Pathogenesis (development of disease)
A genetic predisposition (disposition) is likely. It is theorized that lipedema results from compression of the lymphatic capillaries on the one hand and an accompanying abnormality of the lymphatic capillaries on the other. The pathologically (pathologically) altered fatty tissue also tends to edema (water retention) due to a disturbance in capillary function, which can lead to feelings of tension and pressure pain in the course of the disease.
Histological (fine tissue) evidence shows hyperplasia (enlargement due to increased cell division) and hypertrophy (increase in size due to cell enlargement alone) of fat cells, which are separated from each other by connective tissue septa (partitions). The increased adipogenesis (fat formation) is thought to lead to hypoxia-induced adipose tissue necrosis (“death of adipose tissue due to lack of oxygen“) with consecutive inflammation (inflammation) and activation of adipose tissue stem cells. Furthermore, also as a consequence of hypoxia, angiogenesis (growth of blood vessels, by sprouting or splitting processes from already preformed blood vessels) of pathological vessels occurs. This explains the development of orthostatic edema due to increased fluid and protein accumulation in the interstitium. There is an increased tendency to hematoma (bruising) due to increased capillary fragility (decreased stability of blood capillaries).
Within the pathogenesis of lipedema, involvement of the lymphatic system is not unlikely.
Lipedema develops primarily during periods of hormonal change.
Lipedema affects almost exclusively women. In men, the disease occurs almost only in very severe hormonal disorders. Obesity (being overweight), which often occurs along with the disease, can worsen lipedema.
Etiology (causes)
Biographic causes
