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Lipedema and obesity are chronic, frequently progressive disorders that can present with increased adipose-tissue volume, functional impairment and reduced quality of life. Although often approached as differential diagnoses, they frequently coexist and may aggravate one another. This narrative review addresses how lipedema and obesity interact biologically and clinically and what evidence supports a staged interdisciplinary approach to diagnosis and management. Obesity is increasingly conceptualized as an adiposity-based chronic disease characterized by excess adipose, abnormal adipose-tissue distribution or dysfunction, and associated medical or functional impairment. Obesity can impair lymphatic morphology and function, whereas lymphatic dysfunction may promote subcutaneous adipose-tissue expansion and fibrosis. Literature was identified through iterative PubMed searches and focused supplementary searches in Embase and the Cochrane Library. Publications were selected purposively for their relevance to predefined clinical and mechanistic domains; no systematic screening or formal risk-of-bias assessment was performed. This review synthesizes clinical overlap, biological evidence, diagnostic implications, and staged management for predominantly adult women with suspected or confirmed lipedema, including those with coexisting overweight or obesity. The proposed framework is intended to support clinical reasoning rather than serve as a formal guideline.

PURPOSE: Individuals with lipoedema may experience negative impacts that are not often identified through current quality-of-life measures. The aim of this study was to explore the experiences of individuals living with pre-existing lipoedema and their perceptions of how these experiences influence quality of life. METHODS: Participants with a prior diagnosis of lipoedema participated in a single semi-structured interview or focus group. These interviews/focus groups were transcribed verbatim, allowing for an inductive thematic analysis to be conducted. RESULTS: Sixteen participants were included and four main themes were identified. These included: the ongoing work of living with lipoedema, living with a restrictive and overwhelming condition, caught between self-acceptance and social judgement, and forced to navigate lipoedema alone. Across the four themes, 21 sub-themes emerged to convey the quality-of-life concerns experienced by individuals with lipoedema. CONCLUSIONS: Individuals living with lipoedema experience impacts on their quality-of-life across physical, psychological, and social aspects of life. This study highlights how the ongoing burden of physical symptoms, social perceptions, and healthcare-related challenges contributes to reduced quality-of-life for individuals living with lipoedema. Increased knowledge and awareness amongst healthcare providers is needed to improve care received by individuals living with this condition.

Rare adipose disorders are abnormal subcutaneous adipose tissue diseases that present as a spectrum of soft tissue abnormalities that may be encountered by plastic surgeons. Presentation ranges from distinct subcutaneous masses in characteristic distributions in the body to large generalized fatty deposits. It is imperative to recognize these rare adipose disorders, as they are typically refractory to standard treatment approaches to obesity, such as weight loss, lifestyle modifications, pharmacologic therapy, and bariatric surgery. In this review, we provide a complete and updated review of lipedema, Madelung disease, familial multiple lipomatosis, and Dercum’s disease as well as present a case series highlighting our surgical approach to rare adipose disorders.

Timely diagnosis of lipoedema remains challenging, with prolonged delays contributing to reduced quality of life. The aim of this study was to analyse the time from first symptom onset to diagnosis, and identify factors associated with diagnostic intervals.

Lipedema is a chronic disorder of subcutaneous adipose tissue characterized by symmetrical fat accumulation of the extremities and resistance to conventional weight loss. Therapeutic options remain limited, and clinical data on nutritional interventions are scarce. A 37-year-old woman with stage II lipedema underwent a ten-day medically supervised fasting program embedded in a multimodal intervention that also included physical activity after limited response to standard conservative management. Body weight decreased from 78.7 to 73.7kg, and C-reactive protein from 22.5 to 0.82mg/L. Limb circumferences decreased at the calves (48 to 44–44.5cm) and thighs (65 to 58cm). Subcutaneous tissue thickness, measured by ultrasound, decreased at the medial malleolus (22 to 12–15mm) and at the mid-thigh (44 to 34.5mm), while remaining stable in the gluteal region (98mm). Elastography showed a persistent heterogeneous fibrosclerotic pattern. The patient reported a marked reduction in pain (approximately 80% during fasting, sustained at ~50% for over one month). No adverse events occurred. Altogether, this case is notable because objective ultrasound measurements and inflammatory biomarkers improved after a structured fasting intervention in a condition usually considered resistant to weight loss. Because the intervention was multimodal, the contribution of fasting cannot be isolated and controlled studies are warranted. This suggests that medically supervised fasting may improve inflammatory status and tissue structure in lipedema and warrants further investigation in controlled studies.

Lipedema is a chronic adipose tissue disorder characterized by pain and disproportionate fat distribution. Although exercise is an important component of lipedema management, evidence regarding exercise behavior, physical activity, and related barriers remains limited. This study aimed to investigate exercise behavior, physical activity level, and perceived barriers in women with lipedema compared to healthy controls.

A previously healthy 35-year-old woman developed recurrent syncope and dyspnoea two days after extensive thigh liposuction for lipedema. CT pulmonary angiography revealed a large saddle embolus with peripheral emboli. Fat embolism was initially suspected; however, imaging findings and laboratory parameters supported a thromboembolic origin. Treatment with anticoagulation was complicated by postoperative bleeding. This case report highlights the importance of considering both fat embolism and thromboembolic pulmonary embolism after liposuction.

Lipedema is a chronic, progressive, and often underdiagnosed disease characterized by the pathological, bilateral, and symmetrical accumulation of adipose tissue. This distribution results in disproportionate and painful swelling of the limbs. Typically extending distally from the hips, this predominantly female condition is frequently misidentified as lifestyle-induced obesity or bilateral lymphedema. This review aims to provide a comprehensive overview of the current understanding of structural and functional abnormalities in myocardial dimensions, mechanics, valves, and major arteries in patients with lipedema. According to the existing literature, left atrial enlargement, left ventricular rotational abnormalities, mitral annular dilation, and increased aortic stiffness have been identified in patients with lipedema. These findings suggest latent but significant alterations in left heart physiology. Although current data remain limited and are primarily focused on the left heart and the aorta, the rapid evolution of cardiac imaging technologies suggests that both clinical knowledge and the body of research in this field are poised for significant expansion.

BACKGROUND: Lipedema is a common, female-predominant disorder characterized by disproportionate, painful lower-limb adipose tissue, and it still lacks an objective biomarker, a disease-modifying therapy, or consensus on whether its core lesion is inflammatory. Its molecular literature is openly contradictory, reporting both immune enrichment and immune down-regulation in the same gluteofemoral depot. Because the dominant morbidity is pain rather than adipose mass, this ambiguity carries direct clinical cost. We therefore asked the following three questions: whether the reported molecular hallmarks survive control for cell-type composition, whether pain and adipose volume behave as separable endpoints, and what the germline architecture implies about the primary lesion. MATERIALS AND METHODS: From a theory-neutral standpoint, we reprocessed the largest publicly deposited adipose bulk RNA-seq dataset of lipedema (14 women with lipedema versus seven controls, paired by depot) with Salmon (College Park, MD: University of Maryland) and DESeq2 (Seattle, WA: Bioconductor Project), estimated cell-type composition by single-sample gene-set enrichment (ssGSEA), and refitted differential expression with leukocyte and erythroid composition covariates to test identifiability. We also synthesized published treatment cohorts (pain versus volume) and reviewed the architecture of germline genome-wide association studies (GWAS). RESULTS: There is no transcriptional lipolytic brake (ADRA2A +0.001; lipases unchanged or mildly up). The apparent immune down-regulation is not identifiable from blood content; adjusting for tissue composition reduces genome-wide-significant genes from 1,501 to four, with blood content correlated with disease at r approximately -0.7, so bulk data can neither establish nor exclude immune involvement, including the NLRP3 inflammasome. Pain and adipose volume are dissociable across treatments, so body weight is a confounded endpoint. The germline architecture reported to date (GRB14-COBLL1, VEGFA, RSPO3, ADAMTS9) is adipo-vascular and extracellular-matrix-based rather than immune, although the largest contributing study defined cases by a bioimpedance proxy rather than by clinical diagnosis. CONCLUSIONS: Lipedema's inflammatory status is currently undecidable from composition-confounded bulk tissue rather than settled, which explains the field's contradictory literature; the germline evidence, limited by its case definitions, supports as a hypothesis an adipo-vascular and connective program rather than a primary immune lesion; and pain, not weight, should anchor trials. We specify, but do not perform, the single decisive experiment - paired thigh-versus-abdomen single-nucleus RNA-seq with explicit composition control.

Lipedema is a chronic disorder characterized by the abnormal and disproportionate accumulation of painful subcutaneous adipose fat, primarily affecting the lower limbs and occurring almost exclusively in women. The aim of this controlled cross-sectional study was to compare body image, psychological distress, and psychological well-being in women with (n = 77) and without lipedema (n = 32). Psychological functioning was assessed using validated measures of depressive symptoms (PHQ-9), eating attitudes (EAT-26), perceived stress (PSS), medically unexplained symptoms (M.U.S.), psychological well-being (WHO-5), life satisfaction (SWLS), psychological flexibility (AAQ-II), pain intensity (VAS), together with measures of body image, lifetime psychological burden, maladaptive cognitive beliefs, symptom severity, and anthropometric parameters. Compared with controls, women with lipedema reported significantly greater body image dissatisfaction, perceived distress, M.U.S., depressive symptoms, disordered eating attitudes, and pain, together with lower psychological well-being, life satisfaction, and psychological flexibility (all p < 0.001). Within the lipedema group, PHQ-9 scores were significantly predicted by M.U.S. scores, maladaptive cognitions, and pain intensity (VAS), whereas EAT-26 scores were predicted by PHQ-9 scores and maladaptive cognitions. These findings indicate that lipedema is associated with a substantial psychological burden and support integrating psychological assessment and intervention into multidisciplinary care.

Lipedema and obesity are often misdiagnosed or clinically confused yet arise via distinct mechanisms, complicating diagnosis and treatment. This review synthesizes evidence differentiating these conditions across genetic, hormonal, inflammatory and mechanical pathways to identify therapeutic targets. Lipedema may involve genetic predisposition (forkhead box C2 [FOXC2], prospero homeobox 1 [PROX1]), hormonal dysregulation with aberrant aromatase activity, and altered adipogenesis (peroxisome proliferator-activated receptor gamma [PPARγ], CCAAT/enhancer-binding protein [C/EBP]). A proinflammatory microenvironment with macrophage M1/M2 imbalance, elevated interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), and extracellular matrix remodeling is hypothesized to drive fibrosis. Emerging evidence implicates gut-derived endotoxemia (lipopolysaccharide [LPS]-toll-like receptor 4 [TLR4]-nuclear factor kappa-B [NF-κB]) and mechanotransduction (Yes-associated protein [YAP]/transcriptional coactivator with PDZ-binding motif [TAZ]) in adipocyte hypertrophy and treatment resistance. Obesity involves systemic metabolic dysfunction with visceral adiposity and cardiometabolic comorbidities. Lipedema patients maintain metabolic health, exhibit gluteofemoral fat distribution and experience neuropathic pain via nociceptor sensitization (transient receptor potential vanilloid 1 [TRPV1] and ankyrin 1 [TRPA1]) with central amplification. Weight-loss interventions are ineffective, necessitating targeted strategies. Promising targets include TLR4 antagonism, vascular endothelial growth factor C/vascular endothelial growth factor receptor-3 (VEGF-C/VEGFR3) modulation for lymphatic enhancement, YAP/TAZ inhibition and neuromodulators for pain. Physical therapy functions as a biological modifier targeting inflammation, lymphatic drainage and mechanotransduction. This review highlights promising but largely hypothesis-generating molecular insights and calls for validated biomarkers, rigorous clinical trials, and mechanism-based therapies. Many of the pathways discussed require further confirmation in human studies.

Background: Lipedema is a chronic disorder of subcutaneous adipose tissue characterized by symmetrical fat accumulation in the extremities, pain, and orthostatic edema. Objectives: This study aimed to assess whether high-resolution cutaneous ultrasound can detect measurable tissue-level changes in subcutaneous tissue over six months. Methods: A retrospective, single-center, real-world longitudinal observational cohort study was conducted in 60 women with lipedema followed at three timepoints (baseline, 3 months, 6 months). High-resolution ultrasound (18–20 MHz) measured subcutaneous and dermal thickness at standardized anatomical sites. Results: All primary ultrasound parameters decreased significantly over six months of conservative multicomponent management, which included individualized nutritional counseling and physical activity. Medial proximal thigh subcutaneous thickness declined by 18.7% (48.2 to 39.2 mm; p < 0.001). Edema prevalence fell from 100% to 55.0%. Echogenicity improved significantly between 3 and 6 months, suggesting a delayed structural remodelling effect distinct from early volumetric reduction. Ultrasound reductions were inversely correlated with weight loss, suggesting that ultrasound captures tissue-level information not fully reflected by anthropometric measures alone. Conclusions: Standardized cutaneous high-resolution ultrasound detected consistent tissue-level modifications over six months of routine clinical follow-up, capturing changes beyond anthropometric measures and representing a candidate monitoring tool warranting evaluation in controlled study designs.

Background: Lipedema is a chronic progressive condition affecting approximately 10% of women, characterized by disproportionate subcutaneous adipose tissue accumulation and pain in the lower extremities. Standardized assessment methods for pain evaluation in lipedema remain limited. The Progressive Pain Check (PPC) method represents a potentially valuable tool for standardized pain assessment in lipedema patients. Objective: To evaluate the inter-rater reliability of the PPC method for clinical assessment of evoked pain in lipedema patients. Methods: Two independent assessors performed PPC evaluations. Inter-rater reliability was assessed using the Intraclass Correlation Coefficient [ICC(2,1), two-way random-effects, absolute agreement, single-measurement] with 95% confidence intervals (CI). Results: This study included 429 women diagnosed with lipedema (mean age 41.2 ± 11.5 years, mean disease duration 27.2 ± 12.6 years). Patient characteristics revealed mean BMI of 29.5 ± 6.9 kg/m2, predominantly Type III lipedema presentation, and disease onset during adolescence (mean age 14 ± 9.3 years). The PPC method demonstrated excellent inter-rater reliability between two independent assessors across all examined anatomical districts. Conclusions: The PPC method shows promise as a simple, repeatable, and standardized clinical tool for evoked pain assessment in lipedema patients. The demonstrated inter-rater reliability supports its potential utility in clinical practice. Further research is warranted to evaluate its intra-rater reliability, concurrent validity, and responsiveness in monitoring treatment effects.

The aesthetic-functional planning of the lower limbs is frequently conducted empirically, using idiosyncratic markings and limited standardization among specialists who work in this field. The absence of a common topographic language restricts clinical communication, technical reproducibility, documentation of results, and the integration between the aesthetic approach and the vascular/lymphatic assessment of the segment. This is a descriptive study of methodological development. Based on a review of the anatomic and surgical literature and prospective clinical application during body-contour consultations, six topographic zones of the lower limbs were defined: gluteal, trochanteric (saddlebag), thigh (anterior, medial, and posterior subunits), knee, crural (calf), and talocrural (ankle), each delimited by reproducible surface bony and muscular landmarks. Onto this map, the cartography of the zones of adherence, superficial and deep adipose planes separated by the superficial fascia, saphenous venous axes, and main lymphatic collector pathways was overlaid. A four-stage marking protocol was defined (orthostatism, marking of bony landmarks, zone delimitation, and coding of plane and intensity), with standardized photographic documentation. For each zone, the following are presented: anatomic boundaries, muscular and adipose content, vascular and lymphatic correlates, zones of adherence to be preserved, recommended working plane (deep, intermediate, or superficial), specific risks, and expected aesthetic outcomes. The map provides a common nomenclature among surgeons and enables technology to be prescribed by anatomic zone rather than by generic "region". This anatomofunctional zone-based marking provides a simple, low-cost, and reproducible instrument to structure the therapeutic planning of the lower limbs, aligning the aesthetic objective with the anatomic, vascular, and lymphatic constraints of the segment. Interobserver reliability studies and comparative clinical outcome studies are the necessary next step toward validation.

Lower extremity swelling has a broad differential diagnosis, including lymphedema, obesity-induced lymphedema, phlebolymphedema, and lipedema. Although these conditions may appear similar clinically, their pathophysiology and lymphoscintigraphic findings differ. Obesity, venous insufficiency, and abnormal adipose tissue can complicate image interpretation. We present four representative cases to illustrate characteristic imaging patterns across these conditions. These cases highlight the importance of interpreting lymphoscintigraphy in a clinical context.

BACKGROUND: Lipedema is a chronic disorder characterized by excessive, bilateral, and symmetrical deposition of subcutaneous adipose tissue, predominantly in the lower extremities. Despite its prevalence, lipedema is frequently misdiagnosed as lymphedema, and lymphoscintigraphy is commonly used to differentiate between the two. This systematic review synthesizes the available evidence regarding the most common lymphoscintigraphy findings in patients with lipedema. METHODS: This systematic review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. A comprehensive search was performed across the MEDLINE/PubMed, Embase, and Web of Science databases. Studies were included if they reported lymphoscintigraphy findings in patients with lipedema and provided a clear description of the imaging protocol. Extracted data included patient demographics, lymphoscintigraphy protocols, and imaging findings. RESULTS: Seven studies met the inclusion criteria, encompassing 470 patients, of whom 311 had lipedema. The mean age was 47.4 years, and all patients were women. The mean body mass index was 32.6 kg/m2. Lymphoscintigraphy findings were normal in 61.4% of patients with lipedema. Tortuous lymph vessels were the most common abnormality (56.8%), followed by collateral lymph vessels (49.1%) and popliteal node visualization (44.0%). Dermal backflow (3.8%) and secondary lymphedema (11.8%) were less frequent. CONCLUSIONS: Lymphoscintigraphic alterations in patients with lipedema seem to reflect lymphatic overload rather than frank insufficiency. However, significant heterogeneity in study methodologies precluded a quantitative meta-analysis. Future research should focus on establishing standardized, consensus-based imaging protocols to better define the role of lymphoscintigraphy in the diagnosis and staging of lipedema.

Background: Endometriosis and lipedema are chronic female-predominant disorders characterized by persistent pain that is frequently disproportionate to anatomical lesion burden. Although traditionally interpreted within distinct lesion-centered frameworks, both conditions exhibit striking clinical and epidemiological parallels, including hormonally modulated symptom dynamics, overlap with central pain syndromes, weak correlation between structural disease severity and pain intensity, and symptom clustering during reproductive transitions such as puberty, pregnancy, and menopause. Methods: This study aims to synthesize clinical, molecular, neuroimmune, and endocrine evidence on the interrelationship between endometriosis and lipedema, and to propose a hypothesis-generating neuroimmune framework linking both conditions. This integrative narrative review conducted a non-systematic literature search in PubMed/MEDLINE, Scopus, and Web of Science, focusing on mechanisms related to chronic pain, mast cell biology, TRPV1 signaling, CGRP-mediated neurogenic inflammation, intracrine steroidogenesis, and peripheral and central sensitization. Results: The review identifies convergent biological characteristics between the two diseases, including mast cell activation, macrophage polarization, endothelial dysfunction, fibrosis, angiogenesis, intracrine estrogen metabolism, and persistent inflammatory signaling. In endometriosis, direct evidence demonstrates increased sensory innervation, nerve growth factor expression, TRPV1 sensitization, CGRP-positive fibers, and mast cell-nerve interactions. In lipedema, convergent upstream mechanisms, including mast cell infiltration, elevated histamine levels, adipose tissue inflammation, and local estrogen activation, support the plausibility of a functionally analogous neuroimmune organization, despite incomplete direct neural characterization. In this context, the mast cell-TRPV1-CGRP axis is proposed as a biologically plausible framework, directly supported in endometriosis and currently hypothetical in lipedema, connecting peripheral sensitization, neurogenic inflammation, hormonal chronodependence, and central nociceptive amplification. The model further conceptualizes pain crises as transient events of instability within a sensitized neuroimmune network and proposes mechanistic phenotypes that integrate gastrointestinal, inflammatory, central, and hormonal triggers. Conclusion: Endometriosis and lipedema may represent topographically distinct manifestations of a shared neuroimmune process operating within hormone-sensitive tissues. Although the evidentiary basis remains asymmetric, with stronger mechanistic support in endometriosis than in lipedema, this framework provides a biologically plausible and experimentally testable model integrating endocrine, immune, neural, and vascular contributors to chronic pain amplification. This perspective supports coordinated translational investigation across reproductive biology, endocrinology, and pain medicine and may contribute to future mechanism-based stratification and therapeutic development. This work is hypothesis-generating and is not intended to establish causality or to provide clinical recommendations; all proposed mechanistic and therapeutic inferences require prospective experimental validation.