Lower body wasting type is a clinical symptom of lower body wasting caused by diseases such as progressive lipodystrophy. It is one of the clinical symptoms of progressive lipodystrophy. Progressive lipodystrophy (progressivelipodystrophy) is also known as cephalothoracic lipodystrophy; Simons disease; Seip-Laurence syndrome. It is a rare autonomic disorder characterized by disorders of adipose tissue metabolism. The clinical and histological features are slowly progressive bilateral distribution of largely symmetrical, well-defined, subcutaneous adipose tissue atrophy or loss. The extent of lipodystrophy can be divided into limited lipodystrophy (Simons or cephalothoracic lipodystrophy) and generalized lipodystrophy (Seip-Laurence syndrome). What causes progressive lipodystrophy? The cause is unknown. Sissons found that some patients have a combination of glomerulonephritis and hypocomplementemia (C3). A small number of patients have a family history. Progressive lipodystrophy is a rare autonomic disorder characterized by impaired adipose tissue metabolism. It is characterized clinically and histologically by slowly progressive bilaterally distributed, largely symmetrical, well-defined, subcutaneous adipose tissue atrophy or loss, sometimes combined with limited adipose tissue hyperplasia and hypertrophy. Due to the extent of lipodystrophy, it can be divided into limited lipodystrophy (Simons disease or cephalothoracic lipodystrophy) and generalized lipodystrophy (Seip-Laurence syndrome). Most patients start around the age of 5 to 10 years, and it is more common in females, with a slow onset and progression. At the beginning of the disease, the patient presents with loss of adipose tissue in the face or upper extremities, and later extends downward to the buttocks and femur, with a roughly symmetrical distribution. The course of the disease lasts 2 to 6 years and can stop on its own. The patient’s face is characterized by concavity of the cheeks and temporal areas on both sides, skin relaxation, loss of normal elasticity, and loss of fat around the cheeks and orbits, giving the patient a special appearance. Some patients may have obvious hyperplasia and enlargement of subcutaneous tissue in the buttocks and hips, but the hands and feet are often unaffected. Patients may have a combination of autonomic dysfunction such as skin moisture changes, abnormal sweating, polyuria, reduced glucose tolerance, tachycardia, vasomotor instability, vascular headache, abdominal pain, vomiting, dystrophic skin and nail disorders, etc. Individual cases may be combined with endocrine dysfunction such as genital hypoplasia, thyroid dysfunction, acromegaly and menstrual disorders. The symptoms usually stabilize within 5-10 years after the onset of the disease. Patients have normal muscles, bones, hair, mammary glands and sweat glands, no muscle strength disorders, most patients’ physical strength is not affected, and somatic and mental development are not affected during the progressive course of the disease. Recently, it has been reported that Hodgkin’s disease and scleroderma can be complicated. In addition to the subcutaneous and peri-visceral adipose tissue of the head, face, neck, trunk and limbs, the disease may also be associated with hyperlipidemia, diabetes, hepatosplenomegaly, skin pigmentation, cardiac and muscle hypertrophy.