A paradoxical increase in resting energy expenditure in malnourished patients near death: the king penguin syndrome

Citation
D. Rigaud et al., A paradoxical increase in resting energy expenditure in malnourished patients near death: the king penguin syndrome, AM J CLIN N, 72(2), 2000, pp. 355-360
Citations number
29
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
AMERICAN JOURNAL OF CLINICAL NUTRITION
ISSN journal
00029165 → ACNP
Volume
72
Issue
2
Year of publication
2000
Pages
355 - 360
Database
ISI
SICI code
0002-9165(200008)72:2<355:APIIRE>2.0.ZU;2-4
Abstract
Background: The metabolic expression of extreme starvation on the verge of death is unknown in humans. Objective: The objective was to compare the resting energy expenditure (REE ) of 5 extremely malnourished dying patients [body mass index (in kg/m(2)): 9.77 +/- 0.1] with that of 16 less-malnourished anorexia nervosa (AN) pati ents. Design: REE was measured by indirect calorimetry and body composition was m easured by anthropometry and dual-frequency bioelectrical impedance analysi s. Fasting serum insulin, thyroid hormone, and catecholamine concentrations were also determined. Results: At the start of refeeding, REE was high in each of the 5 extremely malnourished dying patients, whereas it was low in the 16 AN patients ((x) over bar +/- SD: 5174 +/- 391 kJ/d compared with 3844 +/- 619 kJ/d; P < 0. 05). The high REE value in the 5 extremely malnourished dying patients was associated with almost no fat mass (FM), high urinary nitrogen loss (16.4 /- 2.9 g/d), low serum fatty acid concentrations (0.36 +/- 0.23 mmol/L), an d low or normal serum insulin, thyroid hormone, and catecholamine concentra tions. During the first 2-4 wk of refeeding, REE and nitrogen loss decrease d, whereas fatty acid concentrations increased in each of the 4 surviving p atients; REE and urinary nitrogen output increased in the 16 AN patients. Conclusion: In malnourished persons near death, there is an increase in REE and in protein catabolism. The reason for this increase is unknown but cou ld relate to consumption of the last mobilizable muscle mass and to disease d cellular membranes.