Prevalence of eunatremic, eukalemic hypoadrenocorticism in dogs with signs of chronic gastrointestinal disease and risk of misdiagnosis after previous glucocorticoid administration.

BACKGROUND: Dogs with eunatremic, eukalemic hypoadrenocorticism (EEH) typically show signs of chronic gastrointestinal disease (CGD). Previous glucocorticoid administration (PGA) can give false-positive results on the ACTH stimulation test (ACTHst). HYPOTHESIS/OBJECTIVES: To determine the prevalence of EEH in dogs with signs of CGD, and to identify clinical and clinicopathological features for EEH and PGA. ANIMALS: One hundred twelve dogs with CGD (101 non-PGA and 11 PGA), 20 dogs with EEH. METHODS: Multicenter prospective cohort study. Basal serum cortisol (BSC) concentration was measured in dogs with signs of CGD. When BSC was <2 µg/dL and in PGA dogs, ACTHst plus measurement of endogenous ACTH (eACTH) were performed. Records of dogs with EEH from 2009 to 2021 were reviewed. RESULTS: The BSC concentration was <2 µg/dL in 48/101 (47.5%) non-PGA and in 9/11 (82%) PGA dogs. EEH was diagnosed in 1/112 dog (prevalence 0.9%; 95% CI, 0.1%-4.8%); the ACTHst provided false-positive results in 2/11 PGA dogs. PGA dogs showed lower C-reactive protein-to-haptoglobin ratio (median 0.01, range 0.003-0.08; P = .01), and higher haptoglobin (140, 26-285 mg/dL; P = .002) than non-PGA dogs (0.04, 0.007-1.5; 38.5, 1-246 mg/dL, respectively). eACTH was higher (P = .03) in EEH (396, 5->1250 pg/mL) than in non-PGA dogs (13.5, 7.3-46.6 pg/mL). Cortisol-to-ACTH ratio was lower (P < .0001 and P = .01, respectively) in EEH (0.002, 0.0002-0.2) than in non-PGA (0.1, 0.02-0.2) and PGA dogs (0.1, 0.02-0.2). CONCLUSIONS AND CLINICAL IMPORTANCE: The prevalence of EEH in dogs with signs of CGD was lower than previously reported. The clinical and clinicopathological features herein identified could increase the index of suspicion for EEH or PGA in dogs with an unclear history of glucocorticoid administration.

Acute adrenal necrosis in a young female cat.

CASE DESCRIPTION: An 18-month-old spayed female domestic short haired cat was presented for poor appetite, lethargy, exaggerated swallowing, and regurgitation 2 weeks after endoscopic retrieval of gastric foreign material. CLINICAL FINDINGS: The cat was quiet with tacky mucous membranes on physical examination. Point-of-care blood testing identified mild azotemia, moderate hypercalcemia, and a sodium-to-potassium ratio of 26. An ultrasound examination the next day identified moderate to marked bilateral adrenomegaly. Cytology of a fine needle aspirate of the adrenal glands was consistent with necrosis and associated inflammation. Hypoadrenocorticism was diagnosed by a confirmatory adrenocorticotropic hormone stimulation test. TREATMENT AND OUTCOME: The cat normalized both clinically and biochemically after treatment with prednisolone and desoxycorticosterone pivalate. CLINICAL RELEVANCE: Acute adrenal necrosis has been well documented in human medicine after anesthetic events. To our knowledge, hypoadrenocorticism caused by cytologically confirmed acute adrenal necrosis has not been previously reported in dogs and cats.

A case-control survey study of environmental risk factors for primary hypoadrenocorticism in dogs.

BACKGROUND: Primary hypoadrenocorticism in dogs is thought to be multifactorial with roles for both genetic and environmental factors. The contributions of environmental factors remain unexplored. OBJECTIVE: Identify environmental and lifestyle exposures associated with primary hypoadrenocorticism in 2 dog breeds with high risk of developing the disease. ANIMALS: Animals were not used in this study. Owners of Standard Poodles (STPDs) and Portuguese water dogs (POWDs) participated in a survey. METHODS: Retrospective case-control study. Dog owners were invited to participate in an online survey through convenience sampling. Questions regarded the demographics, health histories, and indoor/outdoor environments in which their dogs live and play. Responses for dogs with primary hypoadrenocorticism were compared to those without the disease using univariate and multivariate logistic regression models. RESULTS: Five thousand forty-seven responses (358 cases, 4689 controls) met initial inclusion criteria. Significant associations with modest effect size were found for community type, ingestion of canned food, and use of lawn fertilizer in some analysis models. Reproductive (spay/neuter) status exhibited the strongest association with high effect size across all models with adjusted odds ratio (OR) 2.5 (95% confidence interval [CI], 1.4-4.5; P = .003) for spayed females and 6.0 (95% CI, 2.6-13.9; P < .001) for neutered males. CONCLUSIONS AND CLINICAL IMPORTANCE: The large effect size for reproductive status reflects its high potential clinical relevance, whereas modest effect sizes for other environmental variables suggest lower potential clinical relevance. These findings are associations and do not necessarily imply causation. Before any actionable recommendations are warranted, additional evidence regarding biological mechanisms is needed.

Possible development and resolution of dilated cardiomyopathy phenotype secondary to atypical hypoadrenocorticism in a dog.

OBJECTIVE: To report the possible occurrence of dilated cardiomyopathy phenotype associated with atypical hypoadrenocorticism and subsequent marked improvement with treatment in a mixed breed dog. CASE SUMMARY: A 4.5-year-old, neutered male mixed breed dog was evaluated for a history and clinicopathological changes consistent with atypical hypoadrenocorticism. The dog was being fed a grain-free diet. While hospitalized for supportive care and diagnostics, the patient developed and was diagnosed with biventricular congestive heart failure secondary to dilated cardiomyopathy phenotype and IV fluid administration. The left-sided congestive heart failure resolved with discontinuation of IV fluid therapy and short-term administration of diuretics. After treatment of atypical hypoadrenocorticism with glucocorticoid supplementation, and while continuing to be fed varying grain-free diets, the patient's dilated cardiomyopathy phenotype largely resolved. The patient fully recovered and did not require any long-term cardiac medications. NEW OR UNIQUE INFORMATION PROVIDED: Development of dilated cardiomyopathy phenotype has not been described in dogs as a sequela of untreated hypoadrenocorticism but has been reported in human literature. Given the fact that standard management of hypoadrenocorticism typically involves aggressive fluid resuscitation, awareness of this potential sequela is important for patients that fail to respond or develop signs consistent with volume overload.

Urine electrolytes do not predict desoxycorticosterone pivalate efficacy in dogs with hypoadrenocorticism.

OBJECTIVE: To determine if urine electrolyte assessments can be used to monitor the adequacy of mineralocorticoid therapy in dogs with hypoadrenocorticism (HA). ANIMALS: 29 dogs with naturally occurring glucocorticoid- and mineralocorticoid-deficient HA. PROCEDURES: Urine sodium and potassium concentrations, sodium-to-potassium ratios, sodium-to-creatinine ratios, and potassium-to-creatinine (K:Cr) ratios were evaluated in dogs with newly diagnosed HA that were treated with desoxycorticosterone pivalate (DOCP). Dogs underwent measurements of urine and serum sodium, potassium, and creatinine concentrations and plasma renin activities twice monthly for up to 3 months. Regression analyses and calculation of coefficients of determination (R2) were performed to investigate potential associations between urine and serum variables. Urine variables also were compared between dogs considered to be undertreated or overtreated based on plasma renin activities. RESULTS: Urine K:Cr ratios were significantly associated with serum potassium concentrations 10 to 14 days (P = .002) and 30 days (P = .027) after the initial DOCP injection, but R2 values were only 0.35 and 0.17, respectively. Urine K:Cr ratios (median [IQR]) also were higher in dogs that were overtreated with DOCP (1.3 [0.7 to 2.3]) as compared to those dogs that were undertreated with DOCP (0.8 [0.5 to 0.9]) at 10 to 14 days after the initial DOCP injection (P = .039) but not at 30 days after the initial injection. Other urine variables were not significantly different between undertreated and overtreated dogs. CLINICAL RELEVANCE: Measures of urine electrolytes were not useful for assessing the adequacy of mineralocorticoid therapy in HA dogs that were treated with DOCP.

Prevalence of hypercalcemia in primary hypoadrenocorticism in dogs: Multicenter, retrospective study.

BACKGROUND: Hypoadrenocorticism is an important differential for hypercalcemia. The etiology of hypercalcemia in hypoadrenocorticism in dogs is unclear. OBJECTIVE: To review the prevalence of hypercalcemia and use statistical models to identify clinical, demographic, and biochemical variables associated with hypercalcemia in dogs with primary hypoadrenocorticism. ANIMALS: One hundred ten dogs with primary hypoadrenocorticism; 107 with recorded total calcium (TCa), 43 recorded ionized calcium (iCa). METHODS: Multicenter retrospective observational study at 4 UK referral hospitals. Univariable logistic regression analyses were performed to assess the association between independent variables of signalment, hypoadrenocorticism type (glucocorticoid only deficient hypoadrenocorticism [GHoC] vs glucocorticoid and mineralocorticoid deficient hypoadrenocorticism [GMHoC]), clinicopathological variables and hypercalcemia. Hypercalcemia was defined as elevated TCa, an elevated iCa, or both elevated TCa and iCa (Model 1) or as elevated iCa (Model 2). RESULTS: Overall prevalence of hypercalcemia was 34.5% (38/110). The odds of hypercalcemia (Model 1) were increased (P < .05) in dogs with GMHoC ([vs GHoC], OR [odds ratio] = 3.86, 95% confidence interval [CI] 1.105-13.463), higher serum creatinine (OR = 1.512, 95% CI 1.041-2.197), and higher serum albumin (OR = 4.187, 95% CI 1.744-10.048). The odds of ionized hypercalcemia (Model 2) were increased (P < .05) with reduced serum potassium concentration (OR = 0.401, 95% CI 0.184-0.876) and younger age (OR = 0.737, 95% CI 0.558-0.974). CONCLUSIONS AND CLINICAL IMPORTANCE: This study identified several key clinical and biochemical variables associated with hypercalcemia in dogs with primary hypoadrenocorticism. These findings aid understanding of the pathophysiology and etiology of hypercalcemia in dogs with primary hypoadrenocorticism.

Adrenocortical hypoperfusion detected by contrast-enhanced ultrasound in a dog with trilostane-induced hypoadrenocorticism.

A 12-year-old neutered male Chihuahua dog was diagnosed with pituitary-dependent hypercortisolism and treated with trilostane. Eighty-nine days later, the dog showed lethargy accompanied by hyponatraemia and hyperkalaemia. Hypoadrenocorticism due to trilostane was suspected, but the result of the adrenocorticotropic hormone stimulation test was not conclusive. Contrast-enhanced ultrasound showed loss of adrenocortical blood flow in both adrenal glands, indicating adrenocortical hypoperfusion and isolated hypoadrenocorticism. Treatment with fludrocortisone acetate improved the condition and electrolyte abnormalities. Thirteen months later, the dog showed alopecia, and an adrenocorticotropic hormone stimulation test revealed increased cortisol concentration, indicating hypercortisolism recurrence. The dog died due to progressive deterioration 22 months after the initial presentation. Post-mortem examination revealed focally extensive necrosis with marked calcification in the parenchyma of the adrenal glands and regeneration of the cells in the zona fasciculata with severe fibrosis. Adrenocortical hypoperfusion detected by contrast-enhanced ultrasound can support the diagnosis of adrenal necrosis and hypoadrenocorticism.

Canine hypoadrenocorticism: Insights into the Addisonian crisis.

Objective: Primary objectives of this study were to determine presenting complaints, physical examination, clinicopathologic findings, and hospitalization time of dogs with spontaneous hypoadrenocorticism presenting with critical disease; and to compare those end points to dogs with a more stable presentation. Secondary objectives were to evaluate the shock index and to identify precipitating stressors. Animals: Eighty-four dogs at the Western College of Veterinary Medicine between 1998 and 2018 were included. Procedure: Data were retrieved from the medical records. Results: Collapse and depression were more common among critically ill dogs. Hyperlactatemia was rare despite a diagnosis of hypovolemic shock, and a shock index was ineffective in this patient subset. Isosthenuria, total hypocalcemia, and more severe acidosis were more common (P < 0.05) in critical dogs. Owner separation was the most common precipitating stressor. Conclusion and clinical relevance: We concluded that the critical Addisonian dog has unique characteristics that may aid in early disease identification.

Hypoadrénocorticisme canin : aper ç u de la crise Addisonienne. Objectif: Les principaux objectifs de cette étude étaient de déterminer les motifs de présentation, l'examen physique, les résultats clinico-pathologiques et la durée d'hospitalisation des chiens atteints d'hypoadrénocorticisme spontané présentant une maladie critique; et de comparer ces paramètres aux chiens avec une présentation plus stable. Les objectifs secondaires étaient d'évaluer l'indice de choc et d'identifier les facteurs de stress déclencheurs. Animaux: Quatre-vingt-quatre chiens du Western College of Veterinary Medicine entre 1998 et 2018 ont été inclus. Procédure: Les données ont été extraites des dossiers médicaux. Résultats: L'effondrement et la dépression étaient plus fréquents chez les chiens gravement malades. L'hyperlactatémie était rare malgré un diagnostic de choc hypovolémique, et un indice de choc était inefficace dans ce sous-groupe de patients. L'isosthénurie, l'hypocalcémie totale et l'acidose plus grave étaient plus fréquentes (P < 0,05) chez les chiens critiques. La séparation du propriétaire était le facteur de stress déclencheur le plus courant. Conclusion et pertinence clinique: Nous avons conclu que le chien addisonien critique a des caractéristiques uniques qui peuvent aider à l'identification précoce de la maladie.(Traduit par Dr Serge Messier).

Evaluation of the effect of glucocorticoid treatment on adrenocortical functions by monitoring endogenous hydrocortisone in horses.

Glucocorticoid preparations have anti-inflammatory effects, and are commonly used in the equine clinical setting; however, such treatments can cause a number of side effects. Adrenal insufficiency is an adverse effect induced by the suppression of adrenal function following drug administration. This study aimed to investigate the influence of two glucocorticoid preparations, dexamethasone and hydrocortisone, on adrenocortical function in horses. The usual doses of dexamethasone and hydrocortisone preparations in equine practice were administered intramuscularly to six horses, and peripheral blood was collected at different time points. Concentrations of dexamethasone and hydrocortisone in the plasma, before and after drug administration, were measured using liquid chromatography-tandem mass spectrometry. Considering circadian rhythms in endogenous hydrocortisone levels, hormone concentrations, before and after drug administration, were compared at the same time of the day. Plasma dexamethasone concentrations were below the limit of quantification at 72 hr post-administration. Plasma hydrocortisone concentrations were significantly lower from 1 to 72 hr after administration. After hydrocortisone preparation administration, plasma hydrocortisone levels were significantly higher until 9 hr, and significantly lower at 24 and 48 hr. The suppression rate of endogenous hydrocortisone ranged over 2.2-5.3% with dexamethasone treatment and 17.5-45.7% with hydrocortisone treatment. The study clearly indicated the effects of glucocorticoids on adrenocortical function in horses and provided basic knowledge about the selection and prescription of glucocorticoid preparations and setting the withdrawal times in equine clinical setting.

Diagnostic predictivity of transtubular potassium gradient for primary hypoadrenocorticism in hyperkalemic dogs: a cross-sectional study.

OBJECTIVES: Transtubular potassium gradient has never been evaluated in the diagnosis of primary hypoadrenocorticism in dogs. The objective of this study is to evaluate the diagnostic utility of transtubular potassium gradient for the diagnosis of primary hypoadrenocorticism in dogs with serum K+ > 5.5 mol/L. MATERIALS AND METHODS: Cross-sectional study including dogs with primary hypoadrenocorticism and dogs with other disease. Differences in signalment and laboratory parameters between groups were assessed by binary logistic regression modelling. Variables significantly associated with primary hypoadrenocorticism were evaluated for their diagnostic accuracy of this condition by receiver operator characteristic curve analysis and by multivariable logistic regression analysis, respectively. RESULTS: Dogs with primary hypoadrenocorticism (n=39) were significantly younger than hyperkalemic dogs without primary hypoadrenocorticism (n=41). Moreover they had higher serum and urinary concentrations of Na+ and Na+ :K+ , but lower transtubular potassium gradient than hyperkalemic dogs without hypoadrenocorticism. Serum Na+ (sNa+ ) had the highest diagnostic accuracy (area under the curve [AUC]: 0.87, 95% confidence interval, 0.78 to 0.96), followed by the transtubular potassium gradient (AUC: 0.81, 0.72 to 0.91), however the accuracy of the two AUCs was not statistically different. The transtubular potassium gradient-sNa+ additive index (i.e. transtubular potassium gradient+sNa+ /10) had a greater accuracy (AUC: 0.88, 0.79 to 0.94) than transtubular potassium gradient or sNa+ , although it was not statistically superior to the latter. The multivariable logistic regression model showed that transtubular potassium gradient (adjusted odds ratio [aOR]: 0.51, 0.3 to 0.84), sNa+ (aOR: 0.86, 0.78 to 0.95) and spayed female (aOR: 24.96, 2.32 to 267.66) were associated with primary hypoadrenocorticism. CLINICAL SIGNIFICANCE: Transtubular potassium gradient-sNa+ additive index can contribute to decision-making on diagnosis of primary hypoadrenocorticism in dogs presenting with hyperkalaemia.

Iatrogenic symptomatic hypoadrenocorticism after treatment with trilostane for hyperadrenocorticism in dogs: eight cases (2008-2019).

OBJECTIVES: Trilostane is the medical treatment of choice for hyperadrenocorticism. Iatrogenic hypoadrenocorticism is thought to be rare, with most cases being transient and only a few cases of permanent hypoadrenocorticism have been reported. This study reports findings from eight cases of iatrogenic hypoadrenocorticism and examines the presence of concurrent diseases at the time of diagnosis. MATERIALS AND METHODS: Medical records of dogs treated for hyperadrenocorticism with trilostane since 2008 were reviewed, and cases of clinical iatrogenic hypoadrenocorticism were extracted. Cases were considered permanent if long-term replacement therapy was required. RESULTS: Eight dogs met the inclusion criteria. The time between the beginning of trilostane treatment and the diagnosis of hypoadrenocorticism ranged from 4 days to 13 months, and the dosage of trilostane ranged between 1 and 8 mg/kg/day. Six dogs had a suspicion of concurrent disease at the time of hypoadrenocorticism diagnosis. The trilostane dose was decreased in two dogs; trilostane was withdrawn in one case without further relapse of hyperadrenocorticism; and glucocorticoids with or without mineralocorticoid supplementation were prescribed in five dogs. Two of these five dogs were lost to follow-up, and the other three had a diagnosis of permanent hypoadrenocorticism. Adrenal gland ultrasonography in these three dogs showed a progressive reduction in gland sizes with heterogeneous echogenicity. CLINICAL SIGNIFICANCE: Iatrogenic hypoadrenocorticism is a rare but potentially life-threatening complication of trilostane treatment in dogs with hyperadrenocorticism. The occurrence of a concurrent disease might trigger the development of clinical signs of hypoadrenocorticism in previously subclinical dogs.

Clinical features and long-term management of cats with primary hypoadrenocorticism using desoxycorticosterone pivalate and prednisolone.

BACKGROUND: Primary hypoadrenocorticism (PH) is rare in cats and knowledge about treatment is sparse. OBJECTIVE: To describe cats with PH with a focus on long-term treatment. ANIMALS: Eleven cats with naturally occurring PH. METHODS: Descriptive case series with data on signalment, clinicopathological findings, adrenal width, and doses of desoxycorticosterone pivalate (DOCP) and prednisolone during a follow-up period of >12 months. RESULTS: Cats ranged from 2 to 10 years (median 6.5); 6 cats were British Shorthair. Most common signs were reduced general condition and lethargy, anorexia, dehydration, obstipation, weakness, weight loss, and hypothermia. Adrenal glands on ultrasonography were judged small in 6. Eight cats could be followed for 14 to 70 months (median: 28). Two were started on DOCP doses ≥2.2 mg/kg (2.2; 2.5) and 6 < 2.2 mg/kg (1.5-2.0 mg/kg, median 1.8) q28 days. Both high-dose cats and 4 low-dose cats needed a dose increase. Desoxycorticosterone pivalate and prednisolone doses at the end of the follow-up period were 1.3 to 3.0 mg/kg (median: 2.3) and 0.08 to 0.5 mg/kg/day (median: 0.3), respectively. CONCLUSIONS AND CLINICAL IMPORTANCE: Desoxycorticosterone pivalate and prednisolone requirements in cats were higher than what is currently used in dogs; thus, a DOCP starting dose of 2.2 mg/kg q28 days and a prednisolone maintenance dose of 0.3 mg/kg/day titrated to the individual need seems warranted. Small adrenal glands (width < 2.7 mm) on ultrasonography in a cat suspected of hypoadrenocorticism can be suggestive of the disease. The apparent predilection of British Shorthaired cats for PH should be further evaluated.

Laboratory Diagnosis of Thyroid and Adrenal Disease.

Diagnosis of thyroid and adrenal disease can be confusing. Whereas the definitive diagnosis of hyperthyroidism and hypoadrenocorticism are relatively straightforward, hypothyroidism and naturally occurring Cushing's syndrome (NOCS) are more complicated. In a patient with compatible clinical signs, a single increased tT4 is enough to confirm hyperthyroidism, but a low tT4 alone is never enough to confirm hypothyroidism. A flatline result (post-stimulation cortisol <2 ug/dL) on an ACTH stimulation test (ACTHst) confirms hypoadrenocorticism, but not all dogs with NOCS have increased ACTHst results. This article explains which diagnostics should be pursued for these endocrinopathies, and how to interpret them.

Atypical hypoadrenocorticism with intact zona glomerulosa of the adrenal cortex after long-term observation: a case report of a dog.

An 8-year-old intact male pointer presented with lethargy and hypoalbuminemia. On abdominal ultrasonography, both adrenal glands were reduced in thickness. Based on the ACTH stimulation test results and the absence of electrolyte abnormalities, the dog was diagnosed with atypical hypoadrenocorticism. After treatment with low-dose prednisolone, his general condition improved, and blood tests normalized. The dog died 818 days later, and a complete autopsy was performed. Histologically, the architecture of the zonae fasciculata and reticularis was disrupted in both adrenal glands; however, the zona glomerulosa remained relatively normal. In summary, in this study, we detailed the pathological presentation of atypical hypoadrenocorticism without electrolyte abnormalities.

Characterization of clinicopathologic and abdominal ultrasound findings in dogs with glucocorticoid deficient hypoadrenocorticism.

BACKGROUND: Clinical findings of glucocorticoid-deficient hypoadrenocorticism (GDH) can overlap with other diseases, presenting a diagnostic challenge. OBJECTIVES: Describe clinicopathologic and ultrasonographic features of dogs with GDH and those suspected of having GDH that had the disease ruled out. ANIMALS: Six hundred twenty-three dogs. METHODS: Records from dogs with suspected GDH between 2003 and 2018 were reviewed. Dogs with hyperkalemia or hyponatremia were excluded. Dogs were categorized as controls when the resting serum cortisol or post-ACTH cortisol concentration were > 2 µg/dL. Clinicopathologic and ultrasonographic features were compared between groups. The optimal cut-point, area under the receiver operating characteristic curve (AUC), sensitivity, and specificity were calculated for individual features used to detect GDH. RESULTS: Dogs were categorized as GDH (n = 29) or controls (n = 594). Lymphocyte count (>1750 cells/L; sensitivity, 96.6%; 95% confidence interval [CI], 82.8%-99.8%; specificity, 60.3%; 95% CI, 56.3%-64.1%; AUC, 0.828; 95% CI, 0.762-0.894) and albumin/globulin ratio (<1.081; sensitivity, 86.2%; 95% CI, 69.4%-94.5%; specificity, 78.8%; 95% CI, 75.3%-81.9%; AUC, 0.886; 95% CI, 0.827-0.944) had the highest discriminatory power between groups. Left adrenal gland width <0.39 cm was 80% (95% CI, 58.4%-91.9%) sensitive and 82.4% (95% CI, 74.2-88.4) specific for GDH. Serum cobalamin concentrations and ultrasonographic abnormalities of the GI tract were not different between groups. CONCLUSION AND CLINICAL IMPORTANCE: No single variable could be used to confidently rule out GDH and obviate the need for cortisol testing in dogs with a clinical presentation consistent with GDH.

Successful use of a benchtop fluorescent enzyme immunoassay analyzer to measure serum cortisol concentration as a screening test for hypoadrenocorticism in dogs.

OBJECTIVE: To assess the diagnostic performance of a benchtop fluorescent enzyme immunoassay analyzer (AIA-360; Tosoh Bioscience Inc) for the measurement of serum cortisol concentration as a screening test for hypoadrenocorticism in dogs. ANIMALS: 173 client-owned dogs (20 with hypoadrenocorticism and 153 with nonadrenal illness). PROCEDURES: Medical records of all dogs that underwent an ACTH stimulation test between June 2015 and October 2019 were reviewed retrospectively. Dogs were excluded if the ACTH stimulation test was performed on the basis of a suspicion of hypercortisolism, serum cortisol concentrations were measured using an analyzer other than the one assessed in the present study, or dogs had received medication known to affect the pituitary-adrenal axis in the 4 weeks1,2 preceding ACTH stimulation testing. The diagnostic performance of the benchtop analyzer was evaluated by calculating sensitivity, specificity, and likelihood ratios at various cutoff points. RESULTS: Serum resting cortisol cutoff point concentrations of 0.8 µg/dL (22 nmol/L), 1 µg/dL (28 nmol/L), and 2 µg/dL (55 nmol/L) had a sensitivity of 100%. An optimal serum resting cortisol cutoff point of 0.58 µg/dL (16 nmol/L) had a sensitivity, specificity, and positive and negative likelihood ratios of 100%, 97%, and 30.6 and 0.0, respectively. CLINICAL RELEVANCE: Findings indicated that previously derived cutoff points could be used with excellent sensitivity to exclude hypoadrenocorticism in this population of dogs when serum cortisol concentration was measured with the evaluated benchtop analyzer. An ACTH stimulation test may need to only be performed to diagnose hypoadrenocorticism if resting serum cortisol concentration is ≤ 0.58 µg/dL when measured with the evaluated benchtop analyzer.

Acquired Systolic Dysfunction and Subsequent Congestive Heart Failure Following Treatment of Hypoadrenocorticism in Two Dogs.

Acquired cardiomyopathies have been described in human patients with hypoadrenocorticism. Several mechanisms have been described to explain the cardiac effects of primary adrenal insufficiency, but, clinically, these manifestations may be underappreciated in dogs. In humans, there is an infrequently described, reversible dilated cardiomyopathy in patients with hypoadrenocorticism. Two dogs were presented to a single referral center for evaluation of weakness or collapse and were subsequently diagnosed with hypoadrenocorticism after a full diagnostic workup. Following the diagnosis of hypoadrenocorticism and administration of glucocorticoids and desoxycorticosterone pivalate, both dogs developed left-sided congestive heart failure and had systolic dysfunction diagnosed by echocardiogram. Both dogs were euthanized; one because of recurrent congestive heart failure and another because of a concern for poor long-term prognosis and decreased quality of life. The purpose of this case report is to document multiple cases of hypoadrenocorticism-associated systolic dysfunction and subsequent cardiogenic pulmonary edema in dogs.

Evaluation of a machine learning tool to screen for hypoadrenocorticism in dogs presenting to a teaching hospital.

BACKGROUND: Dogs with hypoadrenocorticism (HA) have clinical signs and clinicopathologic abnormalities that can be mistaken as other diseases. In dogs with a differential diagnosis of HA, a machine learning model (MLM) has been validated to discriminate between HA and other diseases. This MLM has not been evaluated as a screening tool for a broader group of dogs. HYPOTHESIS: An MLM can accurately screen dogs for HA. ANIMALS: Dogs (n = 1025) examined at a veterinary hospital. METHODS: Dogs that presented to a tertiary referral hospital that had a CBC and serum chemistry panel were enrolled. A trained MLM was applied to clinicopathologic data and in dogs that were MLM positive for HA, diagnosis was confirmed by measurement of serum cortisol. RESULTS: Twelve dogs were MLM positive for HA and had further cortisol testing. Five had HA confirmed (true positive), 4 of which were treated for mineralocorticoid and glucocorticoid deficiency, and 1 was treated for glucocorticoid deficiency alone. Three MLM positive dogs had baseline cortisol ≤2 µg/dL but were euthanized or administered glucocorticoid treatment without confirming the diagnosis with an ACTH-stimulation test (classified as "undetermined"), and in 4, HA was ruled out (false positives). The positive likelihood ratio of the MLM was 145 to 254. All dogs diagnosed with HA by attending clinicians tested positive by the MLM. CONCLUSIONS AND CLINICAL IMPORTANCE: This MLM can robustly predict HA status when indiscriminately screening all dogs with blood work. In this group of dogs with a low prevalence of HA, the false positive rates were clinically acceptable.

Presumptive nontraumatic adrenal hemorrhage preceding hypoadrenocorticism in a dog.

Nontraumatic adrenal hemorrhage (NTAH) has been associated with stress-induced catecholamines release in underlying conditions such as sepsis and recent surgery in humans. It can lead to primary hypoadrenocorticism (HOAC) when both adrenal glands are involved, with nonspecific clinical signs and laboratory findings that can lead to a missed diagnosis. Bilateral thickening of the adrenal glands with periadrenal fat stranding was identified in a 10-year-old male Maltese dog after abdominal surgery. The dog showed clinical signs and biochemical changes consistent with HOAC, but treatment for presumed critical illness-related corticosteroid insufficiency was initiated. Clinical signs relapsed with a 3-week dose reduction of hydrocortisone, and a reduction in adrenal size was observed on follow-up ultrasound examination. Hormonal testing confirmed HOAC in the dog. To the best of our knowledge, HOAC caused by spontaneous NTAH has not been reported in the veterinary literature. This report describes a dog that developed HOAC with presumed adrenal atrophy after suspected spontaneous bilateral NTAH.