ObjectivesExclusive enteral feeding reduces inflammation and improves well being, nutrition and growth in children with active Crohn disease. Whether improved growth and increases in growth-related proteins are a consequence of improved nutrition or a reduced inflammation is not known. This

Anti-inflammatory and growth-stimulating effects precede nutritional restitution during enteral feeding in Crohn disease.

Intestinal failure is a specific disease entity resulting from intestinal resection or disease-associated malabsorption and characterized by the inability to maintain protein-energy, fluid, electrolyte or micronutrient balance. We performed a MEDLINE search (1966-2006) to identify relevant articles, using keywords intestinal failure, parenteral or enteral nutrition, intestinal fistula and short bowel syndrome. Causes of intestinal failure are varied, with self-limiting or 'Type 1' intestinal failure occurring relatively commonly following abdominal surgery, necessitating short-term fluid or nutritional support. The rarer, 'Type 2' intestinal failure, is associated with septic, metabolic and complex nutritional complications, usually following surgical resection in patients with Crohn's or mesenteric vascular disease. A multidisciplinary approach to the management of patients with Type 2 intestinal failure is crucial: resolution of sepsis is required before adequate nutritional repletion can be achieved, and it is important to optimize nutritional status, not only through enteral or parenteral supplementation, but also by addressing complications of short bowel syndrome, before considering definitive surgical reconstruction. A structured approach to the management of Type 2 intestinal failure should reduce the likelihood of these complex patients developing 'Type 3' intestinal failure, which is characterized by the need for long-term parenteral nutrition.

https://www.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-2036.2006.02941.x

Review article: intestinal failure

Anorexia nervosa is often characterized by progressive deterioration in many different organ systems. Most medical complications are the result of starvation and can be reversed with a well-planned refeeding program. While some of the complications of anorexia nervosa are predictable physiologic adaptations to the self-imposed starvation, many others are potentially life threatening. It is therefore incumbent upon all primary care physicians to become familiar with this disorder, because it is increasing in incidence and is commonly burdened by substantial chronicity and recidivism.

Medical complications of anorexia nervosa.

In anorexia nervosa, under-nutrition and weight regulatory behaviours such as vomiting and laxative abuse can lead to a range of biochemical problems. Hypokalaemia is the most common electrolyte abnormality. Metabolic alkalosis occurs in patients who vomit or abuse diuretics and acidosis in those misusing laxatives. Hyponatraemia is often due to excessive water ingestion, but may also occur in chronic energy deprivation or diuretic misuse. Urea and creatinine are generally low and normal concentrations may mask dehydration or renal dysfunction. Abnormalities of liver enzymes are predominantly characterized by elevation of aminotransferases, which may occur before or during refeeding. The serum albumin is usually normal, even in severely malnourished patients. Amenorrhoea is due to hypogonadotrophic hypogonadism. Reduced concentrations of free T4 and free T3 are frequently reported and T4 is preferentially converted to reverse T3. Cortisol is elevated but the response to adrenocorticotrophic hormone is normal. Hypoglycaemia is common. Hypercholesterolaemia is a common finding but its significance for cardiovascular risk is uncertain. A number of micronutrient deficiencies can occur. Other abnormalities include hyperamylasaemia, hypercarotenaemia and elevated creatine kinase. There is an increased prevalence of eating disorders in type 1 diabetes and the intentional omission of insulin is associated with impaired metabolic control. Refeeding may produce electrolyte abnormalities, hyper- and hypoglycaemia, acute thiamin depletion and fluid balance disturbance; careful biochemical monitoring and thiamin replacement are therefore essential during refeeding. Future research should address the management of electrolyte problems, the role of leptin and micronutrients, and the possible use of biochemical markers in risk stratification.

https://journals.sagepub.com/doi/pdf/10.1258/acb.2011.011185

The clinical biochemistry of anorexia nervosa.

Among osteotrophic nutrients, proteins play an important role in bone development, thereby influencing peak bone mass. Consequently, protein malnutrition during development can increase the risk of osteoporosis and of fragility fracture later in life. Both animal and human studies indicate that low protein intake can be detrimental for both the acquisition of bone mass during growth and its conservation during adulthood. Low protein intake impairs both the production and action of IGF-I (Insulin-like growth factor-I). IGF-I is an essential factor for bone longitudinal growth, as it stimulates proliferation and differentiation of chondrocytes in the epiphyseal plate, and also for bone formation. It can be considered as a key factor in the adjustments of calcium-phosphate metabolism required for normal skeletal development and bone mineralization during growth. In healthy children and adolescents, a positive association between the amount of ingested proteins and bone mass gain was observed in both sexes at the level of the lumbar spine, the proximal femur and the midfemoral shaft. This association appears to be particularly significant in prepubertal children. This suggests that, like for the bone response to either the intake of calcium or weight-bearing exercise, the skeleton would be particularly responsive to the protein intake during the years preceding the onset of pubertal maturation.

Protein Intake and Bone Growth

Anorexia nervosa (AN) and bulimia nervosa (BN) are potentially fatal eating disorders which primarily affect adolescent females. Differentiating eating disorders from primary gastrointestinal (GI) disease may be difficult. GI disorders are common in eating disorder patients, symptomatic complaints being seen in over half. Moreover, many GI diseases sometimes resemble eating disorders. Inflammatory bowel disease, acid peptic diseases, and intestinal motility disorders such as achalasia may mimic eating disorders. However, it is usually possible to distinguish these by applying the diagnostic criteria for eating disorders and by obtaining common biochemical tests. The primary features of AN are profound weight loss due to self starvation and body image distortion; BN is characterized by binge eating and self purging of ingested food by vomiting or laxative abuse. GI complications in eating disorders are common. Recurrent emesis in BN is associated with dental abnormalities, parotid enlargement, and electrolyte disturbances including metabolic alkalosis. Hyperamylasemia of salivary origin is regularly seen, but may lead do an erroneous diagnosis of pancreatitis. Despite the weight loss often seen in eating disorders, serum albumin, cholesterol, and carotene are usually normal. However, serum levels of trace metals such as zinc and copper often are depressed, and hypophosphatemia can occur during refeeding. Patients with eating disorders frequently have gastric emptying abnormalities, causing bloating, postprandial fullness, and vomiting. This usually improves with refeeding, but sometimes treatment with pro-motility agents such as metoclopromide is necessary. Knowledge of the GI manifestations of eating disorders, and a high index of suspicion for one condition masquerading as the other, are required for the correct diagnosis and management of these patients.

Gastrointestinal and nutritional aspects of eating disorders

Anorexia nervosa (AN) can result in extreme malnutrition, and these patients frequently require inordinately large amounts of calories to gain weight during refeeding therapy. Insulin-like growth factor-I (IGF-I) is a polypeptide that mediates many of the anabolic effects of growth hormone. Low levels of IGF-I have been associated with malnutrition and can cause poor weight gain. To clarify the potential relationship of IGF-I to weight gain, serial serum IGF-I, retinol-binding protein and prealbumin levels were measured at admission, 2 weeks and 4 weeks, in 14 consecutive consenting patients admitted for treatment of AN. Baseline IGF-I levels were lower in the patients compared to age-matched controls (mean 20.8 +/− 2.5 vs 32.9 +/− 2.9 nmol/L, p < 0.01). In patients with no weight gain, IGF-I levels were static. There was a stepwise increment in the IGF-I values related to weight gain. Retinol-binding protein and prealbumin, proteins commonly used to assess nutritional status, did not demonstrate importan...

L L Humphries

Papers

Gastrointestinal and nutritional aspects of eating disorders

Serum insulin-like growth factor-I concentrations in the recovery of patients with anorexia nervosa.