Severe Anorexia Nervosa Treated with Total Parenteral Nutrition: Clinical Course and Influence on Clinical Chemical Analyses

Croner, S.; Larsson, Jörgen; Schildt, B.; Symreng, Tommy

doi:10.1111/j.1651-2227.1985.tb10955.x

Cited by 15 publications

(5 citation statements)

References 23 publications

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“…On the other hand, increases in transaminases have been reported following the start of nutritional therapy in patients with anorexia without a history of paracetamol consumption (Hutteroth et al, 1977;Croner et al, 1985;Fukusako et al, 1995). Minor increases in transaminases with a return to normal when body weight normalized have been observed in smaller series (Nordgren & von Scheele, 1977;Rivera-Nieves et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Decreased glutathione in patients with anorexia nervosa. Risk factor for toxic liver injury?

et al. 2004

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Lower plasma concentrations of glutathione suggest lower intracellular concentrations of the tripeptide. Higher homocysteine, glycine and glutamine concentrations point to a decreased utilization of these amino acids for glutathione synthesis and an impairment of trans-sulfuration. Consequently, the capacity of patients with anorexia nervosa to detoxify electrophilic metabolites and reactive oxygen species via glutathione may be impaired.

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Section: Discussionmentioning

confidence: 99%

Decreased glutathione in patients with anorexia nervosa. Risk factor for toxic liver injury?

et al. 2004

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“…60 -65 Abnormalities may occur before refeeding 56,64,66,67 and improve as nutrition improves 60,67 or arise during the course of refeeding. 68 These abnormalities are commonly referred to as 'nutritional hepatitis' but the cause is not established. Possible mechanisms include liver hypoperfusion and ischaemia, 63,66 hepatocyte autophagy 69 and depletion of glutathione.…”

Section: Liver Functionmentioning

confidence: 99%

“…60–65 Abnormalities may occur before refeeding 56,64,66,67 and improve as nutrition improves 60,67 or arise during the course of refeeding. 68…”

Section: Liver Functionmentioning

confidence: 99%

The clinical biochemistry of anorexia nervosa

Winston

2012

Ann Clin Biochem

116

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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.

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“…However, for ventilated subjects with moderate levels of phosphate in serum, for patients with severe hypophosphatemia ( ! 0.3 mmol/l), and for cancer or critically ill patients requiring total parenteral nutrition (TPN) for extended periods, the intravenous supplementation of phosphate can be of significant importance [3][4][5] . In these subjects, hypophosphatemia is easily overcome by use of phosphorus additives either as inorganic sodium phosphate or glycerophosphate.…”

Section: Introductionmentioning

confidence: 99%

Glycerophosphate Is Interchangeable with Inorganic Phosphate in Terms of Safety and Serum Pharmacokinetics

et al. 2011

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Objective: The primary aim of the present investigation was to determine and compare the pharmacokinetic (PK) profiles of inorganic phosphate in serum and urine after intravenous administration of sodium glycerophosphate and inorganic sodium phosphate. Additionally, study product safety profiles were evaluated. Subjects and Methods: In total, 27 healthy, white volunteers (17 male/10 female) were enrolled in this double-blinded, randomized, 2-sequence, crossover study and were assigned to receive an organic test drug (sodium glycerophosphate) and an inorganic reference preparation (sodium phosphate) on 2 occasions. Validated analytical methods were used, and concentrations of total inorganic phosphate in serum and urine were determined over 24 h following a single 4-hour continuous intravenous infusion of test and reference drugs at a dose of 80 mmol. Study days were separated by washout periods of 7 days. An analysis of variance, based on population means and 90% confidence intervals (CIs), was used for testing bioequivalence (BE; range 0.8–1.25) between investigational products. Results: The geometric means of the ratio of the point estimates and corresponding 90% CIs for the area under the concentration-versus-time curve of inorganic serum phosphate from 0 to 24 h (AUC_0–24), the phosphate’s maximum concentration in serum (C_max) and the total amount of inorganic phosphate excreted in urine over 24 h corrected for individual baseline values (Ae_{0–24 bc}) were estimated. The test/reference ratios for inorganic phosphate were 1.04 (CI 1.00–1.07), 0.85 (CI 0.84–0.87) and 0.84 (CI 0.77–0.92) for AUC_0–24, C_max in serum and Ae_{0–24 bc} in urine, respectively. Hence, standard BE criteria were met for AUC_0–24 and C_max in serum, while Ae_{0–24 bc} marginally failed to demonstrate BE. After drug administration, a total of 15 subjects reported the occurrence of at least 1 treatment emergent adverse event (AE). All AEs were classified as mild to moderate in severity, and the two treatment groups were equally affected. No serious AEs occurred. Conclusion: The serum PK profiles of inorganic phosphate were almost superimposable following intravenous administration of equimolar doses of test and reference drugs. Thus, we conclude that the two study drugs are essentially similar in terms of serum PK profiles, safety and tolerability.

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Severe Anorexia Nervosa Treated with Total Parenteral Nutrition: Clinical Course and Influence on Clinical Chemical Analyses

Cited by 15 publications

References 23 publications

Decreased glutathione in patients with anorexia nervosa. Risk factor for toxic liver injury?

Decreased glutathione in patients with anorexia nervosa. Risk factor for toxic liver injury?

The clinical biochemistry of anorexia nervosa

Glycerophosphate Is Interchangeable with Inorganic Phosphate in Terms of Safety and Serum Pharmacokinetics

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