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OBJECTIVE: The aim of this study is to compare tissue sodium and fat content in the upper and lower extremities of participants with lipedema versus controls using magnetic resonance imaging (MRI). METHODS: MRI was performed at 3.0 T in females with lipedema (n = 15, age = 43.2 ± 10.0 years, BMI = 30.3 ± 4.4 kg/m2 ) and controls without lipedema (n = 14, age = 42.8 ± 13.2 years, BMI = 28.8 ± 4.4 kg/m2 ). Participants were assessed for pain and disease stage. Sodium MRI was performed in the forearm and calf to quantify regional tissue sodium content (TSC, mmol/L). Chemical-shift-encoded water-fat MRI was performed in identical regions for measurement of fat/water (ratio). RESULTS: In the calf, skin TSC (16.3 ± 2.6 vs. 14.4 ± 2.2 mmol/L, P = 0.04), muscle TSC (20.3 ± 3.0 vs. 18.3 ± 1.7 mmol/L, P = 0.03), and fat/water (1.03 ± 0.37 vs. 0.56 ± 0.21 ratio, P < 0.001) were significantly higher in participants with lipedema versus control participants. In the forearm, skin TSC (13.4 ± 3.3 vs. 12.0 ± 2.3 mmol/L, P = 0.2, Cohen's d = 0.50) and fat/water (0.65 ± 0.24 vs. 0.48 ± 0.24 ratio, P = 0.07, Cohen's d = 0.68) demonstrated moderate effect sizes in participants with lipedema versus control participants. Calf skin TSC was significantly correlated with pain (Spearman's rho = 0.55, P = 0.03) and disease stage (Spearman's rho = 0.82, P < 0.001) among participants with lipedema. CONCLUSIONS: MRI-measured tissue sodium and fat content are significantly higher in the lower extremities, but not upper extremities, of patients with lipedema compared with BMI-matched controls.

BACKGROUND: Lymphatic insufficiency might play a significant role in the pathophysiology of lipoedema. Liposuction is up to now the best treatment. As liposuction is invasive, the technique could destruct parts of the lymphatic system and by this aggravate the lymphatic component and/or induce lymphoedema. We investigated the function of the lymphatic system in lipoedema patients before and after tumescent liposuction and thus whether tumescent liposuction can be regarded as a safe treatment. METHODS: Lymphoscintigraphy was performed to quantify the lymph outflow of 117 lipoedema patients. Mean clearance percentages of radioactive protein loaded after 1 min with respect to the total injected dose and corrected for decay of the radiopharmaceutical in the subcutaneous lymphatics were used as functional quantitative parameters as well as the clearance percentages and inguinal uptake 2 h post injection. The results of lymphatic function in lipoedema patients were compared with values obtained from normal healthy volunteers. We also compared 50 lymphoscintigraphies out of the previous 117 lipoedema patients before and six months after tumescent liposuction. RESULTS: In 117 lipoedema patients clearance 2 h post injection in the right and left foot was disturbed in 79.5 and 87.2% respectively. The inguinal uptake 2 h post injection in the right and left groin was disturbed in 60.3 and 64.7% respectively. In 50 lipoedema patients mean clearance and inguinal uptake after tumescent liposuction were slightly improved, 0.01 (p = 0.37) versus 0.02 (p = 0.02), respectively. This is statistically not relevant in clearance. CONCLUSION: Lipoedema legs have a delayed lymph transport. Tumescent liposuction does not diminish the lymphatic function in lipoedema patients, thus tumescent liposuction can be regarded as a safe treatment.

Lipedema is a chronic, progressive disease of adipose tissue with lack of consistent diagnostic criteria. The aim of this study was a thorough comparative characterization of extracellular microRNAs (miRNAs) from the stromal vascular fraction (SVF) of healthy and lipedema adipose tissue. For this, we analyzed 187 extracellular miRNAs in concentrated conditioned medium (cCM) and specifically in small extracellular vesicles (sEVs) enriched thereof by size exclusion chromatography. No significant difference in median particle size and concentration was observed between sEV fractions in healthy and lipedema. We found the majority of miRNAs located predominantly in cCM compared to sEV enriched fraction. Surprisingly, hierarchical clustering of the most variant miRNAs showed that only sEVmiRNA profiles - but not cCMmiRNAs - were impacted by lipedema. Seven sEVmiRNAs (miR-16-5p, miR-29a-3p, miR-24-3p, miR-454-p, miR-144-5p, miR-130a-3p, let-7c-5p) were differently regulated in lipedema and healthy individuals, whereas only one cCMmiRNA (miR-188-5p) was significantly downregulated in lipedema. Comparing SVF from healthy and lipedema patients, we identified sEVs as the lipedema relevant miRNA fraction. This study contributes to identify the potential role of SVF secreted miRNAs in lipedema.

BACKGROUND: Selenium is a trace element, which is utilized by the human body in selenoproteins. Their main function is to reduce oxidative stress, which plays an important role in lymphedema and lipedema. In addition, selenium deficiency is associated with an impaired immune function. The aim of this study was to determine the prevalence of selenium deficiency in these conditions, and if it is associated with disease severity and an associated medical condition such as obesity. METHODS: This cross-sectional study is an anonymized, retrospective analysis of clinical data that was routinely recorded in a clinic specialized in lymphology. The data was comprised from 791 patients during 2012-2019, in which the selenium status was determined as part of their treatment. RESULTS: Selenium deficiency proved common in patients with lymphedema, lipedema, and lipo-lymphedema affecting 47.5% of the study population. Selenium levels were significantly lower in patients with obesity-related lymphedema compared to patients with cancer-related lymphedema (96.6 ± 18.0 μg/L vs. 105.1 ± 20.2 μg/L; p < 0.0001). Obesity was a risk factor for selenium deficiency in lymphedema (OR 2.19; 95% CI 1.49 to 3.21), but not in lipedema. CONCLUSIONS: In countries with low selenium supply, selenium deficiency is common, especially in lymphedema patients. Therefore, it would be sensible to check the selenium status in lymphedema patients, especially those with obesity, as the infection risk of lymphedema is already increased.

Lipedema is a frequently unrecognized and misdiagnosed disorder of the fatty tissue of extremities and hips, which affects almost purely women. The beginning of the disease usually occurs with hormonal changes, such as puberty, pregnancy, or menopause. Women suffer from pain, easy bruising, and disfigurement, which may lead to early immobility and social stress. Accurate diagnosis and treatment are essential. The differentiation between obesity and lipedema is difficult, as these two different entities often occur together. Other differential diagnoses are lymphedema, benign lipohypertrophy, and Dercum’s disease. A therapy targeting the underlying cause of lipedema is not available because the exact etiology of the disorder is not clarified yet. Decongestive physical therapy is the basic conservative treatment, which is usually necessary lifelong. However, liposuction has led to a paradigm shift in the treatment of lipedema. The purposes of this article are to describe the symptoms and treatment options of the still fairly unknown disease Lipedema and to show the distinctions to its differential diagnoses.

OBJECTIVE: Lipedema is a disorder of adipose tissue characterized by abnormal subcutaneous fat deposition, leading to swelling and enlargement of the lower limbs and trunk. The aim of this study was to evaluate the lipedema phenotype by investigating the role of polymorphisms related to IL-6 (rs1800795) gene in people with diagnosis of lipedema. The second aim was to identify indicators of body composition, useful for a differential analysis between subjects with lipedema and the control group. PATIENTS AND METHODS: Two groups are involved in the study, 45 women with lipedema (LIPPY) and 50 women randomly chosen from the population as Control (CTRL). Clinical and demographical variables recorded include weight, height, body mass index (BMI) and circumference measurements. Body composition (Fat mass, FM; lean mass, LM) was assessed by Dual-energy X-ray Absorptiometry (DXA). The genetic tests for IL-6 (rs18oo795) gene were performed for both groups, using a saliva sample. RESULTS: The study of the relationship between the IL-6 (rs1800795) gene polymorphism, the anthropometric values and the body composition indices has provided the following significant results: subjects with diagnosis of lipedema present statistically significant increased values with regard to weight, BMI, waist, abdomen and hip circumferences, arms, legs and whole FM (% and kg), gynoid FM (kg), legs LM (kg) and ASMMI. Moreover, the value of the waist hip ratio was found to be decreased. CONCLUSIONS: For the first time, we suggested that IL-6 gene polymorphism could characterize subjects with lipedema respect to Normal Weight Obese and obese subjects. The intra-group comparisons (LIPPY carriers vs. LIPPY non-carriers and CTRL carriers vs. CTRL non-carriers) showed no statistically significant values. In contrast, the inter-group comparisons (LIPPY non-carriers vs. CTRL non-carriers and LIPPY carriers vs. CTRL carriers) resulted statistically significant. We have identified other indices, such as leg index, trunk index, abdominal index, total index, that could be promising clinical tools for diagnosis of the lipedema phenotype and for predicting the evolution of the disease.

Lipedema is a painful loose connective tissue disorder characterized by a bilaterally symmetrical fat deposition in the lower extremities. The goal of this study was to characterize the adipose-derived stem cells (ASCs) of healthy and lipedema patients by the expression of stemness markers and the adipogenic and osteogenic differentiation potential. Forty patients, 20 healthy and 20 with lipedema, participated in this study. The stromal vascular fraction (SVF) was obtained from subcutaneous thigh (SVF-T) and abdomen (SVF-A) fat and plated for ASCs characterization. The data show a similar expression of mesenchymal markers, a significant increase in colonies (p < 0.05) and no change in the proliferation rate in ASCs isolated from the SVF-T or SVF-A of lipedema patients compared with healthy patients. The leptin gene expression was significantly increased in lipedema adipocytes differentiated from ASCs-T (p = 0.04) and the PPAR-γ expression was significantly increased in lipedema adipocytes differentiated from ASCs-A (p = 0.03) compared to the corresponding cells from healthy patients. No significant changes in the expression of genes associated with inflammation were detected in lipedema ASCs or differentiated adipocytes. These results suggest that lipedema ASCs isolated from SVF-T and SVF-A have a higher adipogenic differentiation potential compared to healthy ASCs.

The growth and differentiation of adipose tissue-derived stem cells (ASCs) is stimulated and regulated by the adipose tissue (AT) microenvironment. In lipedema, both inflammation and hypoxia influence the expansion and differentiation of ASCs, resulting in hypertrophic adipocytes and deposition of collagen, a primary component of the extracellular matrix (ECM). The goal of this study was to characterize the adipogenic differentiation potential and assess the levels of expression of ECM-remodeling markers in 3D spheroids derived from ASCs isolated from both lipedema and healthy individuals. The data showed an increase in the expression of the adipogenic genes (ADIPOQ, LPL, PPAR-&gamma; and Glut4), a decrease in matrix metalloproteinases (MMP2, 9 and 11), with no significant changes in the expression of ECM markers (collagen and fibronectin), or integrin A5 in 3D differentiated lipedema spheroids as compared to healthy spheroids. In addition, no statistically significant changes in the levels of expression of inflammatory genes were detected in any of the samples. However, immunofluorescence staining showed a decrease in fibronectin and increase in laminin and Collagen VI expression in the 3D differentiated spheroids in both groups. The use of 3D ASC spheroids provide a functional model to study the cellular and molecular characteristics of lipedema AT.

Lipedema is a disease with high prevalence but low recognition. It is often misdiagnosed and underdiagnosed. Obesity and lymphoedema are the most common differential diagnoses and can also coexist in patient with lipedema. Its broad range of presentation and fat distribution types contribute to this confusion. It is likely that lipedema symptom variations and presentation forms are often associated with hormonal variations, chronic low-grade systemic inflammation, and wide polygenic variations. This paper presents a theory regarding the clinical evolution of lipedema clinical and its involvement with other diseases, suggesting a three-phase approach for treatment.

The metabolic consequences of obesity arise from local inflammation within expanding adipose tissue. In pre-clinical studies targeting various inflammatory factors, systemic metabolism can be improved through reduced adipose inflammation. Lymphatic vessels are a critical regulator of inflammation through roles in fluid and macromolecule transport and immune cell trafficking and immunomodulation. Lymphangiogenesis, the expansion of the lymphatic network, is often a necessary step in restoring tissue homeostasis. Using Adipo-VD mice, a model of adipocyte-specific, inducible overexpression of the potent lymphangiogenic factor vascular endothelial growth factor-D (VEGF-D), we previously identified that dense de novo adipose lymphatics reduced immune accumulation and improved glucose homeostasis in obesity. On chow diet, however, Adipo-VD mice demonstrated increased adipose tissue immune cells, fibrosis, and inflammation. Here, we characterize the time course of resident macrophage accumulation and lymphangiogenesis in male and female Adipo-VD mice fed chow and high fat diets, examining multiple adipose depots over 4 months. We find that macrophage infiltration occurs early, but resolves with concurrent lymphatic expansion that begins robustly after 1 month of VEGF-D overexpression in white adipose tissue. In obesity, female Adipo-VD mice exhibit reduced lymphangiogenesis and maintain a more glycolytic metabolism compared to Adipo-VD males and their littermates. Adipose lymphatic structures appear to expand by a lymphvasculogenic mechanism involving lymphatic endothelial cell proliferation and organization with a cell source we that failed to identify; hematopoietic cells afford minimal structural contribution. While a net positive effect occurs in Adipo-VD mice, adipose tissue lymphangiogenesis demonstrates a dichotomous, and time-dependent, inflammatory tissue remodeling response.

Lipomas are defined as a common subcutaneous tumor composed of adipose (fat) cells, often encapsulated by a thin layer of fibrous tissue.[1] In fact, these are the frequently encountered neoplasms by the clinicians. [2] Clinically, they often present in the body's cephalic part, specifically in the head, neck, shoulders, and backs of patients. However, they can less commonly be seen elsewhere, for example, the thighs. The tumors typically lie in the subcutaneous tissues of patients. The masses are often benign, and while the age of onset can vary. There is usually no reason for treatment. They pose no threat to the patient unless they are uncomfortable due to being located on joints or rapidly growing, which is uncommon, as the typical lipoma growth is slow. Lipomas can sometimes, though rare, be associated with certain disorders such as multiple hereditary lipomatosis, Gardner syndrome, adiposis dolorosa, and Madelung disease.[3] [4] Some unconventional forms of lipomas include the following: angiolipoma, chondroid lipoma, lipoblastoma, myolipoma, pleomorphic lipoma/spindle cell lipoma, intramuscular and intermuscular lipoma, lipomatosis of nerve, lipoma of the tendon sheath and joint, lipoma arborescens, multiple symmetric lipomatosis, diffuse lipomatosis, adiposis dolorosa, and hibernoma.

Purpose To quantify chemical exchange saturation transfer contrast in upper extremities of participants with lymphedema before and after standardized lymphatic mobilization therapy using correction procedures for B0 and B1 heterogeneity, and T1 relaxation. Methods Females with (n = 12) and without (n = 17) breast cancer treatment-related lymphedema (BCRL) matched for age and body mass index were scanned at 3.0T MRI. B1 efficiency and T1 were calculated in series with chemical exchange saturation transfer in bilateral axilla (B1 amplitude = 2µT, Δω = ±5.5 ppm, slices = 9, spatial resolution = 1.8 × 1.47 × 5.5 mm3). B1 dispersion measurements (B1 = 1-3 µT; increment = 0.5 µT) were performed in controls (n = 6 arms in 3 subjects). BCRL participants were scanned pre- and post-manual lymphatic drainage (MLD) therapy. Chemical exchange saturation transfer amide proton transfer (APT) and nuclear Overhauser effect (NOE) metrics corrected for B1 efficiency were calculated, including proton transfer ratio (PTR'), magnetization transfer ratio asymmetry , and apparent exchange-dependent relaxation (AREX'). Nonparametric tests were used to evaluate relationships between metrics in BCRL participants pre- versus post-MLD (two-sided P &lt; 0.05 required for significance). Results B1 dispersion experiments showed nonlinear dependence of Z-values on B1 efficiency in the upper extremities; PTR' showed &lt; 1% mean fractional difference between subject-specific and group-level correction procedures. PTR'APT significantly correlated with T1 (Spearman's rho = 0.57, P &lt; 0.001) and body mass index (Spearman's rho = −0.37, P = 0.029) in controls and with lymphedema stage (Spearman's rho = 0.48, P = 0.017) in BCRL participants. Following MLD therapy, PTR'APT significantly increased in the affected arm of BCRL participants (pre- vs. post-MLD: 0.41 ± 0.05 vs. 0.43 ± 0.03, P = 0.02), consistent with treatment effects from mobilized lymphatic fluid. Conclusion Chemical exchange saturation transfer metrics, following appropriate correction procedures, respond to lymphatic mobilization therapies and may have potential for evaluating treatments in participants with secondary lymphedema.

Lipedema is a chronic and progressive disease of adipose tissue caused by abnormal fat accumulation in subcutaneous tissue. Although there is no known cure for lipedema, possible complications can be prevented with conservative and surgical treatments. One of the conservative treatment options is physiotherapy and rehabilitation (PR). When the literature is examined, few studies focusing on the efficacy of PR were found for this patient group. The purpose of this review is to provide a better understanding of the effectiveness of PR applications by compiling existing studies. A bibliographic PubMed search was performed for published studies regarding PR in lipedema management in June 2019 including the last 58 years (1951-2019). Articles were chosen by reading the abstracts and subsequently data were analyzed by reading the entire text through full-text resources. A total of 15 studies met inclusion criteria. Results document how lipedema patients are benefited by PR and the effectiveness of different types of PR programs. The current review also showed that complex decongestive physiotherapy, gait training, hydrotherapy, aerobic exercise, and resistance exercise training each have value in the management of lipedema. The effects of PR for the treatment of lipedema are variable among studies, although overall PR seems to be effective in lipedema management. Although physiotherapy applications have a potentially important role in the management of lipedema, they should be used in combination with other treatment modalities. More studies with higher quality are needed to fully demonstrate the effect and efficacy of PR in lipedema patients.

Lipedema can cause chronic pain and increases patients’ risk for conditions such as lymphedema and venous disease. This author explores how lipedema affects the body, why its effects are disproportionate in the lower body, and how to diagnose and manage the condition.

Obesity is a leading cause of cardiovascular diseases and cancer. Body mass is regulated by the balance between energy uptake and energy expenditure. The etiology of obesity is determined by multiple factors including genetics, nutrient absorption, and inflammation. Lymphatic vasculature is starting to be appreciated as a critical modulator of metabolism and obesity. The primary function of lymphatic vasculature is to maintain interstitial fluid homeostasis. Lymphatic vessels absorb fluids that extravasate from blood vessels and return them to blood circulation. In addition, lymphatic vessels absorb digested lipids from the intestine and regulate inflammation. Hence, lymphatic vessels could be an exciting target for treating obesity. In this article, we will review our current understanding regarding the relationship between lymphatic vasculature and obesity, and highlight some open questions.

Lipedema is a chronic, progressive, painful, increased deposition subcutaneous fat tissue in women with a clear disproportion between the trunk and extremities. Lipedema offen lead to oedema, which are worsened by orthostasis, and hematoma after minor injury. The pathogenesis is unknown and no curative treatment is available. Conservative therapy consisting of lymphatic drainage and compression stockings is often recommended, but is only effective against the edema component. Some patients show a short-term improvement when treated in this way. Permanent reduction of the pathological subcutaneous fat on the legs and arms has become possible by employing advanced liposuction techniques using microcannula technology in local tumescent anaesthesia.

Genetic or acquired defects of the lymphatic vasculature often result in disfiguring, disabling, and, occasionally, life-threatening clinical consequences. Advanced forms of lymphedema are readily diagnosed clinically, but more subtle presentations often require invasive imaging or other technologies for a conclusive diagnosis. On the other hand, lipedema, a chronic lymphatic microvascular disease with pathological accumulation of subcutaneous adipose tissue, is often misdiagnosed as obesity or lymphedema; currently there are no biomarkers or imaging criteria available for a conclusive diagnosis. Recent evidence suggests that otherwise-asymptomatic defective lymphatic vasculature likely contributes to an array of other pathologies, including obesity, inflammatory bowel disease, and neurological disorders. Accordingly, identification of biomarkers of lymphatic malfunction will provide a valuable resource for the diagnosis and clinical differentiation of lymphedema, lipedema, obesity, and other potential lymphatic pathologies. In this paper, we profiled and compared blood plasma exosomes isolated from mouse models and from human subjects with and without symptomatic lymphatic pathologies. We identified platelet factor 4 (PF4/CXCL4) as a biomarker that could be used to diagnose lymphatic vasculature dysfunction. Furthermore, we determined that PF4 levels in circulating blood plasma exosomes were also elevated in patients with lipedema, supporting current claims arguing that at least some of the underlying attributes of this disease are also the consequence of lymphatic defects., , Characterization of plasma-circulating exosomes from mouse models and patients with lymphatic dysfunction indicate that PF4 is a promising biomarker for the diagnosis of lymphatic disorders.