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Abstract Background The relationship between collapse and a diagnosis of hypoadrenocorticism is not well understood in dogs. Hypothesis To assess the prevalence of episodes of collapse in dogs screened for hypoadrenocorticism, and to assess the prevalence of confirmed hypoadrenocorticism in dogs presenting with reported collapse. Animals Seventy‐three client‐owned dogs with resting cortisol concentrations were measured and presented to a University teaching hospital for collapse. Methods Retrospective review of medical records of dogs at a single center. Results The prevalence of episodes of collapse in dogs that had a resting cortisol measurement was 73/856 (8.5%; 95% confidence interval [95% CI], 6.7%‐10.6%). Resting cortisol concentration was 2 μg/dL (>55 nmol/L). The most common diagnosis was vasovagal syncope (10/73), followed by sick sinus syndrome and third‐degree atrioventricular block (2/73). The final diagnosis was unknown in 24/73 dogs. Conclusions and Clinical Importance Hypoadrenocorticism was the final diagnosis in 1 of 73 dogs presented to a teaching hospital either in a collapsed state or with a previous history of episodes of collapse. No dog presenting as cardiovascularly stable for intermittent collapse was found to have hypoadrenocorticism.

Abstract Background Evidence indicating the optimal treatment protocol for dogs in adrenal crisis is lacking. Objectives Compare outcomes of dogs presented in adrenal crisis treated with either hydrocortisone (HC) continuous rate infusion (CRI) or intermittent dexamethasone (DEX) administration. Animals Thirty‐nine client‐owned dogs. Methods Multi‐institutional retrospective observational study (July 2016‐May 2022) including dogs diagnosed with adrenal crisis and with available sequential blood work during hospitalization. Dogs were excluded if already on treatment with exogenous corticosteroids. Outcomes assessed included duration of hospitalization, survival, number of repeat measurements of electrolyte concentrations, and time to normalization of electrolyte and acid‐base status. Results No significant difference was found between the groups for hospitalization time (P = .41; HC median [range] 48 h [19‐105 h]; DEX 57 h [17‐167 h]) nor case fatality rate 2/28 in the DEX group and 0/11 in the HC group (P = 1), nor in number of measurements of electrolyte concentrations (P = .90; HC 4 [2‐10]; DEX 4.5 [2‐15]). No significant differences were found between the 2 treatment groups in time to normalization of serum Na (P = .30; HC 33 h [7‐66 h]; DEX 16 h [1.5‐48 h]), K (P = .92; HC 17 h [4‐48 h]; DEX 16 h [1.25‐60 h]) or Na/K ratio (P = .08; HC 17 h [8‐48 h]; DEX 26 h [1.5‐60 h]). Conclusions This study detected no difference in outcomes for dogs in adrenal crisis treated with either DEX boluses or HC CRIs.

Abstract Background Metabolic profiles differ between healthy humans and those with inflammatory bowel disease. Few studies have examined metabolic profiles in dogs with chronic enteropathy (CE). Hypothesis Serum metabolic profiles of dogs with CE are significantly different from those of healthy dogs. Animals Fifty‐five dogs with CE and 204 healthy controls. Methods A cross‐sectional study. The serum concentrations of 99 metabolites measured using a canine‐specific proton nuclear magnetic resonance spectroscopy platform were studied. A 2‐sample unpaired t‐test was used to compare the 2 study samples. The threshold for significance was set at P

Abstract Background Resting cortisol concentrations are routinely measured in dogs with chronic gastrointestinal signs to rule out hypoadrenocorticism based on a concentration >2 μg/dL (>55 nmol/L). Hypothesis/Objectives To assess the cross‐sectional prevalence of hypoadrenocorticism in a group of dogs with chronic gastrointestinal signs presented to a referral internal medicine service. Animals Two‐hundred and eighty‐two client‐owned dogs with chronic gastrointestinal signs and with resting cortisol concentration testing performed. Methods Retrospective review of medical records (final diagnosis, resting cortisol concentration, and adenocorticotropic hormone [ACTH] stimulation test results) of a referral population of dogs between May 2013 and September 2017. Results Resting cortisol concentration was 2 μg/dL (>55 nmol/L). Overall, the most common diagnosis was chronic primary inflammatory enteropathy (176/282, 62.4%), followed by extragastrointestinal neoplasia (17/282, 6%), protein‐losing enteropathy, pancreatitis and megaesophagus (10/282, 3.5% each). Conclusions and Clinical Importance Although dogs with hypoadrenocorticism can present with chronic gastrointestinal signs, it was the final diagnosis in only 1 of 282 dogs presenting to a referral internal medicine service for signs of chronic enteropathy. Repeated resting cortisol concentration may be considered as a test to try and exclude hypoadrenocorticism.

Abstract Background Canine hypoadrenocorticism is an immune-mediated endocrinopathy that shares both clinical and pathophysiological similarities with Addison’s disease in humans. Several dog breeds are overrepresented in the disease population, suggesting that a genetic component is involved, although this is likely to be polygenic. Previous research has implicated CTLA4 as a potential susceptibility gene. CTLA4 is an important regulator of T cell function and polymorphisms/mutations in CTLA4 have been associated with a number of autoimmune phenotypes in both humans and rodent models of autoimmunity. The aim of the current study was to undertake a case:control association study of CTLA4 promotor polymorphisms in three dog breeds, cocker spaniels, springer spaniels and West Highland white terriers (WHWT). Results Polymorphisms in the CTLA4 promoter were determined by PCR and sequence-based typing. There were significant associations with three promoter haplotypes in cocker spaniels (p = 0.003). A series of SNPs were also associated with hypoadrenocorticism in cocker spaniels and springer spaniels, including polymorphisms in predicted NFAT and SP1 transcription factor binding sites. Conclusions This study provides further evidence that CTLA4 promotor polymorphisms are associated with this complex genetic disease and supports an immune mediated aetiopathogenesis of canine hypoadrenocorticism.

Canine hypoadrenocorticism likely arises from immune-mediated destruction of adrenocortical tissue, leading to glucocorticoid and mineralocorticoid deficiency. In humans with autoimmune Addison's disease (AAD) or autoimmune polyendocrine syndrome (APS), circulating autoantibodies have been demonstrated against enzymes associated with adrenal steroid synthesis. The current study investigates autoantibodies against steroid synthesis enzymes in dogs with spontaneous hypoadrenocorticism. Coding regions of canine CYP21A2 (21-hydroxylase; 21-OH), CYP17A1 (17-hydroxylase; 17-OH), CYP11A1 (P450 side-chain cleavage enzyme; P450scc) and HSD3B2 (3β hydroxysteroid dehydrogenase; 3βHSD) were amplified, cloned and expressed as 35S-methionine radiolabelled recombinant protein. In a pilot study, serum samples from 20 dogs with hypoadrenocorticism and four unaffected control dogs were screened by radio-immunoprecipitation assay. There was no evidence of reactivity against 21-OH, 17-OH or 3βHSD, but five dogs with hypoadrenocorticism showed immunoreactivity to P450scc compared with controls. Serum samples were subsequently obtained from 213 dogs diagnosed with hypoadrenocorticism and 110 dogs from a hospital control population. Thirty control dogs were randomly selected to establish a threshold for antibody positivity (mean + 3 × standard deviation). Dogs with hypoadrenocorticism were more likely to be P450scc autoantibody positive than hospital controls (24% vs. 1.2%, respectively; p = 0.0016). Sex was significantly associated with the presence of P450scc autoantibodies in the case population, with 30% of females testing positive compared with 17% of males (p = 0.037). Significant associations with breed (p = 0.015) and DLA-type (DQA1*006:01 allele; p = 0.017) were also found. This cross-sectional study indicates that P450scc autoantibodies are present in a proportion of dogs affected with hypoadrenocorticism.