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DOI: 10.12687/phleb2413-2-2018
Obesity and chronic inflammation in phlebological and lymphatic diseases
Article in several languages: deutsch | EnglishPublication History
Eingereicht:
08 February 2018
Angenommen:
12 February 2018
Publication Date:
02 April 2018 (online)
Summary
The prevalence of obesity has continued to rise considerably during the last 15 years. There is a striking increase of cases with morbid obesity (BMI over 40 Kg/m2), especially among the elderly. Since venous thromboembolic events, chronic venous insufficiency and secondary lymphoedema also increase with age, the number of patients who suffer from these conditions and, at the same time, are obese and often multimorbid, rises disproportionately. Obesity, especially if it is visceral, causes all sorts of oedema to deteriorate, increases the risk of thromboembolic events and postthrombotic syndrome and can be the sole cause of the so called obesity-associated dependency- syndrome, or rather the obesity-associated functional venous insufficiency without obstruction or reflux, as it ought to be called, with its skin lesions characteristic of CEAP stages C4 to C6. Among the various causes of secondary lymphoedema obesity is by now the most common. Of patients suffering from lipoedema more than 50 percent are obese, with the secondary lymphoedema often to be seen in those cases being the direct consequence of obesity, not the lipoedema itself. In all the conditions mentioned above symptoms can be ameliorated by weight loss. Aside from mechanical factors like intraabdominal and intertriginous pressure which in turn raise the intravenous pressure in the legs, it is foremost the metabolic, proinflammatory and procoagulatory effects of the augmented visceral fat tissue which can explain the correlation between obesity and thrombosis, oedema and, probably, the skin changes, too. These effects can be identified by low levels of adiponectin, which has antiinflammatory and vasoprotective qualities, and high levels of leptin, characteristic of leptin resistance, inflammation and insulin resistance, insulin and intact proinsulin (precursor of insulin, indicating β-cell insufficiency). Plasminogen Activator Inhibitor-1 (PAI-1), preventing fibrinolysis, and proinflammatory cytokines like Interleukin-6 (Il-6), Interleukin-8 (Il-8) and Tumour Necrosis Factor-α (TNF-α) are also found to be raised. In addition to treating the acute or chronic symptoms by anticoagulation, compression, manual lymphdrainage and wound care, therapeutic measures must endeavour to sustainably reduce visceral fat tissue, and thus hyperinsulinaemia, insulin resistance and inflammation.
English version available at: www.phlebologieonline.de