Calcinosis
Cutis, Calcium Circumscripta, Canine Gout
Fred Lanting
The subject ailment 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.
In 1998, I wrote the first version of this paper as a response to requests
for information by a British friend who phoned and said he was afraid
he would lose his 18-month-old German Shepherd Dog, which had been limping
badly on several limbs. England has a lower population than the United States
does, both in humans and dogs, so it is natural for us to see more incidences
of any particular health problem or genetic anomaly in the U.S.A. Also,
his GSD is of the “Alsatian persuasion” (style dating back to the go-it-alone
and anti-German breeding of the post-war era), and this style has been
decreasing numerically in proportion to the “Germanic” or what I prefer
to call the international style in the past decade or more. So it was not
surprising that he had not heard of any cases, even though the veterinary
literature includes work of the ailment in his own country. The dog’s feet
were extremely sore, and a whitish fluid exuded from the pads; it was analyzed
and the diagnosis in the U.K. 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 what he
then called gout, but for the life of me, I could not remember what the
medication was, or what variety of gout he meant. I was on the road when
the call from England 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 England, but would be “downgraded”
to “uncommon” in the U.S.A.
According to Carroll Weiss, Director of the Study Group on Urinary
Stones, Health & Research Committee, Dalmatian Club of America, the
term “gout” in the U.S. (and within medical schools, hospitals, medical
libraries, and medical dictionaries), is very specifically defined. It
is the deposition within tissue of insoluble uric acid or purines (or
metabolites) due to an inborn defect in the normal production of urine
within the liver and kidneys. Within both human and canine health circles,
it is traditionally treated and controlled with one of several treatments,
especially an anti-urate drug, “Allopurinol”. This drug would be totally
inappropriate for conditions like calcinosis cutis that mimic true gout.
It acts pharmacologically on the defect of abnormally producing insoluble
uric acid and is indicated only for urate-induced gout, abnormal urinary
crystals, or stones. Other conditions certainly resemble “gout” if minerals
other than urates are deposited. But “gout” is exclusively reserved for
urates and purines. Dalmatian owners will probably want to go to website
for more on these disorders as seen in their breed. Thank you, Carroll.
Gout in humans has often been the subject of cartoonist humor, and
I used to read many examples in the “funny papers” of the 1940s and for
many years after. Maggie may have had the only chance of keeping Jiggs
from sneaking out for a night with the boys when he was suffering from
gout. The history of this cartoon goes far back to the Elizabethan era,
when the British cartoonist Hogarth had a series entitled “Marriage a la
Mode.” It showed the husband with his gout-afflicted foot bandaged and
on a cushioned stool. This was to be copied up to the modern era, in drawings
and stage plays. However, as my son found out when he had a “bout with gout”,
it is most assuredly not funny to the sufferer. In this disorder, the insoluble
uric acid or its chemical relations are deposited within tissues where, untreated,
they can result in almost intolerable pain and even bone degeneration. The
most common site for the deposits are probably localized areas in the foot
where they can become visibly detected as tophi, which are deposits of uric
acid (or its metabolites or salts, like urates) within the tissues about
joints. Deposits of calcium carbonate and/or other calcium salts within
tissues can resemble or even mimic tophi. Weiss says tophi look like bunions.
The word comes from the Latin word for sandstone, which is what it
probably looks and feels like.
Dalmatians suffer from true urate gout. It is rare but it also seems
to be specific to this breed. More commonly seen is its urinary stone manifestation
problem in the breed. Dalmatians are apparently the only breed of dog
born with the defect in their kidneys and livers that can result in uric
acid or “chemical relations” becoming insoluble and precipitating out in
urine as crystals or “stones”. Two other species have the same inborn defect:
man and apes. In humans, more develop the familiar gout than develop urinary
stones.
Weiss says that when humans do indeed have urinary stones, they form
more in the kidneys than in the bladder — unlike dogs — where over 95%
form in the lower urinary tract, where which is far more treatable and
responsive to current non-surgical methods than if found in the kidneys.
Parenthetically, this is the reason why the DCA Study Group prefers the
term “Dalmatian urinary stones” rather than the incorrect, misleading,
and more serious problem of “kidney stones.” Urinary stones form more in
canines than in humans. Breeds other than Dalmatians can form urate crystals/stones
but not for the same inborn reasons, according to Weiss.
The main subject of this article, however, is the calcinosis seen in
other breeds, more in certain ones. It 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 Boston Terriers are predisposed
to it on the ear and cheek. Calcinosis cutis circumscripta in humans is
most often seen as nodules in the skin of the extremities, especially the
hands (scleroderma). In the canine, it seems to be more variable in location
and manifestation, but still frequently in areas of increased wear, though
most researchers now discount any idea that trauma has any significance.
Treating the dog with drugs designed to fight hyperglucocorticoidism is
helpful in many but not all of the varieties or locations. As described
above, there are other crystal-related joint disorders referred to as gout
or calcium pyrophosphate-dihydrate disease (pseudo-gout), and calcific periarthritis/tendinitis,
which are managed by uric-acid-lowering medication. You may have met some
people like my son, who have suffered from one of these. A diet lower in
meat and certain other foods is usually prescribed.
Histologically, the canine calcinosis disorder often 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 in all of those cases, chronic kidney disease
has been observed. 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 telltale sign in the haircoat
may be loss of hair, or hairs easily pulled out of the follicles.
Whether associated with glucocorticoid abnormality (sometimes found
in puppies) or from an idiopathic (unknown, spontaneous) cause (in which
case it almost always shows up after a year of age), Calcinosis cutis may
take a year to clear it up, with drugs in the former cases or spontaneously
in the latter. 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. Over-mineralization (too much calcium in the diet)
should be considered a suspected factor in gout as well as in so many orthopedic
disorders.
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 that imbalanced hormonal condition
known as hyperglucocorticoidism or hyperadrenocorticism, and if this becomes
severe, an imbalance in minerals also occurs. 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; in humans, these
glands are mainly in the area of hair follicles. Researchers have held differing
ideas regarding the involvement, if any, of these glands. The renowned
dermatologist Dr. Danny Scott, whom I profiled several years ago in my
Dog World article, “Itch!”, has discounted the involvement of apocrine
gland origins. Similar glands are found elsewhere in the integument, such
as merocrine sweat glands in the pads, where the secretion is more watery,
although a small amount of perspiration is possible in the rest of the skin.
In the dog, other similar glands are found in the tongue.
How does canine calcinosis 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 this once-called-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
American Animal Hospital Association, “found no indication of familial occurrence”
in their study of idiopathic calcinosis circumscripta.
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 footpad. 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 less than two years of age when
diagnosed, as was the British GSD, yet most cases show up after one year
of age, so it is just when a show career might be starting that the problem
does, too. It is usually a benign disorder, with normal serum calcium levels
(amount of calcium compounds circulating in the blood and lymph). However,
the disorder can be cancerous and with the metastatic form of the disease,
these levels will be abnormal, as is the metabolism of calcium and phosphorus.
If the calcinosis is widespread, it is probably due to hyperglucocorticoidism
or diabetes or else it has already metastasized.
If there is no apparent damage to tissues, and even if no abnormalities
are seen in blood hormone levels, the calcium salt deposits may likewise
be either localized or generalized. The benign 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 granular material, but this can be from
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 England, my friend
informed me that his dog was being successfully treated and I later learned
that it recovered completely, thanks to the surgical removal of the deposits.
Although foot pad involvement in other breeds may indicate the metastatic
variety, localized calcinosis circumscripta and successful surgical removal
has been reported several times now in the German Shepherd Dog, and in
breeds less often afflicted.
Copyright
2001, Fred Lanting. Use requires permission.
[ Author Fred Lanting <mr.gsd@netscape.com> is an SV and
international show judge for many registries, presents seminars and consults
worldwide on such topics as Gait & Structure, Orthopedic Disorders,
Training Techniques, and the GSD. Fred invites all to join his annual non-profit
Sieger Show and sightseeing tour. He actively trains in schutzhund and
breeds occasionally. Most articles can now be found on www.angelfire.com/de3/jagenstadt/vonsalixforsale.html
, siriusdog.com/lanting.htm, or others by a Google search for his name.
Reprint permission of these copyright pieces can be requested and should
carry this or a similar notice at the end.] Looking for a gift item for
your veterinarian or “doggie” friends?
Books are available, autographed by the author:

The new Canine Hip Dysplasia and Other Orthopedics Disorders book.
It's here! The long-awaited revision of the popular HD book by Fred
Lanting is finished. (The first 1980 book sold 10,000 copies!) This one
covers all joints plus many bone disorders, and includes genetics, diagnostic
methods, treatment options, and the role that environment plays. $68,
plus $4 Book Rate postage & packaging in the U.S. and another $2 for
Canada; or for overseas shipments in “M-bag” economy surface mail, $11
for the first 11 pounds, and $1 for each additional pound, with a maximum
of 66 pounds per bag. If you order several copies to one address, we can
save considerably on postage by using the “M-bag”.
This new book is a comprehensive (nearly 600 pages), amply illustrated,
annotated, and monumental work that is suitable as a coffee-table book,
reference work for breeders and vets, and a study adjunct for veterinary
students. It is equally valuable for the dog trainer and the general dog owner
of any breed, as there is no breed that does not have some sort of orthopedic,
bone, or spinal disorder. Do not confuse it with the out-of-print 1980 edition,
which was much smaller. This new one is published by Los Perros. The author
has been described by a former OFA director as the world’s leading non-veterinarian
authority on hip dysplasia, and has lectured in some 30 countries.
Don’t wait! Be informed. Postal money orders or cashier’s checks are
fast but may be expensive. If in Canada, send your U.S.-Federal-Reserve-approved
money order or an international postal money order to: Willow Wood, 3565
Parches Cove, Union Grove, Alabama 35175-8422 USA. Other foreign
buyers may prefer payment by PayPal — that can be arranged. Add $3 for
their charge. You only need the e-mail address, support@mrgsd.com . However,
Moneygram is by far the easiest and

most economical method:
http://www.moneygram.com/index.htm
. Your First-Edition copy will be mailed as soon as the money order
or other suitable payment form arrives and is processed. All will be mailed
from the USA.
ALSO THINK ABOUT GETTING, IN THE SAME BOX, THE
TOTAL GERMAN SHEPHERD DOG
by the same author; 17 of its 20 chapters are applicable to all breeds.
For USA shipments: You can send a money order for $54 U.S., and get an autographed,
postpaid copy. ($50 plus postage) Use the address above. Make it
$56 for mail to Canada.
***********************