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Background: Emerging evidence suggests that lipedema may share hormonal, inflammatory, and genetic mechanisms with gynecologic diseases, particularly endometriosis. However, the extent and nature of these interrelationships remain poorly characterized, supporting the need for this scoping review. Objectives: To map and synthesize the available evidence on the clinical, pathophysiological, and epidemiological interrelationships between lipedema in women, endometriosis, and other gynecologic diseases. Methods: Searches were conducted in international and regional health databases, including MEDLINE (PubMed), CINAHL, Scopus, Embase, Web of Science, the Cochrane Library, LILACS/VHL, APA PsycInfo, SciELO, Epistemonikos, and La Referencia, as well as grey literature sources and relevant institutional websites. There were no language restrictions. The search period began in 1940, the year in which lipedema was first described by Allen and Hines. Study selection followed a two‐stage process conducted independently by two reviewers, consisting of title and abstract screening followed by full‐text review. Data extraction was performed using a predeveloped and peer‐reviewed instrument covering participants, concept, context, study methods, and main findings. The review protocol was registered in the Open Science Framework (https://doi.org/10.17605/OSF.IO/D65GS). Results: Twenty‐five studies from ten countries were included. Synthesis of the available evidence indicates that lipedema is consistent with a systemic condition involving metabolic and hormonal dimensions, characterized by onset related to reproductive milestones, a high frequency of gynecologic and endocrine comorbidities, and molecular features overlapping with steroid‐dependent pathologies. These findings reflect a recent shift from a predominantly lymphovascular paradigm toward a more integrated endocrinometabolic framework. Conclusions: The findings indicate that lipedema clusters with hormone‐sensitive gynecologic and endocrine features across reproductive life stages.
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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.