumors. [Pg.453]

Haimowitz, J., Margolis, D. (1997). Moist wound healing. In D. Krasner, D. Kane (Eds.), Chronic wound care A clinical source book for healthcare professionals. Wayne, PA Health Management Publications. [Pg.467]

Chronic Morphine s Role on Innate Immunity, Bacterial Susceptibility and Implications in Wound Healing... [Pg.337]

The pharmacokinetics of bevacizumab demonstrate a terminal half-life of 21 days, with a volume of distribution consistent with limited extravascular distribution.34 Bevacizumab has shown clinical activity in the treatment of colorectal, kidney, lung, breast, and head and neck cancer. Patients may develop hypertension requiring chronic medication during therapy. Impaired wound healing, thrombolembolic events, proteinuria, bleeding, and perforation are serious side effects. [Pg.1294]

Trace elements are essential cofactors for numerous biochemical processes. Trace elements that are added routinely to PN include zinc, selenium, copper, manganese, and chromium. There are various commercial parenteral trace element formulations that can be added to PN admixtures (e.g., MTE-5 ). Zinc is important for wound healing, and patients with high-output fistulas, diarrhea, burns, and large open wounds may require additional zinc supplementation. Patients may lose as much as 12 to 17 mg zinc per liter of gastrointestinal (GI) output (e.g., from diarrhea or enterocutaneous fistula losses) however, others have demonstrated that 12 mg/day may be adequate to maintain these patients in positive zinc balance.18 Patients with chronic diarrhea, malabsorption, and short-gut syndrome may have increased selenium losses and may require additional selenium supplementation. Patients with severe cholestasis should have copper and manganese... [Pg.1498]

Recently, the notion that the chronicity of inflammation may not actually drive the fibrogenic process has been widely appreciated (Tables 1, 2, and 3). Some propose that it is indeed the alteration of the mesenchymal cell phenotypes that disrupts the balance between collagen synthesis and degradation in the wound-healing process, highlighted by clinical evidence that shows unsuccessful treatment of fibrosis with anti-inflammatory or immunosuppressive drugs (18,19). One scenario is that mesenchymal cells (myofibroblasts and fibroblasts) are phenotypically altered and thus do not undergo apoptosis after resolution. [Pg.297]


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