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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.
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Lipoedema is a chronic adipose tissue disorder mainly affecting women with excess subcutaneous fat deposition on the lower limbs, associated with pain and tenderness. There is often a family history of lipoedema, suggesting a genetic origin, but the contribution of genetics is not well studied. We conducted a genome-wide association study (GWAS) for this disorder in a clinically ascertained cohort from Spain and performed a meta-analysis with the UK lipoedema cohort GWAS. We then used the results of this study as a replication of the inferred UK Biobank “lipoedema phenotype” study. Whilst our meta-analysis alone did not identify any genome-wide significant associations, our clinical cohorts provide support for three loci identified through the UKBB study: the chr2q24.3 GRB14-COBLL1 locus (rs6753142, PMETA=1.64x10-6), chr6p21.1 VEGFA locus (rs4711750, PMETA=8.99x10-7) and the chr5q11.2 ANKRD55-MAP3K1 locus (rs3936510, PMETA=1.67x10-5). We identify numerous rare SNPs with strong association signals in our meta-analysis (P<1x10-6) with support in both UK and Spanish datasets, three of which also show nominal support in the UKBB (P<0.05). These findings provide a starting point towards understanding the genetic basis of clinical lipoedema and demonstrate the utility of the interplay of large-scale biobanks genetic data and clinically ascertained cohorts to elucidate the genetic architecture of lipoedema.
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