Hypoadrenocorticism is a clinical syndrome resulting from deficiency of glucocorticoids, mineralocorticoids, or typically both. The most common cause of hypoadrenocorticism in dogs is complete loss of adrenal gland cortical function, although selective destruction of the zona fasciculata resulting in glucocorticoid, but not mineralocorticoid, deficiency has been reported.1-5 Glucocorticoid deficiency may also result from impaired secretion of ACTH by pituitary gland corticotrophs but is uncommon in dogs.3-5
Hypoadrenocorticism is most commonly diagnosed in young female dogs.1,4,6 In 1 retrospective study4 involving 225 dogs with hypoadrenocorticism, 71% were female and the median age at diagnosis was 4.0 years (25th to 75th percentile, 2.5 to 6.5 years). Breeds reported to be at increased risk for hypoadrenocorticism include Great Dane, Portuguese Water Dog, Rottweiler, Standard Poodle, West Highland White Terrier, Soft Coated Wheaten Terrier, Bearded Collie, and Leonberger.4,7-10 The narrow-sense heritability of hypoadrenocorticism in Bearded Collies, Standard Poodles, and Portuguese Water Dogs has been estimated as 0.76, 0.75, and 0.49, respectively, with both sexes equally affected.7-9 Narrow-sense heritability is a measure of how a trait or disease will respond to selection and is measured on a scale of 0 to 1. In Standard Poodles and Portuguese Water Dogs, hypoadrenocorticism is likely influenced by a major locus with an autosomal recessive mode of inheritance8,9; however, the mode of inheritance in Bearded Collies is less definitive.7 Research is ongoing to determine the genes involved in hypoadrenocorticism in these breeds.7-9,12
The NSDTR is a relatively rare breed that was developed in Nova Scotia, Canada, to lure (toll) waterfowl to the shoreline and retrieve them for hunters. The breed was accepted into the AKC in July 2003, and AKC records indicate that 347 NSDTR puppies were registered in 2005.13 Hypoadrenocorticism in 5 related NSDTRs was reported in 1997,14 and a recent health survey of NSDTRs performed by the Toller Health Coalition identified hypoadrenocorticism in 12 of 1,180 NSDTRs.15 At the time of diagnosis, the mean age was 2.35 years and the youngest age was 15 weeks. Four of the 12 affected NSDTRs died at a mean age of 3.25 years.15 This information suggests a genetic basis for hypoadrenocorticism in NSDTRs. The purpose of the study reported here was to evaluate the clinical features and examine the heritability and mode of inheritance of naturally occurring hypoadrenocorticism in NSDTRs.
Nova Scotia Duck Tolling Retriever
American Kennel Club
Highest density region
SOLAR (Sequential Oligogenic Linkage Analysis Routines), version 4.0.5 for Linux, Southwest Foundation for Biomedical Research, San Antonio, Tx. Available at: www.sfbr.org/solar/. Accessed Sep 8, 2006.
iBay, version 1.0, Janss Biostatistics, Leiden, Netherlands. Available at: www.lucjanss.com. Accessed Mar 20, 2006.
Janss LLG. MAGGIC. A package of subroutines for genetic analyses with Gibbs sampling (abstr), in Proceedings. 6th World Congr Genet Appl Livest Prod 1998;27:459–460.
Florinef acetate, Global Pharmaceuticals, Philadelphia, Pa.
Willard MD, Schall WD & McCaw DE, et al. Canine hypoadrenocorticism: report of 37 cases and review of 39 previously reported cases. J Am Vet Med Assoc 1982;180:59–62.
Rakich PM, Lorenz MD. Clinical signs and laboratory abnormalities in 23 dogs with spontaneous hypoadrenocorticism. J Am Anim Hosp Assoc 1984;20:647–649.
Lifton SJ, King LG, Zerbe CA. Glucocorticoid deficient hypoadrenocorticism in dogs: 18 cases (1986–1995). J Am Vet Med Assoc 1996;209:2076–2081.
Peterson ME, Kintzer PP, Kass PH. Pretreatment clinical and laboratory findings in dogs with hypoadrenocorticism: 225 cases (1979–1993). J Am Vet Med Assoc 1996;208:85–91.
Sadek D, Schaer M. Atypical Addison's disease in the dog: a retrospective survey of 14 cases. J Am Anim Hosp Assoc 1996;32:159–163.
Feldman EC, Nelson RW. Hypoadrenocorticism (Addison's disease). In:Canine and feline endocrinology and reproduction. 3rd ed. St Louis: Elsevier Saunders, 2004;396–397.
Famula TR, Belanger JM, Oberbauer AM. Heritability and complex segregation analysis of hypoadrenocorticism in the standard poodle. J Small Anim Pract 2003;44:8–12.
Oberbauer AM, Bell JS & Belanger JM, et al. Genetic evaluation of Addison's disease in the Portuguese Water Dog. BMC Vet Res 2006;2: 15.
Chase K, Sargan D & Miller K, et al. Understanding the genetics of autoimmune disease: two loci that regulate late onset Addison's disease in Portuguese Water Dogs. Int J Immunogenet 2006;33:179–184.
American Kennel Club Web site. Dog registration statistics. Available at: www.akc.org/reg/dogreg_stats.cfm. Accessed Apr 12, 2006.
Burton S, DeLay J & Holmes A, et al. Hypoadrenocorticism in young related Nova Scotia Duck Tolling Retrievers. Can Vet J 1997;38:231–234.
Nova Scotia Duck Tolling Retriever Health Survey Web site. Available at: www.tollerhealth.com/SurveySummary.html. Accessed May 12, 2004.
Lynch M, Walsh B. Threshold characters. In:Genetics and analysis of quantitative traits. Sunderland, Mass: Sinauer Associates, 1998;727–744.
Duggirala R, Williams JT & Williams-Blangero S, et al. A variance component approach to dichotomous trait linkage analysis using a threshold model. Genet Epidemiol 1997;14:987–992.
Lynch M, Walsh B. Detecting major genes. In:Genetics and analysis of quantitative traits. Sunderland, Mass: Sinauer Associates, 1998;364–375.
Elston RC, Nasmboodrii KK & Glueck CJ, et al. Studies of the genetic transmission of hypercholesterolemia and hypertriglyceridemia in 195 member kindred. Ann Hum Genet 1975;39:67–87.
Kadarmideen HN, Janss LLG. Evidence for a major gene from Bayesian segregation analysis of liability to osteochondral diseases in pigs. Genetics 2005;171:1195–1206.
Morton NE, MacLean CJ. Analysis of family resemblance. III. Complex segregation of quantitative traits. Am J Hum Genet 1974;26:489–503.