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Lipedema is a chronic and progressive adipose tissue disorder characterized by disproportionate fat accumulation, microvascular dysfunction, chronic inflammation, and progressive fibrosis. Despite its prevalence and significant impact on quality of life, current therapeutic approaches remain largely symptomatic and fail to address the underlying biological mechanisms of the disease. Emerging evidence suggests that lipedema should be understood as a multifactorial condition involving genetic susceptibility, endothelial alterations, immune dysregulation, and extracellular matrix remodeling. In this context, pharmacological strategies targeting these pathways have gained increasing attention. Metformin, through activation of AMP-activated protein kinase (AMPK), exerts antifibrotic and immunometabolic effects, including inhibition of TGF-β signaling, reduction of extracellular matrix deposition, and modulation of adipose tissue inflammation. In parallel, incretin-based therapies, particularly glucagon-like peptide-1 (GLP-1) receptor agonists and dual GLP-1/GIP agonists such as tirzepatide, have demonstrated pleiotropic effects that extend beyond weight reduction, including improvements in metabolic homeostasis, reduction of systemic inflammation, and enhancement of endothelial function. These therapies appear to act through complementary mechanisms, with metformin primarily targeting tissue remodeling and fibrosis, and incretin-based therapies exerting broader systemic effects on metabolism, inflammation, and vascular integrity. This review proposes a hypothesis-generating mechanistic framework, supporting a shift from weight-centric and symptomatic approaches toward disease-modifying strategies. Although current evidence in lipedema is largely indirect, the convergence of experimental and clinical data provides a strong rationale for further investigation. Future studies should focus on evaluating combined therapeutic approaches and identifying biomarkers that reflect fibrosis, inflammation, and microvascular dysfunction, with the aim of developing targeted and personalized treatments for this complex disorder.
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Background: The aim of the study was to verify the effectiveness of a 5-week intensive protocol of multilayer bandaging alone or in combination with diet, applied to the clinical practice of lipedema. Methods: 114 women with lipedema were studied, divided into three groups: 35 women were treated with multilayer bandaging in biweekly sessions for 5 weeks, 48 were treated with the same bandaging protocol combined with an anti-inflammatory diet, and 31 women received no treatment. The effect on anthropometry, lower limb volume, pain caused by the tissue fold, and subjective symptoms were evaluated. Results: Women who completed the 5-week intensive protocol of multilayer bandaging showed a statistically significant reduction in all observed parameters: body weight, waist and hip circumference, lower limb volume, pain, and subjective symptoms. The group of women treated with multilayer bandaging and diet showed a significantly greater reduction in lower limb volume and body weight. The treatments were effective regardless of age, BMI, clinical stage, and the presence of fovea in both groups. The wearing time with the multilayer bandage had a positive correlation in the group treated with bandage in combination with diet. Conclusion: A 5week intensive protocol of multilayer bandaging of the lower limbs is an effective treatment for reducing the symptoms and clinical signs of lipedema at all stages of the disease, even in the absence of edema. Adding nutritional therapy during the bandaging cycle increases the effectiveness of the treatment on the volume of the affected extremities and body weight.