How to treat lipoatrophy

Most people have heard of muscle atrophy, but have you heard of fat atrophy? This is not a joke. Fat can also atrophy. The full name is subcutaneous fat atrophy. The direct cause is fat malnutrition. There is also a saying that fat atrophy is caused by genetics or viral infection. So, what is the situation of patients with subcutaneous fat? Let me give you a detailed introduction below.

Overview

Lipodystrophy is also known as subcutaneous fat atrophy and lipodystrophy. In 1885, Weir-Miechell first reported partial lipodystrophy. Later, it was reported that patients had lipodystrophy in the neck, arms, chest and abdomen, accompanied by increased fat deposition in the hips and legs. In 1946, Lawrence reported complete lipodystrophy. The patients had systemic distribution of fat malnutrition, which was complete or patchy. The lack of fat was often accompanied by a series of metabolic disorders.

Causes

Causes

Congenital lipodystrophy is an autosomal recessive inheritance, and 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.

Pathogenesis

The pathogenesis of this disease is still unclear. Various hypotheses proposed from epidemiological, genetic and clinical studies mostly believe that: systemic lipodystrophy is related to 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.