I. Overview Pediatric intestinal malabsorption syndrome refers to the small intestine digestion and/or absorption function is reduced so that one or more nutrients in the intestinal lumen can not be smoothly transported to the body, but from the feces excretion, so that the child occurs nutritional deficiency. The deficiency is often caused by the absorption of multiple nutrients to varying degrees. Malabsorption of certain nutrients often has its own specific clinical manifestations. Any factor that can affect one or several links in the 3 periods of nutrient digestion and absorption process (intracavitary period, mucosal period and operation period) can cause malabsorption syndrome. Third, clinical manifestations 1, malabsorption of common clinical manifestations (1) diarrhea is often the main complaint of malabsorption syndrome, caused by unabsorbed nutrients affect the function of the intestine. Sugar fermentation in the colon produces bloating and loss of appetite, and slow absorption of water can lead to increased nocturnal urination. It is often accompanied by abdominal discomfort and active bowel sounds. Abdominal pain is mostly seen in chronic pancreatitis, intestinal obstructive lesions or intestinal ischemia. (2) Weight loss, fatigue, edema Due to insufficient absorption of nutrients and loss of appetite, weight loss or weight loss, lethargy, fatigue are often manifested. Severe and persistent malnutrition can manifest as progressive malnutrition, growth retardation, and even cachexia. Chronic protein malabsorption and continuous loss of plasma protein from the intestinal lumen can cause hypoproteinemia and peripheral edema. In severe diarrhea, disorders of water, electrolytes and acid-base balance may occur; in prolonged disease, malnutrition, anemia and growth disorders often occur. (3) Vitamin and mineral deficiencies such as anemia due to iron, folic acid or vitamin B12 malabsorption, bleeding tendency due to fat-soluble vitamin K malabsorption and hypoprothrombinemia, hand-foot convulsions due to long-term vitamin D, calcium and magnesium deficiency, osteoporosis or pathological fractures in patients with steatorrhea, secondary hyperparathyroidism due to chronic hypocalcemia, and hyperparathyroidism due to malabsorption. Chronic hypocalcemia can lead to secondary hyperparathyroidism, malabsorption patients can show night blindness, skin roughness and hyperkeratosis due to vitamin A deficiency. 2, the main nutrients malabsorption of special performance (1) sugar malabsorption can be divided into primary and secondary two categories, causing primary sugar malabsorption diseases such as congenital lactose malabsorption, sucrose-isomaltase deficiency, glucose-galactose malabsorption; and diseases that cause damage to the epithelial cells of the small intestinal mucosa and brush border, such as viral enteritis, chronic diarrheal disease, protein-calorie malnutrition The diseases that cause damage to the mucosal epithelium and brush border of the small intestine, such as viral enteritis, chronic diarrheal disease, protein-calorie malnutrition, immunodeficiency disease, and post-surgical small intestine can cause secondary sugar malabsorption. Glucose malabsorption with clinical signs and symptoms is called glucose intolerance. The clinical manifestations are osmotic diarrhea, watery stools, no increase in fecal fat, acidic and frothy stools, abdominal discomfort, bloating and increased exhaustion, and disorders of water, electrolyte and acid-base balance in severe cases. Once dairy foods are stopped or intolerant sugars are removed, diarrheal symptoms can be rapidly relieved, which is one of the characteristics of this disease. (2) Fat malabsorption diarrhea, increased stool volume and frequency, typical stool color, odor, gray, accompanied by abdominal pain, abdominal distension, fat-soluble vitamin deficiency such as vitamin A deficiency eye disease, vitamin D deficiency rickets, vitamin E deficiency resulting in proximal muscle atrophy, vitamin K1 deficiency resulting in bleeding tendency. (3) protein malabsorption Clinically uncommon, mainly occurs when the intestinal mucosa is extensively damaged, manifested as malnutrition edema, ascites, diarrhea, foul-smelling stools, etc. D. Examination 1. Screening test (1) Stool pH determination The pH of fresh stool of glucose intolerant children is more and often lower than 5.5. (2) Stool reducing sugar determination Take 1 part of fresh stool, add 2 parts of water and mix, then centrifuge, take 1 ml of supernatant, add 1 tablet of Clinitest reagent, obtain reducing sugar concentration by colorimetric comparison with standard card, ≥ 0.5g/dl is positive, neonates > 0.75g/dl was considered abnormal. The above supernatant can also be heated with the addition of Benedict’s (Benedict) solution to measure reducing sugars. Since sucrose is not a reducing sugar, it is necessary to add 2 parts of 1N HCl to 1 part of feces, heat the supernatant and then take the supernatant, at this time sucrose has been hydrolyzed into monosaccharide, and then reduce sugar can be measured according to the above method. Since unabsorbed sucrose is often broken down by bacteria into reducing sugars in the colon, it is often not necessary to add HCl to hydrolyze it first, but when treated with acid, the fecal sugars increase significantly compared to untreated sugars. This suggests that the child has sucrose malabsorption. False positives can be presented by the presence of other reducing substances in the stool, such as vitamin C. 2, sugar – breath test method is sensitive, reliable, simple and non-invasive, but requires gas chromatography to measure the hydrogen content in the breath. The human body itself cannot produce hydrogen, and the hydrogen in breath is produced by bacterial fermentation of sugar in the colon. Most of the absorbable sugars are completely absorbed by normal people before they reach the colon, and the fermentation and metabolism of unabsorbed sugars by intestinal bacteria is the only source of hydrogen in human breath, and this principle can be used to determine the malabsorption of sugars in the small intestine. Before and after ingestion of a certain test sugar, the hydrogen or 14CO2 in the breath is measured, and after ingestion of the test sugar, if the exhaled hydrogen is elevated or the exhaled 14CO2 is reduced, it indicates malabsorption of that test sugar. The dose can be reduced to 0.25-0.5g/kg to reduce the induction of glucose intolerance symptoms. Breath was collected every half hour to measure the hydrogen content for a total of 2-3 hours. 3.Small intestinal mucosal biopsy The Crosby intestinal biopsy catheter can be inserted through the endoscope or through the mouth, and thin layers of intestinal mucosa can be cut under negative pressure for histological examination and direct measurement of various disaccharidases, which is especially beneficial to the diagnosis of congenital sugar malabsorption. 4, dextrose absorption test In the case of normal renal function, the measurement of urinary xylose excretion can reflect the absorption function of the small intestine. The test has a positive rate of more than 70% for the diagnosis of malabsorption due to generalized damage to the small intestinal mucosa; positive xylose test for pancreatic diseases and diseases involving only the ileum; false positives can occur in cases of renal insufficiency or delayed gastric emptying. Method: Take 5g of dextrose (dissolved in 250ml of water) on an empty stomach, then drink 200-300ml of water, collect the urine for 5h, and determine the urinary xylose content. Normal value (1.51 ± 0.21) g, if the excretion of 1 ~ 1.16g is suspicious, <1g is abnormal. If it is not easy to collect urine for infants and young children, the xylose content in the blood can be measured after 1 hour, and if it is <200mg/L, it is considered as malabsorption. 5.Vitamin B12 absorption test or Schilling test Inject 1mg of vitamin B12 intramuscularly first to saturate the body stock, then take 2µg of 60Co (cobalt) or 57Co labeled vitamin B12 orally, collect urine for 24 hours, and measure the radioactive content in urine. The amount excreted via urine in normal people should be greater than 8% to 10% of the oral dose. Below this value is malabsorption, which is common in malabsorption at the end of ileum or after being resected, bacterial overgrowth in the intestine (such as blind loop syndrome) and pernicious anemia due to lack of internal factors, etc. 6.Intestinal fluid examination Intubate the duodenum or jejunum to extract intestinal fluid for microscopic examination or bacterial culture; determine the activity of pancreatic enzymes in intestinal fluid to evaluate the function of the pancreas, etc. 7, sweat chloride measurement Sweat chloride > 60 mmol/L can help diagnose cystic fibrosis of the pancreas. 8.Other such as glucose tolerance test, after taking 2g/kg of sugar orally, if the glucose tolerance curve is low and flat, it indicates the presence of malabsorption, but blood sugar can be affected by a variety of factors, the results need to be combined with clinical significance. Fecal sugar can be measured by chromatography, and different kinds of sugar can be distinguished, and lactose in feces can also be measured by lead acetate method, and these methods have reference significance for diagnosis. V. Treatment Treatment principles: treatment for the cause, correction of nutritional deficiencies and the use of the necessary metabolic therapy. 1. Etiological treatment (1) Discontinue intolerant diet For example, stop eating lactose-containing food if lactose is malabsorbed. (2) Supplement the lack of digestive enzymes such as lactase for lactose malabsorption and pancreatic enzymes for pancreatic insufficiency. (3) Chronic enteritis due to bacterial infection Antibiotics can be used as appropriate, and microecological preparations can be used as appropriate. After the cause is removed, most of the symptoms can be relieved. 2. Nutritional treatment In principle, high-calorie, high-protein, low-fat food should be used. Severely ill patients are often anorexic, poor digestion and absorption, and the food and drugs they eat are often excreted intact in the feces. At this time, parenteral nutrition can be used first, and after the symptoms improve, it can be changed to elemental diet orally, that is, the application of easily digestible or already semi-digestible food. Such as fat with medium-chain triacylglycerol, sugar made of maltose dextrin or glucose, protein made of hydrolyzed protein or amino acids. Smaller and more frequent meals, incremental and gradual. At present, there are lactose-free milk powder and hydrolyzed protein elements in the diet. (1) Supplement the necessary vitamins, inorganic salts and trace elements. (2) Timely correction of water, electrolytes and acid-base balance disorders. Prognosis Most patients have a good prognosis. Children with secondary malabsorption syndrome can recover if the cause is removed. Children with primary malabsorption syndrome are mainly treated symptomatically.