In recent years, with the continuous improvement of people’s living standards and changes in dietary structure, the number of people suffering from obesity and hyperlipidemia is increasing, and the number of cases of acute pancreatitis caused by hyperlipidemia is also gradually increasing. Hyperlipidemia (HL) is one of the causes of acute pancreatitis (AP), and the resulting pancreatitis is called “hyperlipidemic acute pancreatitis” (HLAP). Hyperlipidemic acutepancreatitis (HAP) is closely related to serum triglyceride (TG) value, but less related to serum cholesterol value.Among the causes of AP, hyperlipidemia accounted for 1.3%-3.8%, while 12%-38% of the patients with AP were accompanied by elevated blood TG value. Therefore, HL is both the cause of AP and a common complication of AP metabolic disorders, and the two often form a vicious circle. The clinical features of this type of pancreatitis are different from those of the most common biliary pancreatitis and alcoholic pancreatitis, and sometimes it is very easy to cause misdiagnosis. The author combines clinical experience and refers to domestic and international literature on the etiology and pathogenesis, clinical features and diagnosis, treatment options and prevention to make some brief comments for the benefit of readers.1. The etiology and pathogenesis of HAP HL is mainly divided into five types, HAP-related for the I, IV, V. Primary HL is commonly found in familial pancreatitis, which is characterized by the presence of a large number of patients with HL. Primary HL is commonly characterized by familial lipoproteinase (LPL) deficiency and familial apo-cII deficiency. The main causes of secondary HL are alcoholism, diabetes mellitus, obesity, hemophagocytic syndrome, high-fat diet, administration of drugs such as triamcinolone acetonide, diuretics, and pregnancy.The pathogenesis of HAP is complex, and HL triggers HAP mainly by affecting pancreatic fluid secretion, inducing pancreatic microcirculation disorders, and damaging pancreatic follicular cells: (1) HL can put pancreatic blood in a hypercoagulable state, which is conducive to thrombus formation; plus serum lipid The aggregation of serum lipid particles blocked the pancreatic microvessels, thus inducing pancreatic microcirculation disorder. (2) HL activates platelets, releasing a large amount of thromboxane A2 (TXA2) with strong vasoconstriction effect, and at the same time damages the pancreatic vascular endothelial cells, so that the secretion of prostacyclin (PGI2) with strong vasodilatation effect is reduced, leading to TXA2/PGI2 imbalance, and aggravating pancreatic microcirculation disorder. (3) Excessive celiac particles embolize in the pancreatic microvessels or pancreatic parenchyma to form yellow tumors, leading to pancreatic microcirculation disorder. (4) In HL, the high concentration of TG in the pancreas and peripancreas was hydrolyzed by pancreatic lipase, locally producing a large amount of free fatty acids (FFA), inducing acidosis, activating trypsinogen, and exacerbating pancreatic auto-digestion. (5) FFA produces direct cytotoxic effects on pancreatic alveolar cells and capillary endothelial cells, and enhances the toxic effects of cytokines such as tumor necrosis factor, causing biofilm damage, increased permeability, resulting in mitochondrial swelling and deformation, aggravating the pancreas’ persistent ischemia and necrosis. 2. Clinical features and diagnosis of HAP HAP is similar to pancreatitis caused by other triggers in terms of clinical manifestations, and is characterized by persistent epigastric pain. HAP is similar to other causes of pancreatitis in terms of clinical manifestations, mainly characterized by persistent epigastric pain, which may radiate to the lower back, abdominal distension, nausea, vomiting, etc. However, there are still differences. However, there are differences. Patients with hyperlipidemic pancreatitis may have a history of alcoholism, obesity, pregnancy, diabetes mellitus, and in a small percentage of patients, a family or personal history of hypertriglyceridemia. Hyperlipidemic pancreatitis has a rapid onset, HAP patients have mild clinical symptoms, manifested as a transient elevation of amylase, few complications, most of them are mild AP, but there is a tendency to recur.AP with HL patients have more severe clinical symptoms, often accompanied by serious metabolic disorders in vivo (such as blood glucose acute elevation, multiorgan insufficiency syndrome, etc.), many complications, poor prognosis. When the blood TG value is extremely elevated, HAP patients will have severe abdominal pain, inducing fulminant AP or even death; and HAP combined with pancreatic abscess, fatty liver and the incidence of low-density lipoproteinemia is also correspondingly higher.In HAP, there exists a kind of plasma inhibition of blood amylase activity of non-lipid inhibitory factors, which can be passed through the kidneys into the urine to inhibit the activity of urinary amylase. Therefore, blood and urine amylase activities are often not significantly elevated in patients with HAP. The disease should be highly suspected in the presence of severe abdominal pain during pregnancy when other etiologies are excluded. For patients who are clinically suspected of HAP but have no or insignificant elevation of blood and urine amylase, ultrasound, CT or MRI can be used to help diagnose the pancreas and peripancreas, especially dynamic enhanced CT, which is of greater reference value for the pancreas with or without necrosis.The diagnosis of HAP mainly relies on the combination of typical clinical manifestations and the detection of blood TG, and the diagnosis is based on the combination of the typical clinical manifestations and the blood TG, and the diagnosis is based on the fact that, once pancreatitis has been established, the TG > 11.3 Once pancreatitis is established, TG>11.3mmol/L or TG5.65~11.3mmol/L and serum is celiac, and exclude other causes of pancreatitis can be diagnosed as hyperlipidaemic pancreatitis (HAP), for the blood lipids are higher than the range of the reference value, but serum is not celiac can only be referred to as accompanied by hyperlipidaemic pancreatitis or pancreatitis stress caused by transient elevation of blood lipids.3, the treatment of HAP and the prevention of HAP HAP shows the general characteristics of AP, but also has its own specificity. Although there is no uniform and effective treatment plan for HAP, on the basis of standardized treatment of AP, the key to HAP treatment is to rapidly remove the primary and secondary factors causing HL and reduce the blood TG value. When the blood TG value is reduced to below 5.65 mmol/L, the further development of HAP can be prevented.3.1 Conventional treatment for pancreatitis: conventional treatment includes fasting, gastrointestinal decompression, nutritional support, inhibition of pancreatic exocrine secretion, inhibition of pancreatic enzyme activity, prophylactic use of antibiotics, and maintenance of the water-electrolyte-acid-base balance. It should be noted that fat emulsion should be regarded as a contraindication for parenteral nutritional support in these patients, especially when TG>4.5mmol/L, which will increase the amount of blood lipids in the body and aggravate the condition. At present, there is a standard in the use of fat emulsions, namely: TG1.7~3.4mmol/L can be used, 3.5~4.5mmol/L with caution, in the process of application should also be regularly detected in vivo blood lipid levels. For severe HAP patients, fasting time is long, the general state of patients in the late stage is poor and can not implement enteral nutrition, if the blood TG value is 1.7~3.4mmol/L, under the condition of strict monitoring of blood lipids, the amount of short and medium-chain fat emulsion can be input ≤750mL for 24h, and the amount of long-chain fat emulsion is ≤250mL for 24h, after 12h of inputting the fat emulsion, if the value of blood TG>5.65mmol/L, it should be immediately detected during the application. If the blood TG value is >5.65mmol/L after 12h of fat emulsion input, it should be stopped immediately. During the use of fat emulsion, fat contouring test should be reviewed regularly, and those with positive test should also be discontinued in time.3.2 Application of lipid-lowering drugs: lipid-lowering drugs can be given through nasal feeding tube or enteral nutrition tube. Lipid-lowering drugs can effectively reduce the level of blood TG by 20%~60%, and beta-lipid-lowering drugs are preferred for primary HAP, such as fenofibrate, gemfibrozil, benzapentamide and so on. Its lipid-lowering mechanism is to enhance lipoprotein enzyme activity, promote TG hydrolysis, some data say that beta-lipid-lowering drugs can reduce 50% TG level and increase 20% HDL cholesterol level at the same time.Jain et al. showed that long-term use of fenofibrate can make the serum TG level to maintain normal, and can effectively prevent the recurrence of pancreatitis. Niacin has a significant effect on raising HDL and can reduce serum TG levels by 30%-50% by inhibiting the synthesis of very low-density lipoproteins, so its efficiency in lowering TG is lower than that of fibrates. Statins are not preferred because of their significant effect on hyperlipidemia, which is mainly characterized by elevated cholesterol. Because oral lipid-lowering drugs have a slow onset of action, patients often have abdominal distension during the onset of the disease and should not eat, so they are mostly recommended for prophylactic use.3.3 Blood purification: blood purification, including plasma exchange and hemofiltration, can be considered for patients with severe HAP. Plasma exchange (PE) means that the patient’s blood is withdrawn in stages, the plasma is removed to exclude the contained TG and excessive inflammatory cytokines, the other components of the blood are transfused back to the patient, and fresh frozen plasma and albumin are reintroduced. A few foreign cases reported that patients treated with PE had significant recent improvement and a significantly lower relapse rate.Kyriakidis et al. treated five patients with HAP with plasmapheresis and found it to be effective in lowering lipid levels and improving symptoms. Except for one case who underwent surgery, none of them died of the disease, and none of them had recurrence at a follow-up of 4-28 months. Because PE requires a large amount of plasma and special equipment, which is expensive, it is difficult to be widely carried out at present.The timing of PE is the key to the success of the treatment, and it should be performed as early as possible after the onset of the disease, and is mostly advocated to be carried out within 48-72 h. The treatment should be carried out as early as possible after the onset of the disease. Hemofiltration (HF) is to use the adsorption effect of the filter membrane to remove lipids, replace the filter every 1-2d, generally 4-5 times can reduce the blood TG to 2.3-6.8mmol/L, and effectively reduce the symptoms of abdominal pain.The best time for HF treatment is within 72h after the onset of the disease, the earlier the more obvious the effect. During this period, absolutely prohibit the input of any fat emulsion, so as to avoid further elevation of TG.3.4 Application of heparin and insulin: Lipoprotein lyase (LPL) is the key enzyme of endogenous and exogenous fat metabolism, and plays an important role in the clearance of blood lipids. Continuous intravenous infusion of heparin (or subcutaneous injection of low molecular heparin) and insulin (blood glucose control below 11.1 mmol/L) can activate LPL, accelerate the degradation of chymotrypsin, significantly reduce the value of blood TG, improve the microcirculation of the pancreas, and prevent the activation of neutrophils, which is an effective means of treating HAP.Berger et al. conducted a study on five cases of severe HAP patients with continuous intravenous push of low molecular heparin and Berger et al. continuously pushed low molecular heparin and insulin into the veins of 5 patients with severe HAP, and the blood TG value of all the patients was reduced to less than 2.8mmol/L, and none of them suffered from complications or died.3.5 Traditional Chinese Medicine (TCM) therapy: TCM recognizes HAP as real heat or heat-embedded knots, and the internal organs are not accessible to the qi, and the spleen and stomach are in real heat condition. Therefore, Tongli attack, clearing heat and removing toxins, activating blood circulation and removing blood stasis are the basic principles of treating this disease. In order to maintain effective blood volume, prevent shock, reduce inflammatory reaction, commonly used to benefit the qi and save the yang of the sheng pulse injection, astragalus injection, etc., with low molecular dextrose or corticosteroid drugs. In order to lift intestinal paralysis to enhance intestinal peristalsis and control the translocation of intestinal bacteria, commonly used Tongli tapping method, prescription for large Chengqi soup, Huanglian detoxification soup plus reduction, gentian diarrhea liver soup plus reduction, can also be used to pi nitrate whole abdomen external application or raw rhubarb gastric gavage and other methods, to assist in the absorption of ascites, defecation and bowel movements, reduce intra-abdominal pressure, improve symptoms.3.6 Surgery: Surgical intervention should be avoided in the period of acute reaction, but if the combination of the abdominal cavity ventricular septum syndrome, the intra-abdominal pressure is not relieved by short-term conservative treatment, then open decompression and drainage should be implemented. As for the timing of surgical intervention, the current consensus is that pancreatic necrosis with infection is an absolute indication for surgery, and the main purpose of surgery is to remove necrotic tissue, abdominal lavage and drainage in order to stop the progression of the disease. For patients without infection around the pancreas, but with large amount of peritoneal fluid, abdominal tube drainage and lavage can be used, which can transfer the abdominal exudate rich in pancreatic enzymes and many harmful substances out of the body, dilute the concentration of enzyme toxins in the abdominal exudate, and reduce the local and systemic damages caused by it.4. Prevention of HAP4.1 General prevention: controlling the diet, taking lipid-lowering medicines to reduce the level of blood lipids, and obese people should properly increase exercise and reduce body weight. Increase exercise and reduce weight. Obesity is an independent risk factor for AP, and an important indicator of the prognosis of AP, with a strong correlation with HL.4.2 Prevention for specific groups: Pregnant women should monitor the blood lipids and lipoproteins during the whole period of pregnancy, and once the elevated blood lipids are detected, the blood lipids should be controlled by diet, and it is not advisable to take lipid-lowering drugs. Those who take drugs that can cause elevated lipids should monitor the blood TG level.Glueck et al. believe that those who apply estrogen or triamcinolone should stop taking the drug when the blood TG>7.90mmol/L, and the blood TG>3.39mmol/L is a relative contraindication to the use of the drug. Other drugs such as diuretics, β-blockers, etc., if abnormalities occur during the application process, dietary regulation can be preceded, and the drug should be stopped when it is ineffective.4.3 Gene therapy: For the high TGemia caused by hereditary LPL deficiency, some scholars in foreign countries have proposed the application of gene therapy. This method is still in the research stage. Animal experiments show that after injecting a drug called AAV1-LPLS447X into LPL-deficient felines and rodents, myofibroblasts can produce and secrete LPL with enzyme activity, which can reduce blood TG level by 97% and maintain it for more than 1 year.5 Prospect: With the improvement of the living conditions, the incidence rate of HAP is increasing year by year. Clinicians should attach great importance to it, and lipid determination should be listed as one of the routine examinations for admission of AP, so as to facilitate early diagnosis and timely treatment. It is reasonable to believe that the prognosis of HAP patients will be further improved with the increased attention to HAP by medical workers and researchers and the in-depth study of the correlation between HL and AP.