Your search

To the Editor.— I do not believe that Stallworth et al (228:1656, 1974) have proven their case for a definite clinical entity of "lipedema" in the patients described.The plasma lipid values seem high, but are of no significance unless the controls were patients of comparable sex, age, and mean weight; this is not stated. The origin of tissue lipid values would similarly have to be a group of middle-aged, overweight patients with fat legs but no symptoms, to make their figures valid.I have seen and treated many patients with a clinical picture identical with that described in their paper. Many of these patients have clinical evidence of past phlebitis; others do not. Both groups have episodes of painful, lumpy swellings in their legs, that may be accompanied by redness, heat, and tenderness in the affected areas. This picture frequently takes many weeks to resolve and may leave some ...

A 22 yr old woman with bilateral symmetrical enlargement of her lower extremities since the age of 11 is reported. A diagnosis of lipedema of the legs was made on the basis of history, physical examination, biopsy and phlebography. Lipedema of the legs should be included in the differential diagnosis of symmetrical nonpitting edematous lower extremities. According to Allen and Hines, the characteristic points to be made for a diagnosis of lipedema of the legs included the following: almost exclusively seen in women; always bilateral and symmetrical with minimal involvement of the feet; minimal to absent pitting edems; all parts of the limbs are involved simultaneously; persistent enlargement despite elevation of the extremities. 16% of their patients gave a family history of the disorder; 40% complained of pain in the lower extremities; and approximately half of the patients were obese. The age of onset was variable, from childhood to the sixth or seventh decade. There was no racial preponderance. No patient gave a history compatible with progressive lipodystrophy. Treatment included diet, diuretics, tight stockings, rest and elevation, and massage, but was unsatisfactory in most cases.

Lipoedema was first described by Allen and Hines (1940), and it is characterised by fat legs and orthostatic edema. Generalised obesity may be presend or absent, the mean weight of five illustrative patients in their paper ws 154.5 lbs. Allen and his co-workers (1951) then reported 119 cases of lipoedema at the Mayo Clinic from 1937 to 1946. The condition affects women almost exclusively. Hines (1952) states that the diagnosis of lipoedema can be made easily from observation: (1) The characteristic symmetrical distribution of fat in the lower half of the body, excepting the feet, and (2) the oedema of varying degrees in the more dependent portions of the legs. The condition is briefly mentioned by Martin et al. (1956). The condition is often confused with vascular diseases affecting lower extremities, and lymphoedema (Wold et al., 1951). Furthermore, these workers consider that lipoedema can be distinguished from lipodystrophy progressiva by the extensive loss of subcutaneous fat in the upper half of the body associated with deposition of fat in the buttocks and lower extremities (Whittle, 1944). Two patients are presented with lipoedema, associated with diabetes mellitus. The possibility that lipoedema may be a variatn of lipodystrophy progressive is discussed.

1. Lipoedema is described with an illustration of a recent case. 2. This condition should be distinguished from lymphoedema of the legs. 3. The differential diagnosis is discussed. 4. Comment is made on treatment.

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 .

Introduction. Personal observations (20 cases, 19 photographs). Consideration of special clinical varieties or syndromes—groups of cases. Group I. Adiposis dolorosa. Group II. Obesity. Group III. Nodular circumscribed lipomatosis. Group IV. Diffuse symmetrical lipomatosis (Fetthals, Madelung; adéno-lipomatose symétrique à prédominance cervicale, Launois and Bensaude). Group V. Neuropathic edema, pseudoedema, pseudolipoma and lipoma. Group VI. Adipositas cerebralis (Fröhlich, Madelung and others). Consideration of the combined groups. General summary (including special subjects, arthritism, heredity, etc.). Etiology (including glands of internal secretion). Treatment. Conclusions. Bibliography.The object of this study is to simplify or unify the clinical classification of abnormal subcutaneous fat deposits by correlating the symptomatology and constitutional relations common to the several varieties or clinical groups that have been separated under descriptive designations according to their predominant characteristics. It is with special reference to Dercum's ``adiposis dolorosa'' that this study is undertaken. I shall

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.

Lipedema is a chronic and progressive disorder, a primary lipotrophy characterized by abnormal fat deposition, primarily in the buttocks and legs bilaterally. It is symmetrical and disproportionate. It is estimated to affect 10 to 18% of women in Europe and approximately 12.3% of the Brazilian female population.