Lipodystrophy is a subcutaneous adipose tissue disease of the atrophic or hypertrophic type. Among hypertrophic forms, the most widespread are lipomatous lipodystrophies, Launois-Bensaude’s syndrome, insulin lipodystrophy, and Dercum’s disease (42).
Dercum’s disease shows signs of sequential lipolymphedema with periods of neuropsychological or metabolic disorders and alterations in the lower abdomen and adynamia.
Pathogenesis includes neurovegetative, hypothalamic, and hypophyseal alterations, and might be caused by interstitial phlogosis produced by branches of the nervous system, i. e., by an extracellular matrix pathology accompanied by an increase in lipogenesis.
A similar phenomenon might be assumed for lipolymphedema considering the interstitial phlogosis of nervous and fibrillary branches as the direct or indirect cause of the increase in local lipogenesis. It seems that German authors have identified an intestinal streptococcal microorganism as causing matrix alteration.
In lipolymphedema, there are certainly clear correlations among alterations of the intestinal flora, metabolic acidifying alterations of the extracellular matrix, hyperinsuline-mia, and peripheral hyperestrogenism. Therefore, the adipocyte and the extracellular matrix condition would be affected at least at the initial phases (with regard to the lymphatic or venous system).
Over the superficial fascia at the dermal level, an extremely diffuse lipolymphedema may be noticed, which improves with sun exposure and also when the patient stops wearing elastic hose.
This type of “superficial cellulite’’ might be attributed to superficial vascular alterations due to unnecessary elastic compression, the low energy derived from low arterial flow, lipogenesis, and also cellular oxidation.
Primary vascular alterations would be more evident at the surface than within the subcutaneous tissue, where the extracellular matrix and the lymphoadipose system would be mainly affected.
At the dermal level, microcirculatory turbulences might provide basic conditions for the disease, which might later evolve into liposclerosis.
Therefore, Vage’s observations regarding circulatory factors might be valid, because he says, ‘‘blood and lymphatic flows through adipose tissue are inversely proportional to its growth.’’
From what has been said, it may be concluded that, in accordance with Curri’s formulation, ‘‘slow circulation” involves “lipogenesis,” whereas ‘‘quick circulation’’ involves ‘‘lipolysis’’ (43-45).