Persistent inflammation and immune activation contribute to cholestasis inpatients receiving home parenteral nutrition

Citation
Jm. Reimund et al., Persistent inflammation and immune activation contribute to cholestasis inpatients receiving home parenteral nutrition, NUTRITION, 17(4), 2001, pp. 300-304
Citations number
21
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
NUTRITION
ISSN journal
08999007 → ACNP
Volume
17
Issue
4
Year of publication
2001
Pages
300 - 304
Database
ISI
SICI code
0899-9007(200104)17:4<300:PIAIAC>2.0.ZU;2-7
Abstract
Liver disease is frequent in patients taking home parenteral nutrition (HPN ). but its cause remains unclear. Ongoing inflammation was implicated in HP N-associated cholestasis, so we examined the relation between liver-enzyme concentrations and circulating inflammatory and immune markers in these pat ients, in 17 HPN patients and 10 age- and sex-matched control subjects, we examined erythrocyte sedimentation rate, blood neopterin, soluble interleuk in (IL)-2 receptors, circulating tumor necrosis factor-alpha, IL-6, asparta te and alanine aminotransferases, alkaline phosphatases, and gamma -glutamy ltranspeptidase (GGT) concentrations. Fourteen of 17 patients had abnormal liver function tests with an increase in alkaline phosphatases (P < 0.001), gamma -glutamyltranspeptidase (P < 0.01), and aspartate aminotransferase ( P < 0.01). Alkaline phosphatases were positively correlated to erythrocyte sedimentation late, neopterin, tumor necrosis factor-alpha, and IL-6, gamma -Glutamyltranspeptidase was positively linked to tumor necrosis facotr-alp ha and soluble IL-2 receptors. There was no link between aminotransferases and inflammatory parameters. Liver-enzyme concentrations were correlated to the amount of total intravenous calories and calories originating from car bohydrates but not to infused lipids (median infused lipids . kg(-1) body w eight . d(-1) = 0.62 g) in contrast to recently published data. Our results confirmed that the number of infused calories contributes to liver toxicit y in HPN patients and strongly suggested that sustained inflammation is pro bably a key factor in worsening HPN-associated cholestasis. (C) Elsevier Sc ience Inc. 2001.