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Chronic venous disease and diabetic microangiopathy: pathophysiology and commonalities

Identifikátory výsledku

  • Kód výsledku v IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023001%3A_____%2F21%3A00081949" target="_blank" >RIV/00023001:_____/21:00081949 - isvavai.cz</a>

  • Výsledek na webu

    <a href="https://www.minervamedica.it/en/getfreepdf/NEtEdS9vc3dFRjVKZExEWjNGc0ZTdkJyMlZLQlJCMlBsYlpwaEVwdU1KZTE4WkgveFVrOWE3OElvcUd2WjVxRQ%253D%253D/R34Y2021N06A0457.pdf" target="_blank" >https://www.minervamedica.it/en/getfreepdf/NEtEdS9vc3dFRjVKZExEWjNGc0ZTdkJyMlZLQlJCMlBsYlpwaEVwdU1KZTE4WkgveFVrOWE3OElvcUd2WjVxRQ%253D%253D/R34Y2021N06A0457.pdf</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.23736/S0392-9590.21.04664-2" target="_blank" >10.23736/S0392-9590.21.04664-2</a>

Alternativní jazyky

  • Jazyk výsledku

    angličtina

  • Název v původním jazyce

    Chronic venous disease and diabetic microangiopathy: pathophysiology and commonalities

  • Popis výsledku v původním jazyce

    Chronic venous disease and diabetes mellitus are highly prevalent and debilitating conditions affecting millions of individuals globally. Although these conditions are typically considered as separate entities, they often co-exist which may be important in both understanding their pathophysiology and determining the best treatment strategy. Diabetes mellitus is twice as common in patients with chronic venous disease compared with the general population. Notably, a large proportion of patients with diabetes mellitus present with venous disorders, although this is often overlooked. The etiology of chronic venous disease is multifactorial, involving hemodynamic, genetic, and environmental factors which result in changes to the venous endothelium and structural wall as well as inflammation. Inflammation, endothelial dysfunction and hyperfiltration or leakage, are commonly observed in diabetes mellitus and cause various diabetic microvascular complications. Both diseases are also influenced by the increased expression of adhesion molecules, chemokines, and cytokines, and are characterized by the presence of vessel hypertension. Consequently, despite differences in etiology, the pathophysiology of both chronic venous disease and diabetic microangiopathy appears to be driven by endothelial dysfunction and inflammation. Treatment strategies should take the co-existence of chronic venous disease and diabetic microangiopathy into account. Compression therapy is recommended in inflammatory conditions that have an edema component as seen in both chronic venous disease and diabetes mellitus. Lifestyle changes like weight loss and exercise, will improve metabolic state and lower inflammation and should be promoted in these patients. Additionally, both patient populations may benefit from venoactive drugs. (Cite this article as: Gastaldi G, Pannier F, Roztocil K, Lugli M, Mansilha A, Haller H, et al. Chronic venous disease and diabetic microangiopathy: pathophysiology and commonalities. Int Angiol 2021;40:457-69. DOI: 10.23736/S0392-9590.21.04664-2)

  • Název v anglickém jazyce

    Chronic venous disease and diabetic microangiopathy: pathophysiology and commonalities

  • Popis výsledku anglicky

    Chronic venous disease and diabetes mellitus are highly prevalent and debilitating conditions affecting millions of individuals globally. Although these conditions are typically considered as separate entities, they often co-exist which may be important in both understanding their pathophysiology and determining the best treatment strategy. Diabetes mellitus is twice as common in patients with chronic venous disease compared with the general population. Notably, a large proportion of patients with diabetes mellitus present with venous disorders, although this is often overlooked. The etiology of chronic venous disease is multifactorial, involving hemodynamic, genetic, and environmental factors which result in changes to the venous endothelium and structural wall as well as inflammation. Inflammation, endothelial dysfunction and hyperfiltration or leakage, are commonly observed in diabetes mellitus and cause various diabetic microvascular complications. Both diseases are also influenced by the increased expression of adhesion molecules, chemokines, and cytokines, and are characterized by the presence of vessel hypertension. Consequently, despite differences in etiology, the pathophysiology of both chronic venous disease and diabetic microangiopathy appears to be driven by endothelial dysfunction and inflammation. Treatment strategies should take the co-existence of chronic venous disease and diabetic microangiopathy into account. Compression therapy is recommended in inflammatory conditions that have an edema component as seen in both chronic venous disease and diabetes mellitus. Lifestyle changes like weight loss and exercise, will improve metabolic state and lower inflammation and should be promoted in these patients. Additionally, both patient populations may benefit from venoactive drugs. (Cite this article as: Gastaldi G, Pannier F, Roztocil K, Lugli M, Mansilha A, Haller H, et al. Chronic venous disease and diabetic microangiopathy: pathophysiology and commonalities. Int Angiol 2021;40:457-69. DOI: 10.23736/S0392-9590.21.04664-2)

Klasifikace

  • Druh

    J<sub>imp</sub> - Článek v periodiku v databázi Web of Science

  • CEP obor

  • OECD FORD obor

    30202 - Endocrinology and metabolism (including diabetes, hormones)

Návaznosti výsledku

  • Projekt

  • Návaznosti

    N - Vyzkumna aktivita podporovana z neverejnych zdroju

Ostatní

  • Rok uplatnění

    2021

  • Kód důvěrnosti údajů

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Údaje specifické pro druh výsledku

  • Název periodika

    International angiology

  • ISSN

    0392-9590

  • e-ISSN

  • Svazek periodika

    40

  • Číslo periodika v rámci svazku

    6

  • Stát vydavatele periodika

    IT - Italská republika

  • Počet stran výsledku

    13

  • Strana od-do

    457-469

  • Kód UT WoS článku

    000727449200002

  • EID výsledku v databázi Scopus

    2-s2.0-85121823089