Dechra Brand Guidelines

Support piece front cover

Support piece inside spread

Case Study

Figure 1.Ultrasonographicpicturedemonstrating the small adrenalglands in this case

History and clinical signs Poppy, an8-year-old female neutered JapaneseAkita (BW36 kg)waspresented for further investigationofweight loss, lethargy and intermittent inappetanceof 3months duration.Onphysical examination, shewas underweightwith abody condition score of 3/9 and hermucousmembraneswerepalepink. A reviewof the clinical history showed no evidenceofprevious steroid administration. Diagnostic work up Thediagnostic investigationswere startedwith routinebloodwork (haematology and serumbiochemistry).This revealed amild non-regenerative anaemia and moderate hypoalbuminaemia. Urinalysis and abile acid stimulation testwereperformeddue to thedetection of hypoalbuminaemia,which excluded liverdysfunction and aprotein losing nephropathy as causesof this.Abdominal ultrasonographywas thenperformed to investigate theweight loss and hypoalbuminaemia.Thisdetectedbilateral small adrenalglands (<2.1mm)only (figure 1).Due to this finding, combinedwith the anaemia and lackof a stress leukogramon haematology and the hypoalbuminaemia, anACTH stimulation testwasperformed. It is important to exclude hypoadrenocorticismbefore investigatingother causesof thedog’s clinical signs andblood results e.g.primarygastro-intestinaldisease.The ACTH stimulation testwas consistentwith hypoadrenocorticismwith lackof cortisol noted.Aldosteronewas alsomeasured in this case as the electrolyteswere normal and thiswas also noted tobeundetectably low. Thedogwasdiagnosedwithprimary hypoadrenocorticism.

Case Study 1 Non-regenerative anaemia and hypoalbuminaemia in hypoadrenocorticism

What is Addison’s disease (hypoadrenocorticism)? Addison’sdisease results from lossofproductionof corticosteroids,principally mineralocorticoids (mainly aldosterone) andglucocorticoids (mainly cortisol). Themost common causeofAddison’sdisease isprimary hypoadrenocorticism, which isnearly alwaysdue to an immune-mediateddestructionof the adrenal glands.This conditionusually results indeficienciesofbothglucocorticoids and mineralocorticoids,however casesof isolatedglucocorticoiddeficiency havebeen reported (atypicalhypoadrenocorticism).

How to recognise Addison’s disease

BecauseAddison’sdisease isn’t so easy to identify,beingmore aware of this condition ishalf thebattle. Addison’sdisease is apotentially life-threatening condition. However as clinical signs associatedwith thedisease arenon-specific, canwax andwane, anddogs can respond to non-specific therapy e.g. intravenous fluid therapy, this condition canbe easilymistaken forother diseases (e.g. kidneydisease,gastroenteritis includingparvovirus infection, neuromuscular andmetabolicdiseases).

Addison’sdisease resemblesmanyother illnesses so itcanbe challenging todiagnose. It isoften referred toas ‘thegreatpretender’.

Addison’s disease The advantages of Zycortal for hypoadrenocorticism.

EmmaRobertsBVetMed (Hons)MRCVS and IanRamseyBVSc,PhD,DSAM,DipECVIM-CA, FHEA,MRCVS SmallAnimalMedicine,UniversityofGlasgow

Secondary hypoadrenocorticism (causedbypituitarydysfunction), results in thedeficiencyof adrenocorticotropic hormone (ACTH). This is a very rare causeof canine hypoadrenocorticism and tends to result inglucocorticoiddeficiencyonly.

Themost common signsofAddison’sdisease are:

Almostallcases

Common

Lesscommon

RegulationofCortisolandAldosterone

Inappetence Lethargy

Weakness Vomiting

Diarrhoea Weight loss Shivering/muscle

Metabolic stress

Hypothalamus

stiffness Polyuria Polydipsia

CRH

ClinicalHistory

Pituitary Gland

relieves

Depression Weakness

Dehydration

Bradycardia Hypothermia

Endocrine tests

Result

Capsule Zona glomerulosa

Gluconeogenesis Protein+ fatmobilisation Immunosuppression

< 6.9 (

Basal cortisol (nmol/l) Post-ACTH cortisol (nmol/l) Post-ACTH aldosterone (pmol/l)

AdrenalGland

Physical

examination

ACTH

Bloodandurine testparameters including reference ranges

Result

Zona fasciculata

Cortisol Aldosterone

Adrenal Gland

Medulla

32.5* 39.6 10.66 7.569 2.132 0.64 0.319 143 4.6 31.1 4.1 57 19* 38 6 10 0.07

Haematocrit (%) 37-55 Reticulocyte count (K/μL)10-110 Whiteblood cell count (x10^9/l) 6-12

Cortisolwasmeasured using a radioimmunoassay test. LLQ=lower levelsofquantification

Cortex

Renin-Angiotensin-System

Kidney

Zona reticularis

Neutrophils (x10^9/l) 3-11.8 Lymphocytes (x10^9/l) 1-4.8 Monocytes (x10^9/l) 0.15-1.35 Eosinophils (x10^9/l)0.1-1.25 Sodium (mmol/l) 136-159 Potassium (mmol/l)3.4-5.8 Sodium:potassium ratio

Kidney

Na + re-absorption K + excretion Water retention

Comments • Dogswith hypoadrenocorticism canpresentwith chronic non-specific signs as shownhere.Although typical casesof hypoadrenocorticism tend to have electrolyte abnormalities i. e. hyponatraemia, hyperkalaemiaor sodium:potassium ratio< 27:1, not all caseswill have these abnormalities as shown in this case 1 . • Hypoalbuminaemia hasbeendocumented tooccur in 38.6%ofdogswith hypoadrenocorticism and is thought tobedue to eithergastro-intestinalblood loss, aprotein-losing enteropathy,malassimilationordecreased albumin synthesis 2 . The hypoalbuminaemia in these cases canbeof varying severity. • Ultrasonographyof the adrenalglands canbe helpful in some cases to increase the suspicionof hypoadrenocorticism, howeverdetectionof the adrenalglandsusing thismodality isoperatordependent.The adrenalglandsof dogswithhypoadrenocorticism havebeen found tobe thinner thannormaldogs, aswell asdogswithdiseases thatmimichypoadrenocorticism, however overlap canoccur 3,4 .

Z Y C O R T A L ® HIDDEN DISEASE. VISIBLE ANSWER.

Z Y C O R T A L ® HIDDEN DISEASE. VISIBLE ANSWER.

Blood vessels

Adrenal medulla

Low blood volume

Depressiondue to Addison’sdisease*

Microcardia secondary to hypovolaemia*

Bilious vomit**

Increased blood volume

Glucose (mmol/l) 3-5.5 Totalprotein (g/l) 50-78

Blood vessels

Stimulating Inhibiting

Z Y C O R T A L ® HIDDEN DISEASE. VISIBLE ANSWER.

Z Y C O R T A L ® HIDDEN DISEASE. VISIBLE ANSWER.

Albumin (g/l) 29-36 Globulin (g/l) 28-42

Pre-prandialbile acids (μmol/l)< 10 Post-prandialbile acids (μmol/l)< 15 Urineprotein: creatinine ratio< 0.2

If leftuntreated,Addison’sdisease canbeacuteand life threatening.

Z Y C O R T A L ® HIDDEN DISEASE. VISIBLE ANSWER.

Melena**

Masticatorymuscle loss*

Youngpuppywith Addison’sdisease*

Z Y C O R T A L ® HIDDEN DISEASE. VISIBLE ANSWER.

*Abnormal results in red andbold

*CopyrightofUniversityofGlasgow **Permission fromBMJ InPractice2003;25:18-25

26

27