|
Canine Gout |
|
by Fred Lanting |
Canine gout is an imbalance in mineral
assimilation resulting in abnormal deposits, sometimes between bones, often in
layers of the skin or integument.
Calcium deposits in the skin can be the result of injury, of metabolic
changes, or of unknown factors. Since mineralization (calcium deposits) in skin
can occur in a wide variety of unrelated diseases, a common thread among them
is not easy to establish. One form of the condition is related to, or could be
an early indication of, a canine version of the disorder which in humans is called Cushing’s Disease, although many
dogs will never develop the distended abdomen, susceptibility to hematomas and bruising, or over-pigmented, sparsely-coated
skin. Indeed, that may be a sufficiently
different disorder that it should be classified as a separate variety of hyperadrenocorticism or hyperglucocorticoidism.
A British friend phoned and said he was
afraid he would lose his 18-month-old German Shepherd
Dog, who had been limping badly on several limbs. The dog’s feet were extremely sore, and a
whitish fluid exuded from the pads; it was analyzed and the diagnosis was
“calcium circumscripta”, which I thought I knew
simply as “gout”. Many years ago, my
friend and HD mentor, Dr. John Bardens, told me about
a remedy or treatment he had devised for gout, but for the life of me, I could
not remember what it was, or what variety of gout he meant. I was on the road when the call came in, but
when I returned I consulted some references and was convinced that it was not
this type. I told my English friend it
may have been considered “rare” by his vet in
Canine gout can be either generalized (a
few to several areas) or localized (one or two spots). Considered a tumor ( which word could refer to a cancer, a nodule, a cyst, or
an impacted gland), the condition when found in the skin is also known as Calcinosis Cutis, which means calcified skin. It is usually a non-neoplastic
(benign, not cancerous) disorder there.
Boxers and
Histologically,
the disorder appears as an amorphous granular material with fibrous trabecula (“bone”) cells and inflammation around it. As the lesion progresses, ulceration often
occurs. Sometimes it starts or occurs at
injection sites or where ears are cropped.
If the calcinosis develops in injured tissue,
it could be localized, in which case some have surmised it to be often
associated with demodex, TB, staph
infection, or granuloma caused by a foreign body such
as grit or sand imbedded beneath the skin, or it could be connected with epidermoid cysts or malignant tumors.
If it is localized, it could still be
considered coincidental that it is found at wound sites. If it is widespread, it is probably due to
either hyperglucocorticoidism (hyperadrenocorticism)
or diabetes. If there is no apparent
damage to tissues, and no abnormalities seen in blood hormone levels, the
calcium salt deposits may likewise be either localized or generalized. In the above types of the disorder, serum
calcium levels (amount of calcium compounds circulating in the blood and lymph)
are not abnormal, as is the metabolism of calcium and phosphorus. If, however, the disorder metastasizes
(travels from original location to others by means of abnormal cells being
transported via the bloodstream), there have been seen abnormal calcium levels
and a connection with chronic kidney disease.
According to Muller, Kirk, & Scott’s text on Small Animal
Dermatology, “No therapy is beneficial” if it develops into the metastatic form.
Considering all variations, we see such cutaneous
mineralization in 40% of all dogs with hyperadrenocorticism. A tell-tale sign in the haircoat
may be loss of hair or hairs easily pulled out of the follicles.
Atop the kidneys sit the adrenal glands
(whence comes the word “adrenaline”), the cortex layer of which produces
hormones known as corticosteroids. One
of these hormones is glucocorticoid, which affects
the metabolism of glucose, a form of sugar taken in or even manufactured by the
body. If the body makes too much, it
results in an imbalanced condition known as hyperglucocorticoidism
or hyperadrenocorticism, and if this becomes severe,
an imbalance in minerals occurs and the calcinosis
cutis could be widespread, appearing in any or all of the following: skin along
the back, armpit, groin, flanks, over bony protuberances such as foot bones and
vertebrae, and {reportedly} apocrine (sweat)
glands. In the dog, these apocrine glands are found primarily in the tongue and pads,
although a small amount of perspiration is possible in the rest of the
skin. Researchers have held differing
ideas regarding the involvement, if any, of these glands. The renowned dermatologist Dr. Danny Scott,
whom I profiled several year ago in my Dog World article, “Itch!”, has discounted the involvement of apocrine gland
origins.
How does canine gout come about? Well, etiologically speaking, it could be
that there develops an abnormal breakdown of hydrocortisone in the
genetically-predisposed dog or even from an almost entirely environmental
cause, which leads to molecular structural changes in proteins such as collagen
and elastin so that the tissue chemically attracts
and binds calcium. Also there may be
unseen mineralization in lungs, stomach wall, and skeletal muscles, where there
may be tissue damage at a later time. A
good argument for neutering an affected dog is that almost everything is
“genetic” to some degree. There
are references in the literature about gout occurring in related dogs, such
as Dr. L. N. Owen’s
1967 article on Irish Wolfhounds in Volume 8 of Journal of Small Animal
Practice, although you probably want to remember that there are different types
and that which occurs in the hock possibly could have a different heritability
than in other locations. Drs. Scott and Buerger, in the Nov./Dec. 1988 volume
of the Journal of the
One form seems connected with polyarthritis or HOD (see Canine Hip Dysplasia,
by this author, currently out of print, with 2nd edition being
worked on) but in these cases it goes away when those diseases associated with
mineral imbalance or poor metabolism of calcium subside. Those cases usually appear near the shoulder
blades and hip joints. When occurring
over pressure points and bony prominences or bones close to the skin, nearly a
quarter of the lesions are seen in the hock area, almost a fifth in the
phalanges of the toes, about 17% in elbows, and 10% in the lower dorsal neck
area. There is ten to twenty times more
involvement in the tarsal-metatarsal (hock) area than in the foot pad. The dogs
with calcification of the “skin” in the pads possibly are exhibiting a
different form, and since they limp, it is diagnosed faster than if gout appears
elsewhere in the skin as plaques, nodules, or papules (bumps). Typically, a milky or chalky white liquid,
often gritty or paste-like, can be expressed if the pad is lanced or sliced,
and this was the beginning of the definitive diagnosis in the case of my
English friend’s dog. One of my vet-tech correspondents described the hock
lesions in her breed (Wolfhounds) as being sometimes open and weeping,
sometimes closed and cauliflower-like.
Her advice was if it were not open or very painful, “ignore” it for six
months, as they often diminish in size and even disappear without
treatment. She also had one of her pups
develop a lesion on its tongue, and having chosen to delay surgery, found that
it had gone from large-marble size to pea-size in four months. We should not draw conclusions from one type
and apply them to others.
Some 80% of cases of localized idiopathic
calcinosis cutis are in large breeds including many
Great Danes and Irish Wolfhound; over 50% of affected
dogs are German Shepherd Dogs. Most are
under two years of age, as was the case with the British GSD, and most show up
after one year of age. The nodules are
generally up to one-quarter inch in diameter and shaped like domes although
frequently they lie under a layer or more of skin so their shape is not seen
until removed. Typically, treatment for
this form (rather than drugs aimed at the adrenal glands) involves cutting out
the granulous material, but this can be disappointing
to satisfactory, depending on the individual dog, the
degree and type of lesion, and removing the whole lesion. There does not appear to be development of
new lesions in the same place after successful (complete) surgical excision,
and many dogs have gone well over eight years without recurrence in the same location. Treatment of the generalized forms still
involves treating the underlying causes such as skeletal disease or blood
chemistry and metabolism. This may take
a year to clear up, and that is about the same time that it takes for most
cases to spontaneously regress.
Generalized gout, whether associated with glucocorticoid
abnormality (sometimes found in puppies) or from an idiopathic (unknown) cause
almost always shows up after a year of age, and it may take a year to clear it
up, with drugs in the former cases or surgically or spontaneously in the
latter.
Some time after I faxed copies of medical
articles to
