What Is Fat Atrophy?

Fat malnutrition is also known as subcutaneous fat atrophy and lipodystrophy. Weir-Miechell first reported partial lipodystrophy in 1885, and later reported that patients had neck, arms, chest and abdomen lipodystrophy, with increased hip and leg fat deposits, and Lawrence report in 1946 Complete fat dystrophy. Patients with fat dystrophy have a systemic distribution, showing completeness or patchiness. Fat deficiency is often accompanied by a series of metabolic disorders.

Subcutaneous fat atrophy

Fat malnutrition is also known as subcutaneous fat atrophy and lipodystrophy. Weir-Miechell first reported partial lipodystrophy in 1885, and later reported that patients had neck, arms, chest and abdomen lipodystrophy, with increased hip and leg fat deposits, and Lawrence report in 1946 Complete fat dystrophy. Patients with fat dystrophy have a systemic distribution, showing completeness or patchiness. Fat deficiency is often accompanied by a series of metabolic disorders.

Causes of subcutaneous fat atrophy

A) Cause of Onset

Congenital lipodystrophy is an autosomal recessive inheritance, and the patient is related by blood; acquired people may have no genetic basis and often have precursor symptoms of viral infection. Acquired systemic and partial fat malnutrition is considered an autoimmune disease.

(Two) pathogenesis

The pathogenesis of this disease is unclear, and various hypotheses proposed from epidemiology, genetics and clinical research mostly believe that: systemic lipodystrophy is related to a wide range of metabolic and systemic abnormalities, and the enhancement of sympathetic nerve activity may Enhances fat breakdown; pituitary may secrete fat mobilization material, but pituitary resection fails to correct fat malnutrition. Others have found that CRF melanocyte release factor and FSH release factor are increased, so the hypothalamus is considered to be the site of major damage. The autoimmune destruction theory of adipose tissue has also been proposed, but many patients have lesions that appear patchy and difficult to explain with this theory. The relationship between the pathogenesis of kidney disease and lipodystrophy is unknown.

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 often occurs in patients with lipodystrophy, with a 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% are caused by extensive peripheral mesangial migration. The morphological and histochemical characteristics of these two glomerulonephritis are the same as those of patients with non-lipid dystrophy.

A type III variant has been reported. Patients with this phenotype and low serum complement and nephrotic syndrome are sensitive to glucocorticoids.

Because total fat dystrophy often occurs at the same time as diabetes, non-diabetic nephropathy is often found. Its pathological manifestations cannot be distinguished from diabetic nephropathy without fat malnutrition. There have been reports of glomerulonephritis in patients without diabetes. The relationship between lipodystrophy and glomerulopathy is unknown. Tuck et al. Reported that a small portion of their patients had peripheral mesangial implants, subepithelial, and intramembranous deposits, but overall there were no special features. Patients had normal serum complement C3 levels, no proteinuria, and only a slight decrease in renal function.

Subcutaneous fat atrophy test

1. Urine examination shows proteinuria, gross hematuria, microscopic hematuria, pyuria, and a few cases of proteinuria within the scope of nephrotic syndrome.

2. Blood test Hyperlipidemia, hyperproteinemia, hyperglycemia, hyperinsulinemia, urea nitrogen, creatinine elevation, and serum complement C3 decrease.

3 Routine X-ray, B-ultrasound, CT, electromyography, etc., can find the size of the kidneys, abnormal structure and urinary stones.

Differential diagnosis of subcutaneous fat atrophy

1. Muscle atrophy: Human skeletal muscle is generally no less than 434, which accounts for 25% of the total body weight of newborns and 40-45% of adult body weight. All casual activities of a person must be accomplished by muscle contraction. The blood supply required for muscle activity accounts for 12% of the total cardiac output and 18% of systemic oxygen consumption. Muscle is one of the important organs of human metabolism, especially glucose metabolism. The striated muscle is composed of many juxtaposed muscle fibers. The muscle fibers, ie, muscle cells, are cylindrical, with sarcoplasm inside and serosa outside. There are several muscle nuclei in the sarcoplasm, many small cells such as mitochondria and ribosomes, and many longitudinal Transverse tubular sarcoplasmic mesh. Some parts of the sarcoplasmic reticulum store calcium ions. There is a depression and fold on the serosa, and the motor nerve endings form the motor end plate, which is the neuromuscular junction, which is the synapse. When the nerve impulses arrive, the nerve endings release the chemical transmitter acetylcholine, which temporarily binds to the receptor on the end plate, increasing the permeability of the myometrium to sodium there, allowing extracellular sodium ions to enter the cell, so that the terminal The membrane potential of the plate area is depolarized; when a certain threshold is reached, action potentials are generated on the surrounding sarcolemma. The action potential is transmitted to the sarcoplasmic network, prompting it to release calcium ions into the sarcoplasm; the latter can promote the decomposition of adenosine triphosphate, release energy and tightly fit certain protein molecules in muscle cells, causing contraction of muscle cell length.

2. Tonic muscle atrophy: Myotonicdystrophy is a rare family inherited disease, with distal muscle atrophy and muscle rigidity as the main symptoms. Atrophy outside the muscle is often complicated by gonad atrophy, baldness, and cataract. The incidence is mostly in adolescence, but it can also occur in infants and young children. It belongs to chromosomal dominant inheritance.

3. Progressive lipodystrophy: Progressive lipodystrophy is a rare autonomic nervous system disease characterized by metabolic disorders of adipose tissue. Its clinical and histological characteristics are slowly progressive bilateral distribution with basically symmetrical borders. Clear, subcutaneous adipose tissue atrophy or disappear, sometimes combined with limited adipose tissue hyperplasia and hypertrophy.