Fatty diarrhea refers to a clinical syndrome group of nutrient deficiency caused by various causes of reduced digestion and absorption in the small intestine, resulting in incomplete absorption of nutrients and their excretion from the stool, also known as dyspepsia syndrome. Due to the excessive fat excreted in the stool, it is also called small intestine malabsorption and is also known as oily flower-like diarrhea. Causes are common, such as malabsorption syndrome, bile salt and pancreatic digestive enzyme deficiency, small bowel inflammation or diverticulosis, intestinal-derived fat metabolism disorder, gastrinoma, or inability of celiac ducts to absorb fat. The stool of typical steatorrhea is light-colored, voluminous, greasy or foamy, often floating on the water surface, and mostly foul-smelling. What is the differential diagnosis between pediatric steatorrhea and other malabsorption syndromes? 1. lactose intolerance Lactose intolerance is one of the disaccharidase deficiencies. There are two types: congenital and acquired. Congenital lactose intolerance is rare and is a congenital abnormality of sugar metabolism. Acquired lactose intolerance is far more common than congenital lactose intolerance. It develops as a result of temporary deficiency or reduced activity of lactase due to damage to the intestinal mucosa. There are many causes of intestinal mucosal damage, such as enteritis (rotavirus enteritis is known to cause lactase deficiency), dysentery, intestinal parasitosis, gastrointestinal surgery, immunodeficiency syndrome, etc. The digestion and absorption of lactose is in the upper part of the small intestine. Lactase is secreted by the brush border of epithelial cells, which hydrolyze lactose into monosaccharides and absorb them through active cellular transport. Reduced or deficient intestinal lactase activity allows unabsorbed lactose to remain in the intestinal lumen, which, due to its osmotic effect, causes water and Na+ and Cl- to run into the intestinal lumen until the osmotic gradient between the intestinal contents and extracellular fluid is balanced. The increased amount of fluid in the intestinal lumen promotes intestinal peristalsis and accelerates the passage of intestinal contents, causing watery stools. Undigested lactose reaches the terminal ileum and colon and is partially metabolized by bacteria into lactic acid, acetic acid and hydrogen, and these organic acids further increase the osmotic pressure in the intestinal lumen, promoting the onset of diarrhea and, in severe cases, dehydration and acidosis. Clinical manifestations of lactose intolerance: in congenital cases, the onset of the disease is mostly from the beginning of breastfeeding; in late cases, symptoms appear only a few years after birth; in acquired cases, it occurs after a disease causing lactase deficiency. The clinical manifestations are watery, foamy stools, frequent stools, and lack of fecal matter. There may be vomiting, abdominal distention, dehydration, acidosis, and subsequent nutritional and developmental disorders. In severe cases, the disease can be life-threatening. The stool is acidic, with a pH of 5.5 or less. A lactose absorption test can be done to further confirm the diagnosis. If the blood glucose has a low flat curve with a peak value below 200 mg/L, the disease can be considered. In addition, lactose in the stool can be detected, and if lactose or 0.25% or more reducing substances are present in the stool, the diagnosis is supported. If available, a small intestinal biopsy can be done to determine lactase activity, and less than 2 U/g mucosa (wet weight) is considered lactase deficiency. Treatment is mainly dietary therapy, stopping all dairy diets and replacing them with lactose-free foods, such as various legumes (soy milk, soy flour) sucrose, fructose, etc. With age, sick children have some tolerance to carbohydrates, so older children can try a moderate amount of dairy foods. 2, non-tropical sprue (non-tropical disease, celiac disease) This disease is also known as glutin sensitive enteropathy or pediatric celiac disease, also known as “primary malabsorption syndrome” in the past. It may be related to genetic factors, and the disease is familial, with children having a sensitivity to gliadin. The pathogenesis is thought to be due to the lack of a peptidase enzyme in the intestine, which causes a large accumulation of toxic peptides in the wheat gum and damages the intestinal mucosa cells; it is also thought to be due to immune abnormalities, which occurs in the body after eating food containing wheat flour and causes damage to the intestinal mucosa. The pathological changes of the disease mainly occurred in the jejunum, which showed that the jejunal villi became stiff, some fused, some atrophied, or even completely disappeared, the mucosa was flat, the mucosal epithelial cells changed from columnar to rectangular, the number of brush border cells decreased, and the height was reduced or disappeared. Plasma cells and eosinophil infiltration were seen in the lamina propria of the mucosa. The disease starts gradually after the addition of cereal at the age of 6 months, showing a gradual loss of appetite, vomiting, and a large amount of grayish-white corn paste, foul-smelling, and containing foam and fat. There is no weight gain or loss of weight, depressed expression, pale face, distended abdomen and flaccid muscles. Due to malabsorption of protein, fat, fat-soluble vitamins and other nutrients, the child’s growth and development are stagnant, and there may be signs of nutritional deficiency such as malnutrition edema, rickets or osteoporosis, anemia or bleeding tendency. Due to the decreased activity of many hydrolytic enzymes in the brush border of small intestinal epithelial cells, glucose, galactose and fructose are poorly absorbed, resulting in hyperosmolarity in the intestinal lumen, causing hyperosmolar diarrhea. In severe cases, “crisis” occurs, manifested by lack of appetite, vomiting, diarrhea, water loss, acidosis and even shock. Laboratory tests: fecal neutral fat and free fatty acids, xylose absorption test, fat absorption test and small intestine mucosal biopsy can be examined; treatment test can also be done, i.e., the symptoms can be improved after stopping wheat flour food for a few days to a few weeks. Treatment should be a wheat gum-free diet, that is, wheat, barley, oats, rye and other wheat products are prohibited and can be replaced by foods such as milk, rice, eggs, lean meat, beans and bananas. Most patients have significant symptomatic improvement after 1 week of treatment, a few need six months. The wheat-free gum diet should be adhered to for life. Due to the long duration of the disease and high consumption, a high-heat, high-protein diet should be given promptly, with attention to vitamin and inorganic salt supplementation. In severe cases, especially in acute diarrheal attacks with severe dehydration “crisis”, adrenocorticosteroids can be applied to relieve symptoms.