Crohn's disease (CD), a type of inflammatory bowel disease (IBD), is a chronic inflammatory disorder that can affect any part of the gastrointestinal (GI) tract and typically causes symptoms such as abdominal pain, diarrhea, and eating disorders. CD can manifest at any age, with up to a quarter of cases diagnosed in childhood. In recent years, the incidence of CD has been increasing in many countries. For example, recent data from Australia show a tenfold increase in the incidence of CD in the first decade of the 21st century. Other reports also demonstrate an increase in the incidence of CD in various countries and indicate that the disease often manifests at a younger age.  The most accepted hypothesis for the pathogenesis of CD is that uncontrolled inflammation in the GI tract is a consequence of a dysregulated immune response to environmental triggers in individuals with a genetic predisposition [1]. Environmental factors include diet and intestinal microflora. Some nutritional factors, such as breastfeeding in infancy, have a protective effect, while others (such as a high-fat diet) are associated with increased risk.

Crohn's disease (CD), a type of inflammatory bowel disease (IBD), is a chronic inflammatory disorder that can affect any part of the gastrointestinal (GI) tract and typically causes symptoms such as abdominal pain, diarrhea, and eating disorders [1]. CD can manifest at any age, with up to a quarter of cases diagnosed in childhood. In recent years, the incidence of CD has been increasing in many countries. For example, recent data from Australia show a tenfold increase in the incidence of CD in the first decade of the 21st century [2]. Other reports also demonstrate an increase in the incidence of CD in various countries and indicate that the disease often manifests at a younger age [3]. The most accepted hypothesis for the pathogenesis of CD is that uncontrolled inflammation in the GI tract is a consequence of a dysregulated immune response to environmental triggers in individuals with a genetic predisposition [1]. Environmental factors include diet and intestinal microflora. Some nutritional factors, such as breastfeeding in infancy, have a protective effect, while others (such as a high-fat diet) are associated with increased risk.  The development of Crohn's disease in children and adolescents is typically associated with weight loss and can lead to impaired linear growth and delayed puberty. Therefore, treatment of Crohn's disease in this age group requires close attention to nutrition, frequent weight and height measurements [1,4]. Exclusive enteral nutrition allows for remission and optimization of nutrition after diagnosis. Enteral nutrition involves the administration of a liquid dietary formula over a period of time as the only method to promote remission [4]. Enteral nutrition has virtually no side effects and ensures a high rate of mucosal healing. However, like all other currently available treatments for Crohn's disease, enteral nutrition does not lead to a cure. 

Crohn's disease is characterized by acute and chronic inflammatory changes in any part of the gastrointestinal tract. Crohn's disease can be distinguished from ulcerative colitis by the location of the disease, the extent of intestinal wall involvement, the focal nature of the lesions, and the presence of noncaseating granulomas [5]. Crohn's disease in childhood is usually extensive, often involving the entire intestine; in more than half of children, the lesion is located proximal to the terminal ileum [1,6]. The initial signs of Crohn's disease may also include perianal, perioral, or extraintestinal manifestations. Many children diagnosed with Crohn's disease experience classic symptoms: diarrhea, abdominal pain, and weight loss. However, others may experience less obvious symptoms, such as lethargy, isolated joint symptoms, or oral abnormalities.  Many studies show that almost all children with Crohn's disease have a history of either weight loss or plateauing in weight gain: in some studies, these features are observed in over 85% of children [1,7]. This likely reflects early satiety or abdominal discomfort after meals. Circulating proinflammatory cytokines [e.g., tumor necrosis factor-α] also contribute to anorexia [8]. Due to weight changes, some children may also experience disturbances in linear growth. These changes in normal growth patterns may exist many months before diagnosis, sometimes preceding the onset of any specific gastrointestinal symptoms [9]. Measuring weight, height, and body mass to assess growth is essential in making a diagnosis. Also important is reviewing the growth history and interpreting linear growth in the context of familial growth patterns. Once a diagnosis is made, close attention to growth patterns and linear growth velocity is required to ensure adequate growth is achieved and subsequently maintained. 

In addition to changes in weight and height, malnutrition and uncontrolled inflammation also lead to delayed pubertal development. [8] In past generations, the cumulative impact of these growth disturbances typically resulted in reduced final adult height. Therefore, assessment of pubertal status in adolescents and calculation of bone age are important aspects of the ongoing treatment of children with celiac disease, beginning at diagnosis. Micronutrient deficiencies are also observed in children with celiac disease. While iron and vitamin 

D deficiencies are most common, vitamin B12, zinc, and selenium levels may also be low. [10] Although the nutritional consequences of celiac disease may be most pronounced at diagnosis (when inflammation is uncontrolled before treatment), these adverse effects can also occur at any subsequent stage. Given that celiac disease can have adverse nutritional consequences in children, it is not surprising that close attention to nutrition is a critical aspect of patient management. Enteral nutrition plays a significant and vital role in reversing many of the negative nutritional consequences of celiac disease in children and achieving remission [4]. Although the primary focus of enteral nutrition is on inducing remission and initial disease control, other benefits may also follow. Furthermore, continued maintenance enteral nutrition after initial enteral feeding may contribute to the maintenance of remission [11,12]. 

Several studies published over the past 15 years have demonstrated the efficacy of enteral nutrition in children with active Crohn's disease. Generally, enteral nutrition induces remission in approximately 85% of patients. A meta-analysis of pediatric studies found that enteral nutrition produced an equivalent response to corticosteroids in children with active Crohn's disease. [13] One Australian study involving 34 children demonstrated clinical remission in 84% and biochemical remission in 76%, with 58% experiencing an early endoscopic response. [14] A portion of this group also underwent small bowel imaging (magnetic resonance enterography) before and after enteral nutrition: three of these 14 children demonstrated complete transmural healing. 

A recent Spanish study evaluated the treatment outcomes of 40 children receiving enteral nutrition. [15] In an intention-to-treat study, remission occurred in 80% of children after 6–8 weeks of enteral feeding. Of the 34 children who completed the full course of enteral feeding, 32 (92.1%) achieved remission.  A retrospective study conducted in the Netherlands assessed the outcomes of enteral feeding in 77 children [16]. Of the children who completed the course of enteral feeding, 71