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Israel Journal of Veterinary Medicine  Vol. 69 (4)  December 2014 Oron, L. 234
INTRODUCTION
Hypoadrenocorticism is a rare endocrinopathy in cats.
Primary hypoadrenocorticism is hypothesized to result from
immune-mediated destruction of the adrenal cortex, leading
to inadequate glucocorticoid and mineralocorticoid produc-
tion (1,2). At least 85-90% of the adrenal cortices must be
impaired for clinical signs to develop (1,2). Spontaneous,
secondary hypoadrenocorticism, unreported in cats so far, re-
sults from inadequate pituitary adrenocorticotropin (ACTH)
secretion, leading to defcient glucocorticoid secretion (1, 2).
Iatrogenic hypoadrenocorticism can occur after withdrawal
of potent glucocorticoids or progestins, however, clinical
signs are rarely seen in cats (2).
Cats with hypoadrenocorticism typically show lethargy,
anorexia, weight loss, (nonspecifc signs which are common
to many other illnesses) and may also present vomiting, poly-
dipsia and polyuria, while unlike dogs, collapse and brady-
cardia are rare (2-4). Dysphagia occurs uncommonly, and is
believed to result from muscle weakness, secondary to elec-
trolyte disturbances and generalised atrophy (5). Laboratory
abnormalities may include an “anti-stress leukogram” (eosin-
ophilia, lymphocytosis and neutropenia) , anaemia, azotae-
Hypoadrenocorticism Diagnosed by Adrenocorticotropin Stimulation
Test for Aldosterone in a Diabetic Cat
Oron, L.,
1
Mazaki-Tovi, M.,
1
Neri, D.,
2
Aroch, I.
1
and Kelmer, E.
1
1
Hebrew University Veterinary Teaching Hospital, Koret School of Veterinary Medicine, Te Hebrew University of Jerusalem,
P.O. Box 12, Rehovot, 761001, Israel.
2
Ramat Hasharon Veterinary Center, Yaakov Cohen 21, Ramat Hasharon, Israel.
*
Corresponding Author: Dr. Efrat Kelmer, DVM, MS, DACVECC. Tel: 972-3-9688588, Fax: 972-3-9688525, P.O. box 12 Rehovot 761001, Israel.
Email: kelmere1@gmail.com
ABSTRACT
A 6-year-old male neutered cat was referred with a 3-month history of lethargy, chronic constipation,
intermittent vomiting, inappetence, progressive weight loss, dysphagia and polyuria. Previous treatment
with intravenous fuids, antimicrobials, glucocorticoids, laxatives and appetite stimulants [megestrol-acetate
(MgAc)] resulted in partial response. During the treatment course, the cat developed diabetes mellitus
(DM). Physical examination revealed obtundation, cachexia, dehydration, pale mucosal membranes,
generalised muscle atrophy, sialoadenomegaly and thoracolumbar pain as well as pain upon opening the
mouth. Serum electrolyte analysis showed severe hypochloridaemia, hyperkalaemia and hyponatraemia,
with a sodium to potassium (Na:K) ratio of 19.6. As the cat had been chronically treated with prednisolone
at presentation cortisol concentration could not be reliably interpreted. Terefore, ACTH-stimulation
was performed and pre- and post-ACTH aldosterone concentrations were measured, and were consistent
with hypoadrenocorticism. Fludrocortisone treatment was initiated, and the clinical signs and electrolyte
imbalances resolved; however DM persisted. Feline hypoadrenocorticism is rare, and unlike dogs, cats with
this disease may present with dysphagia as a major clinical sign. Although MgAc may induce glucocorticoid
defciency and DM in cats, it has not been reported to induce mineralocorticoid defciency with subsequent
electrolyte imbalance, and its role in the pathogenesis of hypoadrenocorticism in this cat is questionable.
Keywords: Feline; Addison’s Disease; Glucocorticoid; Megestrol-Acetate; Diabetes Mellitus;
Hyperkalaemia; Hyponatraemia; Hypoadrenocorticism.
DECEMBER Book.indb 234 04/12/2014 10:57:17
Israel Journal of Veterinary Medicine  Vol. 69 (4)  December 2014 235 Hypoadrenocorticism in a Diabetic Cat
mia, hyperphosphatemia, hypocholesterolaemia and evidence
of dehydration (1). Hyponatremia is reported in 100% of
cases whilst hyperkalemia occurs in 90% of such cats, and
the Na:K ratio is typically <24 (2).
Defnitive diagnosis of hypoadrenocorticism is mostly
based on measurement of pre- and post-ACTH serum
cortisol concentrations. To the best of our knowledge, an
ACTH stimulation of serum aldosterone concentrations for
confrmation of hypoadrenocorticism in cats was previously
reported only once (4). Te present report describes a case of
hypoadrenocorticism in a diabetic cat, diagnosed using pre-
and post-ACTH serum aldosterone concentrations.
CASE REPORT
A 6-year-old male neutered domestic shorthair cat was
referred to the Hebrew University Veterinary Teaching
Hospital (HUVTH) with chief complaints of chronic con-
stipation, weight loss and intermittent vomiting. During
the three months prior to presentation, the cat was vocal
when defecating, passed overly frm stools, progressively lost
weight, and presented with selective appetite, polyuria and
dysphagia. Te cat appeared to be interested in food, but
had difculties prehending and chewing it. Two weeks after
the initial clinical signs were frst noted, blood samples for
CBC and serum biochemistry (electrolytes measurement ex-
cluded) were performed by the referring veterinarian. Results
were unremarkable, with exception of increased haematocrit
[47.4% reference interval (RI) 30-45%; 0.474 L/L, RI 0.30-
0.45]. Serum cholesterol concentration was low within RI
(68 mg/dL, RI 65-225; 1.76 mmol/L RI 1.68-5.83). Urine
was obtained by cystocenthesis, and urinalysis showed a SG
of 1.025 and mild proteinuria (25 mg/dL). Oral examina-
tion fndings, performed under sedation, thoracic radio-
graphs and abdominal ultrasound were unremarkable. Te
cat was treated at the referring clinic with intravenous (IV)
fuids, cefovecin (Convenia, Zoetis, Madison, NJ, USA; 80
mg SC), lactulose (Avilac, Perrigo, Allegan, MI, USA; 330
mg PO, q12h) and megestrol-acetate (MgAc) (Ovarid, Jurox
Pty Ltd., Silverwater, NSW, Australia; 5 mg PO, q48h for
one week, followed by q72h for four additional weeks and
followed by q96h for two additional weeks). Mineral oil and
an oral fat additive (Nutri-cal, Toymlin, Fort Worth, TX,
USA) were added to the cat’s diet. Despite treatment no
improvement was noted.
Total serum thyroxine concentration, measured seven
days later by the referring veterinarian was within RI (0.9
µg/dL, RI 0.8-4.7; 11.5 nmol/L, RI 10.3-60.4). Te cat con-
tinued to show eating difculties, and was therefore referred
for computed tomography of the head which was reviewed
by a board certifed radiologist, and was unremarkable. Four
weeks after noting the initial signs, prednisolone (Danalone,
Trima, Maabarot, Israel; 6 mg PO, q12h for fve days, fol-
lowed by 6 mg PO q24h) was empirically initiated, and
the cat showed improvement in his eating ability, although
he still sufered from dysphagia and did not gain weight.
Treatments with prednisolone and MaAc overlapped for
three weeks.
After fve weeks of prednisolone treatment, during a
check-up, hyperglycemia was noted, and was persistently
present later on (glucose 223-330 mg/dL, 12.38-18.32
mmol/L measured several times over a 2.5-week period; RI
74-159, RI 4.11-8.82). Serum fructosamine concentration
was increased (634 µmol/L, RI 0-375; 6.34 mmol/L, RI 0 –
3.75). Te cat was tentatively diagnosed with glucocorticoid /
MgAc-induced diabetes mellitus (DM), and treatment with
NPH insulin (Humulin-N, Eli Lilly, IN, USA; 3 IU SC,
q12h) was initiated, and the cat was then referred to the
HUVTH.
At presentation to the HUVTH, the cat showed cachexia
(body condition score: 2-3/9; body weight: 4.06 Kg.), general
muscle atrophy, obtundation, pale mucous membranes, hypo-
thermia (rectal temperature 36.5° C), mild gingivitis, bilateral
sialoadenomegaly and 8% dehydration. Pain was noted upon
palpation of the lumbar-sacral spine and upon opening the
mouth. Abdominal palpation, thoracic auscultation and neu-
rological examination were unremarkable. At presentation,
the cat was still being treated with prednisolone (6 mg PO,
q24h), but had not received MgAc for three weeks.
A CBC showed microcytic normochromic anaemia, lym-
phopenia and eosinopenia, with an unremarkable leucocyte
count (Table 1). Polychromasia was absent upon examination
of a stained blood smear. Abnormal serum biochemistry re-
sults (Table 2) included hyperglycemia, hypertriglyceridemia,
hypochloridemia , hyperkalemia, hyponatremia, decreased
Na:K ratio (19.6, RI 27.0-40.1) and increased fructosamine
and β-hydroxybutyric acid (BHBA) concentrations. Serum
cobalamine and folate concentrations were within RI. Feline
pancreatic lipase like immunoreactivity assay (SNAP fPL,
Idexx, Westbrook, ME, USA) was negative. Fine needle as-
Case Report
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Israel Journal of Veterinary Medicine  Vol. 69 (4)  December 2014 Oron, L. 236
piration from the enlarged salivary glands was cytologically
unremarkable. Abdominal ultrasound revealed increased he-
patic echogenicity, with no other abnormalities.
In view of the low Na:K ratio and the chronic, waxing
and waning clinical signs, hypoadrenocorticism was sus-
pected. As the cat had been treated with prednisolone. the
continued clinical signs were attributed to the lack of min-
eralocorticoid treatment. Because the cat had been treated
with prednisolone continuously for fve weeks at the time
of presentation, measurement of cortisol concentrations
pre- and post-ACTH was deemed unreliable for diagnos-
ing hypoadrenocorticism, due to the expected suppression of
adrenal cortisol secretion (6). Blood samples were collected
pre- and one hour post-ACTH (Cortosyn, Amphastar
Pharms, Rancho Cucamonga, CA, USA; 0.125 mg, IV) ad-
ministration, and the harvested sera were sent, at 2-8°C, to
the Diagnostic Center for Population and Animal Health,
Michigan State University Veterinary School Laboratory,
for measurement of aldosterone concentration. Aldosterone
concentration was not expected to decrease in response to
administration of glucocorticoids as the main determinants
of aldosterone secretion are concentrations of angiotensin
II and potassium (1, 7).
Pending results, fudrocortisone
(Florinef, Pfzer, New York, NY, USA; 0.1 mg PO, q24h)
treatment was initiated, and prednisolone (5 mg, PO, q12h)
and NPH-insulin were continued. Te cat was then referred
back to the referring clinic for further treatment and moni-
toring. Over the next four days, progressive improvement
was noted. Te cat began eating voluntarily, and the diet was
subsequently changed to a diabetic prescription veterinary
diet (DM, Nestlé-Purina PetCare Company, St. Louis, MI,
USA). Electrolytes concentrations four days after initiation
of fudrocortisone were within RI (Table 2), with a Na:K
ratio of 33. Pre- and one hour post-ACTH aldosterone con-
centrations were both below the assay’s detection limit (< 14
pmol/L pre and post- ACTH; RI pre-ACTH 194-388; RI
post-ACTH, 277-721), confrming hypoadrenocorticism.
Follow up was performed by the referring veterinarian.
Te cat progressively improved over the next three months,
and gained 1.5 kg of body weight. Prednisolone was tapered
down several weeks post diagnosis, while fudrocortisone
dose was increased to 0.125 mg PO q24h. He remained
diabetic despite prednisolone tapering, and was therefore
constantly treated with NPH insulin (4 units SC q12h).
DISCUSSION
Primary hypoadrenocorticism is a rare endocrinopathy in
cats, reported sporadically in the veterinary literature (3-
5,8,9). Megastrol-acetate can induce adrenal insufciency
by its glucocorticoid activity (10,11), however, to the best of
our knowledge, it has not not reported to afect adrenocorti-
cal mineralocorticoid production neither in cats and dogs,
nor in humans. Adrenal suppression induced by predniso-
lone, given at a dose of 2 mg/kg q24h, was compared to that
induced by MgAc at 5 mg (total dose) q24h in cats (11). Te
severity of adrenal suppression and the decrease in circulating
serum cortisol levels were more profound when induced by
MgAc compared to prednisolone. Moreover, while adrenal
suppression induced by prednisolone resolved in 85% of the
cats at two weeks after its discontinuation, it was still evident
Table 1: Complete blood count results* of a 6-year-old male cat
with hypoadrenocorticism and diabetes mellitus at presentation at
HUVTH.
Analyte Day 0
RI
1
(US units)
RI
1
(SI units)
White blood cells (x10
3
/µL)
[x10
9
/L]
9.4 6.3 – 19.6 6.3 – 19.6
Red blood cells (x10
6
/µL)
[x10
12
/L]
7.3 6.0 – 10.2 6.0 – 10.2
Haemoglobin (g/dL) [g/L] 9.6 [96] 8.1 – 14.2 81 – 146
Haematocrit (%) [L/L] 27.2 [0.27] 27.7 – 46.8 0.27 – 0.46
Mean corpuscular volume
(µm3) [fL]
37.3 41.3 – 52.6 41.3 – 52.6
Mean corpuscular haemoglobin
(pg)
13.2 12.0 – 16.0 12.0 – 16.0
Red cell distribution width (%) 15.9 15.9 – 19.4 15.9 – 19.4
Haemoglobin distribution width
(g/dL)
2.0 1.6 – 2.9 1.6 – 2.9
Platelets (x10
3
/µL) [x10
9
/L] 272 156 – 626 156 – 626
Mean platelet volume (fL) 16.4 8.6 – 18.9 8.6 – 18.9
Neutrophils (x10
3
/µL)
[x10
9
/L]
7.4 3.0 – 13.4 3.0 – 13.4
Lymphocytes (x10
3
/µL)
[x10
9
/L]
1.7 2.0 – 7.2 2.0 – 7.2
Monocytes (x10
3
/µL) [x10
9
/L] 0.1 0 – 1.0 0 – 1.0
Eosenophils (x10
3
/µL)
[x10
9
/L]
0.1 0.3 – 1.7 0.3 – 1.7
Basophils (x10
3
/µL) [x10
9
/L] 0.02 0 – 0.10 0 – 0.10
Leucocytes (x10
3
/µL) [x10
9
/L] 0 0 – 0.2 0 – 0.2
Reticulocytes (x10
9
/µL)
[x10
9
/L]
1.9 15 – 81 15 – 81
* US units are depicted in parentheses, while SI units (when diferent
from the US ones) depicted in square brackets; 1, reference interval.
Case Report
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Israel Journal of Veterinary Medicine  Vol. 69 (4)  December 2014 237 Hypoadrenocorticism in a Diabetic Cat
in 57% of the MgAc-treated cats at two weeks after its dis-
continuation (11). Nevertheless, no clinical signs of adrenal
insufciency were noted in any of the cats in that study (11).
Signs of hypoadrenocorticism in cats may be noted from
several days and up to four months prior to its diagnosis, as
was seen in this cat. In some cats, the disease is diagnosed
only when a hypoadrenal crisis occurs, which is considered
a medical emergency (2). Te present cat exhibited weak-
ness, weight loss and selective appetite for three
weeks before MgAc therapy was initiated. Overall,
the cat was treated with MgAc for seven weeks
and treatment was discontinued three weeks prior
to presentation to the HUVTH. Terefore it is
unlikely that MgAc treatment contributed to the
electrolyte imbalance noted at presentation. Te
presence of decreased sodium concentration and
increased potassium concentration, along with al-
dosterone defciency is suggestive of primary, rather
than iatrogenic hypoadrenocorticism. Additionally,
MgAc was tapered gradually, decreasing the likeli-
hood of inducing iatrogenic hypoadrenocorticism.
Nevertheless, it is very likely that concurrent MgAc
and prednisolone treatment in this cat had a role in
induction of DM (12,13). Jaw and back pain, ex-
hibited in this cat has not been reported previously
and was attributed to muscle atrophy.
Defnitive diagnosis of hypoadrenocorticism
is based on measurement of low pre- and post-
ACTH stimulation serum cortisol concentrations
(1,2). Combining these with baseline endogenous
serum ACTH concentration or pre- and post-
ACTH stimulation serum aldosterone concentra-
tions allows diferentiation between primary and
secondary hypoadrenocorticism (1).
Prednisolone or methyl-prednisolone adminis-
tration prior to ACTH stimulation testing inter-
feres with the diagnosis, and make interpretation of
the test results difcult to impossible, as both drugs
are detected, along with endogenous cortisol, in the
cortisol assay (6). Moreover, if used long-term, both
glucocorticoids lead to adrenal gland suppression,
thereby resulting in low pre- and post-ACTH
stimulation cortisol concentration, thereby mim-
icking hypoadrenocorticism (14,15). Aldosterone is
the primary hormone responsible for maintaining
sodium, potassium, chloride, and acid-base homeostasis (1),
and its defciency accounts for some of the major clinical
signs of hypoadrenocorticism (1,2). Serum aldosterone con-
centration is seldom measured in the diagnostic work-up of
feline hypoadrenocorticism, mostly because the availability
of the aldosterone assay has been limited for some time (1).
To our knowledge, feline hypoadrenocorticism has been di-
agnosed previously by ACTH stimulation and aldosterone
Table 2: Serum biochemistry results* of a 6-year-old cat with hypoadrenocorticism
and diabetes mellitus at presentation, and repeat electrolyte results four days later.
Analyte Day 0 Day 4
RI
1
(US units)
RI
1
(SI units)
Albumin (g/dL) [g/L] 4.1 [41] 2.0 – 4.6 22 – 46
Alkaline phosphatase (U/L) 39 14 – 71 14 – 71
Alanine transaminase (U/L) 65 27 – 101 27 – 101
Amylase (U/L) 870 500 – 1800 500 – 1800
Aspartate transaminase (U/L) 50 17 – 58 17 – 58
Total bilirubin (mg/dL)
[µmol/L]
0.2 [3.4] 0.0 – 0.2 0.0 – 3.4
Calcium (mg/dL) [mmol/L] 9.6 [2.4] 9.0 – 10.9 2.2 – 2.7
Cholesterol (mg/dL)
[µmol/L]
211 [5.4] 89 – 258 2.3 – 6.6
Creatine kinase (U/L) 60 73 – 260 73 – 260
Chloride (mmol/L) [mEq/L] 91 115 117 – 126 117 – 126
Total CO2
(mmol/L)
[mEq/L]
14.3 15.0 – 21.0 15.0 – 21.0
Createnine (mg/dL) [µmol/L] 0.9 [83.9] 1.1 – 2.2 97.2 – 194.4
Fructosamine (µmol/L)
[mmol/L]
387 [3.87] 0 – 375 0 – 3.75
γ-glutamyl transpeptidase
(U/L)
<0.0 0.0 – 6.0 0.0 – 6.0
Glucose (mg/dL) [mmol/L] 297.6 [16.4] 63.0 – 118.0 3.5 – 6.5
Potassium (mmol/L)
[mEq/L]
6.2 4.6 3.6 – 4.9 3.6 – 4.9
Sodium (mmol/L) [mEq/L] 122 150 151 – 158 151 – 158
Sodium:potassium ratio 19.6 33 >24 >24
Phosphorus (mg/dL)
[mmol/L]
4.8 [1.5] 3.2 – 6.3 1.0 – 2.0
Total protein (g/dL) [g/L] 6.8 [68] 6.6 – 8.4 66 – 84
Triglycerides (mg/dL)
[µmol/L]
377 [4.26] 8.0 – 88.0 0.09 – 0.99
Urea (mg/dL) [mmol/L] 37.4 [13.3] 38.5 – 70.6 13.7 – 25.2
b-hydroxybutyric acid
(md/dL) [mmol/L]
29.8 [2.87] 0 – 4.8 0 – 0.47
Cobalamine (pg/mL)
[pmol/L]
308.8 [227.8] 100.0 – 350.0 73.8 – 258.3
Folate (ng/mL) [nmol/L] 11.7 [26.5] 10.4 – 20.7 23.5 – 46.9
* US units are depicted in parentheses, while SI units (when diferent from the US
ones) depicted in square brackets; 1, reference interval.
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Israel Journal of Veterinary Medicine  Vol. 69 (4)  December 2014 Oron, L. 238
concentration only once (4). Serum aldosterone concentra-
tions in dogs with primary hypoadrenocorticism are usually
below RI, although they overlap the lower RI (16). Similar
data for cats are unavailable. In the present cat, due to the
need to ship the serum samples for aldosterone measurement
overseas, some degradation cannot be completely ruled out,
but was considered unlikely to be signifcant. Nonetheless,
considering the clinical signs and, most importantly, the
excellent response to treatment, the measured aldosterone
concentrations were likely actually very low.
While dogs with hypoadrenocorticism typically re-
spond quickly to treatment, the response of cats may take
up to 3-5 days (2). In the present case, electrolyte con-
centrations normalised within four days from initiation
of fudrocortisone therapy. Hypoadrenocorticism in cats
requires life-long mineralocorticoid and to a lesser ex-
tent glucocorticoid treatment, and can be usually treated
with fudrocortisone (0.05–0.1 mg/cat PO q 12 h) which
supplements both glucocorticoids and mineralocorticoids.
Some cats will require additional glucocorticoid supple-
mentation (e.g., prednisolone at 0.25-1 mg/cat PO, q12h)
either for life, or at times of stress (2). Te prognosis is
usually good to excellent with proper treatment (2), as was
observed in this case.
Increased serum BHBA concentration typically occurs
in cats in states of negative energy balance, such as DM
(i.e., diabetic ketosis), diabetic ketoacidosis (DKA) or he-
patic lipidosis (HL) (17). In this cat, in light of the dys-
phagia, prolonged anorexia and hyperechoic liver it is likely
that hyperketonemia resulted from both DM (or DKA)
and HL; however, additional diagnostic tests, such as fne
needle aspiration of the liver, venous blood gas analysis and
additional serum BHBA measurements overtime were not
performed, being deemed unnecessary in light of the cat’s
clinical improvement.
In conclusion, hypoadrenocorticism should be consid-
ered in cats presenting chronic dysphagia, weight loss and
inappetance, when other causes of dysphagia are ruled out.
If prior glucocorticoid supplementation precludes measure-
ment of pre- and post-ACTH stimulation serum cortisol
concentrations, measurement of pre- and post-ACTH
stimulation serum aldosterone concentrations can aid in the
defnitive diagnosis of hypoadrenocorticism.
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