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      Naturally Occurring Adrenocortical Insufficiency – An Epidemiological Study Based on a Swedish‐Insured Dog Population of 525,028 Dogs

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          Abstract

          Background

          Naturally occurring adrenocortical insufficiency ( NOAI) in dogs is considered an uncommon disease with good prognosis with hormonal replacement treatment. However, there are no epidemiological studies with estimates for the general dog population.

          Objectives

          To investigate the epidemiological characteristics of NOAI in a large population of insured dogs.

          Animals

          Data were derived from 525,028 client‐owned dogs insured by a Swedish insurance company representing 2,364,652 dog‐years at risk ( DYAR) during the period between 1995–2006.

          Methods

          Retrospective cohort study. Incidence rates, prevalences, and relative risks for dogs with NOAI ( AI with no previous claim for hypercortisolism), were calculated for the whole dog population, and for subgroups divided by breed and sex. Mortality rates were calculated and compared in dogs with NOAI and the remaining dogs overall.

          Results

          In total 534 dogs were identified with NOAI. The overall incidence was 2.3 cases per 10,000 DYAR. The relative risk of disease was significantly higher in the Portuguese Water Dog, Standard Poodle, Bearded Collie, Cairn Terrier, and Cocker Spaniel compared with other breeds combined. Female dogs overall were at higher risk of developing AI than male dogs ( RR 1.85; 95% CI, 1.55–2.22; P < .001). The relative risk of death was 1.9 times higher in dogs with NOAI than in dogs overall.

          Conclusion and Clinical Importance

          The data supports the existence of breed‐specific differences in incidence rates of NOAI in dogs.

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          Normal overall mortality rate in Addison's disease, but young patients are at risk of premature death.

          Kristian Løvås, Erik R. Hauge, Johan Svartberg … (2009)
          Primary adrenal insufficiency (Addison's disease) is a rare autoimmune disease. Until recently, life expectancy in Addison's disease patients was considered normal. To determine the mortality rate in Addison's disease patients. i) Patients registered with Addison's disease in Norway during 1943-2005 were identified through search in hospital diagnosis registries. Scrutiny of the medical records provided diagnostic accuracy and age at diagnosis. ii) The patients who had died were identified from the National Directory of Residents. iii) Background mortality data were obtained from Statistics Norway, and standard mortality rate (SMR) calculated. iv) Death diagnoses were obtained from the Norwegian Death Cause Registry. Totally 811 patients with Addison's disease were identified, of whom 147 were deceased. Overall SMR was 1.15 (95% confidence intervals (CI) 0.96-1.35), similar in females (1.18 (0.92-1.44)) and males (1.10 (0.80-1.39)). Patients diagnosed before the age of 40 had significantly elevated SMR at 1.50 (95% CI 1.09-2.01), most pronounced in males (2.03 (1.19-2.86)). Acute adrenal failure was a major cause of death; infection and sudden death were more common than in the general population. The mean ages at death for females (75.7 years) and males (64.8 years) were 3.2 and 11.2 years less than the estimated life expectancy. Addison's disease is still a potentially lethal condition, with excess mortality in acute adrenal failure, infection, and sudden death in patients diagnosed at young age. Otherwise, the prognosis is excellent for patients with Addison's disease.
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            MHC Class II Polymorphisms, Autoreactive T-Cells, and Autoimmunity

            Sue Tsai, Pere Santamaria (2013)
            Major histocompatibility complex (MHC) genes, also known as human leukocyte antigen genes (HLA) in humans, are the prevailing contributors of genetic susceptibility to autoimmune diseases such as Type 1 Diabetes (T1D), multiple sclerosis, and rheumatoid arthritis, among others (1–3). Although the pathways through which MHC molecules afford autoimmune risk or resistance remain to be fully mapped out, it is generally accepted that they do so by shaping the central and peripheral T-cell repertoires of the host toward autoimmune proclivity or resistance, respectively. Disease-predisposing MHC alleles would both spare autoreactive thymocytes from central tolerance and bias their development toward a pathogenic phenotype. Protective MHC alleles, on the other hand, would promote central deletion of autoreactive thymocytes and skew their development toward non-pathogenic phenotypes. This interpretation of the data is at odds with two other observations: that in MHC-heterozygous individuals, resistance is dominant over susceptibility; and that it is difficult to understand how deletion of one or a few clonal autoreactive T-cell types would suffice to curb autoimmune responses driven by hundreds if not thousands of autoreactive T-cell specificities. This review provides an update on current advances in our understanding of the mechanisms underlying MHC class II-associated autoimmune disease susceptibility and/or resistance and attempts to reconcile these seemingly opposing concepts.
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              Pretreatment clinical and laboratory findings in dogs with hypoadrenocorticism: 225 cases (1979-1993).

              P Kintzer, P Kass, Gregory M. Peterson (1996)
              To evaluate clinical and laboratory findings in 225 dogs with naturally occurring hypoadrenocorticism diagnosed over a 14-year period. Retrospective case series. 220 dogs with primary hypoadrenocorticism and 5 dogs with secondary hypoadrenocorticism (primary ACTH deficiency). We reviewed medical records of all dogs with naturally occurring hypoadrenocorticism examined at The Animal Medical Center between 1979 and 1993 or at Tufts University, Foster Hospital for Small Animals, between 1987 and 1993. Dogs ranged from 4 months to 14 years old. Most (71%) were female, and female dogs had a significantly higher relative risk of developing hypoadrenocorticism than did males. Great Danes, Portuguese Water Dogs, Rottweilers, Standard Poodles, West Highland White Terriers, and Wheaton Terriers had a significantly higher relative risk of developing hypoadrenocorticism than did dogs of other breeds. Common owner complaints included lethargy, poor appetite, and vomiting, whereas lethargy, weakness, and dehydration were common abnormalities detected on physical examination. Serum biochemical testing at the time of diagnosis revealed moderate-to-severe azotemia and hyperphosphatemia in most dogs. In 99 of 172 (57.6%) dogs that had a pretreatment urinalysis performed, urine specific gravity was < 1.030 even though dogs were azotemic. Serum electrolyte changes included hyperkalemia (n = 215), hyponatremia (183), hypochloremia (94), and hypercalcemia (69). Five of the 220 dogs with primary hypoadrenocorticism and the 5 dogs with secondary hypoadrenocorticism did not have hyperkalemia at time of diagnosis. In all dogs, ACTH stimulation testing revealed a low to low-normal baseline serum cortisol concentration with little to no rise after ACTH administration. Endogenous plasma ACTH concentration measured in 35 dogs with primary hypoadrenocorticism was markedly high; whereas ACTH concentration was undetectable to low in the 5 dogs with secondary hypoadrenocorticism. hypoadrenocorticism is a rare disease in dogs, most commonly affecting young to middle-aged females; some breeds are at greater risk of developing the disease than others. In general, clinical signs are nonspecific and similar to manifestations of more common diseases. Serum electrolyte disturbances of hyperkalemia and hypernatremia are characteristic in dogs with primary hypoadrenocorticism, but concentrations may be normal in dogs with early or mild primary or secondary hypoadrenocorticism. Diagnosis of hypoadrenocorticism is best confirmed by demonstration of a low baseline serum cortisol concentration with a subnormal or negligible response to ACTH administration. Determination of endogenous plasma ACTH concentrations is valuable in differentiating primary from secondary hypoadrenocorticism, particularly in dogs with normal serum electrolyte concentrations.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Vet Intern Med
                Journal ID (iso-abbrev): J. Vet. Intern. Med
                Journal ID (doi): 10.1111/(ISSN)1939-1676
                Journal ID (publisher-id): JVIM
                Title: Journal of Veterinary Internal Medicine
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 0891-6640
                ISSN (Electronic): 1939-1676
                Publication date (Print): Jan-Feb 2016
                Publication date (Electronic): 18 December 2015
                Volume: 30
                Issue: 1 ( doiID: 10.1111/jvim.2016.30.issue-1 )
                Pages: 76-84
                Affiliations
                [ 1 ] Department of Clinical SciencesSwedish University of Agricultural Sciences UppsalaSweden
                [ 2 ] Science for Life Laboratory Department of Medical Biochemistry and MicrobiologyUppsala University UppsalaSweden
                [ 3 ]B Bonnett Consulting Georgian Bluffs ONCanada
                Author notes
                [*] [* ]Corresponding author: Dr J. Hanson, Department of Clinical Sciences – Companion Animals, Swedish University of Agricultural Sciences, P.O. Box 7054, 750 07 Uppsala, Sweden; e‐mail: jeanette.hanson@ 123456slu.se .
                Article
                Publisher ID: JVIM13815
                DOI: 10.1111/jvim.13815
                PMC ID: 4913634
                PubMed ID: 26683136
                SO-VID: f41a8bb2-a33e-4f58-82ae-6af35e25f2c8
                Copyright © Copyright © 2015 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine .
                License:

                This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                Date received : 22 December 2014
                Date revision received : 19 September 2015
                Date accepted : 16 November 2015
                Page count
                Pages: 9
                Funding
                Funded by: Swedish Research Council
                Funded by: Foundation for Research, Agria Insurance Company
                Categories
                Subject: Standard Article
                Subject: SMALL ANIMAL
                Subject: Standard Articles
                Subject: Endocrinology
                Custom metadata
                source-schema-version-number 2.0
                component-id jvim13815
                cover-date January/February 2016
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:4.9.1 mode:remove_FC converted:17.06.2016

                ScienceOpen disciplines: Veterinary medicine
                Keywords: addison's disease,hypoadrenocorticism,incidence
                Data availability:
                ScienceOpen disciplines: Veterinary medicine
                Keywords: addison's disease, hypoadrenocorticism, incidence

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