WE are always reminded that “cats
are not small dogs” and, amongst
other examples, this is dramatically
illustrated by the very different way
in which they present with thyroid
disease.
Hyperthyroid
disease in cats, since
its emergence in the
late 1970s is now the
most common
endocrine disease seen
in cats with a
prevalence estimated
at 2%. By way of
contrast, hyperthyroid
disease in dogs is
extremely rare and
hypothyroidism is
more common. The
feline equivalent of
this latter disease is
usually iatrogenic and
rarely seen
spontaneously.
Feline hyperthyroidism aetiology
The exact aetiology and pathogenesis
of feline hyperthyroidism remains
unclear. Cats are often presented late in
the course of the disease; many owners
happily live with their cat displaying an
increased appetite and lively
demeanour, thinking it a good thing in an older animal. This can make
investigation of the progression of
normal thyroid tissue to adenomatous
hyperplasia difficult.
Suspicions of a goitrogenic
component in the pathogenesis of the
disease is put down to
several observed
factors: the changes in
thyroid tissue seen at
presentation tend to be
that of benign
hyperplasia rather than
neoplasia; histological
changes are often seen
in both thyroid lobes
at presentation and
cases often progress
from unilateral to
bilateral disease; finally
there is diversity in the
severity of tissue involvement between the lobes.
This, combined with the apparent sudden emergence of the disease at a
time when the husbandry of cats was
changing (an increasing number of
indoor-housed cats along with changes
in the way in which cats were fed), has
led to theories of potential
involvement of environmental and/or
nutritional as well as endogenous factors.
Some epidemiological and case-controlled studies have observed
associations with certain chemicals
including flea sprays, cat litter and
pesticides. It was also observed that
cats fed canned food were at a two- to
three-fold increased risk of developing
the disease.
One subsequent study showed a
possible link with cats fed from “pop-
top” cans and it was suggested that
components from plasticisers, notably
bisphenol A, may have disrupted
endocrine function and increased TSH.
Other suggestions for a goitrogenic
component in the food itself came
from observations that cats fed fish,
liver or giblet-based canned foods also
showed an increased
risk of developing the
disease.
Iodine itself is a
goitrogen and variability
in intake has been
associated with iodine-
induced
hyperthyroidism in
people. Some authors
suggest though that
dietary iodine is less
likely to cause
adenomatous change in
the gland.
Soybean, a common
vegetable ingredient in
cat food, may have a
goitrogenic effect through the
isoflavones genistein and daidzein
causing inhibition of an enzyme
involved in synthesis of thyroid
hormone. One study showed a modest
increase in Total T4 and Free T4
concentrations relative to Total T3
concentrations in healthy cats fed
dietary soy.
Endogenous factors such as auto-
immunity and over expression or
mutation of oncogenes and G protein
genes are also undergoing investigation.
It may be that a combination of
environmental, nutritional, infectious
and genetic factors in susceptible
animals is involved. Future studies will
hopefully clarify any interaction leading
to the development of the disease.
Treatment
Treatment of hyperthyroidism involves
three options: administration of long-
term anti-thyroid medication, surgical
thyroidectomy, and radioactive iodine
therapy.
Choice of treatment is often
influenced by the personal experience of the clinician, the client’s attitude and
ability towards medication, and the
temperament of the cat itself. There
are advantages and disadvantages with
each option.
Medical management is a life-long
treatment and requires ongoing
monitoring and compliance on the part
of the owner. The disease itself will
progress and the patient is likely to
need increasing doses of medication.
Surgical thyroidectomy is also
commonly performed, though
involvement of ectopic thyroid tissue
may mean that euthyroidism is not
achieved in all cases. One study
reported up to a third of surgical cases
not leading to a permanent resolution of the disease in a
retrospective review of
cases from two first-
opinion practices.
Access to
radioactive iodine
facilities is increasing,
though it still requires a
long period of
hospitalisation, which
may be a cause of
significant stress in this
species.
Canine
hypothyroidism
At the other end of
the spectrum, the
pathogenesis of canine
hypothyroidism involves destruction of the thyroid
gland.
Histopathology shows two different
presentations, that of lymphocytic
thyroiditis in about 50% of cases, with
a known genetic and breed-related
component and the other half showing
idiopathic atrophy.
The cause of the atrophy is
postulated to be either a primary
degenerative disorder, or the end-stage
of lymphocytic thyroiditis.
Diagnosis
The challenge for clinicians tends to be
in achieving a clear diagnosis of the
disease and avoiding unnecessary
treatment, rather than in the
management itself.
Clinical signs of thyroid disease in
the dog are non-specific and
sometimes subtle. Non-thyroidal illness
(NTI) or euthyroid sick syndrome can
also be a complicating factor. This is
characterised by a decrease in
circulating thyroid hormone levels but
without an increase in TSH levels.
This physiological phenomenon is seen with many other diseases and is
thought to be a protective mechanism.
Treatment with exogenous thyroxine in
these cases is not advised.
Other non-thyroidal factors may
also lead to suppressed thyroid
hormone levels, often seen as a low
level of TT4 (Total T4). Treatment
with glucocorticoids, anaesthetics,
some NSAIDs and potentiated
sulphonamides, and anti-convulsants
such as phenobarbitone should also be
taken into account when interpreting
results and, where possible, expert
advice sought on either withdrawing
the treatment prior to hormone testing,
or on interpretation of the results
where they have been given
concurrently. Sight hounds and some
older dogs also have lower levels of
thyroid hormones.
Because of the cross-over in
presentation and potential effect of
non-thyroidal factors, endocrine
experts recommend careful evaluation
of the clinical signs and presentation of
the case before embarking on
laboratory testing. Ruling out
concurrent disease helps to allow
clearer evaluation of any test results
subsequently.
There are a number of laboratory
tests available to help in the diagnosis
of hypothyroidism, though no one test
should be used in isolation. Amongst those commonly used and widely
available are measurements of total
thyroxine (TT4) and circulating
thyrotropin (cTSH).
Used in combination in a case with
suggestive clinical signs and free of
other illnesses, these allow a fairly
reliable diagnosis. Confusion can arise
from potential interference by any
thyroglobulin auto-antibodies which
may be circulating at the same time.
These are directed against the protein
thyroglobulin (an intrinsic part of T4
and T3) during the inflammatory
process of lymphocytic thyroiditis, and
can interfere with thyroid hormone
measurement.
Some specialist labs are able to
measure these auto-antibodies directly
(which may help indicate lymphocytic
thyroiditis, if caught early in the
disease) and advise on interpretation.
Most of the time, following careful
pre-assessment, a combined finding of
high cTSH and low TT4 is reliable
diagnostically, and further tests are not
needed.
The finding of a low TT4 with a
“normal” cTSH is more challenging,
and measuring free thyroxine (not
protein-bound) FT or auto-antibody
levels may be helpful. The FT4 result
will help to rule out NTIs and the
auto-antibody tests can help to confirm
thyroid disease.
Treatment
Treatment of the disease in dogs is
usually straight-forward and
associated with few side-effects.
Administration of synthetic thyroid
hormone, levothyroxine (L-
thyroxine), in titrated once or twice
daily doses (depending on the
preparation used) usually leads to clinical improvement within 4-6 weeks.
Measurement of both “peak” (4-6 hours post treatment) and “trough”
(immediately before the next dose is
due) T4 levels is recommended every
six months after stabilisation.
- Further reading available on
request from the author.
