Comparison of clinical, clinicopathologic, and histologic variables in dogs with chronic inflammatory enteropathy and low or normal serum 25‐hydroxycholecalciferol concentrations

Abstract

Background The cause of low serum vitamin D concentrations in dogs with chronic inflammatory enteropathy (CIE) is not well understood. Objective Improve understanding of pathogenesis of low serum vitamin D concentrations in dogs with CIE by comparing several clinical, clinicopathologic, and histologic variables between CIE dogs with low and normal serum 25‐hydroxyvitamin D concentrations (25[OH]D). Animals Fifteen dogs with CIE and low serum 25[OH]D concentrations; 15 dogs with CIE and normal serum 25(OH)D concentrations. Methods Prospective cohort study. Clinical and clinicopathologic variables were compared between groups. Correlations between serum 25(OH)D concentration and histopathologic variables were assessed. Results Dogs with CIE and low serum 25(OH)D concentrations had higher canine chronic enteropathy clinical activity index scores (P = .003), lower serum α‐tocopherol (P < .001), cholesterol (P < .001), and albumin (P < .001) concentrations and higher serum C‐reactive protein (P = .004) concentrations compared to CIE dogs with normal serum 25(OH)D concentrations. Serum concentrations of vitamin D‐binding protein (VDBP) were not different between groups (P = .91). Duodenal morphologic and inflammatory histopathological scores (P = .002 and P = .004, respectively) and total histopathological scores in duodenum and combined duodenum and ileum negatively correlated with serum 25(OH)D concentration. Conclusions and Clinical Importance The pathogenesis of low serum vitamin D concentrations in dogs with CIE is likely multifactorial. Fat malabsorption deserves further study in dogs with low serum vitamin D concentration and CIE. Loss of VDBP does not appear to be an important cause of low serum vitamin D concentration in dogs with CIE.

Coagulation status, fibrinolysis, and platelet dynamics in dogs with chronic inflammatory enteropathy

“…Both CIE-N and CIE-PLE dogs had higher MA, lower LY30, lower LY60, and longer CLT compared to HC (Table 2) Median CCECAI score for CIE dogs was 9 (range, 2-19). Median CCECAI scores for CIE-PLE and CIE-N dogs were 11.5 (range, [5][6][7][8][9][10][11][12][13][14][15][16][17] and 8 (range, 2-19), respectively. The CIE dogs had a median serum 27 as well as a decrease in fibrinolysis activators (such as tPA) 28 have been described.…”

“…Previous studies in dogs with chronic small intestinal disease have identified an association between decreased serum 25(OH)D concentrations and increases in intestinal inflammation and markers of systemic inflammation. 14,15 Therefore, the inflammatory state in dogs with CIE may be contributing to the decrease in 25(OH)D concentrations and the increase in MA, prompting the relationship between them.…”

“…[11][12][13] Decreased serum 25-hydroxyvitamin D (25[OH]D) concentrations also have been reported in dogs with chronic gastrointestinal disease, especially dogs with PLE. [14][15][16][17] Alterations of the coagulation system identified in humans with IBD include decreases in anticoagulant factors, increases coagulation factors, increased platelet aggregation, hypofibrinolysis, and alterations in TEG variables. 5,18 Platelet aggregation and fibrinolysis have not been evaluated in dogs with CIE with and without PLE.…”

Association between vitamin D metabolites, vitamin D binding protein, and proteinuria in dogs

“…affect 25(OH)D status 35,36 44 In rats, urinary VDBP was shown to potentially be a biomarker for tubulointerstitial disease. 49 A recent study evaluated the use of urinary VDBP as a biomarker of renal tubular injury in dogs.…”

“…[53][54][55] Decreased vitamin D status previously has been correlated with hypoalbuminemia in dogs with chronic enteropathies. 36,56 Loss of albumin complexed with 25(OH)D partially may explain this finding, but given that only about 10% to 15% of 25(OH)D is bound to albumin in the circulation, it seems more likely that it is simply a reflection of general protein loss, including VDBP and its complexed vitamin D metabolites, rather than a causal link between albumin loss and hypovitaminosis D. Low vitamin D status also could affect albumin by its effects on inflammation. 57,58 Thus, the lack of vitamin D's immunomodulation actually may result in hypoalbuminemia, independent of urinary loss of albumin.…”