Trasforma la Tua Vita con il Lipedema

BACKGROUND: Lipedema is a chronic adipose tissue disorder predominantly affecting women, often misdiagnosed as obesity or lymphedema. Emerging evidence points to microvascular dysfunction and chronic inflammation in its pathophysiology. This study aimed to compare complete blood count (CBC) parameters and derived inflammatory indices between women with lipedema and age-matched healthy controls, focusing on the potential diagnostic value of platelet indices such as PDW and MPV.

METHODS: We conducted a retrospective observational study including 45 women with clinically confirmed lipedema and 40 age matched healthy controls. CBC parameters and derived inflammatory indices were compared between groups without adjustment for body mass index (BMI).

RESULTS: The study included 45 women with lipedema and 40 healthy controls with similar age distributions. No statistically significant between group differences were observed in complete blood count parameters after correction for multiple comparisons, although PDW and MPV were numerically higher in the lipedema group.

CONCLUSION: In this exploratory study, PDW and MPV were numerically higher in women with lipedema than in controls, but these differences lost statistical significance after correction for multiple comparisons. These findings argue against PDW or MPV as standalone diagnostic markers of lipedema and indicate that future research should prioritize larger, BMI-matched cohorts and multimodal approaches that integrate platelet indices with tissue-level or imaging markers.

BackgroundLipedema is an adipose disorder associated with multiple impairments. Conservative treatments remain the mainstay of management, yet evidence regarding the effects of physical therapies on clinical, imaging, and body composition outcomes is limited. Radial extracorporeal shock wave therapy (rESWT) has been proposed as a non-invasive therapeutic option, although its impact is not fully established.MethodsThis was a prospective, longitudinal, within-patient study conducted in women with clinically diagnosed lipedema. One lower limb was treated with radial extracorporeal shock wave therapy (rESWT), whereas the contralateral limb served as an internal control. A total of 16 patients were initially assessed, of whom 12 completed the full follow-up and were included in the final analysis. rESWT was applied over six sessions (two sessions per week) using standardized parameters. Clinical outcomes (LEFS, EQ-5D, SF-36 Physical Function, and IPAQ) were assessed at baseline, 6 weeks, and 3 months. Ultrasound and elastography were used to evaluate subcutaneous tissue thickness and stiffness at predefined leg and thigh sites, while segmental bioimpedance analysis assessed body composition and fluid distribution. Longitudinal changes were analyzed using mixed-effects models.ResultsSignificant improvements were observed in functional capacity, quality of life, and physical activity levels at both 6 weeks and 3 months compared with baseline ( < .05). In contrast, no statistically significant changes were detected in ultrasound-derived tissue thickness, elastography measurements, or bioimpedance parameters over time, and no significant differences were detected between treated and control limbs within the constraints of the available sample size.ConclusionsrESWT was associated with meaningful clinical and functional improvements in patients with lipedema, despite the absence of detectable changes in tissue thickness, stiffness, or body composition. These findings suggest that the benefits of rESWT may be mediated through symptom modulation and functional adaptation rather than structural tissue modification, supporting its role as part of conservative, symptom-oriented treatment strategies in lipedema.

BackgroundLipedema is a chronic and progressive disorder of subcutaneous adipose tissue that predominantly affects women and is frequently misdiagnosed as obesity, lymphedema, or venous disease. Increasing evidence indicates that lipedema represents a systemic vascular-lymphatic-inflammatory disorder rather than a cosmetic or metabolic condition. Delayed diagnosis often results in progressive fibrosis, lymphatic dysfunction, chronic pain, and functional impairment.ObjectiveThis review aims to present a structured, clinically applicable framework for the diagnosis and multimodal management of lipedema within phlebology practice, with an emphasis on stage-specific assessment and integrated therapeutic strategies.MethodsA narrative clinical review of peer-reviewed literature in phlebology, vascular medicine, lymphatic disorders, and adipose tissue pathology was conducted. Diagnostic criteria, clinical staging, and differential diagnostic features were synthesized into a practical, stage-based framework. A multilayer therapeutic approach targeting inflammation, lymphatic function, adipose tissue pathology, extracellular matrix remodeling, and post-treatment rehabilitation is proposed.ResultsAccurate diagnosis of lipedema relies primarily on clinical evaluation, including pain assessment, tissue palpation, characteristic fat distribution, and exclusion of lymphedema and simple obesity. Early-stage identification enables effective intervention focused on inflammation control and lymphatic unloading, potentially preventing irreversible fibrosis. Advanced stages require targeted adipose tissue interventions, fibrosis management, and structured rehabilitation to preserve mobility and quality of life.ConclusionLipedema should be recognized as a systemic vascular-lymphatic-inflammatory disorder within phlebology practice. Early diagnosis and implementation of a structured, stage-specific multimodal treatment framework may significantly alter disease progression and reduce the risk of long-term disability.

BACKGROUND: Postoperative fibrosis is a frequent complication following liposuction for lipedema. Serrapeptase, a proteolytic enzyme with purported anti-inflammatory and antifibrotic effects, is used empirically, but robust evidence supporting its efficacy is lacking. This study aimed to assess the clinical effectiveness of postoperative serrapeptase supplementation in reducing fibrosis following lower limb liposuction for lipedema.

METHODS: This retrospective, observational cohort study included 50 female patients with a confirmed diagnosis of lipedema undergoing tumescent liposuction. Patients were allocated to either a serrapeptase group (n = 25), receiving 60,000 IU daily for 4 weeks, or a control group (n = 25) receiving standard care alone. The primary outcome was tissue stiffness measured by quantitative ultrasound elastography (QUS). Secondary outcomes included B-mode ultrasonography, patient-reported pain (VAS), and clinical assessment of induration. Evaluations were performed at baseline, 4 weeks, and 3 months.

RESULTS: Baseline characteristics were comparable between groups. No statistically significant differences were observed in the primary outcome of tissue stiffness at 4 weeks (14.8 ± 3.1 kPa vs. 15.2 ± 3.0 kPa; p = 0.62) or 3 months (13.7 ± 2.9 kPa vs. 14.0 ± 3.2 kPa; p = 0.78). Similarly, no significant benefits were seen in secondary outcomes, including fibrotic changes on ultrasound, VAS pain scores, or clinical induration (p > 0.05 for all). Serrapeptase was well-tolerated with no adverse events reported.

CONCLUSIONS: Oral serrapeptase supplementation did not demonstrate measurable efficacy in preventing postoperative fibrosis or improving patient-reported outcomes following liposuction for lipedema. These findings do not support its routine use in this clinical setting.

LEVEL OF EVIDENCE III: This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors   www.springer.com/00266 .

BACKGROUND: Lipedema is an abnormal accumulation of subcutaneous fat that usually affects the lower extremities. Inflammation due to adipose tissue may negatively affect body structure and functions.

OBJECTIVE: This case-control study aimed to assess lower extremity muscle strength, endurance and function, functional exercise capacity, pressure pain threshold, and edema in women with lipedema and compare with healthy women.

METHODS: Women with lipedema and healthy women of similar age and body mass index (BMI) were included in the study. Lower extremity muscle strength, muscle endurance, functionality, functional exercise capacity, pressure pain threshold, and edema (local tissue water) were assessed with digital dynamometer, 30-Second Sit to Stand Test (30-SSTS), Lower Extremity Functional Scale (LEFS), 6 Minute Walk Test (6MWT), manual algometer and skin moisture meter, respectively.

RESULTS: Twenty-four women with lipedema (mean age: 47.9 ± 1.8 years, median BMI: 30.62 (19.03-41.20) kg/m) and 20 healthy women (mean age: 47.2 ± 12.1 years, median BMI: 28.12 (23.23-39.66) kg/m) participated in the study. Muscle strength for all assessing lower extremity muscles, 30-SSTS repetition number, LEFS score, pressure pain threshold of all assessing regions, percent of predicted 6MWT distance ( < .001) and 6MWT distance ( = .001) were significantly lower in women with lipedema compared to healthy controls. No significant difference was in terms of local tissue water percentage ( > .050).

CONCLUSION: Lower extremity muscle strength, muscle endurance, functionality, functional exercise capacity and pressure pain threshold decrease in women with lipedema. It is recommended that these changes be taken into account when developing rehabilitation strategies.

BACKGROUND: Lipedema is a chronic female disease characterized by a painful accumulation of adipose tissue in the limbs. Plasma fatty acid (FA) composition has been proposed as a potential modulator of pain. However, the pathophysiology behind lipedema pain remains uncertain. The primary objective of this secondary analysis was to compare changes in plasma concentrations of FAs between low-energy diets either low in carbohydrates or low in fat, in females with lipedema and obesity. A secondary objective was to investigate potential associations between changes in pain and changes in the concentration of several FAs. METHODS: Females with lipedema and obesity (BMI 30–45 kg/m2) were randomized to isocaloric low-energy diets, either low-carbohydrate diet (LCD) or low-fat diet for 8 weeks. Plasma concentrations of FAs were quantified using gas chromatography and subjective pain using the Brief Pain Inventory, before and after the intervention. RESULTS: 70 females were included in the analyses, with a mean BMI of 37 ± 5 kg/m2 and mean age of 47 ± 11 years. Significant decreases in the concentration of the saturated FAs (SFAs) myristic, stearic, and behenic acids, and the polyunsaturated FAs (PUFA) gamma-linolenic (GLA), dihomo-gamma-linolenic (DGLA), alpha-linolenic (ALA), eicosapentaenoic (EPA), and docosapentaenoic acids (DPA) were seen in both groups. A reduction in the SFA arachidic acid, and the monounsaturated FAs (MUFA) palmitoleic and oleic acids was seen in the LCD group only, while an increase in the SFA lignoceric acid and a decrease in the PUFA linoleic acid was seen only the low-fat diet group. Changes in myristic and palmitic acids (SFAs) were positively associated with changes in pain. CONCLUSION: A reduction in most FAs was found after energy restricted LCD and low-fat diets in females with lipedema and obesity. Notably, reductions in SFAs seem to be associated with the reduction in pain seen in the LCD group, especially myristic acid. These findings suggest that FA composition may play a role in pain reduction in females with lipedema. TRIAL REGISTRATION: NCT04632810, Effect of Ketosis on Pain and Quality of Life in Patients With Lipedema (Lipodiet).

Lipedema is a chronic, progressive adipose tissue disorder characterized by disproportionate subcutaneous fat accumulation, pain, edema, and resistance to conventional weight-loss strategies. Although traditionally conceptualized as a disease of adipose expansion, increasing clinical and imaging evidence suggests that functional impairment in advanced lipedema cannot be explained by adipose pathology alone. This narrative, hypothesis-generating review proposes an integrated pathophysiological framework in which inflammatory myosteatosis serves as a mechanistic bridge between lipedema progression and dynapenia. We examine how chronic adipose inflammation, microvascular dysfunction, and impaired lipid mobilization may promote ectopic lipid deposition within skeletal muscle, leading to mitochondrial inflexibility, oxidative stress, and reduced contractile efficiency. Within this model, lipedematous dynapenic myosteatosis may explain the paradox of reduced muscle strength despite preserved or increased limb volume, particularly during the transition from Stage 2.5 to Stage 3. Unlike obesity-associated dynapenia, which is primarily driven by systemic metabolic overload, lipedema-related muscle dysfunction may involve localized adipose-muscle inflammatory crosstalk and mechanical intolerance to exercise. This framework reframes advanced lipedema as a disorder of coupled adipose-muscle dysfunction rather than isolated adipose excess. The model is conceptual and intended to generate testable hypotheses, highlighting the need for future studies incorporating objective measures of muscle quality, mitochondrial function, and inflammatory signaling to clarify mechanisms underlying functional decline.

Lipedema is a lipodystrophic disease characterized primarily by a disproportionate increase in lower body subcutaneous fat. Although moderate weight loss decreases lower body fat mass in women with obesity and lipedema, it is possible that this decrease is due to a reduction in normal subcutaneous fat, rather than lipedema-affected fat. We evaluated the effect of moderate (11%) diet-induced weight loss on body fat mass and distribution, assessed by dual-energy X-ray absorptiometry and magnetic resonance imaging, in a 56-year-old woman with lipedema who was normal weight (body mass index: 23.9 kg/m) at baseline. Approximately 85% of the decrease in body weight comprised body fat. The relative reduction in upper body fat (abdominal subcutaneous, arm and trunk fat) was similar to the relative reduction in lower body (total leg fat and thigh subcutaneous fat). Accordingly, weight loss did not change the proportion of total body fat comprising leg fat (44.8% and 45.1% before and after weight loss, respectively) or arm fat (9.1% and 9.6% before and after weight loss, respectively). These data suggest weight loss decreases lipedema-affected adipose tissue and demonstrate the therapeutic effect of weight loss on body composition in women with lipedema even if they are normal weight.

Lipedema is a chronic disorder characterized by disproportionate subcutaneous fat accumulation and pain, with an incompletely understood inflammatory component. It remains unclear whether this inflammatory profile is disease-specific or primarily driven by coexisting adiposity. This study aimed to evaluate systemic inflammatory markers in women with lipedema compared with women with obesity and normal-weight controls. This retrospective study included 229 women aged 30-65 years: 78 with lipedema, 76 with obesity without lipedema, and 75 normal-weight controls. Demographic and laboratory data were obtained from medical records. Inflammatory indices, including the neutrophil-to-lymphocyte ratio, monocyte-to-lymphocyte ratio, platelet-to-lymphocyte ratio, systemic immune-inflammation index, C-reactive protein-to-albumin ratio, and C-reactive protein-albumin-lymphocyte index, were calculated. Group comparisons were performed using one-way analysis of variance with appropriate post hoc tests. Age was similar across groups, whereas body mass index was significantly higher in the lipedema and obesity groups than in controls (<0.001). The erythrocyte sedimentation rate, C-reactive protein level, and CAR were significantly higher in both the lipedema and obesity groups compared with controls, whereas no significant differences were observed between lipedema and obesity groups. The neutrophil-to-lymphocyte ratio, monocyte-to-lymphocyte ratio, platelet-to-lymphocyte ratio, systemic immune-inflammation index, and C-reactive protein-albumin-lymphocyte index did not differ significantly among groups. Inflammatory indices were generally comparable across lipedema grades. These findings suggest that lipedema is associated with low-grade systemic inflammation; however, its inflammatory profile largely overlaps with obesity, indicating shared inflammatory mechanisms rather than a distinct systemic inflammatory phenotype. Among the evaluated markers, C-reactive protein-based parameters, particularly the C-reactive protein-to-albumin ratio, appeared to better reflect inflammatory burden than hematological composite indices.

BACKGROUND/AIM: Although various distinctive morphological features such as hyperproliferation of adipocytes, fibrosis, and inflammation have been described in the progression of lipedema, the underlying mechanisms of these changes are not yet fully understood. In this study, we aimed to investigate the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), mean platelet volume (MPV), and platelet distribution width (PDW) to demonstrate the role of inflammation in lipedema.

METHODS: The retrospective study consisted of 60 lipedema patients (Group 1) and 40 healthy controls (Group 2). The age, height, weight, and body mass index (BMI) of all participants were recorded, along with the lipedema type and stage for Group 1. Laboratory results, including complete blood count, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR), were obtained for all participants. Hemoglobin, leukocyte, lymphocyte, neutrophil, and platelet counts, NLR, PLR, MPV, PDW, CRP, and ESR were evaluated.

RESULTS: The mean age was 45.45 ± 10.17 years in Group 1 and 44.90 ± 10.69 years in Group 2; the BMI was 32.15 ± 5.05 in Group 1 and 30.94 ± 4.98 in Group 2, with no significant difference between the groups ( > 0.05). The most common type was Type 2 lipedema. Platelet counts, CRP, NLR, and PLR levels were significantly higher in Group 1 than in Group 2 ( < 0.05). There was no difference between groups in MPV and PDW values ( > 0.05). There was a positive correlation between BMI and both leukocyte count and CRP levels ( < 0.05).

CONCLUSION: In our study investigating inflammation in lipedema-an etiology that is still not fully understood-NLR, PLR, platelet count, and CRP levels were found to be significantly higher in the patient group. The increase in BMI was correlated with leukocyte count and CRP levels. This finding is important for elucidating the etiopathogenesis of the disease, and we believe it may guide future research in this area.