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Background/Objectives: Lipedema is a chronic and progressive adipose tissue disorder characterized by the abnormal accumulation of subcutaneous fat, predominantly in the legs and occasionally in the arms. The symptom that most signi cantly affects the quality of life is pain. Ultrasound elastography is an imaging technology that allows for measuring tissue stiffness quantitatively. This study aims to evaluate the relationship between accompanying pain in patients with lipedema and tissue elasticity measured using shear-wave elastography (SWE). Methods: Our study was designed as an observational, analytical and cross-sectional study. The visual analog scale (VAS) was used to assess pain, while the PainDetect questionnaire was utilized to evaluate neuropathic pain. The evaluation of tissue elasticity and brosis was conducted using the SWE method. Results: This research assessed thirty- ve patients, revealing an average age of 45.2 years and an average VKI of 33.6 kg/m². 60% of the patients had a lipedema diagnosis in their family history. Both age (p<0.01) and BMI (p<0.001) values were moderately correlated with all subcutaneous adipose tissue measurements, while no correlation was observed in SWE measurements. Only the level of the thigh in the SWE-Elasticity (SWE-E) values was related to VAS (p=0.03). Additionally, PainDetect data revealed correlations with SWE-Velocity (SWE-V) and SWE-E in both the right and left thighs. Conclusions: While SWE measurements were not correlated with skin adipose tissue, SWE measurements were correlated with pain and neuropathic pain in patients with lipedema. This nding highlights a potentially important relationship between tissue elasticity and pain, which may warrant further exploration.
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Lipedema is a chronic, estrogen-sensitive adipose tissue disorder characterized by disproportionate subcutaneous fat accumulation, fibrosis, inflammation, and resistance to fat mobilization. Despite its high prevalence, lipedema remains poorly understood and frequently misdiagnosed. This narrative review proposes a novel pathophysiological model in which menopause acts as a critical turning point in the progression of lipedema, driven by estrogen receptor imbalance (ERβ predominance over ERα), intracrine estrogen excess, and adipose tissue dysfunction. We demonstrate how menopauseinduced estrogen deficiency amplifies adipose tissue dysfunction by suppressing ERα signaling, enhancing ERβ activity, and disrupting mitochondrial function, insulin sensitivity, and lipid oxidation. Concurrently, the upregulation of aromatase and 17β-HSD1, combined with the suppression of 17β-HSD2, sustains localized estradiol excess, perpetuating inflammation, fibrosis, and immune dysregulation. The molecular signature observed in lipedema closely mirrors that of other estrogen-driven gynecological disorders, such as endometriosis, adenomyosis, and uterine fibroids. Understanding these molecular mechanisms highlights the pivotal role of menopause as a catalyst for disease progression and provides a rationale for targeted therapeutic strategies, including hormonal modulation and metabolic interventions. This review reframes lipedema as an estrogen receptor– driven gynecological disorder, offering a new perspective to improve clinical recognition, diagnosis, and management of this neglected condition.