Name
Addison's Disease
Short Description
Canine
hypoadrenocorticism
Affected Animals:
Female dogs are more
likely to develop
Addison's disease.
Younger dogs of an
average age of four to
five years are more
commonly affected than
older dogs. Any breed
of dog can develop
Addison's disease,
although in some
studies, the majority
of affected dogs were
of mixed breeding.
Veterinarians have
observed that Labrador
retrievers,
Rottweilers, and West
Highland white
terriers seem to be
diagnosed with
Addison's disease at a
higher frequency than
other breeds.
Overview:
Clinically known as
canine
hypoadrenocorticism,
Addison's disease
results from the
decreased production
of steroid hormones by
the adrenal glands.
The common symptoms of
Addison's disease are
not very specific, and
can include lethargy,
weakness,
gastrointestinal
upset, and poor
appetite. Often these
symptoms appear
intermittently during
an extended period of
time.
Although some dogs may
be diagnosed while in
a relatively stable
condition, most are
diagnosed when an
Addisonian crisis
develops -- a severe
stage of the disease
in which shock and
collapse can occur. If
a dog is treated
successfully for an
Addisonian crisis,
however, the long-term
outlook is excellent,
as most dogs can be
controlled with oral
or injectable
medications to replace
the deficient
hormones.
Clinical Signs:
Clinical signs include
anorexia, or an absent
appetite, a thin body
condition, depression,
vomiting, diarrhea,
weakness, collapse,
polyuria, or increased
thirst, signs that
come and go over time,
trembling or shaking,
and abdominal pain.
Symptoms:
See Clinical Signs.
Description:
Addison's disease
refers to the syndrome
that results from
failure of the adrenal
glands to produce the
hormones that they
normally make. The
adrenal glands are two
small structures
located alongside each
kidney. The main
hormones produced by
the adrenal gland are
steroids. There are
two major classes of
these steroids:
mineralocorticoids and
glucocorticoids.
Aldosterone, the main
hormone in the
mineralocorticoids
class, plays a major
role in regulating
sodium, potassium, and
water balance.
Cortisol, the main
hormone in the
glucocorticoids class,
acts on almost every
major tissue in the
body, helping to
regulate glucose
production and
metabolism,
influencing fat and
protein breakdown,
stimulating red blood
cell formation,
helping to regulate
blood pressure,
counteracting stress,
and suppressing
inflammation.
Despite their
different control
mechanisms, both
classes of steroids
usually are affected
by primary adrenal
gland failure in
Addison's disease.
However, some animals
will have symptoms
primarily related to
mineralocorticoid
deficiency, while
others will experience
problems primarily
from glucocorticoid
deficiency. Although
sex hormones such as
estrogens and
androgens also are
produced by the
adrenal glands, signs
due to deficiencies of
these hormones do not
occur in dogs with
Addison's disease.
Destruction of 85 to
90 percent of the
steroid-producing
cells in the adrenal
gland appears
necessary for signs to
develop secondary to
deficiencies of
mineralocorticoids and
glucocorticoids. This
destruction is most
commonly due to immune
system-mediated
destruction of the
adrenal glands. Less
frequently,
infections,
inflammation, cancer,
drug therapy, or
abnormalities in blood
supply to the adrenal
gland can contribute
to the development of
Addison's disease.
Secondary adrenal
gland failure due to
problems that affect
the hypothalamus or
pituitary gland may
also occur, resulting
in the signs seen with
Addison's disease.
Symptoms of Addison's
disease may follow an
intermittent course,
often coming and going
over a long period of
time before the
illness is suspected.
Occasionally,
Addison's disease can
be diagnosed in dogs
with relatively mild
symptoms. However, it
is common for dogs not
to be diagnosed until
a life-threatening
crisis due to
Addison's disease
develops. Severe signs
of illness including
shock and collapse
characterize these
crises. Usually, the
animal can be
stabilized
successfully if it
receives immediate
treatment with fluid
resuscitation and
medications to improve
electrolyte and
acid-base system
abnormalities and to
replace deficient
glucocorticoids. Once
the initial crisis
passes, maintenance
treatment with either
oral or injectable
mineralocorticoids,
and for many dogs,
oral glucocorticoids
will be necessary for
life. Despite the
serious nature of
Addison's disease, the
vast majority of dogs
can be well controlled
with medication.
However, supplementing
some dogs with
glucocorticoid
insufficiency will be
necessary during any
stressful period.
Atypical Addison's
disease refers to
primary or secondary
adrenal gland failure
in dogs that do not
exhibit the classic
symptoms or
electrolyte
abnormalities usually
seen in Addison's
disease. Animals
diagnosed with this
condition may have
more subtle changes on
blood tests and other
diagnostic procedures.
Although these dogs
will not have the
classic findings with
Addison's disease,
they will exhibit
abnormally low
responses to ACTH on
the ACTH stimulation
test, and generally
they will respond to
treatment with
glucocorticoids alone,
since the sodium and
potassium regulation
will remain normal.
Diagnosis:
In many cases, changes
on routine screening
tests, including the
complete blood count,
biochemistry profile,
and urinalysis, will
trigger the suspicion
of Addison's disease.
Chest x-rays may
reveal a reduced heart
size and esophageal
enlargement. An
electrocardiogram may
show changes if the
potassium
concentration is
elevated.
A
definitive diagnosis
depends on the results
of a test of adrenal
gland function called
the ACTH stimulation
test. Serum
concentrations of
cortisol, one of the
main hormones produced
by the adrenal gland,
are measured before
and after the
administration of
either synthetic or
natural ACTH.
Measurements of
another hormone called
aldosterone, which
helps regulate the
sodium and potassium
balance, also can be
checked, although this
procedure is fairly
uncommon. Measurement
of aldosterone may be
helpful in
distinguishing primary
failure of the adrenal
glands from secondary
adrenal gland failure
due to abnormalities
in the hypothalamus or
the pituitary gland.
Similarly, measurement
of yet another
hormone, called
adrenocorticotropic
hormone, also may be
used to distinguish
between primary and
secondary adrenal
failure.
Prognosis:
With appropriate
medical treatment, the
long-term outlook for
dogs with Addison's
disease is excellent.
Effective
communication between
the owner and
veterinarian is vital
in managing dogs with
Addison's disease, and
owners should always
have prednisone on
hand in case it is
needed in a crisis
situation.
Transmission or
Cause:
Addison's disease most
commonly is caused by
primary failure of the
adrenal gland to
secrete adequate
amounts of
mineralocorticoids,
glucocorticoids, or
both. It is thought
that immune
system-mediated
destruction of the
adrenal gland is the
most common cause of
primary adrenal gland
failure. Other causes
can include infection
or inflammation in the
adrenal gland;
abnormalities in blood
supply to the adrenal
gland or bleeding
within the gland;
infiltration of cancer
cells within the
adrenal gland; the
deposition of abnormal
proteins within the
adrenal gland; and
physical trauma to the
glands. Rapid
withdrawal of drugs
such as prednisone
after chronic
administration and
overdoses of drugs
used to treat
Cushing's disease can
result in adrenal
gland failure.
Secondary adrenal
gland failure can
occur due to primary
problems in either the
hypothalamus or the
pituitary gland.
Treatment:
The treatment of dogs
with Addison's disease
depends on the
severity of the
presenting signs. Many
dogs diagnosed with
Addison's disease are
severely ill at the
time of presentation,
often with potentially
life-threatening fluid
deficits and abnormal
serum electrolyte
concentrations. These
animals must receive
immediate medical
attention, since rapid
treatment is extremely
important to stabilize
dogs experiencing an
Addisonian crisis. The
main goals of
treatment are to
correct fluid volume
deficits, to improve
blood vessel
integrity, to provide
a source of
glucocorticoids, to
correct electrolyte
and acid base
abnormalities, and to
confirm the diagnosis.
Fluid volume deficits
are addressed most
appropriately with
intravenous fluid
administration;
usually, saline is
used. If low blood
sugar concentrations
are known or
suspected, then the
fluids should be
supplemented with
dextrose.
Glucocorticoids
usually are given via
injection.
Glucocorticoids that
will not affect ACTH
stimulation test
results are better
used than those that
might make it
difficult to confirm a
diagnosis of Addison's
disease if they are
given prior to the
ACTH stimulation test.
Electrolyte imbalances
are corrected with the
intravenous fluids and
with administration of
mineralocorticoid
replacement drugs.
These drugs generally
are not used until the
diagnosis is
confirmed, since the
other measures used to
treat a dog in crisis
are usually successful
in stabilizing a dog
in an Addisonian
crisis. Sometimes it
will be necessary to
take specific measures
to lower dangerously
high serum potassium
concentrations, such
as the administration
of glucose and
insulin, calcium, and
sodium bicarbonate.
Bicarbonate also can
be used to treat
animals with extreme
acid-base system
disturbances. Most
dogs in crisis will
improve within one to
two hours with
appropriate treatment.
Intravenous fluids
often are maintained
for 24 to 48 hours,
until the dog is
eating and drinking on
its own without
vomiting. Injectable
medications can then
be switched to oral
medications
Once the crisis period
has passed, dogs are
given either oral or
injectable
mineralocorticoids.
The oral medications
need to be given on a
daily basis, usually
twice a day, and
sometimes very high
doses are needed to
control the disease.
The injectable
mineralocorticoid used
most commonly is
called DOCP. It is
given via injection
approximately every 25
days, and is almost
always effective. For
many dogs, especially
large breed dogs, the
injectable drug is
much less expensive
than the oral form.
Most dogs with
Addison's disease do
well clinically with
mineralocorticoid
replacement alone, but
others will require
glucocorticoid
supplementation with
prednisone as well. As
many as 50 percent of
dogs on injectable
DOCP also will require
prednisone
administration. For
any dog with Addison's
disease that may be
undergoing stress,
surgery, or that
develops a non-adrenal
gland dependent
disease, prednisone
should be considered
on a short-term basis.
Dogs that are used as
working dogs also
should take prednisone
on a short-term basis.
Prevention:
There is no known way
to prevent the
development of
Addison's disease,
except for cases in
which it is caused by
rapid withdrawal of
prednisone or other
steroids that have
been used for long
periods of time.
Slowly tapering the
doses of such drugs
before discontinuing
them is almost always
effective in
preventing the
development of
Addison's disease in
these patients.
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