Short bowel syndrome

Introduction to short bowel syndrome Short bowel syndrome (shortbowelsyndromle) refers to the malabsorption syndrome after the extensive small bowel resection (including partial colectomy), the residual functional intestine can not maintain the nutritional needs of patients, clinically with severe diarrhea, weight loss, progressive malnutrition and Water and electrolyte metabolism disorders are characteristic, affecting the body's development, and the mortality rate is high. At present, nutritional support and small bowel transplantation are mainly used, but the efficacy is not certain. The quality of life of the patient still depends on the remaining small intestine length and its functional status. basic knowledge The proportion of sickness: 0.002%-0.003% Susceptible people: no special people Mode of infection: non-infectious Complications: malnutrition

Cause of short bowel syndrome

Intestinal torsion (55%):

There are many different causes of adult short bowel syndrome, mainly due to mesenteric vascular embolization or thrombosis, and acute intestinal torsion leading to extensive small bowel resection (75% or more), leading to mesenteric vascular embolization or thrombosis: Old age, long-standing congestive heart failure, atherosclerosis and heart valve disease, long-term diuretic application, hypercoagulable state, oral contraceptives; ileal short-circuit surgery in patients with morbid obesity can also occur short bowel syndrome symptoms; short Less common causes of bowel syndrome are: abdominal injury, primary or secondary tumor of the intestine, radiation-induced intestinal disease; rare cases: medical errors in the treatment of peptic ulcer will be gastric-ileal anastomosis, resulting in a wide range Similar clinical symptoms of small bowel resection.

Intestinal ectopic (35%):

The cause of short bowel syndrome in children can be divided into pre-natal and post-natal causes. The main cause of small bowel obstruction before birth, small intestinal ectopic fixation or abnormal torsion caused by poor rotation of the midgut can occur in the uterus or at any time after birth. Neonatal necrotizing enteritis gradually increased, has been considered as the main cause of neonatal short bowel syndrome, in addition, less common factors after birth are congenital megacolon disease and small intestine, mesenteric vascular embolism or thrombosis, Radiation enteritis or Crohn's disease can also cause this syndrome, but it is mainly found in children of older age groups.

Pathogenesis

After extensive resection of the small intestine, a series of pathophysiological changes will occur in the function of the digestive tract, resulting in a group of syndromes with nutrient malabsorption as the main symptom. The severity depends on the following factors: the extent and location of the intestine; Retaining the ileocecal valve; the functional state of the residual intestinal tube and other digestive organs (such as the pancreas and liver); the remaining small intestine, the compensatory capacity of the large intestine.

1. The extent of resection of the intestine: the wider the range of the resected small intestine, the more the absorption area of nutrients, water and electrolytes is lost (both active absorption and passive diffusion absorption), and the length of the small intestine has obvious individual differences ( 365 ~ 700cm), the length of the residual intestine and the functional status are far more important than the amount of the intestine segment, so it determines the incidence of postoperative short bowel syndrome and the level of mortality. It is reported that there is no intestinal In the case of nutritional support, the residual jejunum length is less than 30cm, it is difficult to survive, but now more and more reports of residual small intestine 20cm can also achieve long-term survival; therefore, even if the small intestine is removed, the nutrients needed for survival can be maintained. Excision of 75% or more of the small intestine, almost all malabsorption, difficult to handle, it is currently believed that patients with normal intestinal mucosa should have a small intestinal intestine with 50 to 70 cm and retain the entire colon, and some even think that 35 cm empty ileum is required. Retaining the ileocecal valve and part of the colon, after compensation, can rely on the intestine to maintain the body's required nutrients, and the colon resection should have a residual intestinal tube of 110 to 150 cm; Patients intestinal mucosal lesions such as Crohn's disease, we need to retain more of the intestine.

2. Resection of the intestine: the removal of the small intestine is also important for postoperative metabolism. Protein, carbohydrates, fat and most water-soluble vitamins, trace element absorption is closely related to the location of small intestine resection, especially in the ten In the digestive and jejunum, when the proximal small intestine is removed, the normal ileum will replace the entire absorption function. Because the proximal small intestine is also the place where cholecystokinin and the secretion of secretin synthesis, the removal of this small intestine will lead to bile secretion and pancreas. The secretion of exocrine is reduced, further aggravating the transportation of intestinal contents and absorbing obstacles.

The ileum is a specific occasion for absorbing combined bile salts and endogenous factor-binding vitamin B12. The metabolic disorder caused by resection is obviously heavier than that of the jejunum. Excision of 100 cm ileum will result in decreased absorption of bile salts, and unabsorbed bile salts enter the colon, resulting in bile salts. Sexual diarrhea, reduced intestinal-hepatic circulation of bile salts, and the liver compensates for loss of bile salts by increasing bile salt synthesis. Therefore, steatorrhea caused by fat malabsorption can be moderated (fat <20g/d); but more extensively removed The ileum (>100cm) will cause severe disturbance of bile salt metabolism, and the ability of liver compensatory synthesis of bile salts is also limited (4 to 8 times increase), resulting in severe steatorrhea (fat > 20g / d), Excision of the shorter ileum (<50cm), the patient is usually able to absorb the intrinsic factor-binding vitamin B12, which does not cause absorption disorder. When the ileum is removed, the ileum will cause obvious absorption disorder. This vitamin deficiency will lead to megaloblastic anemia. And peripheral neuritis, eventually leading to subacute spinal cord degeneration.

Clinical trials show that simultaneous resection of the small intestine and large intestine will produce more serious complications than small bowel resection. Under normal circumstances, adults consume nearly 2L/d of digestive juice, producing about 7L of endogenous fluid (stomach pancreas, bile, small intestine secretion), only Less than 2% (100 ~ 200ml) of liquid is not absorbed back, the large intestine is an important part of the absorption of water and electrolytes, in addition to the absorption of certain nutrients such as short-chain fatty acids, when a large range of small bowel resection parallel to the colon part, most After resection, severe water, sodium, and potassium are lost.

3. Preservation of ileocecal valve: When partial or total colectomy is performed, resection of the ileocecal valve will lead to metabolic disorders. Resection of the ileocecal valve will result in shortened residence time of the small intestine contents, affecting bacterial reproduction and gallbladder in the residual small intestine. The decomposition of salt, thereby reducing the absorption of fat and fat-soluble vitamins, the increase of bile salts into the colon, due to the increase of bacteria in the small intestine, vitamin B12 is partially metabolized, further reducing its absorption, therefore, if the ileocecal valve can be retained, even The residual small intestine is shorter and the patient is often tolerated.

4. Status of residual intestinal tract and other digestive organs: After intestinal resection, the function of residual intestinal tract is essential for the patient's survival and quality of health. For example, patients undergoing small bowel resection due to Crohn's disease, lymphoma, and radiation enteritis, The functional damage of the disease itself still exists, the absorption function will be further reduced, and it is very difficult to handle. The endocrine function of the pancreas will be significantly damaged in patients with extremely poor nutrition; the gastric acid secretion will occur after extensive small bowel resection, making The decrease in pH in the small intestine cavity directly affects the exocrine digestive function of the pancreas.

5. Residual large, small intestine adaptability:

(1) Structure and function after small bowel resection: After partial resection of the small intestine, changes in the morphology and function of the remaining intestine have been extensively studied in animals, but similar reports have rarely been reported in humans, in the rat, proximal and middle small intestine After resection, the remaining ileum circumference becomes larger, the intestinal wall becomes thicker, the villi becomes higher (Fig. 1), the acceleration of cell proliferation and transformation, and the shortening of the cell division cycle. In the ileal resection, a similar phenomenon is found in the jejunum, but it is not as good. The above is obvious, in humans, proximal intestinal biopsy after intestinal resection revealed intestinal mucosal cell proliferation.

Animal experiments have shown that the ileal mucosal hyperplasia results in an increase in absorption function (mainly for the absorption of glucose, maltose, sucrose, cholic acid and calcium), compensating for the loss of the length of the small intestine, and the increase in absorption function is the amount of epithelial cells per unit length or The increase in mucosal weight is increased, rather than the enhancement of the absorption function of each cell. Some people think that the function of some cells is still in an immature stage.

After the proximal small intestine resection of the animal, the enzyme and metabolism also changed with the proliferation of the mucosa. The specific activity of the sodium-potassium pump depends on the activity of adenosine triphosphate, hydrolase, enterokinase, DNase and pyrimidine synthase. On the contrary, the disaccharidase activity of each cell is decreased; the glucose metabolism of the pentose phosphate pathway is increased in the proliferating mucosa. After extensive intestinal resection in humans, studies have shown that the residual intestinal tract can gradually improve the fat, internal factors and carbohydrates, especially Absorption of glucose.

After human or animal small bowel resection, the study of colonic adaptive changes is still in its infancy. The available data show that the colon can increase the absorption of glucose and calcium after small bowel resection or morbid obesity.

(2) Factors affecting the adaptive changes after small bowel resection: After intestinal resection, the following factors may affect the adaptation of the small intestine:

1 contact between food nutritive substances and non-nutritive substances and residual intestinal tubes;

2 bile and pancreatic juice stimulation, nutritional effects of intestinal hormones or other factors;

3 stimulating effects of parenteral growth factors, hormones, polyamines, etc.;

4 The increase in residual small intestine blood flow.

Available data indicate that nutrients in the remaining intestine play an important role in the adaptive changes of the small intestine, such as no stimulation of the intestinal lumen by nutrients, although there will be proliferative changes in the intestinal wall (in patients with short bowel syndrome, TPN patients can be seen However, this mechanism is still unclear), but the intestinal tract does not produce adaptive changes (increased villus height, depth of recess, and amount of DNA in mucosal cells). At the same time, animal experiments have shown that mixed foods stimulate the small intestine more than the elemental diet. Adaptation changes to demonstrate the synergistic effect of nutritious and non-nutritive foods on adaptive adaptation of the small intestine.

Nutrients in the small intestine, especially higher concentrations of nutrients can stimulate the secretion of bile and exocrine pancreatic juice, and directly stimulate the proliferation of mucous membranes. When bile or pancreatic juice enters the ileum, it can obviously stimulate the proliferation of mucosa, and the pancreatic juice is produced in the stimulation of mucosal hyperplasia. The more obvious effect is that pancreatic juice can also change the activity of intestinal brush border enzyme. However, how these factors promote the proliferation of intestinal mucosa after small bowel resection is still unclear. Some people think that intestinal nutrient is stimulated by the nutrition of small intestine. The release of enteric trophic hormones and other factors may also be due to the removal of intestinal inhibitory factors by small bowel resection, resulting in an increase in the effects of trophic factors. The role of gastrin in many enteral nutritional hormones has been accepted by most scholars. It is recognized that gastrin seems to have only an effect on the adaptive changes of the stomach and proximal small intestine, but has little effect on the adaptation of the distal intestinal tract. Enteroglucagon plays a leading role in stimulating intestinal adaptation. Recent reports suggest that its precursors seem to play a more important role, Druckers study found animal models Glucagon-like peptide (glucagon-like peptide) can significantly stimulate the proliferation of intestinal villi, which is considered to be the main hormone that stimulates intestinal adaptation; in total parenteral nutrition, parenteral administration of pancreatic enzyme and cholecystokinin can be Stimulating mucosal hyperplasia, these hormones may act by stimulating bile, pancreatic juice secretion, rather than direct action; likewise, prostaglandins, epidermal growth factor and growth hormone releasing factor can stimulate intestinal epithelial cell proliferation.

Growth-related factors such as polyamines, putrescine, spermidine, and spermine have become more and more important for the changes in the fit of small intestine after small bowel resection. The initial study showed that ornithine decarboxylase is in polyamine biosynthesis. The role of rate-limiting enzymes plays an important role in intestinal adaptation. It is now believed that other biosynthetic enzymes related to the level of polyamines, such as s-adenyl-methionine decarboxylase, may play a more important role in The study of amine adaptation to small bowel resection is still in its early stages, and the final conclusions are urgently needed for further study.

Other mechanisms, such as residual intestinal innervation or changes in blood flow, may also play an important role in adaptive changes in the small intestine and need further confirmation.

Little is known about the functional adaptation of the colon after small bowel resection, and the colon may have increased absorption of glucose and amino acids.

From the current study, the adaptive changes after small bowel resection are affected by many factors, usually completed within a few months to one year after surgery, which has an important impact on the health, nutrition and survival of patients with short bowel syndrome.

Short bowel syndrome prevention

Among the factors related to the occurrence of this disease, the most important is the scope of surgical resection and the site of resection of the small intestine. When the small intestine is resected to 50% or more, significant malabsorption can be caused, and more than 70% of resection can occur, and severe symptoms or even death can occur. Duodenum, proximal jejunum, distal ileum is the main intestinal segment for digestion and absorption of the small intestine. As long as the above intestinal segment is retained, even if 50% of the small intestine is removed, the patient can still tolerate it, but if the distal ileum is removed, the ileum is 2 /3, or removal of the ileocecal valve and 25% of the jejunum can cause severe diarrhea and malabsorption, so in the implementation of small bowel resection, it is sufficient to keep the main part of the small intestine as much as possible to ensure the patient's life is basically safe. Length, active intestinal tube is an important measure to reduce the occurrence of this disease, affecting common factors of short bowel syndrome.

Complications of short bowel syndrome Complications malnutrition

There may be hand and foot spasm, coagulation mechanism disorders, bone softening, malnutrition and so on.

Symptoms of short bowel syndrome Common symptoms Hypokalemia, gallstones, stenosis, intestinal stenosis, hypoproteinemia, bleeding tendency

1. Clinical stage: The clinical process of short bowel syndrome goes through three stages:

(1) acute phase: general performance 1 to 3 months after surgery, due to a large number of diarrhea, fluid and electrolyte loss, balance disorder, severely endanger the patient's life, peak in 2 to 3 weeks, 2.5 liters of liquid lost from the stool every day 5 liters, in addition to diarrhea, there are still fatigue, oliguria and dehydration, electrolyte deficiency, acid-base balance disorder, low calcium and low magnesium convulsions.

(2) Adaptation period: an adaptation stage of initial oral intake and gradually increasing intake, often lasting for several months to one year. The diarrhea is obviously relieved during this period, and the water and electrolyte imbalance is alleviated. The most prominent clinical manifestation is Malnutrition, weight loss, severe hypoproteinemia and edema, night blindness due to vitamin and mineral deficiency, peripheral neuritis, coagulative bleeding tendency, anemia and osteomalacia.

(3) Stabilization period: Generally, it will be stable after about 1 year after surgery. Because the residual intestinal tube can be compensated to the maximum extent, the condition is gradually stable and can maintain relatively normal family life, but there may still be fat-soluble vitamins. The lack of calcium and other trace elements, excessive ileal resection, patients may have vitamin B12 deficiency, some patients can not reach the stage of complete oral nutrition, need to rely on family parenteral nutrition.

2. Clinical features

(1) diarrhea: diarrhea can be seen after extensive small bowel resection, the cause of diarrhea is multi-factor, including: shortened passage of food contents (due to shortened intestinal tube after intestinal resection and postoperative intestinal motility disorder); secondary to Lactose and other carbohydrates absorb dysfunction of intestinal contents, osmotic pressure changes, bacterial overgrowth, reduce intestinal cell brush border membrane disaccharide activity, increase water and electrolyte secretion, different diarrhea in patients with short bowel syndrome The classification can be used to analyze the different causes of this clinical symptom, so that the corresponding food, drug treatment program is adopted.

(2) High secretion of gastric juice and peptic ulcer: The high gastric secretion state after extensive small bowel resection in humans and animals is an important feature, which not only causes severe peptic ulcer disease, but also causes further absorption of short bowel syndrome. Damage, resulting in diffuse mucosal damage, low pH leads to inhibition of pancreatic enzymes, reduces the formation of fat microcapsules, reduces lipid digestion in the intestinal lumen; another role of high secretion state is a large amount of gastric juice exacerbation after surgery, diarrhea, gastric juice The high-secretion state can occur 24 hours after extensive small bowel resection, and it will cause different degrees of damage with time. The application of drug therapy can be controlled, and surgical treatment is rarely needed. The serum in the stomach after human and dog small bowel resection Elevated secretion, suggesting that the high secretion state of the stomach is secondary to the stimulation of this hormone or its nutritional effects on the gastric mucosa; it is also reported that small bowel resection may affect the catabolism of gastrin or affect the inhibition of gastrin. Hormone secretion; however, in other high-secretion states after intestinal resection, serum levels of gastric secretion have not been elevated, and even some patients have performed after bowel resection. The real reason for the low acid state, therefore, lead to small bowel resection of gastric hypersecretion is not clear.

(3) Nutritional disorders: After extensive resection of the small intestine, almost all obstacles to the absorption of nutrients, including proteins, especially fats and carbohydrates, are caused by insufficient absorption of calories, resulting in weight loss, fatigue, and children. Can lead to slow development, fluid loss in the first few weeks after surgery, the stool often exceeds 5L / d, especially in patients with partial or complete colectomy at the same time, the liquid loss is more obvious, the treatment is not timely can be low Blood volume, hyponatremia, hypokalemia, over time, other electrolyte and nutrient absorption barriers will gradually manifest, calcium and magnesium secondary to fatty acid absorption barriers (formation of fatty acids with these divalent cations) A deficiency in fatty acid salts will also occur.

In addition to vitamin B12 and folic acid, patients with short bowel syndrome rarely lack water-soluble vitamins. Vitamin B12 is absorbed in the ileum (the membrane receptor on its surface can recognize the internal factor-B12 complex). If 90% of the ileum is removed, Xilin ( Schilling) experiments often show malabsorption. Due to ileal resection, vitamin B12 entero-hepatic circulation is broken, accelerating the development of malabsorption; giant cell anemia caused by folate deficiency is relatively rare, but in the treatment of Crohn's disease, therapeutic Sullicylazo sulfapynidine (SASP) is a competitive inhibitor of folic acid absorption, so folic acid deficiency is more common in patients with short bowel syndrome, and other water-soluble vitamins can be absorbed throughout the small intestine, such as niacin malabsorption. The resulting pellagra, vitamin C deficiency symptoms can only be seen after extensive small bowel resection.

In patients with short bowel syndrome, the fat-soluble vitamin deficiency is more obvious. The fat-soluble vitamin is absorbed by bile acid microencapsulation. After a large number of ileal resection, the bile salt pool is significantly reduced, which affects the absorption of fat-soluble vitamins. Lead to reduced fat-soluble vitamin absorption, the most common is vitamin D deficiency, vitamin A, K, E absorption disorders, vitamin D deficiency and osteochondralization have been considered Crohn's disease ileal resection and morbid obesity Common complications after short circuit, vitamin D deficiency and steatorrhea cause calcium malabsorption, after small bowel resection, calcium absorption in the large and small intestine can be compensated to a certain extent, but it is difficult to meet the needs of the human body, plus short bowel syndrome Patients often have other minerals that are prone to fractures; low calcium can lead to increased secretion of parathyroid hormone. Because such patients are accompanied by calcium and magnesium deficiency, the release of this hormone will lead to further magnesium deficiency; these two Reduced absorption of valence cations can cause weakness and excessive fatigue, and short bowel syndrome can also cause night blindness caused by vitamin A deficiency. It should be noted that the level of vitamin A in serum can not truly reflect the degree of vitamin A deficiency. Functional determination, such as night adaptation ability, should be used to understand the true degree of vitamin A, which leads to vitamin K deficiency, but it is also rare. Occurred, manifested as purpura and hemorrhage, vitamin E deficiency leads to imbalance of the nervous system.

Like water-soluble vitamins, the absorption of trace elements in small patients after small bowel resection can be compensated. 25% to 50% of patients with short bowel syndrome have iron deficiency, especially those with persistent bleeding such as Crohn's disease. More obvious; zinc deficiency is directly proportional to the degree of diarrhea, most patients have zinc malabsorption, zinc deficiency and taste loss and pellagra, can be seen in patients with extensive small bowel resection, evaluation of zinc nutritional status Difficulties, because the level of zinc in the blood is affected by the amount of zinc ingested, it is also related to serum protein levels and inflammatory mediators. The latest methods such as blood cell zinc and zinc-dependent enzymes can provide a more accurate evaluation method. The lack of trace elements such as copper, selenium, chromium, and molybdenum can also occur in patients with short bowel syndrome.

(4) Intestinal high oxalic acid and kidney stones: the incidence of kidney stones increased after ileal resection and ileal diseases, high calcium oxalate urine is often secondary to the increase of oxalic acid absorption in the food, and the following two mechanisms in the intestine and the increase of oxalic acid absorption Relatedly, firstly, due to the increase of fatty acid in the colon cavity after extensive small bowel resection, it forms a complex with calcium, which reduces the formation of insoluble calcium oxalate and leads to an increase in intestinal oxalic acid absorption. Second, bile salts and fatty acids cause colonic mucosal infiltration. Sexual changes further increase the absorption of oxalic acid. Based on this, it is believed that the absorption of oxalic acid in the colon is through passive diffusion rather than active transport. Calcium oxalate stones are still related to other factors, including calcium-binding anion concentrations in the urine such as phosphate ions and Citrate is significantly reduced.

(5) excessive bacterial growth: inflammatory bowel disease such as Crohn's disease or radiation enteritis caused by intestinal fistula, small intestine stenosis, ileal short circuit and ileocecal resection after the patient is prone to bacterial overgrowth, empty ileal short circuit due to blind sputum Increased internal siltation can cause bacterial overgrowth; patients with ileocolectomy may be associated with loss of ileocecal valve function, which may cause a large amount of colonic bacteria to flow back into the small intestine, but some people think that the ileocecal valve has no bacteriological blocking ability; other research tips Changes in intestinal kinetics after resection of the terminal ileum or ileocecal can lead to excessive bacterial growth.

(6) gallstones: people have noticed that the incidence of gallstones increased by 2-3 times after ileal resection, due to biliary acid absorption disorder after ileal resection to the interruption of intestinal-hepatic circulation, stimulated liver synthesis increased, cholesterol synthesis will also Enhancement, the cholesterol in the bile is supersaturated, thereby inducing the formation of gallstones, but some recent studies are contradictory, for example: more than 40% of patients after ileocecal resection are calcium-containing radioactively developed stones; other studies also It is suggested that with the increase of bile acid loss in the stool, the cholesterol in the bile is not saturated. In addition, the interruption of hepatobiliary circulation is more likely to form pigmented stones. In short, the mechanism of the increase of gallstone after ileal resection needs further clarification.

3. Air-ileal short-circuit complications: Although vaccination short-circuit has been used as an effective method to treat morbid obesity instead of gastric short-circuit surgery, gastricplasty surgery, but due to its volume and function of the small intestine more than 90%, complications It has also increased, many complications have been said in the short bowel syndrome, such as electrolyte imbalance caused by diarrhea, especially low potassium, low magnesium, fat-absorbed vitamin deficiency caused by fat malabsorption, metabolic bone disease, kidney stones and Retinopathy, deficiency of folic acid and vitamin B12, malabsorption of protein and carbohydrates, and gallstones. Other complications are unique or more common complications after a short circuit. The exact etiology is not fully understood and may be secondary. Excessive hyperplasia of intestinal bacteria after short circuit, can be called short-circuit post-intestinal syndrome; secondary to the increase in lactate produced by bacteria and brain lesions caused by lactic acidosis, immune complex deposition-mediated certain Lesions, such as pustular papules or nodular skin lesions, cirrhosis, myalgia and non-arthritis, focal interstitial nephritis, tubular necrosis, hemolytic depletion Blood, these complications occur more than 1 year after short circuit, Hocking et al believe that these complications may also be delayed until 5 years later.

Examination of short bowel syndrome

1. Blood routine examination: The patient may have iron deficiency anemia or giant cell anemia.

2. Blood biochemical examination: There may be electrolyte imbalance and acid-base balance imbalance, negative nitrogen balance; plasma protein, lipid reduction, lipid content increased.

3. Prothrombin can be reduced.

4. The small intestine can reduce the sugar, protein, and fat absorption tests.

5. Pancreatic function tests and urinary acid excretion measurements can be performed if necessary.

6. Suspected intestinal contamination syndrome can be used for bacterial culture and counting of intestinal fluid, such as more than 107/ml.

7. X-ray barium meal examination can determine the length of the residual small intestine, the time of passage of intestinal contents, the fold of intestinal mucosa, and multiple examinations can be used for comparative observation.

Diagnosis and diagnosis of short bowel syndrome

Diagnostic criteria

1. Diagnostic conditions: Diagnosis of short bowel syndrome should have the following three basic conditions:

(1) A history of extensive resection of the small intestine.

(2) Clinical manifestations of malabsorption and malnutrition.

(3) Evidence of malabsorption in the laboratory.

2. Judgment of clinical staging: The diagnosis of short bowel syndrome is not difficult. It is important to judge different clinical stages in the course of the disease, blood routine, electrolytes, acid-base balance, negative nitrogen balance, plasma protein, lipids, prothrombin. Pancreatic function and X-ray barium meal can provide information on nutrition and bile salt metabolism, pancreatic function, intestinal mucosal hyperplasia, etc., to help determine the extent of nutrient deficiency and to determine whether there is excessive gastric acid secretion, bile salt deficiency, and bacterial overgrowth. Reproductive and impaired pancreatic function and many other unfavorable factors for timely symptomatic treatment.

Differential diagnosis

The disease should be differentiated from malabsorption caused by other causes, medical history, enzyme activity in small intestinal mucosa, new small intestine endoscopy plus biopsy or capsule endoscopy, serological determination (enzyme and electrolyte), lymphangiography, etc. Its identification is helpful.

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