The clinical biochemistry of anorexia nervosa

Abstract

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.

Circulating acylghrelin levels are suppressed by insulin and increase in response to hypoglycemia in healthy adult volunteers

“…In that study, insulin incubation directly inhibited ghrelin secretion through an increase in phosphorylated serine-threonine kinase (AKT) and a reduction in intracellular cAMP. Patients suffering from anorexia nervosa are characterized by low systemic insulin levels and hypoglycemia in concomitance with elevated ghrelin levels (18,19), which are in accordance with our experimental data.…”

“…The protocol was registered at Clinicaltrials.gov (ID NCT01919788). Nine healthy men averagely aged 22.5 (18)(19)(20)(21)(22)(23)(24)(25)(26)(27) years with an average BMI of 23.4 (21.7-26.0) kg/m 2 were recruited in this study. All had a normal physical examination.…”

Study of salivary and serum vaspin and total antioxidants in anorexia nervosa

“…This mechanism in AN is unclear but might be partly mediated by starvation [44,45]. Further explanations relate to dehydration, reduced salivary gland output, malabsorption, anemia, and hormonal disorders [40,46,47]. However, we should consider also the central mechanism of salivary gland activity.…”

Gitelman syndrome DD thiazide diuretics abuse

“…Important differential diagnoses for GS are eating disorders, long-term laxative abuse, TD abuse, renal tubular acidosis and Bartter syndrome (BS) [4][5][6]8,[30][31][32][33]. In order to exclude those differential diagnosis without expensive genetic testing, recurrent examinations are necessary [4].…”

“…Sometimes the creatinine level is elevated [4,35]. TD abuse is often found in cases of eating disorders, weight-loss attempts and sport doping [30][31][32][33][34]36].…”