title: Effect of early enteral nutrition on intestinal permeability, intestinal protein loss, and outcome in dogs with severe parvoviral enteritis.
abstract: A randomized, controlled clinical trial investigated the effect of early enteral nutrition (EN) on intestinal permeability, intestinal protein loss, and outcome in parvoviral enteritis. Dogs were randomized into 2 groups: 15 dogs received no food until vomiting had ceased for 12 hours (mean 50 hours after admission; NPO group), and 15 dogs received early EN by nasoesophageal tube from 12 hours after admission (EEN group). All other treatments were identical. Intestinal permeability was assessed by 6-hour urinary lactulose (L) and rhamnose (R) recoveries (%L, %R) and L/R recovery ratios. Intestinal protein loss was quantified by fecal alpha1-proteinase inhibitor concentrations (alpha1-PI). Median time to normalization of demeanor, appetite, vomiting, and diarrhea was 1 day shorter for the EEN group for each variable. Body weight increased insignificantly from admission in the NPO group (day 3: 2.5 +/- 2.8%; day 6: 4.3 +/- 2.3%; mean +/- SE), whereas the EEN group exhibited significant weight gain (day 3: 8.1 +/- 2.7%; day 6: 9.7 +/- 2.1%). Mean urinary %L was increased, %R reduced, and L/R recovery ratios increased compared to reference values throughout the study for both groups. Percent lactulose recovery decreased in the EEN group (admission: 22.6 +/- 8.0%; day 6: 17.9 +/- 2.3%) and increased in the NPO group (admission: 11.0 +/- 2.6%; day 6: 22.5 +/- 4.6%, P = .035). Fecal alpha1-PI was above reference values in both groups and declined progressively. No significant differences occurred for %R, L/R ratios, or alpha1-PI between groups. Thirteen NPO dogs and all EEN dogs survived (P = .48). The EEN group showed earlier clinical improvement and significant weight gain. The significantly decreased %L in the EEN versus NPO group might reflect improved gut barrier function, which could limit bacterial or endotoxin translocation.
authors.affiliation: Department of Companion Animal Clinical Studies, Faculty of Veterinary Science, University of Pretoria, Onderstepoort, South Africa. bmohr@rossvet.edu.kn
authors.forename: Albert J
authors.initials: AJ
authors.lastname: Mohr
authors.forename: Andrew L
authors.initials: AL
authors.lastname: Leisewitz
authors.forename: Linda S
authors.initials: LS
authors.lastname: Jacobson
authors.forename: Jörg M
authors.initials: JM
authors.lastname: Steiner
authors.forename: Craig G
authors.initials: CG
authors.lastname: Ruaux
authors.forename: David A
authors.initials: DA
authors.lastname: Williams
mesh_terms: D000818:Animals; D001835:Body Weight; D004283:Dog Diseases / Q000378:metabolism / Q000628:therapy* / Q000821:virology; D004285:Dogs; D004750:Enteral Nutrition / Q000662:veterinary*; D004751:Enteritis / Q000378:metabolism / Q000628:therapy / Q000662:veterinary* / Q000821:virology; D005243:Feces / Q000201:enzymology; D005260:Female; D007792:Lactulose / Q000652:urine; D008297:Male; D010322:Parvoviridae Infections / Q000378:metabolism / Q000628:therapy / Q000662:veterinary* / Q000821:virology; D017993:Parvovirus, Canine / Q000254:growth & development*; D012210:Rhamnose / Q000652:urine; D012709:Serum Albumin / Q000378:metabolism; D018709:Statistics, Nonparametric; D000515:alpha 1-Antitrypsin / Q000378:metabolism
chemical_list: D012709:Serum Albumin; D000515:alpha 1-Antitrypsin; D007792:Lactulose; D012210:Rhamnose