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Twelve patients with primary lymphedema of the lower limb were examined with computed tomography (CT). A characteristic "honeycomb" pattern of the subcutaneous compartment was seen in 10 of these patients. CT scans in nine other patients with swollen leg secondary to chronic venous disease or lipedema did not show this characteristic pattern. CT may be helpful in the differential diagnosis of a swollen leg, thus obviating venography or lymphangiography.

Lipedema of the lower extremities are diagnosed on the basis of clinical findings . An exact differentiation is necessary since therapeutical considerations are depending on the pathophysiology of the diseases. In lipedema (Allen and Hines) as weil as in erythrocyanosis cruris puellarum (Klingmüller) an examination of the state of the lymphatic vessels is justified. Using isotope lymphography the lymphatic capacitY, of the lower extremities can be assessed without problem. As demonstrated a disturbance of lymphatic transport is not regularly present in these two syndroms. Therefore we can not consider them as lymphedema. The frequent appearance of unilateral lymphostasis with definite clinical differenccs of both extremities indicate on the other band that lipedema is not seldom superimposed by the lymphedema .

Patients with lipoedema of the typus rusticanus Moncorps show a skin elasticity deficit of the skin of the calf. This is partly due to the derma oedema in the skin of these patients and seems partly to be due to an intrinsic connective tissue defect in the skin of such patients. The auteurs put forward the hypothesis that also present calf muscle pump dysfunction in these patients is the result of a connective tissue defect of the fascia of the muscular compartment, as an expression of a more generalized connective tissue defect.

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.

Background:Lipedema, a chronic condition affecting 11% of women, causes abnormal fat buildup in the lower limbs, leading to disproportionate body...

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 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.