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Chinese to French: Faiblesses des marchés financiers chinois General field: Bus/Financial Detailed field: Finance (general)
Source text - Chinese 中国的金融市场对中国经济的融资贡献相对较弱。比如在2005年，股票市值和债券总量分别占中国GDP的27％和40％。金融市场在中国经济中比重不大主要有两个原因：1.中国金融市场方兴未艾，偏向由国企主导金融资产的发行，2.银行信贷依然是主流融资手段 1998年中国放开债券利息管制，中国开发银行首次通过竞标发行债券，不再由政府确定债券定价，而完全通过市场机制运行，从而更好地协调了供需关系。之后，中国进出口银行也通过竞标方式发行债券。但是私募债券市场需要一个更透明的金融环境和更优良的企业管理模式。	Translation - French Les marchés financiers chinois contribuent pour une part relativement faible au financement de l’économie chinoise. La capitalisation boursière et l’encours obligataire en Chine représentaient, en juin 2005, environ 27 % et 40 %, respectivement, du PIB. Cette faiblesse relative du poids des marchés financiers dans l’économie chinoise s’explique à la fois par leur développement récent, leur orientation prépondérante vers des sociétés publiques faiblement rentables, comme principaux émetteurs potentiels d’actifs financiers, et la prééminence du financement par le crédit bancaire. En 1998, après la libéralisation des taux d’intérêt obligataires et la dématérialisation des obligations, la China Development Bank a, pour la première fois, émis des obligations sur la base d’une adjudication compétitive où les prix n’étaient donc plus ﬁxés ex ante par les autorités, mais par le libre jeu des mécanismes de marché, ce qui a permis de réconcilier plus aisément l’offre et la demande. Cette première émission obligataire par adjudication compétitive fut suivie par celle de la China Import and Export Bank. Néanmoins, cette réforme indispensable s’est avérée insuffisante pour permettre un véritable décollage du marché d’obligations privées (freiné par la faiblesse de la gouvernance d’entreprise et la transparence limitée des états financiers). […]
English to Chinese: Lactose Intolerance in Infants, Children, and Adolescents General field: Medical Detailed field: Medical: Health Care
Source text - English Lactose Intolerance in Infants, Children, and Adolescents Melvin B. Heyman and for the Committee on Nutrition Pediatrics 2006;118;1279-1286 DOI: 10.1542/peds.2006-1721 The online version of this article, along with updated information and services, is located on the World Wide Web at: http://www.pediatrics.org/cgi/content/full/118/3/1279 PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly publication, it has been published continuously since 1948. PEDIATRICS is owned, published, and trademarked by the American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk Grove Village, Illinois, 60007. Copyright © 2006 by the American Academy of Pediatrics. All rights reserved. Print ISSN: 0031-4005. Online ISSN: 1098-4275. Downloaded from www.pediatrics.org by on August 17, 2010 CLINICAL REPORT Lactose Intolerance in Infants, Children, and Adolescents Melvin B. Heyman, MD, MPH, for the Committee on Nutrition ABSTRACT The American Academy of Pediatrics Committee on Nutrition presents an updated review of lactose intolerance in infants, children, and adolescents. Differences between primary, secondary, congenital, and developmental lactase deficiency that may result in lactose intolerance are discussed. Children with suspected lactose intolerance can be assessed clinically by dietary lactose elimination or by tests including noninvasive hydrogen breath testing or invasive intestinal biopsy determination of lactase (and other disaccharidase) concentrations. Treatment consists of use of lactase-treated dairy products or oral lactase supplementation, limitation of lactose-containing foods, or dairy elimination. The American Acad- emy of Pediatrics supports use of dairy foods as an important source of calcium for bone mineral health and of other nutrients that facilitate growth in children and adolescents. If dairy products are eliminated, other dietary sources of calcium or calcium supplements need to be provided. INTRODUCTION SIGNIFICANT CHANGES IN our knowledge and approach toward lactose intolerance have occurred over the past quarter century, since the first statement on lactose intolerance was published by the American Academy of Pediatrics Committee on Nutrition.1 Lactose ingestion in certain susceptible individuals can cause abdomi- nal symptoms that are variable and can be treated with dietary restriction or enzyme replacement, depending on the amount of lactose consumed and the degree of lactase deficiency. Pediatricians and other pediatric care providers should maintain awareness of the benefits and controversies related to the consumption of dietary milk products and milk-based infant formula. The lactose content of milk often influences, correctly or not, the ultimate decision about the use or continuation of milk in the diet. Milk and dairy-product avoidance has a negative effect on calcium and vitamin D intake in infants, children, and adolescents. Other nutrients such as protein make dairy products an important source of nutrition for growing children. This revised statement will update the initial statement of 1978 while incorporating changes from the 1990 supplement2 and current state-of-the- art relating to lactose intolerance. Recommendations regarding dietary calcium have been updated recently.3 Lactose, a disaccharide that comprises the monosaccharides glucose and galac- tose, is the primary carbohydrate found exclusively in mammalian milk. Absorp- tion of lactose requires lactase activity in the small intestinal brush border to split the bond linking the 2 monosaccharides. A -galactosidase termed “lactase-phlo- rizin hydrolase” (lactase) accounts for most of the lactase activity in the intestinal Guidance for the Clinician in Rendering Pediatric Care www.pediatrics.org/cgi/doi/10.1542/ peds.2006-1721 doi:10.1542/peds.2006-1721 All clinical reports from the American Academy of Pediatrics automatically expire 5 years after publication unless reaffirmed, revised, or retired at or before that time. Key Words abdominal pain, breath tests, calcium, dietary, dairy products, diarrhea, flatulence, lactase, malabsorption, pediatric PEDIATRICS (ISSN Numbers: Print, 0031-4005; Online, 1098-4275). Copyright © 2006 by the American Academy of Pediatrics PEDIATRICS Volume 118, Number 3, September 2006 1279 Downloaded from www.pediatrics.org by on August 17, 2010 mucosa.4 Lactase is found in the small intestine and localized to the tips of the villi, a factor of clinical im- portance when considering the effect of diarrheal illness on the ability to tolerate milk. Milk intolerance may be attributed to either the lac- tose or the protein content. Lactose intolerance can oc- cur among infants and young children with acute diar- rheal disease, although the clinical significance of this is limited except in more severely affected children. Symp- toms of lactose intolerance are relatively common among older children and adolescents; however, associ- ated intestinal injury is infrequently seen. Lactose intol- erance is a distinct entity from cow milk–protein sensi- tivity, which involves the immune system and causes varying degrees of injury to the intestinal mucosal sur- face. Cow milk–protein intolerance is reported in 2% to 5% of infants within the first 1 to 3 months of life, typically resolves by 1 year of age, and is not the subject of this statement.5,6 DEFINITIONS Following are definitions of terms used in the remainder of this statement: ● Lactose intolerance is a clinical syndrome of 1 or more of the following: abdominal pain, diarrhea, nausea, flatulence, and/or bloating after the ingestion of lac- tose or lactose-containing food substances. The amount of lactose that will cause symptoms varies from individual to individual, depending on the amount of lactose consumed, the degree of lactase deficiency, and the form of food substance in which the lactose is ingested. ● Lactose malabsorption is the physiologic problem that manifests as lactose intolerance and is attributable to an imbalance between the amount of ingested lactose and the capacity for lactase to hydrolyze the disaccha- ride. ● Primary lactase deficiency is attributable to relative or absolute absence of lactase that develops in childhood at various ages in different racial groups and is the most common cause of lactose malabsorption and lac- tose intolerance. Primary lactase deficiency is also re- ferred to as adult-type hypolactasia, lactase nonpersis- tence, or hereditary lactase deficiency. ● Secondary lactase deficiency is lactase deficiency that results from small bowel injury, such as acute gastro- enteritis, persistent diarrhea, small bowel overgrowth, cancer chemotherapy, or other causes of injury to the small intestinal mucosa, and can present at any age but is more common in infancy. ● Congenital lactase deficiency is extremely rare; teleo- logically, infants with congenital lactase deficiency would not be expected to survive before the 20th century, when no readily accessible and nutritionally adequate lactose-free human milk substitute was available. ● Developmental lactase deficiency is now defined as the relative lactase deficiency observed among pre- term infants of less than 34 weeks’ gestation. Primary Lactase Deficiency Approximately 70% of the world’s population has pri- mary lactase deficiency.7,8 The percentage varies accord- ing to ethnicity and is related to the use of dairy products in the diet, resulting in genetic selection of individuals with the ability to digest lactose (Table 1). In populations with a predominance of dairy foods in the diet, particu- larly northern European people, as few as 2% of the population has primary lactase deficiency. In contrast, the prevalence of primary lactase deficiency is 50% to 80% in Hispanic people, 60% to 80% in black and Ashkenazi Jewish people, and almost 100% in Asian and American Indian people.9–11 The age of onset and its prevalence differ among various populations. Approxi- mately 20% of Hispanic, Asian, and black children younger than 5 years of age have evidence of lactase deficiency and lactose malabsorption,12 whereas white children typically do not develop symptoms of lactose intolerance until after 4 or 5 years of age. Recent mo- lecular studies of lactase-phlorizin hydrolase (lactase) have correlated the genetic polymorphism of messenger RNA expression with persistence of lactase activity, demonstrating early loss (at 1–2 years of age) of mes- senger RNA expression and enzyme activity in Thai chil- dren and late (10–20 years of age) loss of activity in Finnish children.11,13 The clinical relevance of these ob- servations is that children with clinical signs of lactose intolerance at an earlier age than is typical for a specific ethnic group may warrant an evaluation for an under- lying cause, because primary lactase deficiency would otherwise be unusual at such a young age. Although primary lactase deficiency may present with a relatively acute onset of milk intolerance, its onset typically is subtle and progressive over many years. Most lactase- TABLE 1 Prevalence of Acquired Primary Lactase Deficiency69 Examples of groups among whom lactase deficiency predominates (60%–100% lactase deficient) Near East and Mediterranean: Arabs, Ashkenazi Jews, Greek Cypriots, Southern Italians Asia: Thais, Indonesians, Chinese, Koreans Africa: South Nigerians, Hausa, Bantu North and South America: black Americans, Latinas, Eskimos, Canadian and American Indians, Chami Indians Examples of groups among whom lactase persistence predominates (2%–30% lactase deficient) Northern Europeans Africa: Hima, Tussi, Nomadic Fulani India: individuals from Punjab and New Delhi 1280 AMERICAN ACADEMY OF PEDIATRICS Downloaded from www.pediatrics.org by on August 17, 2010 deficient individuals experience onset of symptoms in late adolescence and adulthood. Reports that focus on clinical symptoms of lactase deficiency are prone to subjectivity, confounding clinical diagnosis. For instance, when lactase-deficient adults were given 2 glasses of milk or 2 glasses of lactose- hydrolyzed milk per day in a double-blind, crossover study, no statistical differences in symptoms of lactose intolerance were found regardless of whether the indi- vidual described himself or herself as lactose intolerant.14 Even lactose-intolerant adults may find that 1 glass of milk or a scoop of ice cream is tolerated, whereas an additional glass of milk or other milk product may pro- duce symptoms. Because of the variation of dairy intake in each individual’s diet and in the amount of lactose contained in different products, symptoms may vary and be modified by diet and by milk-containing foods (see “Management”). For these reasons, dietary history is an unreliable means to confirm or exclude the diagnosis of lactose intolerance. Secondary Lactase Deficiency Secondary lactase deficiency implies that an underlying pathophysiologic condition is responsible for the lactase deficiency and subsequent lactose malabsorption. Etiol- ogies include acute infection (eg, rotavirus) causing small intestinal injury with loss of the lactase-containing epithelial cells from the tips of the villi. The immature epithelial cells that replace these are often lactase defi- cient, leading to secondary lactose deficiency and lactose malabsorption, although several reports indicate that lactose malabsorption in most children with acute gas- troenteritis is not clinically important.15 Several recent studies and a meta-analysis found that children with rotaviral (and other infectious) diarrheal illnesses who have no or only mild dehydration can safely continue human milk or standard (lactose-containing) formula without any significant effect on outcome, including hydration status, nutritional status, duration of illness, or success of therapy.16–18 However, in the at-risk infant (eg, younger than 3 months or malnourished) who de- velops infectious diarrhea, lactose intolerance may be a significant factor that will influence the evolution of the illness. Giardiasis, cryptosporidiosis, and other parasites that infect the proximal small intestine often lead to lactose malabsorption from direct injury to the epithelial cells by the parasite. Secondary lactase deficiency with clinical signs of lactose intolerance can be seen in celiac disease, Crohn disease, and immune-related and other enteropathies and should be considered in these chil- dren. Diagnostic evaluation should be directed toward these entities when secondary lactase deficiency is sus- pected and an infectious etiology is not found. Young infants with severe malnutrition develop small intestinal atrophy that also leads to secondary lactase deficiency.19 Although uncommon in the United States, malnutrition is associated with lactose malabsorption and carbohydrate intolerance in developing countries.20 Lactose malabsorption has also been associated with poor growth in these countries.21 Most infants and chil- dren with malabsorption attributable to malnutrition are able to continue to tolerate dietary carbohydrates, in- cluding lactose.22 However, the World Health Organiza- tion recommends avoidance of lactose-containing milks in children with persistent postinfectious diarrhea (diar- rhea lasting more than 14 days) when they fail a dietary trial of milk or yogurt.23 Treatment of secondary lactase deficiency and lactose malabsorption attributable to an underlying condition generally does not require elimination of lactose from the diet but, rather, treatment of the underlying condi- tion. Once the primary problem is resolved, lactose- containing products can often be consumed normally, and these excellent sources of calcium and other nutri- ents need not be unnecessarily excluded from the diet. Developmental (Neonatal) Lactase Deficiency In the immature gastrointestinal tract, lactase and other disaccharidases are deficient until at least 34 weeks’ gestation.24 One study in preterm infants reported ben- efit from use of lactase-supplemented feedings or lac- tose-reduced formulas,25 and the use of lactose-contain- ing formulas and human milk does not seem to have any short- or long-term deleterious effects in preterm in- fants.26 Up to 20% of the dietary lactose may reach the colon in neonates and young infants. Bacterial metabo- lism of colonic lactose lowers the fecal pH (5.0–5.5 is normal), which has a beneficial effect, favoring certain organisms (eg, Bifidobacterium and Lactobacillus species) in lieu of potential pathogens (Proteus species, Escherichia coli, and Klebsiella species) in young infants. Antimicro- bial agents may also affect this colonization. Congenital Lactase Deficiency Congenital lactase deficiency is a rare disorder that has been reported in only a few infants.27,28 Affected new- born infants present with intractable diarrhea as soon as human milk or lactose-containing formula is introduced. Small intestinal biopsies reveal normal histologic char- acteristics but low or completely absent lactase concen- trations.29,30 Unless this is recognized and treated quickly, the condition is life-threatening because of dehydration and electrolyte losses. Treatment is simply removal and substitution of lactose from the diet with a commercial lactose-free formula. DIAGNOSIS Symptoms of lactose intolerance, including abdominal distention, flatulence, abdominal cramping, and (ulti- mately) diarrhea, are independent of the cause of lactose malabsorption and are directly related to the quantity of ingested lactose. These symptoms are not necessarily PEDIATRICS Volume 118, Number 3, September 2006 1281 Downloaded from www.pediatrics.org by on August 17, 2010 correlated with the degree of intestinal lactase defi- ciency. Malabsorbed lactose generates an osmotic load that draws fluid and electrolytes into the intestinal lu- men, leading to loose stool. The onset of diarrhea and other symptoms is related to the amount of lactose that is not absorbed. As little as 12 g of lactose (the amount of lactose in an 8-oz glass of milk) may be sufficient to cause symptoms in children with chronic abdominal pain.31 In addition, unabsorbed lactose is a substrate for intestinal bacteria, especially in the colon. Bacteria me- tabolize lactose, producing volatile fatty acids and gases (methane, carbon dioxide, and hydrogen), leading to flatulence. The fatty acids lower the fecal pH, making the fecal pH test a nonspecific but sometimes helpful marker for lactose (or other carbohydrate) malabsorption. When sufficient intestinal gas is produced by the bacterial met- abolic processes to cause stimulation of the intestinal nervous system by intestinal distention, visceral (ab- dominal) cramping results. Initial studies using lactose hydrogen breath tests doc- umented lactose malabsorption in up to 40% of children and adolescents presenting with abdominal pain.32 How- ever, recent studies suggest that the prevalence of ab- dominal symptoms related to lactose intolerance docu- mented by hydrogen breath tests is variable and ranges from 2% in Finnish children to 24% in southern US children.33,34 A good clinical history often reveals a relationship between lactose ingestion and symptoms. When lactose intolerance is suspected, a lactose-free diet can be tried (Tables 2 and 3).35 During a diagnostic lactose-free diet, it is important that all sources of lactose be eliminated, requiring the reading of food labels to identify “hidden” sources of lactose. Generally, a 2-week trial of a strict lactose-free diet with resolution of symptoms and sub- sequent reintroduction of dairy foods with recurrence of symptoms can be diagnostic. In more-subtle cases, the hydrogen breath test is the least invasive and most help- ful test to diagnose lactose malabsorption. The test has been shown to be more reliable than history, because some patients think they are lactose intolerant when they prove not to be, and others prove to be lactose intolerant (lactose malabsorbers) when they think they are not.36,37 The test is performed by administration of a standardized amount of lactose (2 g/kg, up to a maxi- TABLE 2 Lactose and Calcium Content of Common Foods70,71 TABLE 3 Hidden Sources of Lactose72 Bread and other baked goods Processed breakfast cereals Mixes for pancakes, biscuits, and cookies Instant potatoes, soups, and breakfast drinks Margarine Nonkosher lunchmeats Salad dressings Candies and other snacks mum of 25 g, equivalent to the amount of lactose in 2 8-oz glasses of milk) after fasting overnight and then measuring the amount of hydrogen in expired air over a 2- to 3-hour period. An increase ( 20 ppm) in the hydrogen expired after approximately 60 minutes is consistent with lactose malabsorption. Factors that may produce false-negative or false-positive results include conditions affecting the intestinal flora (eg, recent use of antimicrobial agents), lack of hydrogen-producing bac- teria (10%–15% of the population), ingestion of high- fiber diets before the test, small intestinal bacterial over- growth, or intestinal motility disorders. A pediatric gastroenterologist should be consulted to interpret the results of this test. The older lactose-tolerance test was previously relied on as the primary test of lactose malabsorption before the breath hydrogen test became available. Lactose in- tolerance was diagnosed by onset of symptoms and/or positive test results after ingestion of a standard lactose dose (2 g/kg of body weight or 50 g/m2 of body surface area; maximum 50 g in a 20% water solution). If the maximum increase in blood glucose concentration was less than 26 mg/dL after a lactose-tolerance test dose, lactose malabsorption was diagnosed. The lactose-toler- ance test is not sensitive enough to determine if a subject is malabsorbing some lactose. It is also often falsely pos- itive because of lack of an increase of blood glucose concentration attributable to normal insulin response to the carbohydrate load. Given the high rate of false- negative and false-positive results, this test should not be used and has been replaced by the hydrogen breath test. Other tests are available in consultation with a pedi- atric gastroenterologist to diagnose lactose intolerance. If an underlying cause for secondary lactose intolerance is suspected, testing for intestinal etiologies includes stool examination, particularly for parasites affecting the up- per gastrointestinal tract such as Giardia lamblia and Cryptosporidia species, and blood tests for celiac disease (ie, total immunoglobulin A concentration and anti- tissue transglutaminase antibody38,39) or immunodefi- ciency (quantitative immunoglobulins). Intestinal bi- opsy may be needed to uncover an underlying gastrointestinal mucosal problem that is causing the lac- tose malabsorption. Biopsies can yield direct measure- ment of disaccharidase concentrations to document lac- tase deficiency directly and assess the status of the other Dairy Products Yogurt, plain, low fat, 1 cup Milk, whole (3.25% fat), 1 cup Milk, reduced fat, 1 cup Ice cream, vanilla, 1/2 cup Cheddar cheese, 1 oz Swiss cheese, 1 oz Cottage cheese, creamed (small curd), 1 cup Calcium Content, mg 448 276 285 92 204 224 135 Lactose Content, g 8.4 12.8 12.2 4.9 0.07 0.02 1.4 1282 AMERICAN ACADEMY OF PEDIATRICS Downloaded from www.pediatrics.org by on August 17, 2010 brush-border disaccharidases (sucrase, maltase, isomal- tase), which may also be deficient under various circum- stances. However, intestinal lactase concentrations do not seem to correlate well with symptoms of lactose intolerance.40 Newer tests may eventually yield additional detailed information pertaining to the prevalence and signifi- cance of lactose intolerance.41 For example, the [13C]lac- tose breath test is being considered as a test to augment the accuracy of the breath hydrogen test but is still primarily an investigational tool.42,43 In infants with diarrhea in whom lactose (or other carbohydrate) intolerance is suspected, stool can be screened for malabsorbed carbohydrate by testing fecal pH, which decreases with carbohydrate malabsorption as a result of the formation of volatile fatty acids. It should be remembered that fecal pH will normally be lower (5.0–5.5) in infants compared with older children and adolescents because of the physiologic overload of lac- tose in their diets, which in turn helps to favor growth of Lactobacillus species in the colon. Fecal reducing sub- stances can also be measured and become positive by excretion of a reducing sugar in the stools. Reducing sugars include lactose, glucose, fructose, and galactose but not sucrose. Because some patients may only mal- absorb enough carbohydrates, such as lactose, to lower the fecal pH but not increase excretion of carbohydrate in the stool, the pH test is a more sensitive test for carbohydrate malabsorption. MANAGEMENT When children are diagnosed with lactose intolerance, avoidance of milk and other dairy products will relieve symptoms. However, those with primary lactose intol- erance have varying degrees of lactase deficiency and, correspondingly, often tolerate varying amounts of di- etary lactose. Lactose-intolerant children (and their par- ents) should realize that ingestion of dairy products re- sulting in symptoms generally leads to transient symptoms without causing harm to the gastrointestinal tract (as compared with celiac disease or allergic reac- tions, including milk-protein intolerance, that can lead to ongoing inflammation and mucosal damage). Al- though lactose malabsorption does not predispose to calcium malabsorption,44 avoidance of milk products to control symptoms may be problematic for optimal bone mineralization. Children who avoid milk have been doc- umented to ingest less-than-recommended amounts of calcium needed for normal bone calcium accretion and bone mineralization.45,46 Lactose-free and lactose-reduced milks (and lactose- free whole milk for children younger than 2 years) are widely available in supermarkets and can be obtained with WIC (Special Supplemental Nutrition Program for Women, Infants, and Children) vouchers. Although lac- tose-free milk is more expensive than regular milk, some major chain stores sell less-expensive lactose-free milk under their own brand names. Beyond infancy, substitutes for cow milk based on rice, soy, or other proteins are readily available and are generally free of lactose, although the nutrient content of most of these milks is not equivalent to cow milk. Other mammalian milks, including goat milk, are not free of lactose. Tolerance to milk products may be par- tial, so that dietary maneuvers alone may help avoid symptoms in some individuals. Small amounts of lactose in portions of 4 to 8 oz spaced throughout the day and consumed with other foods may be tolerated with no symptoms.47–51 Some children are able to drink 1 to 2 glasses of milk each day without difficulty but cannot tolerate more without developing symptoms.14 Many lactose-intolerant individuals who are intolerant of milk can tolerate milk chocolate52 and/or yogurt (plain better than flavored), because the bacteria in the yogurt par- tially digest the lactose into glucose and galactose before consumption.53,54 In addition, yogurt’s semisolid state slows gastric emptying and gastrointestinal transit, re- sulting in fewer symptoms of lactose intolerance.55 Fur- thermore, ingestion of other solid foods delays gastric emptying, providing additional time for endogenous lac- tase to digest dietary lactose. Aged cheeses tend to have lower lactose content than other cheeses and, thus, may also be better tolerated. Finally, oral lactase-replacement capsules or predigested milk or dairy products with lac- tase are readily available and will often permit a lactose- intolerant individual to be able to take some or all milk products freely.56 Because the vitamin D content in milk- substitute products varies, labels must be checked to verify the vitamin D content of individual brands. Even among population groups with significant lac- tose intolerance, the importance of dietary dairy prod- ucts has been stressed. For example, the National Med- ical Association recently recommended that black people consume 3 to 4 servings per day of low-fat milk, cheese, and/or yogurt and that lactose-free milk be used as an alternative for those who are intolerant of these other products to help reduce the risk of nutrient-related chronic diseases such as hypertension and diabetes.57 Milk and dairy products are often well tolerated by many children with underlying inflammatory conditions of the intestines, including Crohn disease and ulcerative colitis, in whom the prevalence of lactose intolerance does not seem to be any greater than in the general population.58–61 Lactose-Free Formulas In developed countries, even in the case of acute gastro- enteritis, enough lactose digestion and absorption are preserved so that low-lactose and lactose-free formulas have no clinical advantages compared with standard lactose-containing formulas except in severely under- nourished children, in whom lactose-containing formu- PEDIATRICS Volume 118, Number 3, September 2006 1283 Downloaded from www.pediatrics.org by on August 17, 2010 las may worsen the diarrhea and lactose-free formulas may be advantageous.62 Breastfed infants should be con- tinued on human milk in all cases.57 This has also been reviewed recently in the American Academy of Pediat- rics’ practice guideline for acute gastroenteritis.63 The use of lactase in formulas for preterm infants has been noted above. Although lactose-free cow milk–protein-based formulas are readily available and popular, no studies have documented that these formulas have any clinical impact on infant outcome measures including colic, growth, or development.64 Lactose, Calcium Absorption, and Bone Mineral Content Recent evidence indicates that dietary lactose enhances calcium absorption and, conversely, that lactose-free di- ets result in lower calcium absorption.65 Thus, lactose intolerance (and lactose-free diets) theoretically may predispose to inadequate bone mineralization, a problem now recognized in many other disorders affecting pedi- atric patients.45,46 The effects of lactose-free diets in child- hood on long-term bone mineral content and risk of fractures and osteoporosis with aging remains to be clar- ified. Calcium homeostasis is also affected by protein intake, vitamin D status, salt intake, and genetic and other factors, making long-term studies essential to de- termine the risks of each or all of these to bone health. Recent studies suggest that in the future, genetic testing may be useful for identifying individuals at increased risk of lactase deficiency and consequent diminished bone mineral density,66 potentially allowing early inter- vention with dietary manipulation or nutrient supple- mentation. Recent research has even suggested that gene-replacement therapies might someday be available for susceptible individuals.67 SUMMARY Lactose intolerance has been recognized for many years as a common problem in many children and most adults throughout the world. Although rarely life-threatening, the symptoms of lactose intolerance can lead to signifi- cant discomfort, disrupted quality of life, and loss of school attendance, leisure and sports activities, and work time, all at a cost to individuals, families, and society. Treatment is relatively simple and aimed at reducing or eliminating the inciting substance, lactose, by eliminat- ing it from the diet or by “predigesting” it with supple- mental lactase-enzyme replacement. Calcium must be provided by alternate nondairy dietary sources or as a dietary supplement to individuals who avoid milk in- take. CONCLUSIONS 1. Lactose intolerance is a common cause of abdominal pain in older children and teenagers. 2. Lactose intolerance attributable to primary lactase de- ficiency is uncommon before 2 to 3 years of age in all populations; when lactose malabsorption becomes apparent before 2 to 3 years of age, other etiologies must be sought. 3. Evaluation for lactose intolerance can be achieved relatively easily by dietary elimination and challenge. More-formal testing is usually noninvasive, typically with fecal pH in the presence of watery diarrhea and hydrogen breath testing. 4. If lactose-free diets are used for treatment of lactose intolerance, the diets should include a good source of calcium and/or calcium supplementation to meet daily recommended intake levels. 5. Treatment of lactose intolerance by elimination of milk and other dairy products is not usually necessary given newer approaches to lactose intolerance, in- cluding the use of partially digested products (such as yogurts, cheeses, products containing Lactobacillus aci- dophilus, and pretreated milks56,68). Evidence that avoidance of dairy products may lead to inadequate calcium intake and consequent suboptimal bone min- eralization makes these important as alternatives to milk. Dairy products remain principle sources of pro- tein and other nutrients that are essential for growth in children. COMMITTEE ON NUTRITION, 2005–2006 Frank R. Greer, MD, Chairperson Jatinder J. S. Bhatia, MD Stephen R. Daniels, MD, PhD Melvin B. Heyman, MD Marcie B. Schneider, MD Dan W. Thomas, MD Robert D. Baker, Jr, MD, PhD LIAISONS Sue Ann Anderson, PhD, RD Food and Drug Administration Donna Blum-Kemelor, MS, RD US Department of Agriculture Margaret P. Boland, MD Canadian Paediatric Society Laurence Grummer-Strawn, PhD Centers for Disease Control and Prevention Capt Van S. Hubbard, MD, PhD National Institutes of Health Benson M. Silverman, MD Food and Drug Administration STAFF Raymond J. Koteras, MHA REFERENCES 1. American Academy of Pediatrics, Committee on Nutrition. The practical significance of lactose intolerance in children. Pediat- rics. 1978;62:240–245 1284 AMERICAN ACADEMY OF PEDIATRICS Downloaded from www.pediatrics.org by on August 17, 2010 2. 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Accessed August 18, 2005 1286 AMERICAN ACADEMY OF PEDIATRICS Downloaded from www.pediatrics.org by on August 17, 2010 Updated Information & Services References Citations Subspecialty Collections Permissions & Licensing Reprints including high-resolution figures, can be found at: http://www.pediatrics.org/cgi/content/full/118/3/1279 This article cites 65 articles, 22 of which you can access for free at: http://www.pediatrics.org/cgi/content/full/118/3/1279#BIBL This article has been cited by 9 HighWire-hosted articles: http://www.pediatrics.org/cgi/content/full/118/3/1279#otherartic les This article, along with others on similar topics, appears in the following collection(s): Nutrition & Metabolism http://www.pediatrics.org/cgi/collection/nutrition_and_metabolis m Information about reproducing this article in parts (figures, tables) or in its entirety can be found online at: http://www.pediatrics.org/misc/Permissions.shtml Information about ordering reprints can be found online: http://www.pediatrics.org/misc/reprints.shtml Lactose Intolerance in Infants, Children, and Adolescents Melvin B. Heyman and for the Committee on Nutrition Pediatrics 2006;118;1279-1286 DOI: 10.1542/peds.2006-1721 Downloaded from www.pediatrics.org by on August 17, 2010	Translation - Chinese 儿科美国儿科学会官方月刊婴幼儿，儿童和青少年乳糖不耐症梅尔文·B·海曼以及营养委员会《儿科》，2006；118；1279-1286 DOI：10.1542/peds.2006-1721 此篇文章的在线版以及更新信息和服务的网页链接如下： http://pediatrics.aappublications.org/content/118/3/1279 临床报告婴幼儿，儿童和青少年乳糖不耐症梅尔文·B·海曼，医学博士，公共卫生硕士，营养协会摘要美国儿科学会营养委员会提出了对于婴幼儿，儿童和青少年乳糖不耐症的最新探讨。人们讨论了导致乳糖不耐症的原因：原发性，继发性，先天性和即发育乳糖酶缺乏症之间的区别。疑患病的儿童在临床上可以通过膳食中乳糖筛除，或是通过无创性氢呼气试验，再或是侵入性小肠（以及其他双糖酶）活检乳糖酶含量测试来进行评估。治疗方法包括服用乳糖酶处理过的乳制品或是口服补充乳糖酶，限制含乳糖食物食用量或是避免食用乳制品。美国儿科学会支持人们食用乳制品，它们为骨矿物质健康提供重要的来源：钙，以及其他促进儿童和青少年生长的营养物。如果不食用乳制品，那么要确保其他钙膳食来源或是钙补充剂的提供。引言自从美国儿科学会营养委员会发表的第一篇关于乳糖不耐症的报告起，已经过去的四分之一个世纪，在此期间，人们对于乳糖不耐症的认知和处理方法发生了巨大的变化1。一些易感人群摄入乳糖后会导致不同的腹部病症，这些病症根据乳糖摄入量和乳糖缺失程度的不同，可以通过饮食限制或是替代酶的方式来治疗。儿科医生和其他儿童保健服务人员需要对于膳食中食用乳制品和以牛奶为基础的婴儿配方粉的益处与争议保有一定的意识。无论是促进地还是阻碍地，牛奶中的乳糖含量常常会对于饮食中牛奶的食用和持续食用产生最终的影响。不食用牛奶和乳制品对婴幼儿，儿童和青少年的钙和维他命的摄入量会产生一定的负面影响。其他的例如蛋白质的营养物也使得乳制品成为成长中儿童的不可或缺的营养来源。修订的报告将会更新1978年的最初版报告，并整合入自1990年以来与乳糖不耐症相关的补充说明2和当前发展状况。关于膳食钙的建议最近已得到了更新3。乳糖，是一种包含一分子葡萄糖和一分子半乳糖的一种二糖，是只存在于哺乳动物乳汁当中的主要糖类。乳糖靠肠刷状缘的活性乳糖酶分解两个单糖之间的苷键来被人体吸收。β-半乳糖苷酶，又称“乳糖酶-根皮苷水解酶”（乳糖酶）占据了肠粘膜中最主要的活动4。乳糖酶被发现于小肠内部，位于小肠绒毛的顶端，考虑到腹泻疾病对于容忍牛奶能力的影响，乳糖酶是在临床学上十分重要。牛乳不耐症可能归因于体内乳糖亦或是蛋白质的含量。乳糖不耐症有可能发生在患有急性腹泻疾病的婴幼儿或是低龄儿童身上，即便它的临床意义仅限于几例受到严重影响的儿童。乳糖不耐症通常存在于年级稍大的儿童和青少年之中，然而它导致的肠道损伤并不常见。牛乳蛋白过敏由免疫系统和不同程度的肠道粘膜表面损伤引起，乳糖不耐症是牛乳蛋白过敏中一个独特的类型。据报道，牛乳蛋白不耐症发生在2%~5%的婴幼儿出生后的1到3个月内，通常在他们1岁之前就会得到解决，不过这也并非是这份报告的主题5,6。定义以下是这份报告其余术语的定义。 λ 乳糖不耐症的临床症状表现为以下的其中一种或是多种：腹部疼痛，腹泻，恶心，胀气，以及/或是食用乳糖或是含乳糖食品之后产生腹胀。产生这些症状的乳糖量会因个体的不同，摄入乳糖量的不同，乳糖酶缺乏程度不同，以及摄入食品的形式的不同而有差异。 λ 乳糖吸收障碍属于生理问题，它的表现为乳糖不耐症，产生这种问题的原因在于摄取乳糖量和人体内乳糖酶水解二糖能力之间的失衡。 λ 原发性乳糖酶缺乏症的病因在于乳糖酶的相对或是绝对的缺失，这种缺失在不同种族的儿童身上会在不同的年龄产生，它也是乳糖吸收障碍和乳糖不耐症最常见的原因。原发性乳糖酶缺乏常常被称作成人型乳糖酶缺乏，乳糖不抗性，或是遗传性乳糖酶缺失。 λ 继发性乳糖酶缺乏症是为小肠损伤所导致，这些损伤包含急性肠胃炎，持续性腹泻，小肠增生，肿瘤化疗，或是其他原因造成的小肠粘膜损伤。这个症状可能在任何年龄出现，但通常是出现于婴幼儿阶段。 λ 先天性乳糖酶缺乏症十分罕见，按目的论来说，20世纪前，由于不含乳糖而又营养充足的人奶替代品并不易得到，患有这种病症的婴幼儿一般无法存活。 λ 即发育乳糖酶缺乏症现在被定义为发生在妊娠期小于34周的早产婴儿身上的乳糖酶相对缺失。原发性乳糖酶缺乏症原发性乳糖酶缺乏症占全部病例的70%7,8。这个比例因种族不同而有差异，同时它也与人们饮食结构中乳制品的食用量有关，这也导致了个体由于基因选择而产生消化乳糖的能力不同。（表1）。在饮食结构中乳制品占主导地位的人群，尤其是北欧人中，患此病症的比例只有2%。相反，此病的患病率在西班牙裔人群中为50%~60%，在黑种人和德系犹太人中为60%~80%，而在亚裔和美洲印第安人群中则为100%9,10。发病年龄和患病率随人群而异。大约20%的西班牙裔，亚裔和黑人儿童在5岁之前出现乳糖酶缺乏和乳糖吸收不良的症状12，然而白种人群儿童通常直到4,5岁之后才会出现乳糖不耐症状。最近的乳糖酶-根皮苷水解酶（乳糖酶）分子研究表明，乳糖活性的持续性与信使RNA表达时的遗传多态性有关，这也阐明了信使RNA表达和酶活力在泰国儿童早期（1~2岁），以及芬兰儿童后期（10~20岁）体内有所缺失的原因11~13。这些观察结果的临床意义在于，可以对一些特定种族中，判断在正常年龄前就表现出乳糖不耐临床症状的儿童是否有其他潜在疾病，否则，在如此年龄患这种病是不正常的。虽说原发性乳糖不耐症有可能表现为相对急性的牛奶不耐症，但它的发作通常不易被察觉，是多年间逐渐形成的。大多数病患在青春期末期或是成年之后才开始出现病症。表1 后天原发性乳糖酶缺乏症患病情况69 乳糖酶缺失人群占主导位置的种群（60%~100%的人患有乳糖酶缺失症）近东和地中海地区：阿拉伯人，德系犹太人，希腊族塞浦路斯人，意大利人亚洲：泰国人，印度尼西亚人，中国人，韩国人非洲：南尼日利亚人，豪萨人，班图人北美和南美洲：美国黑人，拉丁美裔人，爱斯基摩人，加拿大人，美国印第安人，沙米印第安人乳糖耐受的人群占主导位置的种群（2%~30%的人患有乳糖酶缺失症）北欧人非洲：希马人，图西人，富拉尼游牧人印度：旁遮普组和新德里的一些个人专注于乳糖酶缺失症的报告因一些临床诊断而易带有一定的主观性。例如，采用双盲测试法，每日分别给患有乳糖酶缺失的成年人两杯牛奶和两杯乳糖水解了的牛奶，做交叉对比。无论被测试者自称是否患有乳糖不耐症，人们均未统计出症状差异14。即便是乳糖不耐症患者也可以忍受一杯牛奶或是一勺冰激凌，然而他们若再多食用一杯牛奶或是奶制品则可能会出现一些相关症状。由于每一个个体日常摄入乳制品的量不同，不同食品中的乳糖含量不同，他们的症状也会有所不同，这些症状也可被饮食结构和含奶制品食物所改变（见“管理”）。由于这些原因，一个人过去的饮食习惯并非确诊或是排除乳糖不耐症的一种可靠的手法。继发性乳糖酶缺乏症继发性乳糖酶缺乏症是指潜在的病例生理状态导致的乳糖酶缺失和随后的乳糖吸收障碍。它的病因包含急性感染（如轮状病毒感染）导致的小肠损伤，这种损伤伴有绒毛尖端上含乳糖的表皮细胞的缺失。而代替这些表皮细胞的不成熟表皮细胞通常乳糖酶含量不足，导致了继发性乳糖酶缺乏和乳糖吸收障碍，即便很多报告都表明大多患有急性肠胃炎的儿童的乳糖吸收障碍在临床学上并无重要意义。很多近期的研究和荟萃分析发现感染了轮状性（和其他传染性）腹泻疾病，但没有脱水或只是轻微脱水的儿童可以放心地饮用人奶或是标准（含乳糖）的配方奶，而并不影响他们身体状况，这些状况包含水合状态，营养状态，患病时长或是治疗的成功。然而对于处境危险，患有感染性腹泻的婴幼儿（小于3个月和营养不良的婴儿）来说，乳糖不耐症对他们病情发展的影响很大。贾第虫，隐孢子虫，和其他感染近端小肠的寄生虫通常因直接损伤上皮细胞而导致乳糖吸收障碍。伴有不耐乳糖临床症状的继发性乳糖酶缺乏症可见于麸质过敏症，克罗恩病，免疫先关和其他肠道疾病患者，人们也应当留意患这些病的儿童是否有相关的病症。这些儿童在疑患有乳糖缺乏症而又未找到传染性病因时，诊断评估对象应转向这些寄生虫。患有严重营养不良的幼婴也会因肠道萎缩而诱发继发性乳糖酶缺乏症。虽在美国不常见，但在发展中国家，营养不良与乳糖吸收障碍和醣不耐症有一定的关联20。在这些国家21，乳糖吸收障碍也与生长中营养不良相关。多数因营养不良而患有有乳糖吸收障碍的婴幼儿和儿童是可以忍受在膳食中摄入包含乳糖在内的碳水化合物的22。然而，世界卫生组织建议患有持续性后感染性腹泻的孩童（腹泻时长超过14天）若对牛奶和酸奶产生了不良反应则应该避免食用含乳糖的奶类23。继发性乳糖酶缺乏症和因自身疾病导致的乳糖吸收障碍症的治疗并不需要将乳糖从饮食中除去，而是治疗个体自身疾病就足矣。一旦问题得到解决，患者就可正常地食用含乳糖的食品，而不用刻意排除这些包含钙和其他营养物的上好来源了。即发育（新生儿）乳糖酶缺乏症在新生儿未成熟的胃肠道中，乳糖酶和其他双糖酶在妊娠期达到34周之前都是不足的24。一项关于早产儿的报告中提出了食用补充乳糖酶或是低乳糖配方食品的益处，而食用含乳糖的婴儿食品和人乳也似乎并不会对早产儿产生短期亦或是长期的有害影响26。饮食中20%的乳糖都有可能达到新生儿和幼婴的结肠。结肠内乳糖的细菌代谢课降低粪便的pH值（5.0~5.5是正常值），这其中有一个益处，它对幼婴体内一些微生物（双歧杆菌和乳杆菌属）而非潜在病原体（变形杆菌，大肠杆菌和克雷伯氏菌）有利。抗生素对于这样的移生也会产生影响。先天性乳糖酶缺乏症先天性乳糖酶缺乏症是一种很罕见的紊乱，只发生在很少的几例婴幼儿身上27,28。患病的新生儿一旦食用人乳或是含乳糖的婴儿食品，就会出现难治的腹泻。患儿的小肠粘膜活检显示其组织特征正常，而当中乳糖酶浓度低甚至为零29,30。若不尽快治疗，那么这种状况则会使患儿因脱水和缺失电解质而有生命危险。治疗方法很简单，只需从饮食中除掉乳糖或是食用不含乳糖的商业配方食品即可。诊断乳糖不耐症的症状表现有腹胀，胀气，腹部绞痛和（最终出现地）腹泻，这些症状与引起乳糖吸收障碍的原因无关，而与摄入的乳糖量直接相关。这些症状与肠道内乳糖缺失程度也不一定有关。吸收不良的乳糖会造成渗透负荷，将液体和电解质吸入肠腔，导致粪便稀薄。腹泻和其他症状是由于未被吸收的乳糖引起的。即便是12克的乳糖（一杯8盎司牛奶中的乳糖含量）也足以导致儿童出现长期腹痛症状31。除此之外，未被吸收的乳糖也是肠道内，尤其是结肠内细菌的基底。细菌代谢乳糖，产生挥发性脂肪酸和气体（甲烷，二氧化碳和氢气），从而导致肠胃胀气。脂肪酸降低粪便的pH值，因此，虽无特异性，但有时粪便pH值可以作为乳糖（或是其他碳水化合物）吸收不良的鉴别标志。当细菌代谢产生出足够多的肠道气体后，会造成肠道膨胀，刺激肠道内神经系统，引起内脏（腹部）绞痛。引用乳糖氢呼吸试验的初步研究证明，40%患有乳糖吸收障碍的儿童和青少年都出现了腹痛32。然而最新的研究表明，由乳糖不耐症引起的腹部病症患病率从芬兰儿童中的2%到南美儿童中的24%都有所不同33,34。良好的临床病史常可展现乳糖摄入与症状之间的关系。当疑患有乳糖不耐症时，人们可以尝试采用无乳糖食谱（表2，3）。在采用诊断性无乳糖饮食期间，要确保所有的饮食来源中不含乳糖，这也要求患者需要读取食品标签，以便鉴定“隐藏的”乳糖来源。通常，人们可以通过一个长达两周的严格无乳糖饮食实验分辨出一些症状，随后饮食中再引入乳制品也能诊断出再出现的症状。在一些症状更不易被察觉的案例里，氢呼吸试验是侵入性最小也是最有用的乳糖吸收障碍症的诊断办法。此种方法比临床病史更可靠，因为很多自认为患病的了人做了测试后，发现并未得病，而反过来，一些自认为未得病的病人（乳糖吸收障碍者），做了测试后发现患有乳糖不耐症36,37。该试验的测试者服用一定量的乳糖（2g/kg，最多25g，即一杯28盎司的牛奶中乳糖的含量），禁食一夜之后，测定呼出空气中氢的含量，测试时长为2至3小时。在服用乳糖后60分钟左右，若呼出的气体中氢含量有增加（>20ppm），则为患有乳糖吸收障碍。一些因素如影响肠道菌群的条件（如最近使用的抗微生物药剂），缺失氢生产菌（占人口比例10%~15%），在做测试之前摄入了高纤维膳食，小肠内细菌过度生长或是肠道能动性紊乱均可能导致假阴性或假阳性结果。这个测试的结果应需要咨询儿科胃肠病学专家。表2 常见食物中乳糖和钙含量70,71 乳制品钙含量/毫克乳糖含量/克酸奶，原味，低脂，1杯 448 8.4 牛奶，全脂（脂肪含量3.25%），1杯 276 12.8 牛奶，低脂，1杯 285 12.2 冰激凌，香草，1/2杯 92 4.9 切达干酪，1盎司 204 0.07 瑞士干酪，1盎司 224 0.02 松软干酪，加奶油（小块），一杯 135 1.4 表3 隐藏乳糖来源72 面包和其他烘焙食物加工早餐谷物薄饼，饼干和曲奇饼干调拌料即使土豆，糖，早餐饮料人造黄油非犹太午餐肉沙拉酱糖果等零食在氢呼吸测试面世之前，人们倚赖旧时的乳糖耐受试验作为乳糖吸收障碍的初级测试。测试者摄入标准剂量的乳糖（占体重2‰的乳糖，或是每平米身体表面积50g乳糖，20%的水溶液中最多50克）。若在测试后血糖浓度增值的最大值小于26mg/dL，则可确诊为患有乳糖吸收障碍。乳糖耐受测试并不够敏感，无法决定测试者是否没有乳糖吸收不良。由于胰岛素反应正常而导致血糖浓度并未增加，诊断结果常常呈现为假阳性。由于假阴性结果和假阳性结果的比例过高，人们不应再施行此项测试，而应用氢呼吸测试取而代之。在与儿科肠胃学家商议之后，人们也可实行其他的测试。若疑有患继发性乳糖酶缺乏症，则应进行肠道病原学测试。这些测试包含粪检，尤其检测是否有影响上胃肠道的贾地鞭毛虫和隐孢子虫，还要进行血检，查看是否患有乳糜泻（即总免疫球蛋白浓度和抗组织型谷氨酰胺转移酶抗体38,39）或是免疫缺陷（免疫球蛋白数量）。为了发现引起乳糖吸收不良的潜在的胃肠粘膜病变，需要进行肠粘膜活检。活检可以直接测量出双糖浓度，以直接判断是否有乳糖酶缺失症，并对刷状缘上其他双糖酶（蔗糖酶，麦芽糖酶，异麦芽糖酶）的状态做出评估。然而这种检测也可能因为外界环境不同而产生缺陷。然而小肠内酶浓度与乳糖不耐症的症状似乎并不相关40。新的测试最终会使人们了解到一些关于患病率的额外详细信息，也能阐释乳糖不耐症的重要性41。例如，人们考虑施行13C呼吸试验，以提高氢呼吸试验的准确性，但目前这项测试也还只是临床实验的工具42,43。对于疑患有乳糖（或是其他糖类）不耐症的有腹泻症状婴幼儿，需要筛查他们的粪便，通过检查粪便pH值来看是否有未被吸收的碳水化合物，若有吸收障碍，则pH值会因形成的挥发性脂肪酸而降低。人们应当记住，由于婴幼儿饮食中乳糖含量较高，他们粪便的pH值通常低于（5.0-5.5）年长一些的儿童或是青少年，然而反过来它也有益于结肠中乳酸杆菌的生长。粪便中还原糖的分泌也使得粪便中还原物可被测量并呈现阳性。还原性糖包括乳糖，葡萄糖，果糖和半乳糖，但不包括蔗糖。因为有些病人未吸收的例如乳糖的糖类的量可能恰巧能够降低粪便的pH值，而不增加粪便中糖类的分泌，对于测试碳水化合物吸收障，pH值测试更为灵感。管理在确诊儿童患有乳糖不耐症后，避免食用牛奶和其他乳制品可以缓解病症。然而，原发性乳糖不耐受患者会有不同程度的乳糖酶缺失，相对应的，患者日常饮食中所能忍受的乳糖量并不相同。患有乳糖不耐症的儿童（和他们的家长）应当意识到，食用乳制品引起的病症通常为短暂性的症状，不会对胃肠道造成伤害（相比较而言，腹泻症，过敏，牛奶蛋白不耐症会引起持续的炎症和黏膜损伤）。虽说患乳糖吸收障碍并不易患钙质吸收障碍44，但是若不食用奶制品，骨矿化将无法在理想的状态下进行。有记录证明，不食用牛奶的儿童摄入的钙含量低于正常骨骼钙吸收和骨矿化所需的量44，45。零乳糖和低乳糖的牛奶（以及专给小于2岁的儿童饮用的零乳糖全脂奶）在超市中都有售，也可用WIC（妇女、婴儿及儿童补充营养项目）抵用券来购买。这些牛奶比正常的价格要高，而一些连锁品牌卖的自家品牌的零乳糖的牛奶价格要低一些。婴儿期外，以大米，大豆，牛奶为基础的牛奶替代品通常十分易得，而且通常不含乳糖，然而这些乳剂中的营养成分却不及牛奶。其他的哺乳动物乳汁，例如羊奶，都含有乳糖。患者对于乳制品的耐受度不是完全的，因此这些人也可以通过饮食搭配来避免症状的出现。患者若全天间隔性的摄入少量：4到8盎司的乳糖，并同时摄入其他食物，则不会出现病症47-51。一些儿童可以忍受每天饮用1到2杯牛奶，但若是再多则会出现病症14。很多乳糖不耐症患者不能忍受牛奶但是可以忍受巧克力牛奶52或是酸奶（原味酸奶好过于调味酸奶），因为酸奶中的细菌可以在患者食用前就将乳糖分解为葡萄糖和半乳糖53,54。此外，酸奶由于呈半固态状，因此它可减慢胃肠道清空和运转速度，从而减少乳糖不耐病症的出现55。不仅如此，摄入其他的固体食物可以减缓胃肠道清空速度，留给体内的乳糖酶额外的时间来消化摄入的乳糖。陈年干酪通常比其他奶酪的乳糖含量低，也因此更容易被消化。最后，口服乳糖酶替代胶囊或是乳糖酶预消化乳制或奶制食品十分易得，这也使得乳糖不耐症患者可以无顾虑地食用一些奶制品56。由于不同牛奶替代品中维生素D的含量不同，患者需要查看个别品牌标签中维生素D的成分。即使对于乳糖不耐症较显著的人群中，也应当强调饮食中含有乳制品的重要性。国家医学学会最近建议黑人每日应摄入3至4份的低脂牛奶，乳酪，和/或是酸奶，以及零乳糖牛奶，作为患者的饮食替代品，以减少与营养相关的慢性疾病，例如高血压和糖尿病的危险57。许多自身患有肠道炎症（如克罗恩病和溃疡性结肠炎）的儿童，都可以耐受乳制奶制品，这些儿童中的乳糖不耐症的患病率似乎也不比普通群众中的比例高58-61。零乳糖婴儿食品在发达国家，即使是患有急性肠胃炎的儿童也会摄入并吸收足量的乳糖，致使低乳糖和零乳糖婴儿食品与乳糖含量正常的婴儿食品相比并不具有临床优势，而这不包含营养严重不良的儿童，他们若食用含乳糖的配方食品，则有可能加重他们的腹泻症状，这时食用零乳糖婴儿食品更有益62。母乳喂养的婴儿应当继续母乳喂养57。这件事情美国儿科学会也在最近的急性肠胃炎实践指南中做出了评论。其中也记录了早产儿食用的配方食品中乳糖的使用问题。虽说以牛奶蛋白为基础的低乳糖婴儿食品既易得又流行，并没有研究表明这些配方食品对诸如急腹痛，生长或是发展这些观察指标产生了临床影响64。乳糖、钙的吸收，以及骨矿物质含量最新的证据表明，饮食中含乳糖会促进钙的吸收，反过来，不含乳糖的饮食则会导致体内钙含量低。65 因此，理论上说，患有乳糖不耐症的人也可能患有骨矿化不足，人们现在意识到了这是小儿患者众多的紊乱疾病之一。44,46 无乳糖饮食对于儿童骨骼矿物质含量，以及骨折和随着年龄增长患骨质疏松症的风险是否有长期影响有待阐明。钙稳态也受蛋白质摄入量，维生素D状态，盐摄入量和遗传等因素的影响，这也使针对以上因素对骨骼健康的危害的长期研究显得十分重要。最新的研究表明，今后，可以将基因测试运用于确定个体是否患有乳糖酶缺失以及随之而来的骨密度下降的风险66，这也潜在地允许了早起饮食控制或是营养补充的介入。最新的研究也提出，未来的某天，疑似病患有可能可以采取基因替换的治疗方法。概括很多年以来，全世界都意识到了在很多儿童和成年人当中，乳糖不耐症十分常见。虽说它们很少会危害到生命，但是这种疾病产生的症状可以导致患者感到十分不适，破坏他们的生活质量，导致他们缺席学校的课程，休闲和体育活动，工作，消耗病患，他们的家人和社会的成本。它的治疗方法相对简单，以减少或是去除它当中的“罪魁祸首”，乳糖为目标，从饮食中去除乳糖，或是通过服用乳糖酶替代物来提前分解乳糖。备用的不含乳糖的膳食来源中需要包含钙，或是提供给饮食中不摄入牛奶的患者补充额外的钙。总结 1. 乳糖不耐症是引起稍年长的儿童和青少年腹痛的一个常见原因。 2. 在所有种群中，原发性乳糖酶缺失引起的乳糖不耐症在幼儿2到3岁之前都不常见；如果幼儿在2到3岁之前就出现明显的乳糖吸收障碍，则需要考虑其他的病因。 3. 通过饮食排除和挑战法，人们可以相对容易的诊断出乳糖不耐症。更多正规的测试通常都是无创的，有代表性的例如有水性腹泻症状时粪便pH值测试和氢呼吸测试。 4. 如果施行无乳糖饮食来治疗乳糖不耐症，则应当在饮食中包含入达到日常摄入标准的钙，以及/或是钙补充剂。 5. 鉴于最新出现的对抗乳糖不耐症的治疗方法，目前饮食中筛除奶类和其他乳制品的方法通常并无必要。这些新型的方法包括摄入部分酶解了的食品（如酸奶，干酪，含嗜酸乳杆菌食品和预处理过的牛奶56,68）。证据表明不食用乳制品有可能导致钙的摄入量不足，和随之导致的骨矿化不能在理想状态下进行，这也使其成为十分重要的牛奶替代品。乳制品是有利于儿童成长的蛋白质和其他营养物的重要载体。营养委员会，2005-2006 弗兰克﹒R﹒格利尔，医学博士，主席贾庭﹒J﹒S﹒巴提亚，医学博士史蒂芬﹒R﹒丹尼尔斯，医学博士，哲学博士梅尔文﹒B﹒海曼，医学博士马尔西﹒B﹒施耐德，医学博士丹﹒W﹒托马斯，医学博士小罗伯特﹒D﹒贝克，医学博士，哲学博士联络员苏﹒安﹒安德森，哲学博士，注册营养师食品和药物管理局唐娜﹒百隆﹒凯姆乐尔，理学硕士，注册营养师美国农业部玛格丽特·P·博兰，医学博士加拿大少儿医师协会劳伦斯·格鲁梅尔·斯特朗，哲学博士美国疾病控制与预防中心范·S·哈伯德上校，医学博士，哲学博士国立卫生研究院本森·M·西尔弗曼，医学博士食品和药物管理局员工雷蒙德·J·科特拉斯，医学管理专业硕士参考书目 1. 美国儿科学会，营养委员会：儿童中乳糖不耐症的实际重要性，《儿科》，1978;62:240–245 2. 美国儿科学会，营养委员会：儿童中乳糖不耐症的实际重要性：补充，《儿科》，1990;86:643–644 3. 美国儿科学会，营养委员会：优化骨骼健康和儿童钙摄取，《儿科》，2006;117:578–585 4. 西门扎·G：绒毛刷状缘膜蛋白的锚定和生物合成：糖苷酶，肠肽酶和肾小管，《细胞生物年度评论》，1986;2:255–313 5. 美国儿科学会，营养委员会：低变应原的婴儿食物，《儿科》，2000;106:346–349 6. 侯斯特·A，雅各布森·HP，哈尔肯·S，赫尔门得·D：牛奶蛋白过敏和不耐症的自然历史，《欧洲临床营养学杂志》，1995;49(增刊1):S13–S18 7. 克莱切莫·N，乳糖与乳糖酶，《胃肠病学》，1971;61:805–813 8. 克莱切莫·N，人类发展与小儿学科之间的同源性，《儿科研究》，1968;2:283–286 9. 佩齐·DM，贝里斯·TM, 梅利提斯·ED，戴维斯·L，学龄前黑人儿童的乳糖吸收障碍，《美国临床营养学杂志》，1977;30:1018–1022 10. 劳埃德·ML，奥尔森·WA，双糖吸收障碍，于：豪布里希·WS，夏弗纳·F，伯克·JE，《博克斯胃肠病学》，第5版，费城，宾夕法尼亚州，桑德斯出版社，1995:1087–1100 11. 萨伊·T，成人型乳糖酶缺乏的遗传和流行病学，《北欧胃肠病学杂志-增刊》，1994;202:7–20 12. 渥特基·CE，韦斯·E，杨·EA，墨西哥裔美国儿童中的乳糖吸收障碍，《美国临床营养学杂志》，1976;29:19–24 13. 王·Y，哈维尔·CB,浩勒克斯·EJ及其他，儿童中基因觉得的乳糖负调控，《胃肠病学》，1998;114:1230–1236 14. 苏亚雷斯·FL，塞维雅诺·D，阿尔比希·P，莱维特·MD，自认为患乳糖不耐症个体对于每日两杯的忍耐度，《美国临床营养学杂志》，1997;65:1502–1506 15. 三都·BK,依苏劳利·E，沃克·史密斯·JA及其他，代表欧洲小儿胃肠病学协会和急性肠胃炎营养工作组的跨医疗机构研究；童年时期肠胃炎的早期喂养，《小儿肠胃营养杂志》，1997;24:522–527 16. 巴纳加·KH，布含·MK，辛格·KD，萨克塞纳·SK，谢里夫·M，持续性腹泻中以牛奶为基础的饮食的功效：随机化和受控制的实验，《儿科》，1996;98:1122–1126 17. 斯佩洛托·G，巴里森·EM，鲍尔达奇·ER，冈谷·Y，患急性腹泻和严重脱水症状的儿童的日常治疗中食用未稀释牛奶的影响，《胃肠病学集刊》，1998;35:132–137 18. 布朗·KH，皮尔森·JM，方丹·O，患急性腹泻的幼童饮食管理中非人乳的食用：临川试验的荟萃分析，《儿科》，1994;93:17–27 19. 尼古拉斯·BL，达德利·MA，尼古拉斯·VN及其他，营养不良对儿童乳糖酶表达与活性的影响，《胃肠病学》， 1997;112:742–751 20. 诺斯罗普-克刘易斯·CA，伦恩·PG,道恩斯·RM，冈比亚母乳喂养婴儿的乳糖吸收不，《小儿胃肠病营养学杂志》，1997;24:257–263 21. 沃顿·B，豪厄尔·G，菲利普斯·I，夸希奥科病中的腹泻症状，《英国医学杂志》 1968;4:608–611 22. 哈布特·D，海韦里恩·A，斯太尔·G，夸希奥科病中碳水化合物的吸收不良，《埃塞尔比亚医学杂志》，1973;11:33–40 23. 世界卫生组织，国际持续性腹泻工作小组，一个算法对持续性腹泻的评估，《世界卫生机构公告》，1996;74:479–489 24. 阿洛诺维茨·I, 李班塞尔·E，人类胎儿小肠肠激酶和二糖酶活动的发展模式，《胃肠病学》，1977;72:1299–1303 25.伊拉兹马斯·路德维格-阿瑟尔·HM，派特森·PG，孙·D，桑卡兰·K，食用处理过的乳糖酶对早产儿体重增加的强化：一个随机，双盲，有控制的试验，《儿科杂志》， 2002;141:532–537 26. 舒尔曼·RJ，菲斯特·A，欧·C，早熟儿童中乳糖，高分子葡萄糖的吸收或是结合，《儿科杂志》，1995;127:626–631 27. 丽芙释子·F，先天性乳糖酶缺失，《儿科杂志》，1966;69:229–237 28.萨维拉提·E，劳尼拉·K,库伊图宁·P，先天性乳糖酶缺失：含有16个病人的临床研究，《儿童疾病文献》，1983;58:246–252 29. 爱斯普·NG，达尔克维斯特·A，库伊图宁·P, 劳尼拉·K, 维萨考皮·JK，先天性乳糖缺失中刷毛缘乳糖酶的完全缺失，《柳叶刀》，1973;2(7824):329–330 30. 费拉堡豪斯·AU，施密茨·J,施耐德·M及他人，特定的先天性乳糖酶缺失症中早期乳糖吸收障碍中刷状缘片段的蛋白质模式，《新英格兰医学期刊》，1976;294:1030–1032 31. 格莱姆斯·DA，格里尔·AS, 维塞克·J，迪帕尔玛·JA，与患有乳糖不耐症儿童中乳糖摄入有关的腹部疼痛，《儿科临川学（费城）》，2003;42:341–345 32. 巴尔·RG，莱文·MD，渥特金·JB，童年时期有乳糖不耐症引起的周期性腹部疼痛，《新英格兰医学期刊》，1979;300:1449–1452 33. 柯克楠·J,哈怕来提·M，提卡嫩·S，卡尔图嫩·R，萨维拉提·E，儿童胃肠道疾病和诊断：一个基于全体人口的研究，《儿科学报》，2004;93:880–886 34. 韦伯斯特·RB，迪帕尔玛·JA，格莱姆斯·DA，童年时期周期性腹痛的肠道易激综合征和乳糖消化不良，《南方医学杂志》，1999;92:778–781 35. Drugs.com，无乳糖饮食，可见于: www.drugs.com/ CG/LACTOSEFREEDIET.html. 于2005年8月18日访问 36. 迪帕尔玛·JA，那尔瓦兹·RM，转诊病人中乳糖吸收不良的预测，《消化疾病科学杂志》，1988;33:303–307 37. 苏阿尔兹·FL，萨维亚诺·DA, 莱维特·MD，自我评定患有严重乳糖不耐症患者摄入牛奶或乳糖分解过牛奶后的症状对比，《新英格兰医学期刊》，1995;333:1–4 38. 希尔·ID，迪尔克斯·MH,利普塔克·GS及其他，患腹部疾病儿童的诊断和治疗方针：北美儿科胃肠学协会的建议，肝脏病学和营养，《小儿胃肠营养学杂志》，GS2005;40:1–19 39.国家卫生研究所，国家卫生所对于腹部疾病发展共识，见于: http://consensus.nih. gov/2004/2004CeliacDisease118html.htm. 与2015年8月18日访问 40. 古普塔·SK, 崇·SK, 菲茨杰拉德·JF，儿童体内的二糖酶活动：以症状和组织变化为基础的正常评估和对比，《小儿肠胃营养学杂志》 1999;28:246–251 41. 万克·RJ,林·Y, 克埃特斯·HA以其他，通过13C呼吸试验评估乳糖吸收（不良），《欧洲临床调查期刊》，2000;30:140–146 42. 席勒·M, 古斯·Y, 鲁特吉尔·P, 万川普·G, 卡尔容·H, 艾格蒙特·E. 在13C呼吸测试引用13C自然强化过的乳糖检测有胃肠道疾病患者的乳糖酶缺失，《临床医学实验期刊》，1988;112:193–200 43. 柯哀特斯·HA, 斯戴拉尔·F, 比勒费尔德·CM以其他，运用13CO2和H2 结合呼吸测试无创检测儿童肠道内部的低乳糖酶活性，《北欧胃肠道学杂志》，1999;34:35–40 44. 特里曼·WJ, 纽科莫·AD, 里格斯·BL, 麦吉尔·DB.，患乳糖酶缺失症和体内乳糖酶充足的成年人对牛奶中钙的吸收，《消化疾病科学杂志》，1986;31:376–378 45. 斯大林·VA, 欧的艾弗森·NW, 纽格力·BY, 泽梅尔·BS, 伟伦·R，规定需摄入低乳糖饮食的儿童的骨骼矿物质成分和钙摄入，《小儿肠胃营养学杂志》，994;18:440–445 46.迪史蒂芬诺·M, 威奈托·G, 马勒赛尔维斯· S, 及其他. 乳糖吸收障碍和乳糖不耐症与峰值骨密度，《胃肠道学》，2002;122:1793–1799 47. 麦克斌·LD, 米勒·GD. 减轻对乳糖不耐症的恐惧和谬误，《美国饮食协会杂志》，1998;98:671–676 48. 约翰逊·AO, 赛美雅·JG, 布朝沃思齐·MS, 安沃武·CO, 斯奎木·NS. 乳糖消化不良者对持续摄入牛奶的适应，《美国临床营养学杂志》，1993;58:879–881 49. 海兹勒·SR, 塞维雅诺·DA，乳糖消化不良者结肠对于日常乳糖摄入的适应减缓乳糖不耐症，《美国临床营养学杂志》，1996;64:232–236 50. 普利布拉·BA, 海尔兹乐·SR, 马丁·BR, 维尔·CM, 塞维雅诺·DA，日常摄入富含乳制品饮食的非洲裔美国女青少年对乳糖的消化和耐受的加强，《美国饮食协会杂志》，2000;100:524–528 51. 海尔兹乐·SR, 休因·BC, 塞维雅诺·DA. 多低的乳糖算是低乳糖？，《美国饮食协会杂志》，1996;96:243–246 52. 加尔魏楠·RM, 卢卡斯考尔皮·M, 尤斯图皮亚·MI，有病症的乳糖吸收不良者对于巧克力牛奶中乳糖的耐受，《欧洲临床营养学杂志》，2003;57:701–705 53. 考莱尔·JC, 莱维特·MD, 阿乌及·M, 塞维雅诺·DA，酸奶：乳糖自分解的一个来源，《新英格兰医学期刊》，1984;310:1–3 54. 布达尔·G, 班不阿布德拉·M, 海迟拉夫·W, 布意赛特·M, 的热·JF, 图阿米·M，患有急性腹泻和糖类吸收障碍的儿童食用酸奶和牛奶的结果对比，《小儿胃肠营养学杂志》，2001;33:307–313 55. 拉巴岩·I, 福尔咖·L, 宫泽拉兹·A,勒诺尔-维金库普·I, 努特尔·R，马提纳兹·JA. 乳糖消化，乳糖吸收障碍者日常食用乳制品后胃肠道传送时间和症状间的关系，《营养药理学与治疗学杂志》，2001;15:543–549 56. 梅多尔·MS, 泰克·KD, 纽曼·LJ,贝尔金·S, 格拉斯曼·MS, 斯瓦尔兹·SM.β牛乳糖药片在治疗儿科乳糖不耐症中的作用，《美国儿童消化杂志》，1990;144:1261–1264 57. 乌潭·WJ, 普利斯·W. 非洲裔美国人饮食中乳制品和乳制营养品的角色，《国家医学协会杂志》，2004;96(12增刊):5S–31S 58. 皮傅菲尔孔尔·MD, 菲兹尔德·JF, 克尔非·JM, 古普塔·SK, 科尔金斯·MR, 莫兰斯顿·JP，乳糖不耐症：患有肠道炎的病患率并不比患有慢性腹部疼痛病患的患病率高，《小儿胃肠道营养学杂志》，2002;35:339–343 59. 科尔诗奈尔·BS, 德法瓦罗·MV, 杰森·W，患有肠胃炎的儿童和青少年间的乳糖不耐症，《胃肠道学》，1981;81:829–832 60. 米世金·S，肠道炎中的乳制品敏感度，乳糖吸收障碍和排除饮食疗法，《美国临床营养学杂志》，1997;65:564–567 61. 贝尔斯坦·CN, 阿门特·M, 阿尔缇妮·L, 瑞志威·J, 沙那罕·F，成人结肠炎患者的牛奶耐度，《美国胃肠道协杂志》，1994;89:872–877 62. 库库鲁周维克·RH, 布鲁斯特·DR，急性肠胃炎和营养不良中的牛奶配方：一个随机试验，《美国儿科儿童健康杂志》，2002;38:571–577 63. 美国儿科医学会,质量改进临时委员会, 急性肠胃炎下属委员会，实践参数：儿童急性肠胃炎的管理，《儿科》，1996;97:424–435 64. 赫比·J, 卡拉索夫·R, 莱辛格·K, 以其他，记录给早产的零乳糖和含乳糖的配方食品的有效性和安全性的随机跨研究机构试验，2000;100:212–217 65. 艾布拉姆斯·SA, 格林芬·IJ, 达维拉· PM，含乳糖和零乳糖配方食品中钙和锌的吸收，《美国临床营养学杂志》，2002;76:442–446 66. 欧布玛亚尔·BM, 伯奈利·CM, 渥特·DE及其他，成人乳糖不耐症的基因素质以及它同饮食，骨密度，和骨折的关系，《骨骼矿物质研究杂志》，2004;19:42–47 67. 杜林·MJ, 徐·R, 杨·D, 卡普里特·MG, 诗尔温·RS, 里昂纳·P，通过腺伴随病毒载体的乳糖不耐症口服基因疗法，《自然医学》，1998;4:1131–1135 68. 桑德尔斯·ME, 克莱恩海默尔·TR，嗜酸乳杆菌作为益生素的科学依据，《乳制品科学》，2001;84:319–331 69. 强森·JD，乳糖吸收障碍的区域和名族分布，于: 佩齐·DM, 贝里斯·TM, 乳糖消化：临床上和营养学上的影响，巴尔的摩，马里兰州：约翰·霍普金斯大学出版社，1981:11–22 70. 美国农业部，国家营养参考标准数据库，连接: www.nal.usda.gov/fnic/ foodcomp/search，于2005年8月18日访问 71. 马修·RH, 皮尔森·PR, 法尔哈特-撒贝·M，所选食物中糖含量：个体与总体，美国农业部，人类营养学信息服务部，1987，地址： www.nal.usda.gov/fnic/foodcomp/Data/Other/herr48.pdf. ，于2015年8月18日访问 72. 国家消化疾病信息中心，乳糖不耐症，连接 : http://digestive.niddk.nih.gov/ ddiseases/pubs/lactoseintolerance，于2005年8月18日访问婴幼儿，儿童和青少年乳糖不耐症梅尔文·B·海曼以及营养委员会《儿科》，2006；118；1279-1286 DOI：10.1542/peds.2006-1721 更新信息和服务包含高分辨率图片，连接：http://www.pediatrics.org/cgi/content/full/118/3/1279 参考这篇文章引用了65篇文章，其中的22篇可在免费读取http://www.pediatrics.org/cgi/content/full/118/3/1279#BIBL 引用这篇文章可以见于9篇HighWire网站上刊文l http://www.pediatrics.org/cgi/content/full/118/3/1279#otherartices 附属专业集合这篇文章，同其他一些相似话题的文章，在下列选集中可见：营养与新陈代谢 http://www.pediatrics.org/cgi/collection/nutrition_and_metabolism 许可和比准整篇或部分重述这篇文章的信息（图片，表格）可以见于http://www.pediatrics.org/misc/Permissions.shtml 再版要求再版的信息可以见于http://www.pediatrics.org/misc/reprints.shtml

Years of experience: 10. Registered at ProZ.com: Mar 2017.

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French to Chinese (Beijing Foreign Studies University. Graduate School of Translation and Interpretation)
French to Chinese (Université de Montréal)
English to Chinese (Beijing Foreign Studies University. Graduate School of Translation and Interpretation)
Chinese to English (Beijing Foreign Studies University. Graduate School of Translation and Interpretation)
Chinese to English (International English Language Testing System)

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Aug 15, 2018

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