PDF(Pubmed)
Abstract：
Lactose is the main carbohydrate in human and mammalian milk. Lactose requires enzymatic hydrolysis by lactase into D-glucose and D-galactose before it can be absorbed. Term infants express sufficient lactase to digest about one liter of breast milk daily. Physiological lactose malabsorption in infancy confers beneficial prebiotic effects, including the establishment of Bifidobacterium-rich fecal microbiota. In many populations, lactase levels decline after weaning (lactase non-persistence; LNP). LNP affects about 70% of the world\'s population and is the physiological basis for primary lactose intolerance (LI). Persistence of lactase beyond infancy is linked to several single nucleotide polymorphisms in the lactase gene promoter region on chromosome 2. Primary LI generally does not manifest clinically before 5 years of age. LI in young children is typically caused by underlying gut conditions, such as viral gastroenteritis, giardiasis, cow\'s milk enteropathy, celiac disease or Crohn\'s disease. Therefore, LI in childhood is mostly transient and improves with resolution of the underlying pathology. There is ongoing confusion between LI and cow\'s milk allergy (CMA) which still leads to misdiagnosis and inappropriate dietary management. In addition, perceived LI may cause unnecessary milk restriction and adverse nutritional outcomes. The treatment of LI involves the reduction, but not complete elimination, of lactose-containing foods. By contrast, breastfed infants with suspected CMA should undergo a trial of a strict cow\'s milk protein-free maternal elimination diet. If the infant is not breastfed, an extensively hydrolyzed or amino acid-based formula and strict cow\'s milk avoidance are the standard treatment for CMA. The majority of infants with CMA can tolerate lactose, except when an enteropathy with secondary lactase deficiency is present.
摘要：
乳糖是人和哺乳动物乳中的主要碳水化合物。乳糖需要由乳糖酶酶水解成D-葡萄糖和D-半乳糖才能被吸收。足月婴儿表达足够的乳糖酶以每天消化约1升母乳。婴儿期的生理乳糖吸收不良赋予有益的益生元效应，包括建立富含双歧杆菌的粪便微生物群。在许多人群中,乳糖酶水平在断奶后下降（乳糖酶非持久性；LNP）。LNP影响约70%的世界人口,并且是原发性乳糖不耐受(LI)的生理基础。乳糖酶在婴儿期后的持久性与2号染色体上乳糖酶基因启动子区域中的几个单核苷酸多态性有关。原发性LI通常在5岁之前不在临床上表现。幼儿的LI通常是由潜在的肠道疾病引起的，比如病毒性胃肠炎,贾第鞭毛虫病,牛乳肠病,乳糜泻或克罗恩病。因此,儿童期的LI大多是短暂的，并且随着潜在病理的解决而改善。LI和牛奶过敏（CMA）之间存在持续的混淆，这仍然导致误诊和不适当的饮食管理。此外,感知到的LI可能会导致不必要的牛奶限制和不良的营养结果。LI的治疗包括减少，但不能完全消除，含乳糖的食物。相比之下,疑似CMA的母乳喂养婴儿应接受严格的无牛乳蛋白母体消除饮食试验.如果婴儿没有母乳喂养，广泛水解或基于氨基酸的配方和严格避免牛奶是CMA的标准治疗方法。大多数患有CMA的婴儿可以耐受乳糖，除非存在继发性乳糖酶缺乏症的肠病。
