Decreased secretion or excretion of pancreatic enzymes

Introduction Chronic pancreatitis is a persistent, permanent injury to pancreatic tissue and function due to various factors. Different degrees of acinar atrophy, pancreatic duct deformation, fibrosis and calcification in the pancreas, and varying degrees of pancreatic exocrine and endocrine dysfunction, clinical manifestations of abdominal pain, diarrhea or steatorrhea, weight loss and malnutrition and other pancreatic insufficiency Symptoms. In chronic pancreatitis, the amount of pancreatic juice, sodium bicarbonate, and various pancreatic enzyme secretions or excretions are reduced. Typical chronic pancreatitis is rare in China, and it is difficult to diagnose.

Cause

Causes of decreased pancreatic enzyme secretion or excretion:

(1) Causes of the disease: The cause of chronic pancreatitis is affected by many factors. The common causes are alcohol overdose and biliary diseases (mainly gallstones). In the past 10 years, there are more alcoholic pancreatitis in European and American countries. , accounting for 41% to 78%, cholelithiasis only 0% to 8%, and idiopathic 9% to 45%. Japan reported 71% alcohol, 8% to 11.3% cholelithiasis, and 27% idiopathic, similar to Europe and America. There are few reports of chronic pancreatitis in China. Most reports suggest that gallstones account for about 30% to 50%, and alcohol is less, and some reasons are unknown.

The reasons for the low incidence of alcoholic pancreatitis in Chinese may be: 1 statistical data is incomplete, there should be national statistical results of large-scale cases of unified diagnostic criteria, in order to draw conclusions; 2 people's living habits are different from the West, Japan, Westerners The Japanese use low-alcohol and beer as drinks, and drink it for a long time. The Chinese prefer high-alcohol and drink less.

Other causes of chronic pancreatitis are: trauma and surgery, metabolic disorders, nutritional disorders, genetic factors, endocrine abnormalities, etc., are intended to be described below.

1. Biliary diseases: mainly bile duct stones, which can cause the pancreatic juice stasis caused by Oddi sphincter inflammation and edema caused by stones incarceration or edema, and the pancreatic duct pressure is increased, causing the small pancreatic duct and acinar to rupture. Pancreatic juice penetrates into the pancreatic stroma, and trypsin activation leads to a series of pancreatic enzyme chain reactions and self-digestion. Repeated obstruction and increased secretion of pancreatic juice lead to repeated inflammation of the pancreas, and eventually fibrosis causes chronic pancreatitis. In the clinical ascending cholelithiasis surgery, the surgeon often licks the swelling, hardening, and uneven texture of the chronic inflammation of the pancreatic head, which is typical of biliary pancreatitis.

In addition, bile duct mites, Oddi sphincter edema, hernia, fiber stenosis, deformity, tumors, etc. can cause obstruction of the lower common bile duct and pancreatic duct, leading to chronic pancreatitis.

2. Alcoholism: The cause of chronic pancreatitis caused by alcohol is not fully understood. It is generally considered that: 1 alcohol stimulates the increase of gastric acid secretion, stimulates the secretion of secretin and trypsin from the duodenum, resulting in increased secretion of pancreatic juice. At the same time, alcohol stimulates the duodenal mucosa, causing Oddi sphincter spasm, resulting in increased pancreatic ductal pressure; 2 alcohol-induced pancreatic juice protein and bicarbonate concentration increase, pancreatic juice protein and calcium combine to form a stable sediment, attached to small On the wall of the pancreatic duct, protein emboli are formed, causing stenosis and obstruction of the pancreatic duct, which leads to atrophy and necrosis of the acinar epithelium, inflammation of the interstitial and fibrosis; 3 alcohol directly causes degeneration of the acinar cytoplasm, Mitochondrial swelling, lipid accumulation, pancreatic duct epithelial cell damage, etc.

3. Trauma and surgery: Trauma and surgery are common causes of acute pancreatitis. Chronic pancreatitis may only occur after severe trauma or injury to the main pancreatic duct. Chronic pancreatitis can result from extensive abdominal contusion after abdominal blunt injury or surgery. Lesions near the pancreas or penetrating ulcers in the posterior wall of the stomach can also cause destruction of pancreatic tissue and form chronic pancreatitis.

4. Metabolic disorders: In patients with hyperlipidemia, the incidence of chronic pancreatitis is relatively high. It is believed that there is a higher concentration of chylomicrons and free fatty acids in the pancreatic capillaries during hyperlipidemia, which causes embolism and damage of capillaries. Caused by the inner membrane. It may also be due to hyperlipidemia, increased blood viscosity, increased blood flow resistance in venules and venules, blood stasis, thrombosis leading to pancreatic tissue ischemia, and chronic pancreatitis. Alcohol, pregnancy, oral contraceptives, long-term use of estrogen and vitamin A can cause hyperlipidemia.

5. Nutritional disorders: Low-protein diet can lead to chronic pancreatitis, which is more common in Southeast Asia, Africa and Latin America. In recent years, it has been found that there is a correlation between high-fat intake and the onset of pancreatitis. Animal experiments have also shown that high-fat intake makes the pancreas sensitive and prone to chronic pancreatitis. Patients in Europe, America, and Japan are often associated with high fat intake.

6. Genetic factors: Hereditary pancreatitis is rare, and it is a chromosomal dominant inheritance. Congenital malformations of the biliary tract such as pancreatic duct sepsis, abnormal bile duct and pancreatic duct often accompanied by chronic pancreatitis, mostly due to poor pancreatic drainage.

7. Endocrine abnormalities: hypercalcemia can occur when hyperparathyroidism is hyperthyroidism, and about 7% to 19% are associated with chronic pancreatitis. In hypercalcemia, the amount of calcium in the pancreatic juice is increased, and it is easy to precipitate in the acidic pancreatic juice to form pancreatic stones; high calcium can activate pancreatic enzyme and promote pancreatitis.

When the adrenal cortex is hyperactive, cortisol can increase the secretion and viscosity of the pancreas, leading to pancreatic juice excretion, and increased pressure to cause pancreatitis.

(B) the pathogenesis: due to the severity of the disease, different pathology has a greater change. The surface of the pancreas is smooth but not flat and has a wood or stone hardness. The volume is reduced and the cut surface is white. The main pancreatic duct is narrow and the distal end is dilated. The heavy one can affect the first and second branches. Its ends often form a sac. There are white or colorless liquids in the tube, and most of them have no bacterial growth. It is often seen that protein precipitates as the precursor to the stone. Cysts of varying sizes can be seen in the head and neck, communicating with the main pancreatic duct. The larger one can oppress the surrounding organs and sometimes form a sinus with the surrounding tissue. Peri-pancreatic sclerosis can affect adjacent tissues, such as common bile duct stricture, gastric and duodenal artery stenosis, portal vein compression or thrombosis can cause portal hypertension.

Microscopic examination revealed degeneration and necrosis of glandular cells, intertrochanteric tubule dilation, fibrous tissue hyperplasia, inflammatory cell infiltration, and tissue sclerosis. The vascular changes were not significant, and the islets were affected at the latest. In about 27% of the cases, the gland cells were severely affected or even disappeared, but the islets were clearly visible.

The pathophysiological changes are characterized by a large amount of protein secreted by pancreatic acinar cells, and the liquid and bicarbonate secreted by pancreatic duct cells do not increase. It is speculated that the concentration of pancreatic protein (Lithostathine) secreted by pancreatic acinar cells and GP2 (a type of protein that can form a cast) is easy to precipitate in the pancreatic duct, which is closely related to the formation of chronic pancreatitis.

Changes in extra-pancreatic tissue, often biliary system disease, peptic ulcer disease. Pancreatic vein thrombosis and portal hypertension are not uncommon. A small number of patients have ascites and pericardial effusion. In patients with fatty necrosis, subcutaneous tissue necrosis can occur, forming subcutaneous nodules.

an examination

Related inspection

Pancreatic exocrine function test pancreatic disease ultrasound diagnosis of pancreatic CT examination of pancreatic specific antigen (PaA)

Examination and diagnosis of decreased pancreatic enzyme secretion or discharge:

Clinical manifestations: varying in weight. There may be no obvious clinical symptoms, and there may be obvious clinical manifestations.

1. Abdominal pain: Up to 90% of patients have abdominal pain of varying degrees, with intermittent pain for several months or years. Mostly located in the middle and upper abdomen, it is dull or painful. It can also be left or right, often radiating to the back. The pain site is consistent with the site of inflammation. According to the experiment, the pancreatic head was stimulated by electricity, and the pain occurred in the right upper abdomen, stimulating the tail of the pancreas, and the pain was in the left upper abdomen. In addition to radiation to the back, a small number of lower chest, kidney area and testicles are released. Cross-strained, there may be radiation pain in the shoulder. The pain is persistent and deep. Lighter people only have a sense of weight or burning. There is little feeling like it. Drinking, high-fat, high-protein diet can induce symptoms, accompanied by nausea and vomiting when the pain is severe. The abdominal pain of such patients is often characterized by body position. The patient likes to lie in the supine position, sitting position or forward tilt position, and the abdominal pain is increased in the supine position or upright.

2. Diarrhea: mild patients have no symptoms of diarrhea, but in severe cases, the alveolar destruction is excessive, and the secretion is reduced, that is, symptoms appear. It is manifested as abdominal distension and diarrhea. It has 3 to 4 times of stool every day. The amount is large, the color is light, the surface is shiny and bubbles, and the stench is mostly acidic. The amount of fat in the feces increases due to the digestion and absorption of fat. In addition, there are indigestible muscle fibers in the feces. Due to the loss of large amounts of fat and protein, patients experience signs of weight loss, weakness and malnutrition.

3. Others: Some symptoms of dyspepsia such as bloating, loss of appetite, nausea, fatigue, weight loss, etc. are common in patients with severe pancreatic function impairment. For example, islet involvement can significantly affect glucose metabolism, and about 10% have obvious symptoms of diabetes. In addition, patients with biliary diseases or biliary obstruction may have jaundice. Pseudocyst formation can reach the abdominal mass. Pancreatic ascites can occur in a small number of patients. In addition, chronic pancreatitis can cause upper gastrointestinal bleeding. The reason is: pancreatic fibrosis or cyst formation oppression of the splenic vein, can form portal vein thrombosis caused by portal hypertension. Patients with chronic pancreatitis have a higher probability of having peptic ulcer. Alcoholic gastric mucosal damage can occur in people who continue to drink alcohol. Multiple fat necrosis can occur in patients with chronic pancreatitis. Subcutaneous fat necrosis often occurs in the extremities and forms hard nodules under the skin.

Diagnosis: The clinical manifestations of chronic pancreatitis are variable and non-specific, and the diagnosis is often difficult. Atypical is more difficult to confirm the diagnosis. For patients with recurrent acute pancreatitis, biliary tract disease or diabetes, recurrent or persistent upper abdominal pain, chronic diarrhea, weight loss can not be explained by other diseases, the disease should be suspected. Clinical diagnosis is based on medical history, physical examination and supplemented with necessary X-ray, ultrasound or other imaging examinations, upper gastrointestinal endoscopy and related laboratory examinations. The latest diagnostic criteria for chronic pancreatitis (Japan Pancreas Society, 1995) are as follows:

1. Chronic pancreatitis diagnosis criteria:

(1) There is pancreatic stone in the abdominal B-ultrasound tissue.

(2) CT intracranial calcification confirmed by pancreatic stones.

(3) ERCP: The pancreatic duct and its branches in the pancreatic tissue are irregularly expanded and unevenly distributed; the main pancreatic duct is partially or completely obstructed and contains pancreatic stones or protein emboli.

(4) Secretion test: reduced bicarbonate secretion, accompanied by decreased pancreatic enzyme secretion or discharge.

(5) Histological examination: tissue sections showed destruction and reduction of exocrine tissue in the pancreas, and irregular fibrosis between the lobes, but interlobular fibrosis was not unique to chronic pancreatitis.

(6) ductal epithelial hyperplasia or dysplasia, cyst formation.

2. Highly suspected chronic pancreatitis standards:

(1) Abdominal ultrasonography of the pancreas is abnormal, the pancreatic duct is irregularly expanded or the pancreas outline is irregular.

(2) CT pancreas contour is irregular.

(3) ERC: only the main pancreatic duct is irregularly dilated, and the pancreatic duct is filled with defects, suggesting non-calcified pancreatic stones or protein emboli.

(4) Secretion test: only the secretion of bicarbonate is reduced, or the secretion and discharge of pancreatic enzyme are reduced.

(5) Non-intubation test: The benzoic acid-amide-p-aminobenzoic acid (BT-PABA) test and the fecal chymotrypsin test were abnormal at different times.

(6) Histological examination: tissue sections showed interlobular fibrosis, and one of the following abnormalities: decreased exocrine tissue, Langhans cell cluster separation or pseudocyst formation.

It is not necessary to consider which clinical type is involved in the diagnosis, and try to apply a feasible examination method to determine the cause of the disease. In many cases, chronic pancreatitis can only be temporarily suspected, and the diagnosis is confirmed by long-term treatment and follow-up observation.

Chronic pancreatitis mainly manifests as chronic abdominal pain and pancreatic endocrine and exocrine insufficiency, which is related to the occurrence of pancreatic cancer. It can also trigger a series of other complications. The most common complications are the formation of pseudocysts and mechanical obstruction of the duodenum and common channels. Less common complications include splenic vein thrombosis and portal hypertension. The formation of aneurysms (especially the splenic artery) and pancreatic chest and ascites.

Differential diagnosis

Symptoms of confusing pancreatic enzyme secretion or excretion:

Insufficient pancreatic function: At present, methods for diagnosing PEI include: detection of fecal fat, fecal elastase, fecal chymase, etc., secretin-cholecystokinin test and mixed triglyceride breath test. Among them, there is a very good correlation between the modified carbon (13C) triglyceride breath test and the secretin-cholecystokinin test, with sensitivity and specificity of 100% and 92%, respectively.

Exocrine dysfunction of the pancreas: pancreatic exocrine insufficiency refers to the symptoms of nutrient digestion and malabsorption caused by insufficient secretion of pancreatic enzymes and unsynchronized pancreatic enzyme secretion caused by various reasons.

Islet cell destruction: Diabetes mellitus is a metabolic disorder caused by a decrease in the biological effect of insulin deficiency and (and) insulin. It is a common disease characterized by persistent elevated blood glucose and the presence of diabetes. The incidence rate is 1%. ~2%. Diabetes refers to primary diabetes, which can be divided into insulin-dependent diabetes mellitus (type I diabetes) and non-insulin-dependent diabetes mellitus (type II diabetes) according to its etiology, pathogenesis, pathology, clinical manifestations and prognosis. ).

Insulin-dependent diabetes mellitus can occur at any age, but it usually occurs in children or adolescents. It accounts for less than five percent of all diabetes, but its impact on life is far greater than that of common non-insulin-dependent diabetes. The exact cause of insulin-dependent diabetes is not very clear. It is more certain that the body's immune system is out of order and is against the tissues of the body. The body's immune system creates certain substances that fight insulin in the pancreas. When these cells are destroyed, they cannot secrete insulin.

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