BackgroundIntestinal lymphangiectasia (IL), a type of protein-losing enteropathy (PLE), is a dilatation of lymphatic vessels within the gastrointestinal tract. Dietary fat restriction previously has been proposed as an effective treatment for dogs with PLE, but limited objective clinical data are available on the efficacy of this treatment.Hypothesis/ObjectivesTo investigate the clinical efficacy of dietary fat restriction in dogs with IL that were unresponsive to prednisolone treatment or showed relapse of clinical signs and hypoalbuminemia when the prednisolone dosage was decreased.AnimalsTwenty-four dogs with IL.MethodsRetrospective study. Body weight, clinical activity score, and hematologic and biochemical variables were compared before and 1 and 2 months after treatment. Furthermore, the data were compared between the group fed only an ultra low-fat (ULF) diet and the group fed ULF and a low-fat (LF) diet.ResultsNineteen of 24 (79%) dogs responded satisfactorily to dietary fat restriction, and the prednisolone dosage could be decreased. Clinical activity score was significantly decreased after dietary treatment compared with before treatment. In addition, albumin (ALB), total protein (TP), and blood urea nitrogen (BUN) concentration were significantly increased after dietary fat restriction. At 2 months posttreatment, the ALB concentrations in the ULF group were significantly higher than that of the ULF + LF group.Conclusions and Clinical ImportanceDietary fat restriction appears to be an effective treatment in dogs with IL that are unresponsive to prednisolone treatment or that have recurrent clinical signs and hypoalbuminemia when the dosage of prednisolone is decreased.
Objectives
To compare initial treatment with and without corticosteroids for acute pancreatitis in dogs and investigate the therapeutic efficacy and prognosis.
Materials and Methods
Sixty‐five dogs were included in this non‐blinded, non‐randomised clinical study. Dogs with acute pancreatitis received treatment either with dose of 1 mg/kg/day prednisolone (n=45) or without prednisolone (n=20). Response to treatment was based on changes in the C‐reactive protein concentration, improvement in clinical signs, duration of hospitalisation, mortality and recurrence rate.
Results
From the third day of hospitalisation, C‐reactive protein concentration was significantly lower in the prednisolone group than that in the non‐prednisolone group. The number of days required to reach a C‐reactive protein concentration of <2 mg/dL and clinical score of ≤2 was significantly lower in the prednisolone group. The mortality rate 1 month after discharge was significantly lower in the prednisolone group (11.3% versus 46.1%).
Clinical Significance
In dogs with acute pancreatitis, initial treatment with prednisolone resulted in earlier reductions in C‐reactive protein concentration and earlier improvement of clinical signs.
Background
Nucleotide Oligomerization Domain Two (NOD2) is suggested to be an intracellular pathogen‐associated molecular pattern recognition molecule. NOD2, plays a key role against bacteria by triggering a host defense response through activation of the transcription factor NFkappaB and subsequent proinflammatory cytokine production. NOD2 recently was reported to be overproduced in inflamed colonic mucosa in Crohn's disease, and to be accompanied by a significant increase in NFkappaB activity. However, few studies to date have investigated intercellular signaling molecules in dogs with lymphocytic plasmacytic colitis (LPC).
Hypothesis
NOD2 mRNA expression and NFkappaB activation are increased in mucosal biopsies of LPC dogs as compared with control dogs.
Animals
Five healthy dogs and 19 dogs with LPC.
Methods
Descending colon biopsies were obtained endoscopically. Expression of NOD2 mRNA was evaluated by semiquantitative RT‐PCR in the colonic mucosa. NFkappaB binding activity was assessed by electrophoretic mobility shift assay.
Results
NOD2 mRNA expression was approximately 63% greater in LPC dogs than in healthy controls (P = .019). NFkappaB binding activity was approximately 45% higher in the inflamed colonic mucosa of the LPC dogs, as compared with healthy controls (P = .011). No correlations were observed among NOD2 mRNA expression levels, NFkappaB binding activity, and CIBDAI in LPC dogs.
Conclusions and Clinical Importance
NOD2 mRNA and NFkappaB activity were significantly higher in the inflamed colon of dogs with LPC, as compared with healthy controls. Our data suggest that NOD2 and NFkappaB play an important role in the pathogenesis of LPC.
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