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[Juvenile Addison´s Disease in the Cavalier King Charles Spaniel].

Authors:
Veronika Simerdova at Addicoo
Veronika Simerdova
  • Addicoo
Ivana Fazekasova at KVL SR / Company of veterinary doctors Slovac republic/
Ivana Fazekasova
  • KVL SR / Company of veterinary doctors Slovac republic/
Ivo Hajek at AniCura
Ivo Hajek
  • AniCura
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JUVENILNÍ ADDISONOVA CHOROBA U KAVALÍR KING CHARLES
ŠPANĚLA
Veronika Šimerdová, Ivana Fazekašová, Ivo Hájek
Sibra Centrum, Bratislava
Úvod
Hypoadrenokorticismus (Addisonova choroba) vzniká jako následek
nedostatečné tvorby glukokortikoidů a mineralokortikoidů
v nadledvinách. Mechanismem vzniku tohoto onemocnění je nejčastěji
bilaterální atrofie kůry nadledvin v důsledku autoimunitního procesu.1
Klinické příznaky jsou nespecifické a nejčastěji zahrnují zvracení, průjem,
letargii, anorexii a slabost.2 Neléčená Addisonova choroba může přejít
v tzv. Addisonskou krizi, která je jedním z mála život ohrožujících stavů
ve veterinární endokrinologii.3 Terapie Addisonovy choroby je doživotní
a spočívá v podávání glukokortikoidů a mineralokortikoidů.4
Popis případu
Na Sibra Centrum byl prezentován osmitýdenní Kavalír King Charles
španěl (nekastrovaná fena, 1,85 kg) z důvodu jeden týden trvající
anorexie, letargie a intermitentních průjmů. Vakcinace pacienta byla
nekompletní. Podání antibiotik a infuzní terapie na předchozím pracovišti
nevedly k trvalému zlepšení klinického stavu. Klinickým vyšetřením byla
zjištěna apatie, celková slabost, hypotermie a prodloužené CRT.
V průběhu klinického vyšetření došlo k hematemezi. Hematologickým
vyšetřením byla zjištěna leukocytóza, lymfocytóza a eosinofilie,
biochemickým vyšetřením periferní krve elevace urey, hypoglykemie,
hyponatremie a hyperkalemie (viz tabulka 1). Diagnostický test na průkaz
antigenu parvoviru (WITNESS® CPV, Zoetis) v trusu byl negativní.
Rentgenologickým a ultrasonografickým vyšetřením dutiny břišní byl
zjištěn normální nález. Vyšetřením rektálního výtěru byla zjištěna
polymorfní populace bakterií. Elektrokardiografické vyšetření neodhalilo
žádné abnormality. U pacienta byla zahájena symptomatická terapie
spočívající v umístění na vyhřívanou podložku, podání glukózy, infuzní
terapii a ochranné léčbě sliznic. Tato léčba vedla k mírnému klinickému
zlepšení. Vzhledem k přetrvávajícím změnám v koncentraci sodíku a
draslíku (poměr sodíku a draslíku 19:1, normální hodnota 27:1 až 40:1)
bylo vysloveno podezření na Addisonovu chorobu. Provedení ACTH-
stimulačního testu potvrdilo suspektní diagnózu. Syntetický ACTH
(tetrakosaktid; Synacthen, Novartis) byl podán v dávce 5 µg/kg
intravenózně, krev na stanovení kortizolu byla odebrána před aplikací a
hodinu po aplikaci. Hodnoty jsou uvedeny v tabulce 1. I když se pacient
po podání kortikoidů významně klinicky zlepšil, majitelka odmítla nutnost
doživotní medikace a zvolila eutanázii.
Diskuze
Medián věku diagnózy Addisonovy choroby činí u psů 4 roky.4 Juvenilní
forma tohoto onemocnění byla popsána u Nova Scotia duck tolling
retrívrů s výskytem od 7,5 týdnů věku. Polovina Nova Scotia duck tolling
retrívrů je v době diagnózy mladších 2,5 let.5 Addisonova choroba je u
tohoto plemene dědičná.6 Predispozice k Addisonově chorobě ani
juvenilní Addisonova choroba nebyla u Kavalír King Charles španěla
dosud popsána.
Závěr
Toto sdělení je prvním popisem juvenilní Addisonovy choroby u Kavalír
King Charles španěla. Addisonova choroba by měla být součástí
diferenciální diagnózy letargie a intermitentních gastrointestinálních
příznaků i u velmi mladých psů.
Literatura:
1. SCHAER, M., RILEY, W. J., BUERGELT, C. D., et al. Autoimmunity and Addison´s disease in the dog. J Am Anim Hosp
Assoc 1986;22:789-794.
2. LIFTON, S. J., KING, L. G., ZERBE, C. A. Glu cocorticoid deficient hypoadrenocorticism in dogs: 18 cases (1986 -1995). J Am
Vet Med Assoc 1996;209:2076-2081.
3. KOENIG, A. Endocrine emergencies in dogs and cats. Vet Clin North Am Small Anim Pract 2013;43:86 9-897.
4. KINTZER, P. P., PETERSON, M. E. Treatment and lo ng-term follow-up of 205 dogs with hypoa drenocorticism. J Vet In tern
Med 1997;11:43-49.
5. HUGHES, A. M., NELSON, R. W., FAM ULA, T. R., B ANASCH, D . L. Clinical features and heritability of
hypoadrenocorticism in Nova Scotia Duck Tolling Retri evers: 25 cases (1994-2006). J Am Vet Med Assoc 200 7;231:407-412.
6. HUGHES, A. M., JOKINEN, P., BANNA SCH, D. L., LOHI, H., OBERBAUER, A. M. Association of a dog leukocyte antigen
class II haplotype with hypoadrenocorticism in Nova S cotia Duck Tolling Retrievers. Tissue Antigens 2010;75:684 -690.
Adresa pro korespondenci:
MVDr. PharmDr. Veronika Šimerdová
Sibra Centrum
Na vrátkach 13
84101 Bratislava
email: simerdovav@gmail.com
Tabulka 1. Vybrané biochemické a hematologické parametry u pacienta z kazuistiky.
Laboratorní parametr
Jednotka
Hodnota u pacienta
Referenční rozmezí
Glukóza
mmol/l
1,8 ↓
3,05 – 6,1
Urea
mmol/l
23,2 ↑
3,3 – 8
Draslík
µmol/l
7,3 ↑
3,5 – 5
Sodík
µmol/l
136 ↓
140 – 155
pre-ACTH kortizol
ng/ml
0,5 ↓
5 – 65
post-ACTH kortizol
ng/ml
0,5
< 150
Leukocyty
109/l
32,8 ↑
6 – 17
Lymfocyty
109/l
13,9 ↑
0,9 – 5
Eosinofily
109/l
3,4 ↑
0,1 – 1,5
ResearchGate has not been able to resolve any citations for this publication.
Treatment and Long-Term Follow-up of 205 Dogs With Hypoadrenocorticism
Article
Full-text available
Results of long-term treatment were evaluated in 200 dogs with primary hypoadrenocorticism and 5 dogs with spontaneous secondary hypoadrenocorticism. Fludrocortisone acetate initially was used for mineralocorticoid replacement in 190 of the dogs with primary hypoadrenocorticism. The daily dose of fludrocortisone required in these dogs increased significantly during the treatment period (median, 2.6 years) from an initial median dose of 13.1 μg/kg to a final dose of 22.6 μg/kg. In 27 of the 200 dogs, mineralocorticoid therapy was changed from fludrocortisone to desoxycorticosterone pivalate (DOCP) because of adverse effects, poor response, or financial considerations. The dose of DOCP required in the 33 dogs (27 dogs plus 6 dogs initially given DOCP) increased significantly during the treatment period (median, 3.5 years) from an initial median dose of 1.56 mg/kg to a final dose of 1.69 mg/kg; the interval between DOCP injections ranged from 14 to 35 days (median, 30 days). The dose of prednisone administered to the dogs with primary hypoadrenocorticism decreased significantly from an initial median dose of 0.3 mg/kg to a final dose of 0.2 mg/kg; the drug was discontinued in 22 dogs due to adverse effects. The 5 dogs with secondary hypoadrenocorticism received only glucocorticoid replacement therapy (prednisone) at initial and final daily dosages of 0.41 mg/kg and 0.25 mg/kg, respectively, during a median treatment period of 4.4 years. More than 80% of the dogs were considered to have a good to excellent response to therapy. The median survival time of all 205 dogs was 4.7 years. There were no differences in response to treatment or survival between dogs treated with fludrocortisone and those receiving DOCP, or between dogs with primary hypoadrenocorticism and those with secondary hypoadrenocorticism.
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Endocrine Emergencies in Dogs and Cats
Article
  • Jul 2013
Success in treatment of endocrine emergencies is contingent on early recognition and treatment. Many endocrine diseases presenting emergently have nonspecific signs and symptoms. In addition, these endocrine crises are often precipitated by concurrent disease, further making early identification difficult. This article concentrates on recognition and emergency management of the most common endocrine crises in dogs and cats.
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Association of a dog leukocyte antigen class II haplotype with hypoadrenocorticism in Nova Scotia Duck Tolling Retrievers
Article
  • Jun 2010
  • TISSUE ANTIGENS
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.
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Glucocorticoid deficient hypoadrenocorticism in dogs
Article
  • Dec 1996
  • JAVMA-J AM VET MED A
To characterize naturally developing glucocorticoid deficiency in dogs. Retrospective case series. 18 dogs with glucocorticoid deficiency defined by an inadequate response to stimulation with adrenocorticotropic hormone (ACTH), a normal Na:K ratio (> 27), and no history of receiving corticosteroids for at least 6 weeks. Information including signalment, body weight, clinical signs on admission, historical findings, physical examination findings, results of CBC and serum biochemical analyses, results of ACTH stimulation tests and other ancillary endocrine tests, diagnostic imaging findings, findings from other procedures such as endoscopy and surgery, and information on concurrent diseases, management, and outcome were retrieved from the medical records of dogs with glucocorticoid deficiency treated between 1986 and 1995 at the University of Pennsylvania's School of Veterinary Medicine and 2 dogs from private practices. Most dogs were young (< 7 years) and represented larger breeds (> 20 kg). Clinical signs were nonspecific: lethargy, weight loss, and gastrointestinal disturbances including regurgitation with radiographic evidence of megaesophagus. Hypocholesterolemia, hypoalbuminemia, hypoglycemia, and a mild, nonregenerative anemia were common. Ten of the 18 dogs responded well to glucocorticoid supplementation alone, with only 2 dogs developing electrolyte abnormalities. Four (22%) of the dogs died, with death usually occurring as a result of secondary disease processes rather than hypoadrenocorticism. An ACTH stimulation test should be considered as part of the diagnostic plan in dogs with signs of weight loss, inappetence, and intermittent vomiting and diarrhea. Glucocorticoid-deficient dogs may not require supplemental mineralocorticoids.
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Clinical features and heritability of hypoadrenocorticism in Nova Scotia Duck Tolling Retrievers: 25 cases
  • Jan 1994
  • 407-412
  • A M Hughes
  • R W Nelson
  • T R Famula
  • D L Banasch
HUGHES, A. M., NELSON, R. W., FAMULA, T. R., BANASCH, D. L. Clinical features and heritability of hypoadrenocorticism in Nova Scotia Duck Tolling Retrievers: 25 cases (1994-2006). J Am Vet Med Assoc 2007;231:407-412.