BACKGROUND:Vitamin D modulates the immune response in many species, including dogs. To date, research investigating the immunological effects of vitamin D in dogs is limited to in vitro studies. OBJECTIVES:Provide PO calcifediol supplementation to healthy dogs to evaluate its tolerability and assess its effect on leukocyte production of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-10. ANIMALS:Eleven healthy client-owned dogs with serum 25-hydroxyvitamin-D3 (25(OH)D3) concentrations ≤ 30 ng/mL. METHODS:Prospective, randomized, double-blinded, placebo-controlled crossover study. Dogs were randomized to receive calcifediol at 2.3 μg/kg0.75 (low-dose), 4.6 μg/kg0.75 (high-dose), or placebo for 7 days and crossed over to a different treatment arm after 28-day washout periods. Serum 25(OH)D3 was measured using a modified high-performance liquid chromatography method. Whole blood cultures were performed by incubating blood with lipopolysaccharide (LPS), lipoteichoic acid (LTA), or phosphate-buffered saline (PBS) for 24 h, and TNF-α, IL-6, and IL-10 were measured in supernatant using a canine-specific multiplex assay. RESULTS:Both low-dose (median, interquartile range [IQR]; 62 ng/mL, 59-82) and high-dose (93 ng/mL, 80-113) PO calcifediol supplementation increased serum 25(OH)D3 concentrations from baseline (22.2 ng/mL, 20.3-29.3; both p < 0.0001). Low-dose and high-dose calcifediol supplementation decreased LPS-stimulated IL-6 by 197 pg/mL (95% confidence interval [CI]: -369.0 to -24.0; p = 0.03) and 182 pg/mL (95% CI: -355.0 to -8.0; p = 0.04), respectively. Then LPS-stimulated IL-6 concentrations decreased by 2 pg/mL for every 1 ng/mL increase in serum 25(OH)D3 concentration (95% CI: -3.0 to -0.1; p = 0.03). CONCLUSION AND CLINICAL IMPORTANCE:Calcifediol supplementation for 7 days was well-tolerated and decreased LPS-stimulated IL-6 concentrations. Oral calcifediol supplementation may have anti-inflammatory effects in dogs.

The management of diabetes mellitus (DM) in cats can benefit from an integration of medical and nutritional strategies, based on an understanding of the dynamic nature of the disease, together with an appreciation of the interrelationships between nutritional status and clinical status. In this context, a new classification system for feline DM is proposed, comprising three clinical status categories: those at risk of developing DM, those with clinical DM and those in diabetic remission. The influence of individual dietary components (carbohydrate, protein, fat and water fractions) on clinical outcomes is discussed, followed by overarching principles for the dietary management of diabetic cats, based on both the limited scientific evidence and the clinical experience of the authors. Key aspects of nutritional assessment, the principles of therapeutic weight reduction and feeding practices are covered. Using the classification framework, recommendations for nutritional management are proposed for cats at risk of development of DM, cats with clinical DM and those in clinical remission. Successful implementation of these recommendations can be achieved by using a relationship-centred approach, where owner concerns are addressed and goals for management are agreed in partnership. It is hoped that these perspectives will help guide veterinary professionals in their clinical management decisions, thereby improving health outcomes in cats in all three categories of DM.

Naturally occurring diabetes mellitus (NODM) is one of the most common endocrine disorders in dogs and its etiology closely resembles type 1 diabetes mellitus (T1DM) in people. Human patients with T1DM commonly have cellular derangements consistent with inflammation, impaired immune function, and hypovitaminosis D. There is little information available regarding inflammatory biomarkers, immune function, and vitamin D status in diabetic dogs. Therefore, our objectives were to assess inflammatory biomarkers, vitamin D metabolites, and phagocytic capacity in diabetic dogs and determine whether associations exist with these variables and the level of clinical control or vitamin D metabolites. This was a prospective case–control study that included 20 otherwise healthy diabetic dogs (clinically controlled, n = 10; uncontrolled, n = 10) and 20 non-diabetic, healthy, age (± 2 years), breed, and sex matched controls. Complete blood count, biochemical panel, urinalysis, and fructosamine were performed at a single commercial reference laboratory. Basal plasma tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-8, and IL-10 were measured using a canine-specific multiplex bead-based assay. Serum C-reactive protein (CRP) was measured using a commercially available ELISA kit. Serum 25-hydroxyvitamin (OH)D3 and 24,25-dihydroxyvitamin (OH)2D3 were measured with HPLC. Phagocytosis of opsonized-Escherichia coli (E. coli) was evaluated with flow cytometry. Diabetic dogs had higher serum CRP concentrations than controls (p = 0.02). Plasma IL-8 concentrations were higher in diabetic dogs with uncontrolled clinical disease compared to controls (p = 0.02). Diabetic dogs had a lower percentage of leukocytes that phagocytized opsonized-E. coli (p = 0.02), but an increased number of bacteria phagocytized per cell (p < 0.001) compared to controls. No between-group differences were identified in vitamin D metabolites, nor were associations found between vitamin D and any variables. Fructosamine had a positive association with serum CRP concentration (rho = 0.35, p = 0.03) and number of bacteria phagocytized per cell (rho = 0.45, p = 0.004) in our cohort (n = 40). Like people with T1DM, diabetic dogs have a proinflammatory phenotype and phagocytic dysregulation that may be correlated with glycemic control.

Human patients with type 1 diabetes mellitus (T1DM) are susceptible to several long-term complications that are related to glycemic control and immune dysregulation. Immune function remains relatively unexplored in dogs with naturally occurring diabetes mellitus (NODM). Calcitriol improves various aspects of immune function in a variety of species, but its effect in diabetic dogs remains unexplored. Therefore, the objectives of this study were to (i) evaluate immune function in dogs with NODM and determine if differences exist based on the level of clinical control and (ii) assess the immunomodulatory effects of calcitriol. Twenty diabetic dogs (clinically controlled, n = ten, not controlled, n = ten) and 20 non-diabetic, healthy control dogs were included in this prospective, case–control study. Whole blood was incubated with calcitriol (10−7 M) or negative control, after which the samples were divided for phagocytosis and leukocyte cytokine response experiments. The phagocytosis of opsonized Escherichia coli (E. coli) was evaluated with flow cytometry. The samples for leukocyte cytokine response evaluations were stimulated with lipopolysaccharide (LPS), lipoteichoic acid (LTA), or phosphate buffer solution (PBS; negative control), and tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-8, and IL-10 were measured in supernatant using a canine-specific multiplex bead-based assay. The leukocytes from diabetic dogs produced higher concentrations of IL-10 (p = 0.01), IL-6 (p < 0.0001), and IL-8 (p < 0.0001) than the control dogs while controlling for the intervention and stimulant. Calcitriol decreased the supernatant concentrations of TNF-α (p < 0.001) and IL-8 (p = 0.04) with concomitant increases in IL-6 (p = 0.005). Diabetic dogs had a lower percentage of leukocytes undergoing phagocytosis (p < 0.0001) but a higher number of bacteria phagocytized per cell (p = 0.001) when compared to the control dogs. Calcitriol had no effect on phagocytic capacity. Lastly, the status of clinical control in diabetic dogs did not yield differences in immune function. These results support that dogs with NODM exhibit immune dysregulation and warrant additional investigation.

BackgroundVitamin D deficiency and excess in clinically presented cats conventionally is diagnosed by comparison of patient plasma 25-hydroxyvitamin D (25 (OH)D) concentration with plasma reference intervals determined in healthy adult cats. For immature cats, validity of this vitamin D status assessment method is uncertain.ObjectiveThe overall objective was determination of whether plasma concentration of 25 (OH) D and other vitamin D metabolites in immature cats markedly change with developmental age as has been reported in other species.MethodsFour male and 4 female domestic short-hair kittens from weaning were continuously presented a single nutritionally adequate growth-diet. Concentrations of 25 (OH) D and 24,25-dihydroxyvitamin D (24,25 (OH)2D), and calcitriol were quantified in plasma of jugular venous blood collected at 12, 15, 18, and 21 weeks and 1 year of age. Plasma was liquid and solid-phase extracted and fractionation by normal-phase HPLC, and 25 (OH) D and 24,25 OH)2D quantified by reverse-phase HPLC-UV and calcitriol by RIA.ResultsPlasma 3-epi-25 (OH) D and 25 (OH) D concentrations increased (p < 0.001) with age so that by study end the concentrations rose by 1-and 2-fold, respectively. Concentrations of 3-epi-25 (OH) D relative to 25 (OH) D were 30% at 12 weeks and 20% at 1 year. Between ages 12 and 21 weeks, rises in 25 (OH) D concentration were positively correlated with body weight gains (ρ = 0.952, p < 0.001) and 24,25 (OH)2D concentrations were consistently greater than 25 (OH) D concentrations (p < 0.001). At 1 year of age, concentrations of 24,25 (OH)2D declined below those of 25 (OH) D and 3-epi-24,25 (OH)2D consistency occurred in low concentrations. Vitamin D2 metabolites and sex differences in metabolite concentrations were not observed.ConclusionReliance on quantification of plasma 25 (OH) D concentration for vitamin D status assessment in kittens may be confounded by developmental changes in 25 (OH) D independent of vitamin D intake. High 24,25 (OH)2D concentration and occurrence of 3-epi-25 (OH) D in plasma additionally may interfere with the quantification.

Abstract Background Serum 25‐hydroxyvitamin (OH)D, C‐reactive protein (CRP), and haptoglobin are useful biomarkers in various infectious diseases and inflammatory disorders in dogs, but their utility in histoplasmosis is unknown. Objective Determine if serum 25(OH)D, CRP, and haptoglobin concentrations are different in dogs with histoplasmosis compared to healthy controls and whether serum globulin, albumin, CRP, or haptoglobin are associated with 25(OH)D concentration. Animals Twenty‐two client‐owned dogs (histoplasmosis, n = 12; controls, n = 10). Methods Prospective case‐control study. Dogs with histoplasmosis were categorized as pulmonary, disseminated, or gastrointestinal (GI) tract. Serum 25(OH)D was measured using modified high‐performance liquid chromatography (HPLC). Serum CRP and haptoglobin were measured with ELISA assays. Results Dogs with histoplasmosis were grouped as disseminated (n = 8) and GI tract (n = 4). No dogs had pulmonary tract involvement alone. Dogs with histoplasmosis (median, interquartile range [IQR]; 11.6 ng/mL, 16.8) had lower serum 25(OH)D concentrations than controls (35.7 ng/mL, 17.6; P < .001). Serum CRP and haptoglobin concentrations were higher in dogs with histoplasmosis (CRP: median, IQR; 63.5 mg/L, 37.1 and haptoglobin: 459.7 mg/dL, 419.6) than controls (CRP: 1.9 mg/L, 2; P < .001 and haptoglobin: 85.5 mg/dL, 106.7; P = .003). Serum 25(OH)D concentration was positively associated with fold change in serum albumin concentration (ρ = 0.77; P < .001), and negatively associated with fold change in serum globulin (ρ = −0.61; P = .003) and CRP concentrations (ρ = −0.56; P = .01). Conclusion and Clinical Importance Assay of serum 25(OH)D, CRP, and haptoglobin could have clinical value in dogs with histoplasmosis.

Abstract Background Clinicopathologic variables predictive of disseminated coccidioidomycosis are known in humans but have not been explored in dogs. Serum 25‐hydroxyvitamin (OH)D correlates with severity of disease of various etiologies in dogs but its role in coccidioidomycosis is unknown. Objective Determine whether serum 25(OH)D concentrations are different in dogs with coccidioidomycosis compared with healthy controls and if clinicopathologic variables are associated with extent of disease. Animals Thirty‐five dogs with coccidioidomycosis (pulmonary, n = 13; disseminated, n = 15; uncharacterized, n = 7), and 25 healthy control dogs. Methods Prospective cohort study. Serum 25(OH)D and C‐reactive protein (CRP) concentrations were measured with modified‐HPLC and a commercial ELISA kit, respectively. Results There was no difference in 25(OH)D concentrations between dogs with coccidioidomycosis (median, interquartile range [IQR]; 31.9 ng/mL, 23.3‐49.2) and controls (29.5 ng/mL, 25.6‐40.8, P = .73). Serum 25(OH)D concentration was lower in dogs with coccidioidomycosis and IgG titers ≥1:32 than dogs with titers below this cut‐off (P = .02). Dogs with IgG titers ≥1:32 were more likely to have disseminated disease (OR, 7.5; 95% CI: 1.1‐68; P = .03). Serum CRP concentrations were higher in dogs with IgG titers ≥1:16 (median, IQR; 4474.8 ng/mL, 2885.8‐8236.1) than in those below this cut‐off (151.2 ng/mL, 30.4‐2907.3; P = .02). There was a significant inverse association between serum 25(OH)D and CRP at 25(OH)D concentrations ≤33 ng/mL. Conclusion and Clinical Importance Serum 25(OH)D concentration was lower for dogs with IgG titers ≥1:32, indicating a potential association between semi‐quantitative titers and 25(OH)D concentrations in dogs with coccidioidomycosis. IgG titers ≥1:32 yielded higher odds of disseminated disease, but was inadequate as a standalone test to determine form of disease.

BackgroundTaurine status is impacted by dietary supply of methionine and cysteine (SAA) and possibly intestinal microbial activity, where plasma and whole blood taurine concentrations are currently used to evaluate taurine status.ObjectiveWe determined effects of dietary SAA restriction on rate and extent of taurine depletion of blood and skeletal muscle in dogs of two body sizes, and whether oral antibiotic administration affected the taurine depletion and fecal bile acid excretion of the dogs.MethodsAdult, male, Beagles (n = 6; 10.1–13.1 kg) and larger mixed-breed dogs (n = 6; 28.5–41.1 kg) were given four dry-expanded diets, whereby each successive diet contained lower protein and/or SAA concentration. After receiving the final diet for 44 weeks, all dogs were orally administered a mixture of ampicillin, neomycin sulfate, and metronidazole for 12 weeks. Taurine concentrations were determined every 2–4 weeks in venous blood and voided urine and every 4 to 16 weeks in biopsied semimembranosus muscle. Fecal bile acid excretion before and after antibiotics administration were quantified.ResultsWhen given for 36 weeks the lowest SAA diet, 3.4% methionine and 2.9% cystine, taurine concentrations in whole blood were not different between groups, while taurine in plasma declined (P < 0.05) in large but not in small dogs, and taurine in biopsied muscle decreased (P < 0.05) by 50% in large and by 37% in small dogs. Concentrations of taurine in muscle were lower (P < 0.01) and fecal bile acids greater (P = 0.001) in large than small dogs. Antibiotic administration restored plasma and muscle taurine to initial concentrations and halved fecal bile acid excretion by dogs of both groups.ConclusionsBlood taurine concentration may not be a sensitive indictor of taurine depletion caused by low intake of bioavailable SAA in dogs, especially in large dogs. Taurine status and dietary SAA requirements of dogs may substantively depend on taurine loss mediated by intestinal microbiota.

Objectives The study aimed to evaluate the safety and effectiveness of vitamin D supplementation with dietary 25-hydroxyvitamin D 3 (25[OH]D 3 ) in adult cats. Methods Three levels of dietary 25(OH)D 3 concentrations (4.9, 8.4, 11.8 µg/kg as fed) were received by five adult cats for 9 weeks, each in a randomized complete block design. Effects were determined on plasma or serum concentrations of 25(OH)D 3 , 24,25-dihydroxyvitamin D 3 , calcitriol, parathyroid hormone, ionized calcium, urinary excretions of phosphorus, calcium and magnesium, and clinical hematology and chemistry panels. Results The lowest concentration of dietary 25(OH)D 3 supported elevation of vitamin D status, with no adverse effects. Supplementation of 8.4 µg/kg 25(OH)D 3 had significant effects on the urinary magnesium: creatinine ratio. Increasing supplementation up to 11.8 µg/kg 25(OH)D 3 had significant effects on plasma concentrations of calcium and magnesium, and vitamin D metabolites. Conclusions and relevance Dietary supplementation with approximately 5.0 µg/kg of 25(OH)D 3 or the ingested equivalence of 0.09 µg of 25(OH)D 3 per metabolic body weight (kg 0.67 ) is a safe, potent and effective means for raising vitamin D status in cats. A higher dose with approximately 11.8 µg/kg of 25(OH)D 3 resulted in elevation in C-3 epimers of 25(OH)D 3 and slight elevation in plasma magnesium and calcium concentrations above their respective reference intervals. Keywords 25-Hydroxyvitamin D , 24,25-dihydroxyvitamin D , C-3 epimer , urine , calcium , phosphorus , magnesium

OBJECTIVES:The study aimed to evaluate the safety and effectiveness of vitamin D supplementation with dietary 25-hydroxyvitamin D3 (25[OH]D3) in adult cats. METHODS:Three levels of dietary 25(OH)D3 concentrations (4.9, 8.4, 11.8 µg/kg as fed) were received by five adult cats for 9 weeks, each in a randomized complete block design. Effects were determined on plasma or serum concentrations of 25(OH)D3, 24,25-dihydroxyvitamin D3, calcitriol, parathyroid hormone, ionized calcium, urinary excretions of phosphorus, calcium and magnesium, and clinical hematology and chemistry panels. RESULTS:The lowest concentration of dietary 25(OH)D3 supported elevation of vitamin D status, with no adverse effects. Supplementation of 8.4 µg/kg 25(OH)D3 had significant effects on the urinary magnesium: creatinine ratio. Increasing supplementation up to 11.8 µg/kg 25(OH)D3 had significant effects on plasma concentrations of calcium and magnesium, and vitamin D metabolites. CONCLUSIONS AND RELEVANCE:Dietary supplementation with approximately 5.0 µg/kg of 25(OH)D3 or the ingested equivalence of 0.09 µg of 25(OH)D3 per metabolic body weight (kg0.67) is a safe, potent and effective means for raising vitamin D status in cats. A higher dose with approximately 11.8 µg/kg of 25(OH)D3 resulted in elevation in C-3 epimers of 25(OH)D3 and slight elevation in plasma magnesium and calcium concentrations above their respective reference intervals.

Feline vitamin D status is based on dietary consumption but metabolism of this essential nutrient and the efficacy of supplementation forms are poorly described in cats. The aim of this study was to further elucidate the metabolites of vitamin D 2 in cats and to compare the effectiveness of vitamin D 2 and 25(OH)D 2 for increasing feline vitamin D status. Eight adult male castrated domestic shorthair cats received vitamin D 2 or 25(OH)D 2 in a single crossover design. Vitamin D 2 was dosed daily in a molar equivalent dosage to vitamin D 3 ingested in the diet while 25(OH)D 2 was provided at a daily dose of 20% molar equivalent intake of dietary vitamin D 3 based on its expected higher potency. Plasma concentrations of 25-hydroxyvitamin D epimers were evaluated at baseline then every 2 weeks for a total of 10 weeks. Analysis of multiple vitamin D metabolite concentrations was completed at the end of each supplementation period, followed by a washout period preceding the second phase of the crossover trial. Results showed that supplementation with 25(OH)D 2 more effectively and rapidly raised circulating 25(OH)D 2 levels in cat plasma compared to vitamin D 2 . Formation of C-3 epimers of 25(OH)D 3 , 25(OH)D 2 , and 24,25 R (OH) 2 D 3 , but not 24,25(OH) 2 D 2 , were observed in feline plasma. The abundant concentrations of epimeric forms of vitamin D metabolites found in circulation suggest that these metabolites should be considered during vitamin D analyses in cats. Further studies using 25(OH)D and vitamin D 2 forms are needed to conclude safety and efficacy of these vitamers for supplementation in this species.

OBJECTIVE:To compare the effects of short-term dietary supplementation with vitamin D3 and 25-hydroxyvitamin D3 (25[OH]D3) on indicators of vitamin D status in healthy dogs.ANIMALS:13 purpose-bred adult dogs.PROCEDURES:20 extruded commercial dog foods were assayed for 25(OH)D3 content. Six dogs received a custom diet containing low vitamin D concentrations and consumed a treat with vitamin D2 (0.33 μg/kg0.75) plus 1 of 3 doses of 25(OH)D3 (0, 0.23, or 0.46 μg/kg0.75) once daily for 8 weeks followed by the alternate treatments in a crossover-design trial. In another crossover-design trial, 7 dogs received a custom diet supplemented with vitamin D3 or 25(OH)D3 (targeted content, 3,250 U/kg [equivalent to 81.3 μg/kg] and 16 μg/kg, respectively, as fed) for 10 weeks followed by the alternate treatment. In washout periods before each trial and between dietary treatments in the second trial, dogs received the trial diet without D-vitamer supplements. Dietary intake was monitored. Serum or plasma concentrations of vitamin D metabolites and biochemical variables were analyzed at predetermined times.RESULTS:25(OH)D3 concentrations were low or undetected in evaluated commercial diets. In the first trial, vitamin D2 intake resulted in quantifiable circulating concentrations of 25-hydroxyvitamin D2 but not 24R,25-dihydroxyvitamin D2. Circulating 25(OH)D3 concentration appeared to increase linearly with 25(OH)D3 dose. In the second trial, circulating 25(OH)D3 concentration increased with both D vitamer-supplemented diets and did not differ significantly between treatments. No evidence of vitamin D excess was detected in either trial.CONCLUSIONS AND CLINICAL RELEVANCE:Potency of the dietary 25(OH)D3 supplement estimated on the basis of targeted content was 5 times that of vitamin D3 to increase indicators of vitamin D status in the study sample. No adverse effects attributed to treatment were observed in short-term feeding trials.

Vitamin D insufficiency is associated with various disease processes. We determined whether consumption of a diet supplemented with HyD®, a 25-hydroxycholecalciferol (25(OH)D3) source, would safely increase plasma 25(OH)D3 concentrations in Golden Retrievers with low vitamin D status. We hypothesised that dietary supplementation with HyD® would rapidly increase and sustain plasma 25(OH)D3 levels in healthy Golden Retrievers with low vitamin D status compared with supplementation with vitamin D3. Of fifty-seven privately owned dogs recruited with written owner consent, eighteen dogs with low vitamin D status were identified and sorted between two groups to have similar initial plasma 25(OH)D3 concentrations, sex distributions, ages and body weights. Dogs of each group were fed a dry dog food supplemented with either 16 μg/kg of 25(OH)D3 as HyD® (n 10) or 81 μg/kg of cholecalciferol (D3) (n 8) for 4 months. Plasma 25(OH)D3 concentrations were determined monthly. A significant time effect (P < 0⋅001) and time by group interaction (P = 0⋅0045) were found for monthly determined plasma 25(OH)D3 concentrations. Dogs fed the HyD®-supplemented diet experienced a 40⋅5 % rise in plasma 25(OH)D3 values after 1 month (P < 0⋅001) and no change thereafter. Plasma 25(OH)D3 values of dogs supplemented with vitamin D3 did not increase (P > 0⋅05) and were less than values of dogs supplemented with HyD® (P = 0⋅044). With few exceptions, average haematologic, biochemical and urinalyses results remained within the reference range for both groups. Dietary supplementation with HyD® is sufficient to safely increase and sustain plasma 25(OH)D3 levels in healthy dogs.

There is increasing evidence to suggest that vitamin D plays a role in a wide range of disease processes. It has also been suggested that most privately owned dogs have suboptimal levels of vitamin D needed to reduce the risk of developing a neoplastic disease. The authors examined the effects of dietary supplementation with two metabolites, vitamin D3 and 25-hydroxyvitamin D3, on vitamin D status. Their results suggest that the latter compound is five times more effective at increasing circulating vitamin D levels and there was no evidence of excess vitamin D levels during the trial. These findings may have relevance in treating diseases in which circulating vitamin levels may be low, despite adequate dietary intake.

Elevated concentrations of serum phosphate are linked with progression and increased case fatality rate in animals and humans with chronic kidney disease. Elevated concentrations of serum phosphate can be a risk factor for development of renal and cardiovascular diseases or osteoporosis in previously healthy people. In rodents, an excess intake of dietary phosphorus combined with an inverse dietary calcium : phosphorus ratio (<1 : 1) contributes to renal calcification. Renal injury also has occured in cats fed experimental diets supplemented with highly soluble phosphate salts, especially in diets with inverse calcium : phosphorus ratios. However, not all phosphorus sources contribute similarly to this effect. This review, which focuses on cats, summarizes the published evidence regarding phosphorus metabolism and homeostasis, including the relative impact of different dietary phosphorus sources, and their impact on the kidneys. No data currently shows that commercial cat foods induce renal injury. However, some diets contain high amounts of phosphorus relative to recommendations and some have inverse Ca : P ratios and so could increase the risk for development of kidney disease. While limiting the use of highly soluble phosphates appears to be important, there are insufficient data to support a specific upper limit for phosphate intake. This review also proposes areas where additional research is needed in order to strengthen conclusions and recommendations regarding dietary phosphorus for cats.

A 10-year old, castrated male, Bichon Frise with a history of hyperadrenocorticism and intrahepatic portal vein hypoplasia was diagnosed with superficial necrolytic dermatitis (SND). The dog exhibited thick crusts on the chin, muzzle, prepuce, and paws. In addition, the dorsal surfaces of all paws were erythematous while the palmar/plantar surfaces were hyperkeratotic, hardened, and painful. The dog was treated with intravenous amino acid infusions (AAI), raw egg yolks, as well as zinc and omega-3 fatty acid oral supplements. The dog required AAI once every 2-3 weeks because this coincided with recrudescence of painful skin lesions. The dog was subsequently diagnosed with diabetes mellitus. A consult with the Nutrition Service was pursued 220 days after the original SND diagnosis because of concern for feeding raw eggs and for malnutrition since appetite was variable, muscle condition was reduced, and greater than 50% of ingested calories were from foods that were not nutritionally complete. There was also concern regarding the variability of the diet and the impact it would have on the management of diabetes mellitus. The diet was prepared by the dog owner according to a provided recipe and presented twice daily. The diet was rich in high quality protein and fat. All other treatments including medications, supplements, and bathing schedule remained unchanged at the time of diet modification. The dog was subclinical for SND associated clinical signs approximately 3 weeks after the diet modification, which also coincided with the last AAI. The AAI was postponed and was next administered 7 weeks later (i.e., 10 weeks from the previous infusion). The dog remained subclinical for SND related clinical signs and continued to receive AAI once every 10-12 weeks until he was euthanized 718 days later for complications related to severe multi-drug resistant, skin infections. In conclusion, this report highlights a novel role for nutritionally balanced home-made diets designed by a board-certified veterinary nutritionist could substantially increase time interval between AAI and outcome in dogs with SND.

This study sought to establish a baseline understanding of immune function and its association with serum vitamin D in shelter dogs. Ten apparently healthy shelter dogs housed in the Arizona Humane Society for ≥7 days and 10 apparently healthy, age, breed, and sex-matched control dogs were included. Serum 25-hydroxyvitamin D (25[OH]D), the major circulating vitamin D metabolite, was measured using high performance liquid chromatography. Whole blood samples were stimulated with lipopolysaccharide (LPS), lipoteichoic acid, or phosphate buffer solution, and tumor necrosis factor (TNF)-ɑ, interleukin (IL)-6, and IL-10 were measured using a canine-specific multiplex bead-based assay. Phagocytosis of opsonized-Escherichia coli and E. coli-induced oxidative burst were evaluated with flow cytometry. Shelter dogs had decreased percentages of granulocytes and monocytes (GM) that had phagocytized opsonized-E coli (P = 0.019) and performed E. coli-induced oxidative burst (P = 0.011). There were no significant differences in TNF-α, IL-6, IL-10, or 25(OH)D concentrations between shelter and control dogs. Serum 25(OH)D concentrations had a weak positive association with the intensity of GM E. coli-induced oxidative burst (r2 = 0.23, P = 0.03). There was a moderate inverse association between serum 25(OH)D concentration and LPS-stimulated TNF-ɑ production in shelter dogs (r2 = 0.40, P = 0.04). These results demonstrate immune dysregulation in vitro in shelter dogs housed for ≥7 days when compared to age, breed, and sex-matched control dogs. While serum 25(OH)D concentrations did not differ between shelter and control dogs, significant associations between 25(OH)D concentration and immune function parameters in vitro were identified.