The etiology of hyperlipoproteinemia can be divided into two major categories: primary and secondary. The primary system is caused by lipid and lipoprotein metabolism, congenital defects (or genetic defects), and can also be caused by diet, nutrition and other factors. Secondary patients are mainly secondary to diabetes, hypothyroidism, gout, liver disease, kidney disease and so on.
There are two kinds of molecular defects in type 1 hyperlipoproteinemia. One is congenital deficiency or deficiency of LPL (lipoprotein lipase), because insulin is necessary when LPL is produced, so LPL deficiency may also be secondary to insulin deficiency in diabetes. The other is that ApoC- II is deficient or defective, and ApoC- II is the cofactor of the catalytic action of LPL, and the activity of LPL is low and slow when LPL has not been catalyzed by ApoC- II. The vitality of LPL is insufficient and a large number of CM and VLDL can not be completely hydrolyzed to accumulate in the blood flow. I recently found a LPL and ApoC- II work without any defect, is dominant, which is characterized by non lipoprotein fraction in plasma are inhibited LPL activity substance, type II hyperlipoproteinemia for familial hereditary disease, there are at least three different genetic nature: the family of high cholesterol: gene mutation in the LDL receptor (ApoB.E receptor) is characterized by lack or defect, type IIA hyperlipoproteinemia. Type IIIA patients homozygous LDL receptor cells are not functional, or because the receptor protein deficiency or defect, although some patients have receptors exist, but LDL molecules combined with the receptor defects inside the cell can not sink. The heterozygote patients have the number of receptors in half of normal people, and the excess of LDL in these patients is accumulated in the plasma. 2. Familial hyperlipidemia: probably due to excessive ApoB in the liver. ApoB is the main protein component of VLDL and LDL, and its abnormality can cause the increase of these two lipoproteins or a kind of lipoprotein in the plasma. The polygenic hypercholesterolemia: most of the patients with hereditary LDL levels increased, some patients have abnormal LDL, combined with the receptor poor result in the removal of plasma LDL is affected by multiple genes, however, most patients with hypercholesterolemia, due to other reasons, the effect of LDL removal some patients because of dietary saturated fat and cholesterol caused by abnormal sensitivity. Type III hyperlipoproteinemia, is most common in ApoE deficiency or defect, functional defects of ApoE cannot be liver ApoE receptor recognition, so a lot of chylomicron debris, beta VLDL or IDL deposited in plasma, secondary type III hyperlipidemia disease with low thyroid function and systemic lupus erythematosus, type hyperlipidemia may occur in members affected by familial hypertriglyceridemia or familial combined hyperlipoproteinemia effect. Many patients have primary hypertriglyceridemia. They have excessive generation of VLDL-TG. These patients may have genetic factors. Other patients have lower VLDL clearance rate than others. There are two cases of some patients. Its molecular defects have not yet been proved, perhaps ApoC- II. Or HTGL defects. Secondary type IV hyperlipidemic disease in patients with chronic renal failure, the VLDL-TG clearance decreased, low thyroid function, especially in patients with obesity, VLDL-TG production increased while the low activity of LPL in diabetes mellitus; severe insulin deficiency, the LPL activity decreased in patients with obesity and adult onset diabetes, the VLDL overproduction of TG induced nephropathy; VLDL-TG syndrome of excessive secretion, excessive intake of high calorie foods such as carbohydrates and alcohol liver disease (such as hepatitis HTGL deficiency, ApoA I and A II, VLDL decomposition synthesis disorders) metabolic disorders, may be VLDL and LDL increased.