Elevated urinary amylase

Introduction When pancreatitis and other diseases occur, pancreatic amylase enters the bloodstream and is excreted from the urine due to inflammation and other diseases in the pancreatic tissue, causing the patient's blood amylase to rise and amylase to be detected in the urine.

Cause

(1) Causes of the disease

There are many causes of acute pancreatitis, and there are regional differences. In China, more than half of them are caused by biliary diseases. In Western countries, in addition to cholelithiasis, alcohol abuse is also the main reason.

1. Biliary system diseases: Under normal circumstances, the common bile duct and pancreatic duct open to the Vater ampulla 80%, after confluence into the duodenum, this common pipeline is about 2 ~ 5mm long, in this "common channel" Inside or Oddis sphincter, there are stones, biliary mites or inflammation, edema or spasm, and the gallbladder contracts. When the pressure in the bile duct exceeds the pressure in the pancreatic duct, the bile can flow back into the pancreatic duct to activate the trypsin to cause self-digestion. "common duct theory" (common duct theory), 50% of acute pancreatitis caused by this, especially bile duct stones are the most common; if the gallstones migrate, the common bile duct, ampulla or bile duct inflammation caused Oddis sphincter dysfunction, such as There is duodenal hypertonic pressure, which causes duodenal juice to flow back into the pancreatic duct, activate pancreatic enzyme to produce acute pancreatitis; in addition, when biliary tract inflammation, bacterial toxins release kinins to activate pancreas through the biliary-pancreatic lymphatic traffic branch Digestive enzymes cause acute pancreatitis.

2. Alcohol or drugs: Alcoholism in European and American countries is one of the important causes of acute pancreatitis, and it has also increased in China in recent years. Alcohol can stimulate the secretion of gastrin from the G cells of the antrum, increase the secretion of gastric acid, decrease the pH value in the duodenum, increase the secretion of secretin, and increase the exocytosis of the pancreas. Long-term alcoholism can stimulate the protein content in the pancreas to increase. The protein "embolic" blocks the pancreatic duct; at the same time, alcohol can stimulate the duodenal mucosa to cause edema of the nipple and prevent the discharge of pancreatic juice. The reason is consistent with the "blocking-secretion strong theory". Some drugs and poisons can directly damage pancreatic tissue, or promote exocytosis of pancreatic juice, or promote pancreatic duct epithelial cell proliferation, acinar dilatation, fibrosis or increase blood lipids, or promote Oddis sphincter spasm and cause acute pancreatitis, such as azole Anthraquinone, adrenocortical hormone, tetracycline, thiazide diuretics, L-asparaginase, organophosphorus insecticides, and the like.

3. Infection: Many infectious diseases can be complicated by acute pancreatitis. The symptoms are not obvious. After the primary disease is healed, pancreatitis subsides spontaneously. Common mumps, viral hepatitis, infectious mononucleosis, typhoid fever, sepsis Wait. Aphids enter the bile duct or pancreatic duct, which can not only be brought into the intestinal fluid, but also brought into the bacteria, which can activate the pancreatic enzyme to cause inflammation.

4. Hyperlipidemia and hypercalcemia: The chance of patients with familial hyperlipidemia with acute pancreatitis is significantly higher than that of normal people. During hyperlipidemia, fat embolism of the pancreatic vessels causes ischemia, telangiectasia, and damage to the vessel wall; in patients with primary hyperparathyroidism, 7% of patients with pancreatitis have severe disease and high mortality; 25% ~45% of patients have pancreatic parenchymal calcification and pancreatic duct stones. Stones can block the pancreatic duct, and calcium ions can activate trypsin, which may be the main cause of pancreatitis.

5. Surgical trauma: upper abdominal surgery or trauma can cause pancreatitis. Postoperative pancreatitis is more common in abdominal surgery, such as pancreatic, biliary, gastric, and duodenal surgery, and occasionally in non-abdominal surgery. The cause may be intraoperative pancreatic injury, intraoperative contamination, Oddis sphincter edema or dysfunction, and the use of certain drugs after surgery, such as anticholinergic, salicylic acid preparations, morphine, diuretics, and the like. In addition, ERCP can also be complicated by pancreatitis, which often occurs in the case of selective intubation difficulties and repeated pancreatic duct visualization. Under normal circumstances, the success rate of pancreatic duct intubation in ERCP is above 95%, but occasionally after the pancreatic duct is developed, the selective bile duct intubation is not smooth, resulting in multiple repeated pancreatic duct visualization, stimulation and injury. Pancreatic duct opening; or due to aseptic operation is not strict, injecting infectious substances to the distal end of the obstruction pancreatic duct; or injecting excess contrast agent, even leading to pancreatic acinar, tissue development, induced pancreatitis after ERCP. Foreign scholars believe that repeated pancreatic duct visualization more than 3 times, the incidence of pancreatitis after ERCP increased significantly. Lighter only elevated blood urease amylase, severe cases can occur severe pancreatitis, leading to death.

6. Other

(1) vascular factors: atherosclerosis and nodular arteritis, can cause arterial stenosis, pancreatic blood supply.

(2) Late pregnancy: women are easy to have gallstones, hyperlipidemia, increased uterus can compress the pancreas, can cause pancreatic drainage difficulties, pancreatic duct hypertension.

(3) penetrating ulcer: when the duodenal Crohn's disease affects the pancreas, it can release the pancreatic acinar and release pancreatic enzyme to cause pancreatitis.

(4) Mental, genetic, allergic and allergic reactions, diabetes coma and uremia are also factors that cause acute pancreatitis.

(5) pancreatic duct obstruction, pancreatic duct stones, stenosis, tumors, etc. can cause pancreatic juice secretion, pancreatic duct pressure increased, pancreatic duct small branch and pancreatic acinar rupture, pancreatic juice and digestive enzymes infiltrate the interstitial, causing acute pancreatitis. When a small number of pancreas is separated, the main pancreatic duct and the accessory pancreatic duct are shunted and the drainage is not smooth, and may also be related to acute pancreatitis.

(6) Idiopathic pancreatitis, the cause is unknown 8% to 25%.

(two) pathogenesis

The pathogenesis of acute pancreatitis caused by various causes is different, but it has a common pathogenesis, that is, the pancreas itself is digested by various digestive enzymes of the pancreas.

Under normal circumstances, the pancreas can prevent this self-digestion:

1. Pancreatic juice contains a small amount of trypsin inhibitor to neutralize a small amount of activated trypsin.

2. Pancreatic acinar cells have a special metabolic function that prevents pancreatic enzymes from invading cells.

3. The substance that enters the pancreas contains neutralizing trypsin.

4. The pancreatic duct epithelium has a protective layer of mucopolysaccharide. When in some cases the above defense mechanism is destroyed, it can occur.

Under pathological conditions, pancreatic duct obstruction due to various reasons, pancreatic acinar can still secrete pancreatic juice, which can cause the pancreatic duct pressure to rise, destroying the mucus barrier of the pancreatic duct system itself, and the reverse diffusion of HCO3-, causing the catheter The epithelium is damaged. When the pressure inside the catheter exceeds 3.29 kPa, it can cause pancreatic acinar and small pancreatic duct to rupture. A large amount of pancreatic juice containing various pancreatic enzymes enters the pancreatic parenchyma, pancreatic secretory protease inhibitor (PSTI) is weakened, and trypsinogen is activated. Protease, the pancreatic parenchyma undergoes self-digestion. Among them, trypsin is the strongest, because a small amount of trypsin can activate a large number of other pancreatic enzymes including itself, which can cause edema, inflammatory cell infiltration, congestion, hemorrhage and necrosis of pancreatic tissue.

The relationship between pancreatic phospholipase A and acute pancreatitis has been paid more attention in recent years. Once activated by bile salts, trypsin, calcium ions and enterokinase, this enzyme can hydrolyze lecithin of the gland cell membrane to produce fatty acids and lysolecithin. Promote cell disintegration, release a large amount of pancreatic enzymes in the cells, and aggravate the degree of inflammation. In addition, phospholipase A decomposes phospholipase into fatty acids and lysolecithin, and also produces thromboxane A2 (TXA2). TXA2 is a strong vasoconstrictor. The imbalance of TXA2 and PGI2 may lead to tissue blood circulation disorder. Pathological changes. When lipase is activated, it can lead to fat necrosis and even to the peripancreatic tissue. The lower the blood calcium, the more severe the fat necrosis is, which is a sign of poor prognosis. When the elastic fiber enzyme is activated by trypsin, in addition to the general proteolysis, it has a specific digestive effect on the elastic fiber, so that the elastic fiber of the blood vessel wall is dissolved, the pancreatic blood vessel is necrotic, ruptured and hemorrhage, which is also the development of edema and hemorrhage. The pathophysiological basis of pancreatitis. The vasopressin is activated by trypsin to form a kallikrein, which releases bradykinin and pancreatic agonist, which can increase vasodilation and permeability, and eventually cause shock.

In recent years, domestic and foreign scholars have studied the pathogenesis of acute pancreatitis from the above-mentioned "pancreatic enzyme elimination chemistry" to the organization "inflammatory media theory." A large number of experimental studies have revealed that a series of inflammatory mediators play an important role in the process of pancreatic tissue injury in acute pancreatitis, and the interaction between various inflammations mediates the occurrence and development of acute pancreatitis through different pathways.

In 1988, Rinderknecht proposed the "white blood cell overactivation" theory, the recently elaborated "second strike" theory - the generation of inflammatory factors and its cascade "cascade reaction", suggesting that the pancreatic localized inflammatory response develops into Life-threatening acute pancreatitis (SAP). Different pathogenic factors cause damage to acinar cells, trigger the release of active pancreatic enzymes and activation of monocyte macrophages, over-activate neutrophils, stimulate the release of inflammatory factors, leading to pancreatic necroinflammation, microcirculatory disorders and Increased vascular permeability leads to dysfunction of the intestinal barrier. Intestinal bacterial translocation to the pancreas and blood circulation leads to endotoxemia; endotoxin reactivates macrophages and neutrophils, releasing a large number of inflammatory factors leading to hypercytokines and triggering systemic inflammatory syndrome (systemic inflammatory syndrome) Response syndrome (SIRS), while some inflammatory factors chemotaxis more neutrophils infiltrating the pancreas, lungs and other organs, resulting in multiple organ failure (MOF). Inflammatory factors involved in the occurrence and development of SAP include cytokines such as tumor necrosis factor (TNF-), interleukin (ILS), etc.; inflammatory mediators such as platelet activating factor (PAF), nitric oxide (NO), etc. Chemokines such as macrophage chemoattractant protein-1 (MCP-1). Although these inflammatory factors have different effects, the final effect is to achieve the same goal, leading to the occurrence of SIRS and MOF.

The exact mechanism of intestinal translocation is still controversial, and the most likely route is to penetrate the intestinal wall translocation or blood-borne dissemination. It is generally believed that bacterial endotoxin is a potent activator of mononuclear macrophages and induces secretion of inflammatory factors such as TNF-, IL-1 and IL-6. Endotoxin in the portal vein of normal people is quickly cleared by liver Kupffer cells, preventing the cytokine-like effect of endotoxin on the immune system. Decreased hepatic reticuloendothelial function or inhibition of reticuloendothelial function can lead to systemic endotoxemia and activation of systemic mononuclear macrophages. Clinical studies have shown that the function of the reticuloendothelial system in SAP patients is disrupted and inhibited. It can be seen that endotoxin plays an important role in the development of SAP. By activating macrophages and neutrophils, it causes hyperinflammatory cytokines and oxygen free radicals and neutrophil elastase. The powerful destructiveness ultimately leads to SIRS and MOF. This is the recently proposed "second strike" doctrine.

an examination

Related inspection

Urinary amylase trypsin

1. White blood cell count: In mild pancreatitis, it may not increase or slightly increase, but in severe cases and with infection, it is often significantly increased, and neutrophils are also increased.

2. Amylase assay: This is one of the important objective indicators for the diagnosis of acute pancreatitis, but it is not a specific diagnostic method. In the early stage of the disease, when there is embolism of the pancreatic blood vessels and some hemorrhagic necrotizing pancreatitis, it may not increase due to severe destruction of pancreatic tissue. Amylase may also increase in the case of shock, acute renal failure, pneumonia, mumps, perforation of ulcer disease, and intestinal and biliary infections. Therefore, when there is an increase in amylase, it is necessary to combine the history, symptoms and signs to rule out the increase of amylase caused by non-pancreatic diseases, in order to diagnose acute pancreatitis.

The increase of amylase has a certain relationship with the onset time of pancreatitis. According to clinical observations, there are several performances:

1 After 24 hours of onset, serum amylase reached the highest peak, and the highest peak of urinary amylase appeared after 48 hours.

2 Urinary amylase reaches its peak in the short term after the onset, while serum amylase may not increase or increase slightly.

3 serum amylase and urinary amylase increased at the same time, but gradually returned to normal.

4 The amylase elevation curve is wave-like or long-term increase, revealing the occurrence of complications.

It is worth mentioning that the degree of amylase increase is not necessarily proportional to the severity of inflammation. For example, in edematous pancreatitis, amylase can reach a higher degree. In some necrotizing pancreatitis, due to the massive destruction of pancreatic tissue, Amylase is not increased. Regarding the accuracy of serum amylase and urinary amylase, there are differences in the literature. Some people think that the determination of serum amylase is accurate, some people think that urine amylase is accurate, and urine collection is easy, and it can be checked repeatedly. Therefore, there are many clinically measured urinary amylases.

3. Blood chemistry examination of severe pancreatitis, carbon dioxide binding decreased, blood urea nitrogen increased, indicating that the kidneys have been damaged. When the islets are damaged, there may be an increase in blood sugar, but most of them are transient. In hemorrhagic pancreatitis, blood calcium is often lowered, and when it is less than 7 mg%, the prognosis is often poor.

4. Abdominal puncture for abdominal cavity exudation, abdominal puncture can help the diagnosis of this disease. Most of the puncture fluid is bloody. If the amylase is measured, the disease can be diagnosed.

5. Amylase isoenzyme examination There are two types of amylase isoenzymes, pancreatic isozymes and salivary isozymes (STI). In acute pancreatitis, pancreatic isoenzymes can be significantly increased. For those who are highly suspected of pancreatitis and normal amylase, whether the amylase of hyperamylasemia is derived from the pancreas, the determination of isozymes is more valuable. Some people in China use electrophoresis. From the cathode to the anode, PIA has three kinds of P3, P2 and P1. P3 is a sensitive and reliable indicator for diagnosing acute pancreatitis.

6. Radioimmune trypsin assay (RIA) Because of the amylase assay, there is no specificity for the diagnosis of pancreatitis. With the advancement of immunoassay technology, many scholars are looking for a more accurate diagnostic method, namely pancreatic enzyme radioimmunoassay. Currently, there are roughly the following enzymes.

(1) Immunologically active trypsin (IRT): In acute pancreatitis, pancreatic acinar damage can release a large amount of trypsin and zymogen, which is a protease present only in the pancreas. Therefore, the determination of the concentration of trypsin and zymogen in serum should have a certain specificity. Clinical application proves that serum IRT has a large increase in duration of severe pancreatitis and lasts for a long time, which is helpful for the early diagnosis and differentiation of acute pancreatitis.

(2) Elastase II: Serum immunoreactive amylase (IRE) can be determined by radioimmunoassay. Since the serum IRE can disappear after total pancreatectomy, the enzyme can be assayed for specificity.

(3) Pancreatic trypsin inhibitor (PSTI): PSTI is secreted by pancreatic acinar and can inhibit the activation of pancreatic protease. Because it is a specific trypsin inhibitor, present in pancreatic juice and blood, the determination of its content can not only diagnose acute pancreatitis early, but also identify the severity of the disease, which is conducive to the observation of the disease.

(4) Phospholipase A2 (PLA2): PLA2 is a lipolytic enzyme and is one of the important factors causing pancreatic necrosis. Acute pancreatitis can be elevated early and lasts longer than serum amylase, which is useful for the diagnosis of severe pancreatitis.

Film degree exam

X-ray inspection

(1) Abdominal plain film: The following signs may be seen:

1 The density of the pancreas is increased (due to inflammatory exudation).

2 reflex intestinal stagnation (mainly in the stomach, duodenum, jejunum and transverse colon).

3 diaphragmatic muscle rise, pleural effusion.

4 A small number of cases can be seen with pancreatic stones or biliary stones.

5 The duodenal ring is stagnant, and its inner edge has a flat impression.

6 supine abdominal plain film, showing "transverse colon truncation" sign, that is, colonic hepatic flexion, spleen flexion, even if the position of the transverse colon is still not inflated, which is caused by acute pancreatitis caused by colonic spasm.

(2) Upper gastrointestinal barium meal imaging: The following signs may be seen:

1 The head of the pancreas is enlarged and the duodenal ring is enlarged.

2 The stomach sinus is under pressure.

3 Duodenum has expansion and deposition.

4 duodenal papillary edema or due to pancreatic head enlargement caused by the "3" sign.

5 pancreatic pseudocysts, visible gastrointestinal compression.

2. Ultrasound examination: Ultrasound plays an increasingly important role in the diagnosis of acute pancreatitis, and it has become one of the indispensable routine examination methods, but it is susceptible to gastrointestinal gas accumulation. Ultrasound can be found in the diagnosis of pancreatitis.

(1) Increased pancreas volume: In edematous pancreatitis, the pancreas increases in volume; in severe pancreatitis, it increases, and the contour of the pancreas is blurred, the surface is not smooth, and the deep surface of the pancreas is separated from the splenic vein. Unclear, sometimes the front and back of the pancreas are difficult to identify.

(2) Enhancement of pancreatic echo: In the edematous pancreatitis, the echo of the pancreas is enhanced, but in the case of severe pancreatitis, the interior of the pancreas is largely uneven, with strong echoes and irregular low echo areas.

(3) peritoneal exudate: rare in edematous pancreatitis, but more in severe pancreatitis, most of which are diffuse effusion, but also a localized effusion around the pancreas. Pancreatic abscesses and pseudocysts can also be found after treatment.

According to the above, combined with clinical features, ultrasound can be used as one of the means to identify edema and severe pancreatitis.

3. CT examination: CT scan can also show various pathological changes of the pancreas and its surrounding tissues from mild edema, hemorrhage to necrosis and suppuration. CT can also find effusion around the pancreas and small omentum, edema around the kidney, help early detection and follow-up observation of pancreatic pseudocyst. Because of the influence of gastrointestinal gas and obesity, CT scan is more superior and accurate than ultrasound examination, but it is not expensive because it is expensive.

4. Fiber endoscopy

(1) Fiberoptic endoscopy has no direct diagnostic value. It may be seen that the edema and hyperemia of the gastric duodenal mucosa may be seen in the posterior wall of the stomach (caused by enlarged pancreas).

(2) In addition to the lesions of the duodenal mucosa, the duodenal mucosa can be observed abnormalities or lesions in the duodenal papilla, especially in the case of pancreatitis caused by ampullary incarceration You can see the raised nipple or stone to find the cause directly.

(3) Endoscopic retrograde cholangiopancreatography (ERCP): It is only suitable for the understanding of biliary tract lesions after acute symptom control. Although the judgment of pancreatic duct obstruction can also be made, it may cause pancreatitis to re-emerge and become an injectable pancreatitis, so it is not suitable for routine use.

5. Laparoscopy For the diagnosis of acute upper abdominal pain or severe pancreatitis, laparoscopy may have a certain significance. A series of lesions can be seen through laparoscopy and can be divided into accurate signs and relative signs.

(1) Accurate signs: Refer to the microscope to see the diagnosis of pancreatitis, including:

1 focal necrosis: the result of fat necrosis caused by lipase and phospholipase activation. In the early stage of the disease, this necrosis is found in the small omental cavity of the upper abdomen. Due to the spread of the lesion, it can be found in the greater omentum, small omentum, transverse colon, gastric colon ligament, peri-renal fat sac, and colon. The extent of this grayish white fat necrosis is consistent with the extent of the lesion.

2 exudate: in severe pancreatitis, can be found in 85.5% of cases, the amount of exudate is 10 ~ 600ml, the most pancreatic ascites can reach more than 6L. An increase in the amylase activity of the exudate was determined. The slightly increased case fatality rate is 19%. The amylase is higher than 1024U, and the mortality rate is 59.1%. The color of the exudate is also related to the prognosis.

(2) Relative signs: no independent diagnosis, combined with accurate signs and clinical, in order to make a correct diagnosis.

1 abdominal congestion: often accompanied by abdominal exudate, more found in the upper abdomen. 2 elevation of the stomach position: This is caused by swelling of the pancreas, inflammation of the small omentum or cysts. When the fiber wall is used to contact the stomach wall, a hard pancreas can be felt.

6. Angiography: In order to diagnose vascular or hemorrhagic complications of acute pancreatitis, selective angiography of some patients is also a new development in recent years. Angiography can show vascular lesions (such as aneurysms and pseudoaneurysms) in the pancreas and surrounding pancreas, which can help to develop a treatment plan. If you can perform arterial intubation, you may avoid open surgery due to bleeding control.

7. Radionuclide scanning: more normal in the early stage of the disease, but in the case of severe pancreatitis, uneven or non-developed or localized radioactive defect areas can be seen. Since this inspection method requires a certain amount of equipment, it cannot be used universally.

8. Other examination methods: electrocardiogram, EEG, etc., although there is no direct help in the diagnosis of this disease, but there are many changes in severe pancreatitis, which can be used as an auxiliary examination method for diagnosis and treatment.

Differential diagnosis

Reduced urine specific gravity: Urine specific gravity measurement is used to estimate the concentrating function of the kidney, but the accuracy is poor and there are many factors affected. The measured values are for reference only. The decrease in urine specific gravity is seen in diabetes insipidus and chronic nephritis. The urine specific gravity is low, mostly below 1.020, and is often fixed at 1.010 in the late stage of the disease. Urinary protein traces ~+++. There are often red blood cells and casts in the urine (granular tube type, transparent tube type). There is obvious hematuria or gross hematuria during the acute attack.

Increased urine specific gravity: Urine specific gravity measurement is used to estimate the concentrating function of the kidney, but the accuracy is poor and the affected factors are many. The measured values are for reference only. Increased urine specific gravity is seen in dehydration, diabetes, acute nephritis and so on. The proteinuria is light and heavy (1~3g/d). There are microscopic hematuria. The red blood cells are pleomorphic and diverse. Sometimes, red blood cell casts, granular casts and renal tubular epithelial cells can be seen. Urinary fibrin degradation products (FDP) can be positive. Blood urea nitrogen and creatinine may increase transiently, serum total complement (CH50) and C3 decrease, return to normal within more than 8 weeks, and serum anti-streptolysin "O" titer may increase.

Increased urinary biliary: urinary biliary is derived from the binding of bilirubin. In combination with bilirubin in the lower part of the small intestine and in the colon, it is decoupled by the action of intestinal bacteria. After several stages of reduction, bilirubin becomes urinary biliary and then excreted with feces. A part of urinary biliary is absorbed into the portal vein from the intestine, most of which is taken up by the liver cells and then discharged into the intestinal fluid (intestinal hepatic circulation), and part of it enters the systemic circulation from the portal vein and is excreted from the urine through the kidney. A variety of factors can cause an increase in urinary biliary.

Urine osmotic pressure decreased: Urine osmotic pressure, also known as urinary osmolality, is the number of particles that reflect solute molecules and ions per unit volume of urine. The decrease in osmolality reflects the decrease in the concentration of the distal tubules, as seen in chronic pyelonephritis, chronic interstitial lesions caused by various causes, and chronic renal failure.

The urinary filtration fraction is significantly reduced: the production of urine depends on the filtration of the glomerulus and the reabsorption and secretion of the renal tubules and collecting ducts. Therefore, the regulation of the body's formation of urine is achieved by adjusting the filtration, reabsorption and secretion. The amount of filtrate produced by the two kidneys per unit time is called glomerular filtration rate (GFR), which is about 125 ml/min in normal adults. The ratio of glomerular filtration rate to renal plasma flow is called the filtration fraction. The renal plasma flow rate per minute is about 660 ml, so the filtration fraction is 125/660 x 100% 19%. This result indicates that about one-fifth of the plasma flowing through the kidney is filtered into the sac by the glomerulus to produce primary urine. Glomerular filtration rate and filtration fraction are indicators of renal function. Glomerular capillary blood pressure is significantly reduced, renal vasoconstriction, filtration membrane permeability and changes in filtration area can reduce glomerular filtration rate.

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