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La classification des lymphoedèmes en diverses catégories étiologiques est importante autant pour le diagnostic que pour un programme thérapeutique correct. L'approche diagnostique idéale doit Par conséquent envisager toutes les conditions, autant congénitales qu'acquises, responsables de la perturbation de la circulation lymphatique. Dans toutes les formes l'anamnèse est d'intérêt fondamental pour arriver au diagnostic étiologique alors qdu' e l'exame n c1 m· 1· que su ffii t a· poser le si·m ple iagnostic de lymphoedème.

Lipedema of the legs is a symmetrical thickening of upper and lower leg and topically accentuated fat pads. The back of the foot is usually free of swelling. Pathogenetically it is a disturbance of the distribution pattern of subcutaneous fat tissue. Epidemiologically, the subjects affected are women, starting from puberty. Weight reduction programs do not influence the real deformations. If this abnormal fat tissue is infiltrated by angiological diseases, these manifest themselves in modified form. In particular, all the symptoms are more painful. In arterial ischemic syndromes that taut skin is susceptible to necrosis at atypical locations. For reconstruction of trunk arteries it is advisable to bypass larger bulges for better wound nealing. Venous strips should be peeled out away from fat pads and venous-bridges very carefully to protect the tissue. Acute and chronic phlebothrombosis lead to unusual and asymmetrical forms of swelling. The venous ulcer lies directly beneath a fat-muff in the gaiter region. Since they are hard to compress, free skin transplants should be considered early in the course of development. Surgery of varicose veins calls for most careful technique to ensure wound healing. From the lymphological viewpoint there are clinically and lymphographically mixed forms of lymphedema with lipedema.

This condition, which has the full name of 'erythrocyanosis frigida crurum puella rum' (cold reddish blueness of the legs of girls), is extremely common. It is not always recognized, being misdiagnosed as lymphoedema, vasomotor disease, arterial insufficiency, and other things. The skin of the legs is cold to the touch and exhibits patches of bluish discoloration. There may be chilblains and small superficial ulcerated areas. There is often an abnormally large amount of fat particularly above the ankle and around the tendo Achillis. For this reason it is sometimes called ' lipoedema'. The affected patches are often hypersensitive to light touch and may irritate with changes of temperature. Deeper palpation may reveal tenderness and nodularity of the underlying fat. The condition is usually symmetrical or alsmost so. The feet often remain normal. At typical case is illustrated in Figs. 14.22 and 14.23

While the term cellulitis is incorrect, it is commonly used and deserves a nosological classification. "Cellulitis is a dermohypodermosis and an oedemato-sclerous panniculopathy- It is indeed a true histangiography in which the fibroblastic reaction predominates over capillaro-veinular changes. Adipocytes of exaggerated size interpenetrate into micro- and later into macronodules marked off by more or less structured conjunctive fibrilla, thereby making treatment difficult.

Systemic causes of leg edema include idiopathic cyclic edema, heart failure, cirrhosis, nephrosis and other hypoproteinemic states. Lymphedema may be primary, or secondary to neoplasm, lymphangitis, retroperitoneal fibrosis and, rarely (in the U.S.), filariasis. Thrombophlebitis and chronic venous insufficiency are not uncommon causes. Finally, infection, ischemia, lipedema, vascular anomalies, tumors and trauma can be responsible for the swollen leg.

En último término, el edema de los miembros se produce siempre a través de perturbaciones circulatorias. Estas alteraciones pueden tener un origen central o sistémico: afecciones cardiovasculares, renales, tiroideas o humorales (hipoproteinemia) y pueden también tener un origen periférico: insuficiencia venosa, linfoedema, etc. Uno de los problemas más difíciles de controlar para el médico es el edema de las piernas, de origen periférico, esto es sin relación con alteraciones cardiorrenales, tiroideas o humorales,. en otras palabras el edema consecutivo a la insuficiencia venosa que sucede como grave secuela a las flebotrombosis o flebitis, al linfoedema, etc. En los últimos años se ha avanzado bastante, sin embargo, en la prevención y en el tratamiento de estos edemas de origen periférico merced al mejor conocimiento de la fisiopatología, lo que supone un perfeccionamiento diagnóstico y a favor del uso de nuevos medios de tratamiento como ,los anticoagulantes y las vendas elásticas. Uno de los aportes más interesantes que se han hecho en el diagnóstico y diferenciación de estos sindromes es la descripción de una entidad clínica, hecha en Marzo de 1940 por dos investigadores de la Clínica Mayo: Allen y Hines que denominaron lipoedema de las piernas. Se trata de un aumento de volumen simétrico y generalizado de las piernas por aumento de los depósitos adiposos subcutáneos y por edema, que afecta casi exclusivameñte a las mujeres. A la descripción del cuadro clínico hecha en 1940 hemos sumado como antecedente bibliográfico un trabajo de conjunto que nos ha enviado directamente el Dr. Edgar v. Allen desde la Clínica Mayo, que no se ha publicado aún, y que reúne la experiencia de dicho servicio desde 1937 hasta 1946 .

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, predominantly female disorder characterized by disproportionate regional expansion of subcutaneous adipose tissue, pain, tenderness and easy bruising. Although adipocyte hypertrophy, altered progenitor-cell behavior, microvascular dysfunction, extracellular-matrix remodeling, immune-cell alterations and variable lymphatic abnormalities have been reported, their causal and temporal relationships remain unresolved. Here, we propose that these findings may represent interacting manifestations of dysregulation within an adipovascular unit (AVU) rather than independent pathological processes.

Are you newly diagnosed with lipedema, a painful adipose tissue disorder? Maybe you have had the condition for years and are looking for ideas for self-care from a holistic perspective.In this book you will learn:Treatment goals for lipedema / lipoedemaTips for reducing pain and inflammationHow to boost your lymphatic systemIf you are looking for a research-packed guide to caring for lipedema, read this book!Praise for Lipedema Treatment Guide:Steven Dean, DO, FACP, RPVI, Professor of Clinical Internal Medicine, Ohio State University Wexner Medical Center calls the Lipedema Treatment Guide "incredibly well-written and informative" and has added it to his patient lipedema handout.Jacqui Beutel teaches Decongestive Lymphatic Therapy courses in Australia and New Zealand and gives copies of the Lipedema Treatment Guide to her students.