Exocrine pancreatic insufficiency (EPI) in dogs is diagnosed by observing serum canine trypsin-like immunoreactivity (cTLI) to be less than 2.5 µg/L; affected dogs have severe fat malabsorption. Some dogs with signs of EPI have marginally subnormal serum cTLI (3–6 µg/L) and do not respond to enzyme replacement therapy (subclinical EPI, SEPI), but given their clinical signs, abnormal serum cobalamin or folate, and absence of other detectable non-enteric disease presumably have an idiopathic chronic enteropathy (ICE). Unpublished preliminary data indicate decreased serum tocopherol concentrations in dogs with EPI that do not resolve after pancreatic enzyme supplementation. The objectives of this study were to measure serum tocopherol and retinol in dogs with EPI and those with subclinical EPI and ICE (SEPI/ICE).

Inclusion criteria for the EPI group (n=8) were clinical signs of EPI and serum cTLI concentrations <2.5 µg/L. Dogs in the SEPI/ICE group (n=9) had clinical signs of ICE and serum cTLI concentrations in the 3.0–6.0 µg/L range. Diets of dogs in both groups were supplemented with oral pancreatic enzyme extract. Control samples were collected from 10 healthy dogs before and after 10 days of pancreatic enzyme supplementation. All samples were surplus from another study approved by our institutional ethics committee, and stored at -80 C prior to assay of tocopherol and retinol by high-performance liquid chromatography.

Dogs with EPI and SEPI/ICE had significantly lower serum concentrations of tocopherol (means 14.02 and 16.66 μg/mL; p=0.015 and p=0.0002 respectively) and retinol (means 509 and 673.78 ng/mL; p=0.0003 and 0.004, respectively) than enzyme-supplemented control dogs (means 41.6 μg/mL and 1124.86 ng/mL, respectively). Neither tocopherol nor retinol concentrations were significantly different between the EPI and SEPI/ICE groups, nor were there differences between the control dogs before and after enzyme supplementation.

These findings indicate that dogs with EPI and SEPI/ICE have relative deficiencies in tocopherol and retinol, likely reflecting fat malabsorption, and may share a similar enteropathy that may precede the onset of EPI. The clinical significance of these decreased fat soluble vitamin concentrations is unknown though retinol has been shown to influence enteric mucosal immune responses though its effects on T-cell differentiation, IgA secretion in GALT, and homing of innate lymphoid cells to the gut. Tocopherol is an important antioxidant and studies have revealed increased reactive oxygen species in intestinal biopsies from humans with IBD.

Clinical trials to assess the value of tocopherol and retinol supplementation in dogs with EPI and ICE are warranted.

Disclosures

Disclosures to report.
David Williams is a consultant with IDEXX Laboratories and the GI Laboratory at Texas A&M University, and is involved in a collaborative research study with Nestle-Purina. He is a member of the Nestle-Purina Advisory Board.