Genetic characterization of Addison's disease in Bearded Collies.

BACKGROUND: Primary hypoadrenocorticism (or Addison's disease, AD) is an autoimmune disease that results in destruction of the adrenal cortex and consequent adrenal insufficiency. The disease has been described in purebred and mixed breed dogs, although some breeds, including the Bearded Collie, are at increased risk for AD. Candidate gene approaches have yielded few associations that appear to be breed-specific. A single other genome-wide association study reported no significant regions of association for AD in Standard Poodles. The present study aimed to identify genomic regions of association for canine AD in Bearded Collies. RESULTS: Our study consists of the first genome-wide association analysis to identify a genome-wide significant region of association with canine AD (CFA18). Peaks of suggestive association were also noted on chromosomes 11, 16 and 29. Logistic regression analysis supported an additive effect of risk genotypes at these smaller effect loci on the probability of disease associated with carrying a risk genotype on CFA18. Potential candidate genes involved in adrenal steroidogenesis, regulation of immune responses and/or inflammation were identified within the associated regions of chromosomes 11 and 16. The gene-poor regions of chromosomes 18 and 29 may, however, harbor regulatory sequences that can modulate gene expression and contribute to disease susceptibility. CONCLUSION: Our findings support the polygenic and complex nature of canine AD and identified a strongly associated locus on CFA18 that, when combined with three other smaller effect loci, was predictive of disease. The results offer progress in the identification of susceptibility loci for canine AD in the Bearded Collie. Further studies are needed to confirm association with the suggested candidate genes and identify actual causative mutations involved with AD susceptibility in this breed.

Addison's Disease Secondary to Bilateral Adrenal Gland Metastatic Mammary Carcinoma in a Dog.

A 12 yr old intact female Siberian husky was referred with a 2 wk history of progressive weakness, paraparesis, anorexia, and panting. A 4 cm diameter grade 3 mammary solid carcinoma involving the fifth right mammary gland had been removed 2 days prior to the current visit. While hospitalized, the dog was diagnosed with Addison's disease based on electrolyte disturbances and low serum cortisol levels following adrenocorticotropic hormone stimulation test. An abdominal ultrasound revealed adrenal glands at the upper limit of normal size. Despite treatment, the dog deteriorated and died 4 days after presentation. A postmortem examination revealed a neoplastic infiltrate of epithelial malignant cells in both adrenal glands, popliteal lymph nodes, vertebral bodies, and paralumbar musculature, compatible with metastasis from mammary carcinoma. To our knowledge, this is the first reported case of Addison's disease secondary to metastatic mammary carcinoma in a dog.

DLA class II haplotypes show sex-specific associations with primary hypoadrenocorticism in Standard Poodle dogs.

Addison's disease (AD) is a life-threatening endocrine disorder that occurs spontaneously in both humans and dogs. Associations between MHC class II genes and AD have been shown in several human studies. Our goal was to identify MHC class II associations with AD in a large population of Standard Poodles, a breed highly predisposed to AD. We sequenced exon 2 of the class II genes DLA-DRB1, DLA-DQA1, and DLA-DQB1 in 110 affected and 101 unaffected Standard Poodles and tested for association with AD. After correcting for population structure, two haplotypes were found to confer risk of developing AD in a sex-specific manner: DLA-DRB1*015:01-DQA1*006:01-DQB1*023:01 in males (x2p = 0.03, OR 2.1) and DLA-DRB1*009:01-DQA1*001:01-DQB1*008:01:1 in females (x2p = 0.02, OR 8.43). Sex-specific associations have been previously described in human populations, but this is the first report of this kind in dogs. Consistent with findings in other studies, we found the DLA-DQA1*006:01 allele (x2p = 0.04) to be associated with AD in males independent of haplotype. In females, the haplotype DLA-DRB1*009:01-DQA1*001:01-DQB1*008:01:1 confers a very high risk for developing AD, although its frequency was rare (9 of 124 females) in our study population. Further studies are warranted to validate the findings of this exploratory dataset and to assess the usefulness of this haplotype as a risk marker for AD in female Standard Poodles. Our results highlight the importance of evaluating MHC class II disease associations in large populations, and accounting for both biological sex and population structure.

Lymphocyte Subsets in the Adrenal Glands of Dogs With Primary Hypoadrenocorticism.

Primary hypoadrenocorticism, or Addison's disease, is an autoimmune condition common in certain dog breeds that leads to the destruction of the adrenal cortex and a clinical syndrome involving anorexia, gastrointestinal upset, and electrolyte imbalances. Previous studies have demonstrated that this destruction is strongly associated with lymphocytic-plasmacytic inflammation and that the lymphocytes are primarily T cells. In this study, we used both immunohistochemistry and in situ hybridization to characterize the T-cell subtypes involved. We collected postmortem specimens of 5 dogs with primary hypoadrenocorticism and 2 control dogs and, using the aforementioned techniques, showed that the lymphocytes are primarily CD4+ rather than CD8+. These findings have important implications for improving our understanding of the pathogenesis and in searching for the underlying causative genetic polymorphisms.

Prevalence and clinical features of hypoadrenocorticism in Great Pyrenees dogs in a referred population: 11 cases.

Naturally occurring hypoadrenocorticism (Addison's disease) is uncommon, with an estimated prevalence in the canine population between 0.06% and 0.28%. This retrospective study evaluated the prevalence and clinical features of hypoadrenocorticism in Great Pyrenees (GP) dogs presented to the Centre Hospitalier Universitaire Vétérinaire of the University of Montreal between March 2005 and October 2014. During this period, 100 dogs were diagnosed with hypoadrenocorticism, representing 0.38% [95% confidence interval (CI): 0.26% to 0.5%] of the canine population studied. The highest prevalence was observed in GP (9.73%, 95% CI: 9.12% to 10.35%, P < 0.0001), followed by West Highland white terriers (4.66%, 95% CI: 4.24% to 5.09%, P < 0.0001), Great Danes (1.87%, 95% CI: 1.6% to 2.14%, P < 0.0001), standard poodles (1.76%, 95% CI: 1.5% to 2.02%, P = 0.0001), Saint Bernards (1.72%, 95% CI: 1.47% to 1.98%, P = 0.018), and Jack Russell terriers (1.48%, 95% CI: 1.24% to 1.72%, P = 0.003). Although most clinical features were nonspecific, Great Pyrenees dogs were more frequently presented with anemia, azotemia, and eosinophilia, or with hypotension and cachexia compared with dogs of other breeds.

Prévalence et caractéristiques cliniques de l'hypoadrenocorticisme chez les Montagnes des Pyrénées au sein d'une population référée : 11 cas. L'hypoadrénocorticisme (maladie d'Addison) est une maladie rare dont la prévalence est estimée à 0,06 % à 0,28 % au sein de la population canine générale. L'objectif de cette étude rétrospective est d'évaluer la prévalence et les caractéristiques cliniques de l'hypoadrénocorticisme chez les Montagne des Pyrénées présentés au Centre Hospitalier Universitaire Vétérinaire de l'Université de Montréal entre mars 2005 et octobre 2014. Cent chiens ont été diagnostiqués avec l'hypoadrénocorticisme, représentant 0,38 % (95 % CI : 0,26 % à 0,5 %) de la population canine étudiée. La prévalence la plus élevée est observée pour les chiens Montagnes des Pyrénées (9,73 %, 95 % CI : 9,12 % à 10,35 % P < 0,0001), suivie des West Highland white terriers (4,66 %, 95 % CI : 4,24 % à 5,09 %, P < 0,0001), Grand Danois (1,87 %, 95 % CI : 1,6 % à 2,14 %, P < 0,0001), Caniches standards (1,76 %, 95 % CI : 1,5 % à 2,02 %, P = 0,0001), Saint-Bernards (1,72 %, 95 % CI : 1,47 % à 1,98 %, P = 0,018), et les Jack Russell terriers (1,48 %, 95 % CI : 1,24 % à 1,72 %, P = 0,003). Bien que les caractéristiques cliniques soient non spécifiques, comparativement aux autres chiens atteints d'hypoadrénocorticisme les Montagnes des Pyrénées étaient plus souvent présentés avec une anémie, une azotémie et une éosinophilie, ou encore en hypotension ou cachectique.(Traduit par les auteurs).

Generalized vitiligo in a dog with primary hypoadrenocorticism.

BACKGROUND: Vitiligo is presumed to be an autoimmune disorder in the dog; primary adrenal insufficiency (Addison's disease) is associated with immune-mediated destruction of the adrenal cortex. HYPOTHESIS/OBJECTIVES: In this case report we describe a dog with primary hypoadrenocorticism that developed generalized vitiligo. CASE REPORT: A 4-year-old spayed female cross-bred dog developed signs of Addison's disease and this was confirmed by biochemical testing; the dog was treated with fludrocortisone acetate and then desoxycorticosterone pivalate. Three months after the diagnosis, the dog developed depigmentation of the whole hair coat and of several focal areas of the skin. Histopathological findings were consistent with vitiligo. CONCLUSIONS AND CLINICAL IMPORTANCE: Dogs with immune-mediated disease may develop other manifestations of immune-mediated disease, including a combination of Addison's disease and vitiligo. The cause in this case was not determined.

A suspected case of Addison's disease in cattle.

A 4.75-year old Simmental cow was presented with symptoms of colic and ileus. The clinical signs and blood analysis resulted in the diagnosis of suspected primary hypoadrenocorticism (Addison's disease). Although Addison's disease has been frequently described in other domestic mammals, to our knowledge, this disease has not previously been reported in cattle.

Un cas suspecté de la maladie d'Addison chez le bétail. Une vache Simmental âgée de 4,75 ans a été présentée avec des symptômes de coliques et d'occlusion intestinale. Les signes cliniques et l'analyse sanguine ont conduit à un diagnostic d'hypoadrénocorticisme primaire suspecté (maladie d'Addison). Même si la maladie d'Addison a souvent été décrite chez d'autres mammifères domestiques, à notre connaissance, cette maladie n'a pas été décrite antérieurement chez le bétail.(Traduit par Isabelle Vallières).

Hypoadrenocorticism (Addison's disease) in a Hoffmann's two-toed sloth (Choloepus hoffmanni).

A 22-yr-old, captive-born, presumed female Hoffmann's two-toed sloth (Choloepus hoffmanni) presented in respiratory distress with severe dehydration and symptoms of hypotension. During treatment, dysphagia was noted and oral examination revealed enlarged palatine tonsils and mucosal plaques. Bloodwork showed a decreased sodium:potassium ratio, a low baseline cortisol, a decreased adrenocorticotropin response test, and a blunted aldosterone stimulation test. All values were compared to a healthy male Hoffmann's two-toed sloth at the same facility. Despite aggressive medical management and treatment for hypoadrenocorticism, the sloth was found deceased. Necropsy revealed abdominal effusion, multifocal plaques throughout the upper gastrointestinal tract, and testes. Histopathology showed marked adrenal cortical atrophy and intranuclear mucosal inclusions in the gastrointestinal tract; advanced molecular techniques did not uncover any viral etiologies. This is the first reported case of hypoadrenocorticism in a sloth.

Mineralocorticoid before glucocorticoid deficiency in a dog with primary hypoadrenocorticism and hypothyroidism.

A dog with an unexpected presentation of primary hypoadrenocorticism was evaluated for clinical signs and electrolyte abnormalities characteristic of Addison's disease. Although the initial adrenocorticotropic hormone (ACTH) stimulation test documented serum cortisol concentrations within the reference range, subsequent assessments confirmed hypoaldosteronism. Mineralocorticoid replacement promptly normalized electrolytes and transiently improved clinical illness. Six weeks after initial ACTH stimulation testing, the dog became glucocorticoid deficient. Concurrent primary hypothyroidism was also documented. Hypoaldosteronism preceding hypocortisolemia is a unique presentation of canine Addison's disease.

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.

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.

Evaluation of symmetric dimethylarginine and creatinine in dogs with primary hypoadrenocorticism receiving long-term mineralocorticoid replacement therapy.

OBJECTIVES: To investigate kidney function by determining serum symmetric dimethylarginine (sSDMA) and serum creatinine (sCr) concentrations in dogs with primary hypoadrenocorticism (PH) receiving long-term mineralocorticoid replacement therapy. METHODS: Dogs with PH receiving a minimum of 12 months of either desoxycorticosterone pivalate or fludrocortisone acetate were included in the study provided that banked frozen serum samples were available for sSDMA analysis. sCr concentrations were retrieved from the medical records. In dogs still alive and presented for regular re-evaluations and in newly diagnosed patients, blood was prospectively collected for sSDMA and sCr determination. RESULTS: Thirty-two dogs met the inclusion criteria. The treatment time ranged from 12 to 146 months after initial diagnosis (median, 55.5 months). The majority of dogs had normal sSDMA and sCr concentrations throughout the hormone replacement treatment. Both sSDMA and sCr concentrations were persistently elevated in three of 32 dogs. Further workup confirmed chronic kidney disease (CKD) in all three dogs. CONCLUSIONS: Based on these data, the prevalence of CKD could be higher in dogs with PH receiving long-term mineralocorticoid replacement treatment than in the general dog population. However, additional studies with a larger number of dogs are needed to confirm it.

Adrenocortical insufficiency in horses and foals.

The adrenal cortices produce various steroid hormones that play vital roles in several physiologic processes. Although permanent adrenocortical insufficiency is rare in all species, emerging evidence in both human and equine medicine suggests that transient reversible adrenocortical dysfunction resulting in cortisol insufficiency frequently develops during critical illness. This syndrome is termed relative adrenal insufficiency (RAI) or critical illness-related corticosteroid insufficiency (CIRCI) and can contribute substantially to morbidity and mortality associated with the primary disease. This review discusses the mechanisms, diagnosis, and clinical consequences of adrenocortical insufficiency, with particular focus on the current understanding of RAI/CIRCI in horses and foals.

Association of a dog leukocyte antigen class II haplotype with hypoadrenocorticism in Nova Scotia Duck Tolling Retrievers.

Canine hypoadrenocorticism (Addison's disease) is due to a deficiency of corticosteroids and mineralocorticoids produced by the adrenals. Although this is a relatively uncommon disease in the general dog population, some breeds, including the Nova Scotia Duck Tolling Retriever (NSDTR), are at increased risk for developing hypoadrenocorticism. A prior study has shown that the increased risk is due to a heritable component. This potentially lethal disorder is hypothesized to have an autoimmune etiology, thus the aim of this study was to determine whether genetic susceptibility to hypoadrenocorticism in NSDTRs is associated with genes of the canine major histocompatibility complex [MHC; dog leukocyte antigen system (DLA)]. Samples were collected from NSDTRs diagnosed with hypoadrenocorticism and healthy siblings or country-matched controls. The DLA class II alleles and haplotypes were determined and compared between cases and controls. We found seven different haplotypes of which the haplotype DLA-DRB1*01502/DQA*00601/DQB1*02301 was significantly more prevalent in the diseased dogs (P = 0.044). In addition, these affected dogs also were more likely to be homozygous across the DLA class II region than the control dogs (OR = 6.7, CI = 1.5-29.3, P = 0.011). We also found that homozygous dogs, regardless of their haplotype, tended to have earlier disease onset compared with heterozygous dogs. These data indicate a limited MHC diversity in North American NSDTRs and suggest that the MHC may play a role in the development of hypoadrenocorticism in the NSDTR, supporting the autoimmune origin of the disease.

Canine hypoadrenocorticism: part I.

Hypoadrenocorticism (Addison's disease) has been referred to as "the great pretender," due to its ability to mimic other common diseases in the dog and thereby represent a diagnostic challenge. Naturally occurring hypoadrenocorticism is an uncommon canine disease. Young, female dogs are overrepresented. Hypoadrenocorticism typically results from immune-mediated destruction of all adrenocortical layers, resulting in deficiencies of min-eralocorticoids (aldosterone) and glucocorticoids (cortisol). A small number of dogs suffer from glucocorticoid deficiency only. Dogs suffering from hypoadrenocorticism may present in a variety of conditions, from a mildly ill dog to a shocky and recumbent dog. This review discusses etiology, pathophysiology, history, physical examination findings, and diagnostic findings in the Addisonian patient. A follow-up article (Part II) will discuss the definitive diagnosis and management strategies for these patients.

Canine hypoadrenocorticism: part II.

Dogs with chronic, vague gastrointestinal signs and those with signs and laboratory abnormalities suggestive of an Addisonian crisis should be tested for hypoadrenocorticism. A previous article (Part I; Can Vet J 2009;50:63-69) discussed the etiology, pathophysiology, clinical signs, and diagnostic abnormalities found in these patients. The present article discusses definitive diagnosis and treatment for both the acute and the chronic Addisonian patient. Expedient treatment remains the cornerstone of management for these patients, particularly those in the former category. The long-term prognosis is excellent for these patients, given well-educated, committed, and vigilant owners.

Machine learning algorithm as a diagnostic tool for hypoadrenocorticism in dogs.

Canine hypoadrenocorticism (CHA) is a life-threatening condition that affects approximately 3 of 1,000 dogs. It has a wide array of clinical signs and is known to mimic other disease processes, including kidney and gastrointestinal diseases, creating a diagnostic challenge. Because CHA can be fatal if not appropriately treated, there is risk to the patient if the condition is not diagnosed. However, the prognosis is excellent with appropriate therapy. A major hurdle to diagnosing CHA is the lack of awareness and low index of suspicion. Once suspected, the application and interpretation of conclusive diagnostic tests is relatively straight forward. In this study, machine learning methods were employed to aid in the diagnosis of CHA using routinely collected screening diagnostics (complete blood count and serum chemistry panel). These data were collected for 908 control dogs (suspected to have CHA, but disease ruled out) and 133 dogs with confirmed CHA. A boosted tree algorithm (AdaBoost) was trained with 80% of the collected data, and 20% was then utilized as test data to assess performance. Algorithm learning was demonstrated as the training set was increased from 0 to 600 dogs. The developed algorithm model has a sensitivity of 96.3% (95% CI, 81.7%-99.8%), specificity of 97.2% (95% CI, 93.7%-98.8%), and an area under the receiver operator characteristic curve of 0.994 (95% CI, 0.984-0.999), and it outperforms other screening methods including logistic regression analysis. An easy-to-use graphical interface allows the practitioner to easily implement this technology to screen for CHA leading to improved outcomes for patients and owners.

[Therapy of primary hypoadrenocorticism in dogs with low dose desoxycorticosterone pivalate]. / Therapie des primären Hypoadrenokortizismus beim Hund mit niedrig dosiertem Desoxycorticosteronpivalat.

OBJECTIVE: Since 2016 the only approved drug for the treatment of primary hypoadrenocorticism (Addisons disease) in dogs in Germany is desoxycorticosterone pivalate (DOCP), namely Zycortal®. The initial dose recommended by the manufacturer is 2.2 mg/kg. Our own experience and select publications raise the suspicion that a distinctly lower initial dose would be sufficient. Mainly cost reduction motivates for dose reduction and with it comes a higher owner motivation and compliance. It was the objective of our retrospective study to show that an initial dose of 1.5 mg/kg DOCP is sufficient for controlling canine hypoadrenocorticism. MATERIAL AND METHODS: Dogs with primary hypoadrenocorticism were included if the initial starting dose was 1.5 mg/kg DOCP subcutaneously. The first, second and the last known dose of DOCP were documented. Electrolyte concentrations at the time of diagnosis as well as 10-14 days after the first injection, on the day of the second injection as well as at the last known injection were recorded. A dog was considered medically well-regulated when clinically healthy, sodium and potassium concentrations within the reference ranges, and when the responsible veterinarian did not recommended a dose alteration. RESULTS: All 13 included dogs were clinically healthy after the first or second injection. One dog received 1.6 mg/kg DOCP as last documented dose, all other dogs received ≤ 1.5 mg/kg (median: 1.3, range: 0.4-1.6) DOCP. Eleven dogs were injected once monthly, 2 dogs received injections every 60 days. The dogs were followed at least 7 months (median: 20 months, range: 7-26 months). CONCLUSION AND CLINICAL RELEVANCE: We were able to show that a starting dose of 1.5 mg/kg DOCP (Zycortal®) is sufficient for controlling primary hypoadrenocorticism in dogs. Adjustments of the dose are needed in some dogs. Regular measurement of electrolyte concentrations 10 days after treatment initiation and at the monthly DOCP injection is required for a correct disease management with DOCP.

Randomised clinical non-inferiority trial comparing two formulations of desoxycortone pivalate for the treatment of canine primary hypoadrenocorticism.

BACKGROUND: This clinical trial compared two formulations of desoxycortone pivalate (DOCP) for treating the mineralocorticoid deficit in dogs with primary hypoadrenocorticism (PH). METHODS: At veterinary clinics in the USA and France, dogs with PH (n=152) were randomised (3:1) to receive approximately monthly treatments with either the test product, Zycortal (Dechra), administered subcutaneously (n=113), or the control product, Percorten-V (Novartis Animal Health), administered intramuscularly (n=39), both at an initial dose of 2.2 mg/kg DOCP. Treatment administrators were unblinded; veterinarians assessing clinical signs were blinded; owners were blinded until at least day 90, the primary end point. Veterinarians assessed treatment outcome based on all of the following: clinical signs; sodium concentrations; potassium concentrations. Dogs received concurrent glucocorticoid therapy throughout the trial. Non-inferiority was assessed using a generalised linear mixed model to compare success rates between groups. RESULTS: Success rates at day 90 were similar between groups (per-protocol population at day 90: Zycortal 87/101, 86.2 per cent, Percorten-V 29/34, 85.1 per cent). Zycortal was non-inferior to Percorten-V as the upper limit of the 95 per cent CI for the difference between groups was 13.6 per cent. Polydipsia and polyuria were the most common clinical observations. CONCLUSION: Both products, in combination with glucocorticoid therapy, were safe and effective in treating PH.

Suspected bilateral adrenal gland tumour causing primary Addison's disease in a dog.

A 13-year old miniature poodle presented with a 3-day episode of vomiting, anorexia, and lethargy. Lack of micturition had been noted for 2 days. Clinical examination indicated dehydration and a tense, painful abdomen. Laboratory parameters (severe azotaemia, hyperkalaemia, severe hyponatraemia, hypochloraemia, and hyperphosphataemia with glucosuria and proteinuria) were consistent with anuric acute kidney injury (AKI). Abdominal ultrasound revealed bilateral adrenal masses. ACTH stimulation test was diagnostic for Addison's disease. Computed tomography confirmed bilateral adrenal masses and indicated multifocal liver nodules. Additionally, infiltration of the caudal vena cava with partial luminal occlusion was demonstrated. Surgical removal of the adrenal masses with venous plasty intervention and stenting of the vessels deemed unrewarding in this patient in respect to progressed tumour growth with assumed metastatic spread. The dog was treated for Addison's disease and discharged with good overall condition. Eight weeks later, the dog was euthanized due to progressive caudal vena cava occlusion. Whilst hypoadrenocoticism typically affects young to middle aged dogs, in old dogs primary Addison's disease might be caused by neoplastic bilateral adrenal gland destruction. This is the first case report of hypovolaemia leading to AKI secondary to bilateral adrenal masses causing Addison's disease in a dog.