Pediatric intestinal malabsorption syndrome

Introduction to pediatric intestinal malabsorption syndrome Intestinal malabsorption syndrome (malabsorptionsyndrome) refers to the digestion and/or absorption function of the small intestine, so that one or more nutrients in the intestinal cavity cannot be smoothly transported to the body, and discharged from the feces, causing nutritional deficiency in the child. Often a variety of nutrients have different degrees of absorption barriers. Absorption of certain nutrients often has its own specific clinical manifestations. The cause of malabsorption syndrome is very complicated. In the process of digestion and absorption of nutrients, failure of any link can lead to malabsorption syndrome. There are many classification methods: some are classified according to the absorption of nutrients, such as malabsorption of sugar, malabsorption of fat, malabsorption of protein, etc.; some are classified according to pathophysiological changes of digestion and absorption, such as intracavitary causes (indigestion), Mucosal abnormalities (absorption), abnormal transport (lymphatic or blood flow disorders); also divided into primary, secondary and so on. The primary cases in China are rare, mostly secondary. Common causes are infectious chronic diarrhea and secondary lactose intolerance. In addition, large intestine resection, small intestinal bacterial overgrowth, milk or soy protein allergic bowel disease, inflammatory bowel disease, small intestinal lymphatic dilatation, Hepatobiliary and pancreatic diseases are more common; gluten allergic bowel disease and pancreatic fibrocystic changes are rare, but they occur in European and American whites. Its pathogenesis varies with the primary disease. basic knowledge The proportion of illness: 0.003% Susceptible people: young children Mode of infection: non-infectious Complications: dehydration anemia

Causes of intestinal malabsorption syndrome in children

(1) Causes of the disease

Any factor that affects one or more of the three stages of the process of digestion and absorption of nutrients (intraluminal, mucosal, and operational) can cause malabsorption syndrome.

(two) pathogenesis

The malabsorption of sugar is mainly due to the lack of specific disaccharidase in the small intestinal mucosa, which makes the disaccharide in the food not fully hydrolyzed into monosaccharide to affect its absorption. Occasionally, the monosaccharide absorption disorder occurs. The amylase is rare except for newborns. Does not cause clinical problems.

The carbohydrates ingested by the human body are mainly starch, lactose and sucrose. They must be digested and hydrolyzed into monosaccharides before being absorbed by the small intestine. The starches include both linear and branched chains, all of which are glucose multimers, saliva. And amylase in the pancreas, hydrolyzed starch, decomposed into maltose (containing two molecules of glucose), malt oligofine (composed of several molecules of glucose) and dextrin, dextrin on the brush border of intestinal epithelial cells (ie isomaltase) hydrolyzes dextrin molecules, which further hydrolyze maltose and eventually break down these sugars into glucose for absorption.

Both lactose and sucrose are disaccharides. Lactase in the brush border of small intestinal epithelium can decompose lactose into galactose and glucose. Sucrose can decompose sucrose into fructose and glucose. Glucose and galactose can be actively absorbed in the small intestine. It absorbs quickly and can reverse the concentration gradient, but consumes energy. Fructose is mainly absorbed by the carrier, and the absorption can not be reversed. The xylose (experimental) can only be absorbed by passive diffusion.

Sugar is absorbed more completely in the small intestine, but a small amount of unabsorbed sugar enters the colon, which can be decomposed by the intestinal flora (mainly bifidobacteria, followed by lactobacilli, etc.) and then absorbed.

Types of sugar malabsorption: Sugar malabsorption can be divided into primary and secondary.

1. Primary glucose malabsorption Primary glucose malabsorption, congenital lactase deficiency, sucrose-isomaltase deficiency, and glucose-galactose malabsorption are all autosomal recessive diseases, clinically rare, except Sucrose-isomaltase deficiency can be initiated after adding sucrose in the diet. The rest of the disease occurs soon after birth. The histology of small intestinal mucosa biopsy is normal, and the corresponding disaccharidase activity is decreased, and glucose-galactose is poorly absorbed. The disaccharidase activity was normal, and the malabsorption was caused by the congenital deficiency of Na-glucose and Na-galactose carrier protein, and the fructose absorption of the sick children was good.

There are two other types of primary lactase deficiency, which are all physiologically deficient: 1 developmental lactase deficiency, lactase activity at 30 weeks of fetus is only 30% of full-term children, and gradually increases to It is only fully developed during full-term delivery, so lactase activity in premature infants is low, lactose intolerance is prone to occur, and 2 delayed lactase is lacking. In general, lactoin has sufficient lactase activity in the intestinal epithelial brush border, 3 to 5 years old. After the gradual decline, some children can cause lactase deficiency or lactose intolerance, the incidence rate varies from ethnic to ethnic group. The incidence rate in western and northern European population is about 10% lower, and the incidence rate of oriental people is higher. A 5 to 7-year-old Han Chinese child tested, resulting in 71.6% of lactose malabsorption, and 20.5% of lactose intolerance.

2. Secondary lactase deficiency and monosaccharide malabsorption are more common in clinical practice. Because lactase is distributed at the top of small intestine villi, diseases that can cause damage to intestinal mucosal epithelial cells and their brush borders can be secondary to disaccharidase. Lack, severe lesions, extensive, can also affect the absorption of monosaccharides, such as acute enteritis (especially involving the upper part of the small intestine, such as rotavirus enteritis, blue giardia infection, etc.), chronic diarrhea, protein-heat card malnutrition, Immunodeficiency disease, celiac disease and small bowel surgery injuries.

In the upper part of the jejunum, lactase is mainly found in the brush border of the epithelial cells at the top of the villus. The invertase is abundant in the villus, while the maltase is widely distributed in the intestine and is the most abundant. Therefore, lactose occurs when the small intestine is damaged. The enzyme is the most susceptible, and the recovery is the slowest, the most common clinical; maltase is the least susceptible, and the invertase is rare and rare, and only when the intestinal mucosa is seriously damaged, the activity is decreased. At this time, the lactase activity has been affected, and Often accompanied by a single sugar absorption disorder.

3. Fat Absorption Fat Absorption is also called steatorrhea. It is fat digestion. Syndrome caused by malabsorption can be seen in many diseases, such as pancreas, liver, gallbladder and intestinal diseases, caused by intestinal lesions. Fatty diarrhea, accompanied by malabsorption of other nutrients, is called malabsorption syndrome.

4. Protein malabsorption protein alone is poorly absorbed, clinically rare, usually occurs when the intestinal mucosa is extensively damaged, often accompanied by fat malabsorption, malabsorption syndrome sometimes accompanied by protein malabsorption, exudation by intestinal mucosa Loss, such as milk or soy protein tolerance, celiac disease, blue giardiasis, inflammatory bowel disease and intestinal lymphatic dilatation can occur in the intestinal loss of protein, can be determined by measuring 1 antitrypsin in feces It was confirmed that this protein is present in plasma and cannot be digested and hydrolyzed in the intestinal tract, so when protein leakage occurs in the intestinal mucosa, 1 antitrypsin can be detected in feces.

Prevention of intestinal malabsorption syndrome in children

Because most of them are secondary malabsorption, the cause is complicated. The general preventive measures are to strengthen reasonable feeding, enhance physical fitness, and prevent various diseases of the gastrointestinal tract and nutritional disorders.

Complications of intestinal malabsorption syndrome in children Complications, anemia, anemia

Often complicated by dehydration acidosis, protein thermal dystrophy, hip red, various vitamins and minerals, anemia.

Pediatric intestinal malabsorption syndrome symptoms Common symptoms Hypoproteinemia bleeding tends to loss of appetite accompanied by abdominal pain, ... abdominal distension, night blindness, hypocalcemia, glossitis, nocturia, fatigue

Although the pathogenesis is different, its clinical manifestations and laboratory tests are basically the same, that is, the absorption of fat, protein, sugar, vitamins, minerals and electrolytes.

1. Common clinical manifestations of malabsorption

(1) Diarrhea (diarrhea): often the main complaint of malabsorption syndrome, caused by the absorption of nutrients that are not absorbed by the intestinal function, the fermentation of sugar in the colon produces bloating and loss of appetite, slow absorption of water can cause nocturia Increased, often accompanied by abdominal discomfort and active bowel sounds, abdominal pain is more common in chronic pancreatitis, intestinal obstructive lesions or intestinal ischemia.

(2) weight loss, fatigue, edema: due to insufficient absorption of nutrients and loss of appetite, often manifested as weight loss or weight loss, fatigue, fatigue, severe persistent malnutrition can be manifested as progressive malnutrition, growth retardation, Even dyscrasia, long-term protein malabsorption and constant loss of plasma protein from the intestinal lumen can cause hypoproteinemia and peripheral edema. Water, electrolytes and acid-base balance disorders can occur in severe cases of diarrhea; Poor, anemia and growth and development disorders.

(3) Deficiency of vitamins and minerals: anemia caused by iron, folic acid or vitamin B12 malabsorption, fat-soluble vitamin K malabsorption caused by fat malabsorption and bleeding tendency caused by low prothrombinemia ( Hemorrhagic tendency), long-term vitamin D, calcium, magnesium deficiency caused by tetany, patients with steatorrhea may have osteoporosis or pathologic fracture, chronic hypocalcemia can cause secondary parathyroidism Secondary hyperparathyroidism, malabsorption patients can be characterized by nighttime blindness (nyctalopia) due to vitamin A deficiency, rough skin and hyperkeratosis.

2. Special manifestations of malabsorption of major nutrients

(1) Sugar malabsorption: normal human lactose is absorbed by glucose and galactose by the lipase of the intestinal mucosal brush border, which causes the lack of lactase in the small intestine mucosa, which is unique to milk. Lactose can not be fully hydrolyzed and absorbed in the small intestine, causing lactose malabsorption. The malabsorption of sugar can be divided into two major categories: primary and secondary. The disease causing primary glucose malabsorption has congenital lactose absorption. Poor, sucrose-isomaltase deficiency, glucose-galactose malabsorption, etc.; diseases that cause damage to intestinal mucosal epithelial cells and brush borders, such as viral enteritis, chronic diarrheal disease, protein-calorie malnutrition, immunodeficiency disease, After the small intestine surgery, etc., can cause secondary glucose malabsorption.

Those with clinical signs and symptoms of glucose malabsorption are called sugar intolerance. The clinical manifestation is that children have osmotic diarrhea after eating dairy foods. They are watery stools, no increase in fecal fat, and acid smell. There are foams, often abdominal discomfort, abdominal distension, increased exhaustion, severe water, electrolytes and acid-base balance disorders, once you stop eating dairy foods or remove intolerant sugars, diarrhea symptoms can be quickly relieved, this One of the characteristics of this disease.

1 Laboratory examination of sugar malabsorption:

A. The stool pH is often <5.5, suggesting that the sugar is poorly absorbed.

B. Fecal reducing sugar determination, such as 0.005, indicates poor glucose absorption.

C. Sugar-exhalation test, after ingestion of test sugar, elevated expiratory hydrogen or decreased expiratory 14CO2 indicates poor absorption of sugar for the test.

D. Determination of disaccharidase activity in small intestinal mucosa biopsy, one or several disaccharidase activities decreased.

E. Lactose tolerance test, lactose deficiency blood glucose curve is low, and lactose intolerance appears.

Children with disaccharidase deficiency may have only laboratory abnormalities, but no clinical symptoms. Those with clinical symptoms due to poor glucose absorption are called glyce tolerant, and various glucose intolerances often show similar clinical symptoms.

2 its basic pathophysiological changes:

A. Unabsorbed sugar causes an increase in osmotic pressure in the intestinal lumen to cause osmotic diarrhea.

B. The sugar part is lost from the feces, and some of the organic acid and CO2, H2 and methane are produced by bacterial fermentation in the distal part of the ileum and in the colon. After being partially absorbed, these gases can be excreted by exhalation, so the sick child, especially Infants and young children, after eating foods containing intolerant sugar, often manifest as watery stool diarrhea (called glycogen diarrhea), feces containing foam, with acid odor, acid stools irritating the skin easily cause baby hip red, severe Occasionally, diarrhea is often caused by dehydration, acidosis and other electrolyte disorders, prolonged course can cause malnutrition, and some children often have abnormal hunger after eating and dehydration, and after removing intolerant sugar in fasting or diet. Symptoms such as diarrhea can be quickly improved, which is one of the characteristics of this disease. The clinical symptoms of older children are often mild, and can only be manifested as abdominal distension, abdominal discomfort, intestinal colic or bowel sounds.

(2) Fat malabsorption: The most common symptoms are diarrhea, abdominal pain, bloating, vomiting, etc. The stool is mainly steatorrhea, the amount of feces is large, the color is light, the oily, stench, due to malabsorption, can cause weight Reduce, malnutrition anemia, hypoproteinemia, stomatitis, symptoms of secondary fat-soluble vitamin deficiency, growth and development lag.

Laboratory tests for fat malabsorption:

1 fecal microscopic examination of fat droplets or fatty acids increased.

2 fat absorption test, fat absorption rate <90% or fecal fat> 6g, may indicate fat malabsorption; or oral iodized oil after the determination of urinary iodine excretion, urine iodine < 1:8, fat absorption.

3 Determination of fat absorption coefficient, lower absorption coefficient suggests poor fat absorption.

414C-triacylglycerol breath test, fat malabsorption exhaled 14CO2 below normal.

(3) Protein malabsorption: simple protein malabsorption is rare, generally occurs when the intestinal mucosa is extensively damaged, and occurs simultaneously with fat or sugar malabsorption. The clinical manifestation is that the color of the stool is light and smells of stinky eggs. And symptoms associated with hypoproteinemia, such as edema, ascites, etc., and urine protein is often negative.

Laboratory examination of protein malabsorption:

1 serum total protein, albumin decreased and no urine protein increased.

2 Determination of the discharge rate of 51Cr in the feces, such as increased discharge, suggesting protein absorption.

3 The concentration of 1 antitrypsin in feces was determined, and >2.6 mg was protein malabsorption.

Clinical manifestation

1. Direct performance due to malabsorption

Weight loss, delayed growth and development, pale, may have glossitis, abdominal distension and increased gas production caused by discomfort, and more diarrhea, such as fat indigestion, stool color, soft stool, oily foam-like, the amount, There is stench, this kind of feces tends to stick to the toilet, it is not easy to wash away, such as sudden diarrhea after drinking milk, accompanied by abdominal swelling and gas production, often indicates that the child has lactase deficiency.

2. Performance of various deficiencies secondary to malabsorption

The extent and extent of nutritional deficiencies are related to the severity of the primary disease and the size and size of the affected gastrointestinal tract. Many malabsorbed patients have anemia, usually due to iron deficiency (small cell anemia) and folic acid, vitamins. B12 deficiency (large cell anemia), may have neurological symptoms such as restlessness, restless sleep, easy to be stimulated, etc., may have vitamin D and calcium deficiency, convulsions, hand and foot spasms and bones, tooth growth retardation, fat-soluble vitamins K malabsorption can cause prothrombin reduction and skin purpura and bleeding tendency. Riboflavin deficiency can cause glossitis and angular cheilitis. Protein malabsorption can lead to hypoproteinemia edema, usually seen in the lower limbs.

3. Intestinal digestion and malabsorption secondary to certain diseases

There may be different clinical manifestations of the primary disease, such as biliary obstruction may have jaundice, gastrointestinal inflammation may have infection, intestinal malabsorption caused by surgery may have a history of surgery.

Examination of intestinal malabsorption syndrome in children

Screening test

(1) Determination of stool pH: Fresh stools in sugar-tolerant children have a pH of <6 and often less than 5.5.

(2) Determination of fecal reducing sugar: Take 1 part of fresh feces, add 2 parts of water, mix and centrifuge, take 1ml of supernatant, add 1 piece of Clinitest reagent, and obtain the reducing sugar concentration by 5g/ Dl is positive, neonatal > 0.75g / dl is abnormal, the above supernatant can also be heated with Benedict solution, measuring reducing sugar.

Since sucrose is not a reducing sugar, 1 part of feces should be added with 2 parts of 1N HCl. After heating, the supernatant is taken. At this time, sucrose has been hydrolyzed into monosaccharides, and the reducing sugar can be measured according to the above method. Often in the colon has been broken down into reducing sugar by bacteria, so in fact, it is often not necessary to first add HCl hydrolysis, but if acid treatment, the fecal sugar is significantly increased than untreated, suggesting that the sick children have sucrose malabsorption.

Feces contain other reducing substances, such as vitamin C, which can be false positive.

2. Sugar-expiratory test

The method is sensitive, reliable, simple, and non-invasive, but requires gas chromatograph to measure the hydrogen content in exhaled breath. The human body cannot produce hydrogen by itself. The hydrogen in exhalation is produced by the fermentation of sugar in the colon. Normal people are absolutely great. Most of the absorbable sugars are completely absorbed before reaching the colon, and the carbohydrates that are not absorbed by the intestinal bacterial fermentation metabolism are the only source of hydrogen in the human body. This principle can be used to determine the absorption of sugar by the small intestine.

Before and after ingesting certain test sugars, the hydrogen or 14CO2 in the breath was measured. After the test sugar was ingested, such as elevated expiratory hydrogen or decreased 14CO2 exhalation, the glucose was poorly absorbed in the test, and it was fasted for 8-12 h at night. After the test of hydrogen as a base, then oral test 2g / kg of sugar, up to 50g, it is recommended to reduce the dose to 0.25 ~ 0.5g / kg, to reduce the symptoms of induced glucose tolerance, collected every half hour The content of hydrogen measured by breath is 2~3h. If the total amount of hydrogen exceeds the value of fasting time base 20×10-6ppm, it can be diagnosed as poor absorption of the tested sugar. The antibiotics can inhibit intestinal bacteria and can cause false negatives.

3. Small intestinal mucosa biopsy can be inserted into the Crosby intestinal biopsy catheter by endoscopy or orally, and the thin layer of intestinal mucosa can be cut by negative pressure for histological examination and direct determination of various disaccharidase contents, especially for congenital sugar malabsorption. Diagnosis.

4. dextroxylose absorption test (Dextroxylose absorption test) In the case of normal renal function, the measurement of the amount of xylose in the urine can reflect the absorption function of the small intestine, which is a malabsorption caused by the diagnosis of the common damage of the small intestine mucosa. The positive rate is more than 70%; for pancreatic diseases and diseases involving only the ileum, the xylose test is positive; those with renal insufficiency or delayed gastric emptying may have false positives. Method: fasting dextrose 5g (dissolved) In 250ml water), drink 200~300ml again, collect urine for 5h, measure the xylose content in urine, normal value (1.51±0.21)g, if the discharge amount is 11.16g is suspicious, <1g is abnormal, infants and young children It is difficult to collect urine, and the xylose content in the blood after 1 hour can be measured. For example, <200 mg/L is considered as malabsorption.

5. Vitamin B12 absorption test or Schilling test First intramuscular injection of vitamin B12 1mg to saturate the body's stock, then oral 60Co (cobalt) or 57Co labeled vitamin B12 2g, collect 24h urine To determine the radioactivity level in the urine, the normal person's urine output should be greater than 8% to 10% of the oral dose. Below this value, malabsorption is common. In the end of the ileum, it is often poorly absorbed or excised. Blindness syndrome) and pernicious anemia caused by lack of internal factors.

6.14C-glycocholic acid expiratory test 14C-glycocholic acid expiratory test Oral 14C-glycocholate 370MBq (10mCi), most of the normal people in the ileum absorption, circulate to the liver and then enter the small intestine through the bile duct, only pole A small part can enter the colon and be excreted from the feces, and the other part is metabolized into 14CO2 in the body and exhaled through the lungs. In normal people, the discharge of 14C02 within 4 hours after oral administration of 14C-glycocholic acid is less than 1% of the total amount, and the feces are discharged within 24 hours. Less than 8%, small intestinal bacteria over-reproduced, end-intestinal lesions or surgical resection of exhaled 14CO2 and fecal 14CO2 emissions increased.

7. Intestinal fluid intubation to the duodenum or jejunum to extract intestinal fluid, microscopic examination or bacterial culture; determination of pancreatic enzyme activity in intestinal fluid to evaluate pancreatic function.

8. sweat chlorine determination (sweat chlorine determination) sweat chlorine > 60mmol / L contribute to the diagnosis of pancreatic cystic fibrosis.

9. Others such as glucose tolerance test, after oral administration of 2g/kg test sugar, such as low glucose tolerance curve, suggesting that there is malabsorption, but blood glucose can be affected by many factors, the results need to be combined with clinical significance, using chromatography It can measure fecal sugar and distinguish different kinds of sugars, and also use lead acetate method to determine lactose in feces. These methods have reference significance for diagnosis.

10. Fat malabsorption

(1) Fecal microscopic examination of fat droplets or fatty acid increase: normal people discharge less than 6% of fat per day; light, moderate fat absorption, daily discharge of fat accounts for about 6% to 10% of the intake, the positive rate 75%; severe fat malabsorption, daily discharge of fat >10%, positive rate of more than 90%, but the false positive rate of about 14%.

(2) fat absorption test (fatty absorption test): can accurately reflect the fat absorption, before the test, the diet with a fat content of >70g / d for 3 days, while continuously collecting 72h feces, determination of fecal fat, and calculate the fat absorption rate The formula is: fat absorption rate = (diet fat in the diet - fecal fat) / dietary fat × 100%, fat absorption rate <90% or fecal fat > 6g, may indicate fat malabsorption, or oral lipiodol 0.5ml/kg, 12~18h, the urine iodine excretion diluted by the incremental multiple method was measured, and the urinary iodine was <1:8, which was fat malabsorption.

(3) Fat absorption coefficient measurement: The amount of fat taken in 3 days and the amount of fat discharged from the feces were measured, and the absorption coefficient was calculated, and the decrease in the absorption coefficient indicates malabsorption.

(4) 14C-triacylglycerol breath test: After oral administration of 14C-labeled triacylglycerol, 14CO2 in the exhaled breath is absorbed by ammonium hydroxide, counted in a liquid scintillation counter, and the fat-absorbed person is orally administered with 14C-labeled triacylglycerol. The exhaled 14CO2 was lower than the normal value within 6 hours.

11. Protein malabsorption

(1) Total serum protein, albumin decreased and no urine protein increased.

(2) Determination of 51Cr excretion rate in feces: intravenous injection of 25 ~ 50U 51Cr (chromium) labeled albumin, and then measured the discharge rate of 51 Cr in the feces within 96h, the normal value is 0.001 ~ 0.007, such as increased discharge, suggesting protein absorption bad.

(3) Determination of 1 antitrypsin in feces: 1 antitrypsin is not decomposed in pancreatic enzyme, and is stable even when excreted into feces, so protein can be obtained by measuring the concentration of 1 antitrypsin in blood and feces. The extent of leakage, the normal value of dry manure is 0.8 ~ 1mg, > 2.6mg is protein malabsorption.

Intestinal X-ray examination is a non-specific examination, but it has certain reference value for diagnosis, which can help to detect intestinal morphological or functional changes, such as intestinal lumen enlargement, segmental distribution of tincture, and change of emptying time. , intestinal thickening and so on.

Diagnosis and differential diagnosis of intestinal malabsorption syndrome in children

Lactose intolerance

Lactose intolerance is one of the disaccharidase deficiency, which is divided into congenital and acquired. Congenital lactose intolerance is rare. It is a congenital abnormal glucose metabolism. Acquired lactose intolerance is far more inferior. Congenital more common, due to intestinal mucosal damage caused by temporary lack of lactase or decreased activity, causing intestinal mucosal damage for many reasons, such as various enteritis (known rotavirus enteritis is most likely to cause lactase deficiency ), dysentery, intestinal parasitic diseases, gastrointestinal surgery, immunodeficiency syndrome, etc., lactose digestion and absorption in the upper part of the small intestine, epithelial cells brush edge to secrete lactase, hydrolyzed lactose as a monosaccharide, absorbed by the active transport of cells When the intestinal lactase activity is reduced or deficient, the unabsorbed lactose is retained in the intestinal lumen, and due to its osmotic action, water and Na+, Cl- are moved into the intestinal lumen until the intestinal contents and the extracellular fluid penetrate the gradient. When the balance is reached, the increase in intestinal fluid volume can promote bowel movements, accelerate the passage of intestinal contents, cause watery stools, undigested lactose reaches the terminal ileum and colon, and some are metabolized by bacteria to lactic acid, acetic acid. Hydrogen, these organic acids further increase the osmotic pressure of the intestine, promoting diarrhea, severe cases may have dehydration, acidosis.

The clinical manifestations of lactose intolerance: congenital people usually start from breast-feeding; the late-onset symptoms appear only a few years after birth; the acquired ones occur after the disease causing lactase deficiency, and the clinical manifestations are watery. Foamy feces, frequent stools, lack of feces, vomiting, abdominal distension, dehydration, acidosis, and then nutritional and developmental disorders, severe illness can be life-threatening, stool is acidic, pH is below 5.5, can be made lactose The absorption test is further confirmed. If the blood glucose is low-level curve and the high peak value is lower than 200mg/L, the disease can be considered. In addition, lactose in the stool can be detected. If lactose is present in the stool or 0.25% or more of the reducing substance is supported, the diagnosis is supported. If necessary, small intestinal biopsy can be performed to determine lactase activity, and less than 2 U/g mucosa (wet weight) is lactase deficiency.

Treatment is mainly diet therapy, stop all dairy diets, and replace them with lactose-free foods, such as various kinds of legumes (soybean milk, soy flour), fructose, fructose, etc. As the age increases, the sick children have carbohydrates. It must be tolerated, so older children can try the right amount of dairy food.

2. Non-tropical sprue (celiac disease)

This disease, also known as glutin sensitive enteropathy or pediatric celiac disease, used to be called "primary malabsorption syndrome", may be related to genetic factors, the disease is familial, the child has The sensitive mechanism of gluten, its pathogenesis is believed to be due to the lack of a peptidase in the intestine, which causes the accumulation of toxic peptides in the gluten to damage the intestinal mucosal cells. It is also believed that the patient is due to immune abnormalities. After eating food containing wheat flour, humoral and cellular immune reactions occur in the body, causing damage to the intestinal mucosa. The pathological changes of the disease mainly occur in the jejunum, which is characterized by jejunum villi becoming stiff, some fusion, and some Atrophy, or even complete disappearance, mucosa is flat, mucosal epithelial cells change from columnar to cuboid, the number of brush border cells is reduced, the height is reduced or disappeared, and the mucosal lamina propria is infiltrated by plasma cells and eosinophils.

The disease is more than 6 months after the addition of cereals, and gradually becomes sick. The appetite gradually declines, vomiting, and the amount of feces is large. It is grayish white corn paste, malodorous, contains foam and fat, does not increase or decrease in weight, and has a sad expression. Pale, abdominal swelling, muscle relaxation, due to poor absorption of nutrients such as protein, fat, fat-soluble vitamins, child growth and development stagnation, may have dystrophic edema, rickets or osteoporosis, anemia or bleeding tendency and other nutritional deficiencies Due to the decreased activity of many hydrolase enzymes in the brush border of small intestinal epithelial cells, glucose, galactose and fructose are poorly absorbed, resulting in hyperosmolar state in the intestinal lumen, causing hyperosmolar diarrhea. In severe cases, "crisis" occurs, showing no Appetite, vomiting, diarrhea, loss of water, acidosis or even shock.

Laboratory tests: can check fecal neutral fat and free fatty acids, xylose absorption test, fat absorption test and small intestinal mucosal biopsy; can also be used for therapeutic tests, that is, after stopping the wheat noodles for several days to several weeks, the symptoms are improved.

Treatment should be based on a wheat-free diet, that is, wheat, barley, oats, rye and other wheat products can be banned. Milk, rice, eggs, lean meat, beans, bananas, etc. can be used. Most patients have 1 week after treatment. Obvious symptoms improve, a few need half a year, no wheat gelatin diet should adhere to life, because the disease is long, high consumption, should give high heat, high protein diet, pay attention to vitamin and inorganic salts, serious cases, especially acute diarrhea Adrenal corticosteroids can be used to relieve symptoms when accompanied by severe dehydration.

3. Congenital chloride diarrhea

Congenital loss of chlorine diarrhea, also known as familial chloride diarrhea or Darrow-Gamble syndrome, is a rare autosomal recessive disorder, due to the congenital lack of ileum actively absorbs the normal function of Cl- and HCO3- exchange, Cl - In the distal ileum and the colon, the dysfunction, a large number of stay in the intestinal lumen, so that the osmotic pressure of the contents of the intestinal tract increases, water enters the intestinal lumen and causes diarrhea and a large amount of chloride to be discharged.

The disease occurs mostly in premature infants. The mother has a history of polyhydramnios during pregnancy, and the content of alpha-fetoprotein and bilirubin in the amniotic fluid is increased. The baby develops diarrhea soon after birth, and may have abdominal distension and hyperbilirubinemia. Significant weight loss, feces are watery, diarrhea is persistent, severe dehydration is easy to occur in mild infections, physical examination is common in children with developmental delay, and dehydration is performed. Other common causes of diarrhea should be ruled out in diagnosis, such as family Shi Ke earlier suggested the diagnosis of this disease, the stool contains a lot of chloride, about 30 ~ 100mmol / L (the chloride content of adult feces is only 7 ~ 20mmol / L), blood biochemical test blood potassium and blood chlorine are reduced The blood pH is elevated, showing low alkaloid poisoning, and there is little or no chloride in the urine.

The treatment is mainly to supplement enough water, oral potassium chloride 2 ~ 4mmol / kg per day to maintain normal blood pH and electrolyte content, but only improve the general condition, can not cure diarrhea.

4. Intestinal lymphangiectasia

Small intestinal lymphatic dilatation is a rare intestinal lymphatic abnormal disease, which can be congenital or acquired. Congenital causes are mostly congenital malformations of lymphatic vessels. Acquired can be secondary to pancreatitis and peritoneum. Post-fibrosis, constrictive pericarditis and other diseases.

Congenital onset in neonatal or infancy, often accompanied by abnormal lymphatic vessels in other parts, manifested as limb asymmetry edema, groin, posterior peritoneal lymph node dysplasia, or subcutaneous hemangioma, varicose veins, soft tissue and bone hypertrophy Etc, due to the rupture of lymphatic vessels in the intestinal lumen, resulting in loss of lymph, protein, fat, lymphocytes, steatorrhea, bloating, chyle-like ascites, loss of appetite, weight loss, fat-soluble vitamin deficiency, serum albumin Immunoglobulin, transferrin, protein-bound iodine decreased, peripheral blood lymphocytes were significantly reduced, X-ray showed diffuse roughness and thickening of small intestinal mucosa, gear-like, endoscopic duodenal mucosa thickening, The villi are scattered micro-papillary small nodules, small intestine biopsy, under the light microscope, the villi are shorter and more distorted than normal, and the lamina propria lymphatic vessels are obviously dilated.

The treatment of this disease, such as lymphatic vessel expansion is limited to a segment of the intestine, can be surgically removed radically, the general case should limit fat food and use medium chain triacylglycerol (directly into the hepatic vein after absorption) instead of long-chain fat (after absorption) Lymphatic vessels), acquired lymphangiectal distension is mostly caused by the primary disease, mainly to treat the primary disease.

5. Sucrose-isomaltose deficiency

The disease can be congenital or acquired, congenital is an autosomal recessive hereditary disease, due to lack of sucrase and isomaltase in the small intestine, causing digestive disorders, acquired congenital secondary to damage the small intestinal mucosa The disease, the symptoms occur mostly in the late stages of the baby, the baby is asymptomatic when breastfeeding, but after increasing the supplemental food containing sucrose and starch, diarrhea occurs (a part of the isomaltose is produced after the starch is digested), and if it is born, it is artificially fed. Adding sucrose to the milk can cause diarrhea very early. The mechanism of diarrhea is similar to that of lactase deficiency (see "Lactose intolerance"). After oral administration of sucrose 2g/kg, the blood glucose curve is flat and further diagnosis must be done. Mucosal biopsy of the duodenum and jejunum, the intestinal mucosa was normal, but the enzyme assay showed a decrease in sucrase and isomaltase, while lactase was normal.

Infants should adopt a diet that does not contain sucrose. Larger children can give appropriate amounts of sucrose and starch, but they are not limited to diarrhea after eating. Naturally, they can naturally obtain certain tolerance to sucrose and starch.

6. cystic fibrosis of pancreas

Cystic fibrosis of the pancreas is a disease of autosomal recessive systemic exocrine dysfunction. The incidence rate is high in Caucasians in Europe and America. It is extremely rare in oriental yellow races. 80% of children have trypsin, water and heavy carbon. The reduction of acid secretion, the common symptoms are severe steatorrhea, increased frequency of stools, and a large amount of fat and a special odor. Due to fat absorption disorders, symptoms of fat-soluble vitamin deficiency, such as vitamin A deficiency, cause corneal softening. Vitamin K deficiency causes bleeding tendency, etc., because the stool discharges a lot of fat, the stomach is empty and easy to be hungry, but the weight does not increase, the growth and development are stagnant, about 20% of the neonates have meconium intestinal obstruction or meconium peritonitis, the elderly Children may have constipation, intestinal obstruction and abdominal cramps, often have rectal prolapse, chronic cough in the respiratory system, repeated upper respiratory tract infections, pulmonary X-ray lesions may have scattered atelectasis, emphysema, bronchiectasis or chronic Pneumonia can eventually develop into pulmonary fibrosis or pulmonary heart disease. Because the mucous glands secreted by the systemic mucous glands adhere to the dilated gland and block the orifice, it cannot be drained outward. Finally, the organ is fibrotic. When the original sweat is secreted by the sweat gland, the chloride is not reabsorbed normally. Therefore, the chloride concentration in the sweat is obviously increased. The chloride concentration in the sweat is normally 7 to 49 mmol/L, such as 60 mmol/L. The diagnosis can be confirmed; the normal sodium concentration is 22mmol/L, and the average child is 103mmol/L.

Treatment mainly uses pancreatic enzymes orally, including pancreatic lipase, amylase and protease. The diet should take high protein, high heat and low fat diet.

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