Malabsorption

　　The causes of intestinal malabsorption can be many and complex. Any failure in the process of digestion and absorption of nutrients can lead to malabsorption syndrome. The reasons for the malabsorption of the same type of nutrient elements in the intestines can also be quite different.

　　Malabsorption of carbohydrates is mainly due to the lack of specific disaccharidases in the small intestinal mucosa, which prevents the disaccharides in the food from being fully hydrolyzed into monosaccharides, affecting their absorption. Occasionally, malabsorption of monosaccharides may also occur. Amylase is rare in neonates and is generally not a clinical problem. Carbohydrates ingested orally by humans mainly include starch, lactose, and sucrose, which must be digested and hydrolyzed into monosaccharides before they can be absorbed by the small intestine. Starch includes both linear and branched chains, both of which are polymers of glucose. Amylase in saliva and the pancreas can hydrolyze starch, decomposing it into maltose (containing two molecules of glucose), maltodextrin (composed of several molecules of glucose), and dextrin. Dextrinase on the brush border of small intestinal epithelial cells (i.e., isomaltase) can hydrolyze dextrin molecules, while maltase can further hydrolyze maltose, ultimately decomposing these sugars into glucose for absorption. The types of carbohydrate malabsorption can be divided into primary and secondary types.

　　1. Primary carbohydrate malabsorption:

　　Malabsorption is caused by congenital deficiency of Na-glucose, Na-galactose carrier protein, and the child absorbs fructose well.

　　2. Secondary lactase deficiency and monosaccharide malabsorption:

　　Since lactase is distributed at the top of the villi of the small intestine, any disease that can cause damage to the epithelial cells of the small intestinal mucosa and its brush border can lead to secondary deficiency of disaccharidases. The lesions are severe and extensive, and can also affect the absorption of monosaccharides, such as acute enteritis (especially involving the upper small intestine, such as rotavirus enteritis, giardiasis, etc.), chronic diarrhea, protein-calorie malnutrition, immunodeficiency disease, celiac disease, and small intestinal surgery injury.

　　3. Fat malabsorption:

　　Fat malabsorption, also known as steatorrhea, is a syndrome caused by poor digestion and absorption of fat, which can be seen in various diseases such as pancreatic, liver, bile, and intestinal diseases.

　　Fat malabsorption caused by intestinal lesions often accompanies malabsorption of various nutrients, known as malabsorption syndrome.

　　4. Malabsorption of protein:

　　Protein loss from the intestinal mucosal exudation, such as intolerance to milk or soy protein, celiac disease, giardiasis, inflammatory bowel disease, and intestinal lymphangiectasis, can all cause protein loss from the intestines. This protein can be confirmed to exist in plasma by measuring α1-antitrypsin in the feces, as it cannot be digested and hydrolyzed in the intestines. Therefore, when protein exudes from the intestinal mucosa, α1-antitrypsin can be detected in the feces.

　　Intestinal malabsorption refers to the reduction in the digestive and (or) absorptive function of the small intestine, causing one or more nutrients in the intestinal lumen to be unable to be transported smoothly into the body and excreted in the feces, leading to nutritional deficiency in children. It is often characterized by malabsorption of various nutrients to varying degrees.

　　The complications of intestinal malabsorption are mainly due to various nutrient deficiencies, leading to protein-calorie malnutrition, various vitamin and mineral deficiencies, weight loss, anemia, and so on. Due to the large loss of intestinal fluid, dehydration acidosis and water and electrolyte metabolism disorders often occur. Children with recurrent diarrhea may have symptoms such as erythema perinei and eczema.

　　There are many manifestations of malabsorption of the intestine, which can be divided into general manifestations and specific manifestations. Among them, general manifestations include diarrhea, weight loss, fatigue, and deficiencies of vitamins and minerals, while specific manifestations vary with different nutrients. The specific manifestations are as follows:

　　1. General manifestations

　　(1) Diarrhea: Often the chief complaint of malabsorption syndrome, caused by the effect of unabsorbed nutrients on intestinal function. Carbohydrates fermented in the colon produce 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 more common in chronic pancreatitis, obstructive lesions, or intestinal ischemia.

　　(2) Weight loss, fatigue, edema: Due to insufficient nutrient absorption and decreased appetite, it often manifests as weight loss or no weight gain, fatigue, and weakness. Severe and prolonged malnutrition can manifest as progressive malnutrition, delayed growth and development, and even cachexia. Long-term malabsorption of protein and continuous loss of plasma proteins from the intestinal lumen can cause hypoproteinemia and peripheral edema. Severe diarrhea can lead to water, electrolyte, and acid-base imbalance; patients with prolonged course often present with malnutrition, anemia, and growth and development disorders.

　　(3) Manifestations of vitamin and mineral deficiencies: For example, anemia caused by malabsorption of iron, folic acid, or vitamin B12; malabsorption of fat-soluble vitamin K and hypoprothrombinemia due to malabsorption of fat; tetany caused by long-term deficiency of vitamin D, calcium, and magnesium; osteoporosis or pathological fractures in patients with steatorrhea; secondary hyperparathyroidism due to chronic hypocalcemia; and night blindness, rough skin, and hyperkeratosis due to vitamin A deficiency in malabsorption patients.

　　2. Special manifestations of malabsorption of main nutrients

　　(1) Malabsorption of sugar: Normally, lactose in milk is hydrolyzed into glucose and galactose by lactase on the brush border of the small intestinal mucosa and absorbed. Various reasons cause a lack of lactase in the small intestinal mucosa, making it impossible for the specific lactose in milk to be fully hydrolyzed and absorbed in the small intestine, leading to malabsorption of lactose. Malabsorption of sugar can be divided into two major categories: primary and secondary. Diseases that cause primary malabsorption of sugar include congenital lactose malabsorption, deficiency of sucrose-isomaltase, and glucose-galactose malabsorption; diseases that cause damage to the epithelial cells of the small intestinal mucosa and the brush border, such as viral enteritis, chronic diarrhea, protein-calorie malnutrition, immune deficiency disease, and postoperative small intestine, can all cause secondary malabsorption of sugar.

　　(2) Fat malabsorption: The most common symptoms are diarrhea, abdominal pain, bloating, vomiting, etc. The main symptoms are steatorrhea, with increased fecal volume, pale color, greasy texture, and foul smell. Due to malabsorption, it can cause weight loss, malnutrition anemia, hypoalbuminemia, stomatitis, secondary deficiency of fat-soluble vitamins, symptoms of delayed growth and development, etc.

　　(3) Protein malabsorption: Protein malabsorption alone is rare, generally occurring with widespread damage to the intestinal mucosa, simultaneously with fat or sugar malabsorption. The clinical manifestations are light feces color, an odor of rotten egg, and symptoms related to hypoalbuminemia, such as edema and ascites, while urinary protein is often negative.

　　Since the disease is mostly secondary malabsorption, the causes are complex and it is impossible to carry out targeted prevention. The general preventive measures are to strengthen reasonable feeding, enhance physical fitness, prevent and treat various gastrointestinal diseases and nutritional disorders, etc. The following points should be mainly done:

　　1. Strengthen reasonable feeding and eat more fresh fruits and vegetables rich in vitamins.

　　2. Prevent and treat various gastrointestinal diseases and nutritional disorders, etc.

　　3. Strengthen physical fitness and improve immunity: Pay attention to the combination of work and rest, and participate in more physical exercises.

　　The causes of intestinal malabsorption are very complex. Any fault in the digestion and absorption process of nutrients can lead to malabsorption syndrome. The reasons for the malabsorption of the same type of nutritional elements by the intestines are also quite different. Therefore, a comprehensive examination should be carried out for this disease.

　　1. Screening Test (1) Feces pH Measurement: The pH of fresh feces in children with glucose intolerance is often less than 6, and frequently below 5.5. (2) Feces Reducing Sugar Determination: Take 1 portion of fresh feces, mix it with 2 portions of water, centrifuge, and take 1ml of the supernatant. Add 1 tablet of Clinitest reagent and compare the color with the standard card to obtain a reducing sugar concentration ≥0.5g/dl as positive, and >0.75g/dl in neonates as abnormal. The supernatant can also be heated after adding Benedict's solution for reducing sugar determination. Since sucrose is not a reducing sugar, 1 portion of feces should be mixed with 2 portions of 1N HCl, heated, and the supernatant taken. At this point, sucrose has been hydrolyzed into monosaccharides and can be measured for reducing sugar using the aforementioned method. Since the unabsorbed sucrose is often decomposed into reducing sugars by bacteria in the colon, it is usually not necessary to add HCl for hydrolysis first. However, if acid treatment is added, the fecal sugar content is significantly higher than that without treatment, indicating malabsorption of sucrose in the child. The presence of other reducing substances in the feces, such as vitamin C, can present a false positive.

　　2. Sugar-breathe test: The method is sensitive, reliable, simple, and non-invasive, but it requires a gas chromatograph to measure the hydrogen content in the breath. The human body cannot produce hydrogen, and the hydrogen in the breath is produced by the fermentation of sugar in the colon by bacteria. Most absorbable sugars in the human body can be completely absorbed before reaching the colon, and the fermentation and metabolism of the unabsorbed sugars by intestinal bacteria are the only source of hydrogen in the human breath. By using this principle, malabsorption of sugars by the small intestine can be determined. The hydrogen in the breath or 14CO2 before and after ingesting the test sugar is measured; if the breath hydrogen increases or the breath 14CO2 decreases after ingesting the test sugar, it indicates malabsorption of the test sugar. Breath hydrogen can be measured as a baseline after fasting for 8-12 hours at night, followed by oral administration of the sugar to be tested at a dose of 2g/kg, not exceeding 50g. Some advocate reducing the dose to 0.25-0.5g/kg to reduce the induction of symptoms of sugar intolerance. Breath hydrogen content is collected every half hour for a total of 2-3 hours. If the total hydrogen exceeds 20×10-6ppm over the fasting baseline, it can be diagnosed as malabsorption disease of the tested sugar. Antibiotics can suppress intestinal bacteria, and false negatives may occur.

　　3. Small intestinal mucosal biopsy can be performed by endoscopy or through the oral insertion of the Crosby intestinal biopsy catheter, vacuum-cutting thin layers of intestinal mucosa, and performing histological examination and direct determination of the content of various disaccharidases. This is particularly beneficial for the diagnosis of congenital sugar malabsorption.

　　4. Dextrose absorption test: Under normal renal function, the excretion of dextrose in urine can reflect the absorption function of the small intestine. This test has a positive rate of over 70% in diagnosing malabsorption caused by generalized damage to the small intestinal mucosa; it is positive for pancreatic diseases and diseases that only involve the ileum; incomplete renal function or delayed gastric emptying may result in false positives. Method: Take 5g of dextrose (dissolved in 250ml of water) on an empty stomach, followed by drinking 200-300ml of water, and collect urine for 5 hours to determine the dextrose content in urine. Normal value (1.51±0.21)g; if the excretion is 1-1.16g, it is suspicious; less than 1g is abnormal. It is difficult to collect urine from infants and young children, so the dextrose content in the blood can be measured 1 hour after ingestion, and if it is less than 200mg/L, it is considered malabsorption.

　　5. Vitamin B12 absorption test or Schilling test: first intramuscularly inject vitamin B12 1mg to saturate the body's inventory, then orally take 60Co (cobalt) or 57Co-labeled vitamin B12 2μg, collect 24-hour urine, and determine the radioactive content in the urine. The amount of vitamin B12 excreted through urine in normal people should be greater than 8% to 10% of the oral dose. A value below this indicates malabsorption, which is common in malabsorption at the distal ileum or after resection, excessive bacterial overgrowth in the intestine (such as ileus syndrome), and pernicious anemia caused by lack of intrinsic factor.

　　6.14C-glycocholic acid breath test: orally take 14C-glycocholic acid 370MBq (10mCi), where most of the normal people absorb it in the ileum, circulate to the liver, and enter the small intestine through the bile duct, only a small part can enter the colon and be excreted in feces, and another part is metabolized into 14CO2 and exhaled through the lungs. The amount of 14CO2 exhaled within 4 hours after oral administration of 14C-glycocholic acid by normal people is less than 1% of the total amount, and less than 8% is excreted in the feces within 24 hours. In cases of excessive bacterial overgrowth in the distal ileum, lesions, or surgical resection, the amount of 14CO2 exhaled and 14CO2 excreted in the feces increases.

　　7. Intestinal juice examination: insert a tube into the duodenum or jejunum to collect intestinal juice for microscopic examination or bacterial culture; determine the activity of pancreatic enzymes in the intestinal juice to evaluate pancreatic function, etc.

　　8. Sweat chloride measurement: sweat chloride > 60mmol/L is helpful for the diagnosis of cystic fibrosis of the pancreas.

　　9. Other tests such as glucose tolerance test: after oral administration of 2g/kg of test sugar, if the glucose tolerance curve is flat, it indicates malabsorption, but blood sugar can be affected by various factors, and the results need to be combined with clinical data to be meaningful. Chromatography can be used to determine stool sugar and distinguish different types of sugar. Acetic acid lead method is also used to determine lactose in feces, and these methods are of reference significance for diagnosis.

　　The daily diet of patients plays a very important role in the recovery of the disease, especially for patients with gastrointestinal diseases, where the role of diet is particularly obvious. Patients with this disease should pay attention to: avoid wheat foods, use various vitamins and proteins, reduce fat and carbohydrates, avoid foods with a lot of residue, and provide sufficient water. Starch foods should not be used in the early stage of treatment, and more glucose and fructose should be given. Protein milk and lactic acid dehydrated milk, due to their high protein content, should be used as the main diet. In addition, soy products, egg whites, lean beef, fish, chicken meat, liver, and pork tongue, etc., can be made into paste and easily digestible soft food, gradually increased to maintain the nutrition of the child. Ripe bananas or banana powder can also be given. Pay attention to adding fish liver oil or vitamin A, D preparations, and calcium supplements. Gradually add whole milk, fruit puree, vegetable puree, maltose, and sucrose, and finally add starch foods. Start with lotus root starch products, then try cake powder, rice powder, and milk powder, etc. Caution must be exercised when adding wheat flour products. If malabsorption and poor digestion occur again, the simplest food should be restored, and other foods should be gradually added, just like in the early stage of treatment.

　　According to traditional Chinese medicine, malabsorption syndrome of the intestines belongs to the category of 'deficiency of the qi', 'deficiency', and 'spleen痿' in traditional Chinese medicine, which is often caused by chronic diseases of the digestive system such as gastrointestinal tract, leading to long-term anorexia and chronic diarrhea, eventually causing the weakness of the spleen qi, damage to the kidney qi, deficiency of essence, and malnutrition of the whole body, a deficiency syndrome located in the spleen, stomach, and kidney, with deficiency as the main nature. Traditional Chinese medicine differentiates the syndrome into four types: deficiency of the spleen and blood, deficiency of the spleen and dampness, deficiency of the spleen and stomach cold, and deficiency of spleen and kidney Yang, and treatment is implemented accordingly, achieving relatively satisfactory clinical efficacy.

　　1. Deficiency of Spleen and Blood: Symptoms include long-term loss of appetite, epigastric and abdominal distension, loose stools, emaciation, fatigue, shortness of breath, and dullness in speech, pale tongue, thin white fur, and weak pulse. Treatment should focus on replenishing the spleen and nourishing blood. The prescription is modified Gui Pi Decoction. Medicines include American ginseng, fried astragalus root, fried white atractylodes, Zhu fu shen, fried ju ju ren, longan meat, Guang mu xiang, dang gui, yuan zhi, fried licorice root, ginger, jujube, shou wu, huang jing, etc.

　　2. Deficiency of Spleen and Dampness: Symptoms include epigastric and abdominal distension and pain, intestinal rumbling and diarrhea, nausea and vomiting, emaciation, fatigue, shortness of breath, and dullness in speech, pale and swollen tongue, teeth marks on the edges, white greasy fur, and soft and slow pulse. Treatment should focus on replenishing the spleen and qi, and removing dampness to stop diarrhea. The prescription is modified Bai Cao Er Chen Decoction. Medicines include cang zhu, white atractylodes, fa ban xia, Chen pi, poria, codonopsis pilosula, fried licorice root, sha ren, fried coix seed, and fried mung bean, etc.

　　3. Deficiency of Spleen and Stomach Cold: Symptoms include chronic diarrhea, recurrent attacks, loose stools resembling oil, epigastric and abdominal distension and pain, preference for warmth and pressure, nausea and vomiting, dullness in appetite, aversion to cold and cold limbs, emaciation, fatigue, and possibly edema, pale and swollen tongue, teeth marks on the edges, thin white fur, and deep and slow pulse. Treatment should focus on warming the middle-jiao and dispelling cold, transforming dampness, and stopping diarrhea. The prescription is Liangfu Pill and Hezhong Decoction with modification. Medicines include high-quality ginger, xiang fu, fried white atractylodes, fried astragalus root, dried ginger, codonopsis pilosula, fried licorice root, fried coix seed, and fried mung bean, etc.

　　4. Deficiency of Spleen and Kidney Yang: Symptoms include chronic diarrhea that does not heal, intermittent abdominal pain, intestinal rumbling and distension, loose stools, cold limbs and body, fatigue, decreased appetite, dullness, soreness and weakness in the lower back and knees, pale tongue, white fur, and weak pulse. Treatment should focus on warming and replenishing the spleen and kidney, and consolidating the intestines to stop diarrhea. The prescription is to prepare a decoction for healing the intestines. Medicines include fried persimmon peel, Chinese angelica root, myrobalan,五味子, braised magnolia seed, baked glutinous rice shell, Chinese magnolia flower, jujube, aconite, dried ginger, poria, coix seed, red ochre, yu shi liang, du zhong, lu yang, tai wu, chen xiang, rou gui, xiao hui xiang, etc.