Causes of facial subcutaneous fat atrophy

The harm caused by facial subcutaneous fat atrophy is relatively large, and its impact on appearance is relatively large. There are many reasons for facial subcutaneous fat atrophy. In the past, it was often caused by some recessive chromosomal genetic reasons, or kidney damage and other reasons. At present, if plastic surgery fails, it often leads to this phenomenon. These are the more common causes of fat atrophy.

Causes of facial subcutaneous fat atrophy

1) Cause of the disease Congenital lipodystrophy is an autosomal recessive inheritance, and the patients are blood relatives; acquired ones may have no genetic basis and often have prodromal symptoms of viral infection. Acquired systemic and partial lipodystrophy are considered autoimmune diseases.

(II) Pathogenesis The pathogenesis of this disease is still unclear. Various hypotheses proposed from epidemiological, genetic and clinical studies mostly believe that: systemic lipodystrophy is associated with widespread metabolic and systemic abnormalities, and enhanced sympathetic nerve activity may enhance the decomposition of fat; the pituitary gland may secrete fat mobilizing substances, but pituitary removal fails to correct lipodystrophy. Others have found an increase in CRF melanocyte-releasing factor and FSH-releasing factor, and therefore believe that the hypothalamus is the main site of damage. Some people have also proposed the theory of autoimmune destruction of adipose tissue, but the patchy lesions in many patients seem difficult to explain with this theory. The relationship between the pathogenesis of renal lesions and lipodystrophy is also unclear.

The most prominent serological abnormality of this disease is decreased blood C3, but hypocomplementemia and (or) complement activation are not necessary factors for the occurrence of glomerulonephritis. Renal damage is common in patients with lipodystrophy, with an incidence rate of 15% to 30%. The main type of renal damage is type II membranoproliferative glomerulonephritis or dense deposit disease (80%), and the other 20% is caused by extensive peripheral mesangial migration. The morphological and histochemical features of both glomerulonephritides are the same as those in patients with non-lipodystrophy. A case of type III variant has been reported in a patient with this phenotype and low serum complement and nephrotic syndrome who was sensitive to glucocorticoids. Because complete lipodystrophy often occurs simultaneously with diabetes, nondiabetic nephropathy is often found. Its pathological manifestations cannot be distinguished from diabetic nephropathy without fat malnutrition. There are reports of glomerulonephritis in patients without diabetes. The relationship between lipodystrophy and glomerulopathy is unclear. Tuck et al. reported that their patients had peripheral mesangial implants, subepithelial and intramembranous deposits in a small proportion of capillaries, but overall there were no special features. The patient had normal serum complement C3 levels, no proteinuria, and only slightly reduced renal function.

<<: What causes otolith disease?

>>: How to deal with subcutaneous fat pimples on labia majora