Shasta - A Story About SARDS

Shasta - A Story About SARDS Shasta is a five year old Malamute/Shepherd who loves to be included in life's adventures! She is a true companion and road dog!

Shasta was diagnosed with SARDS one month ago today. SARDS is Sudden Acquired Retinal Degeneration Syndrome, which causes sudden blindness. Although currently there is no known cause or cure for this condition, we are sharing Shasta's story to spread awareness as we learn more about this disease. Just within the month of Shasta's diagnoses we have learned so much just by sharing stories of other d

ogs suffering with this condition we've been able to draw similiarities to what may have caused the blindness and what types of treatment has helped each dog. Unfortunately the answers are not simple and therefore this page is to help others begin their own research, collaborate with others, ask questions and provide answers, along with supplying resources and most importantly to push the veterinarians and specialists for better answers and a cure for not just SARDS, but other illnesses as well. Shasta is currently blind, and even though this disease has undoubtedly inhibited her personality, she is still the beautiful and lovable dog that we will continue to support through this time challenging time in her life to help her adapt and possibly overcome this disease. We will be posting Shasta's story soon.

My dear Shasta, the world is a lot less bright without you in it, but I know you are running around and have your energy...
10/25/2017

My dear Shasta, the world is a lot less bright without you in it, but I know you are running around and have your energy and sight back enjoying all the sights and smells you love so much! You brought your daddy and me so much happiness for almost 9 years. It never would have been long enough, but your legacy will go on through Dr. Plechner's SARDS research and our 2 Hearts Animal Haven rescue. You were very special and made everyone who met you smile. You will be so greatly missed my love bug! xoxo
June 21, 2008 - March 28, 2017
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Alfred J Plechner, DVM, sadly passed away on September 8, 2017, at the age of 79; he was born on April 4, 1938 Dr. Plech...
10/08/2017

Alfred J Plechner, DVM, sadly passed away on September 8, 2017, at the age of 79; he was born on April 4, 1938

Dr. Plechner was a caring and compassionate veterinarian, who had a theory about the immune endocrine imbalance that is occurring in humans and animals. His controversial view has given many veterinarians another option for care for their most difficult cases. His interest in the increasing numbers of cancer cases kept his curious mind challenging the standard understanding of the behavior of the adrenal gland. He described it as Atypical Cortisol Estrogen Imbalance Syndrome (ACEIS), or, as many in the public refer to it, the Plechner Syndrome.

Dr. Plechner graduated from the University of California Davis School of Veterinary Medicine in 1966. He owned and worked at the California Veterinary Hospital in Los Angeles from 1968 to 2004. He also worked at Cedar Sinai Veterinary Hospital 2008-2016. He purchased a 27 acre parcel at the base of the Santa Monica Mountains and started a wildlife preserve called Stone Wood Meadows ,which provided free treatments and relocation for indigenous species. His passion for wildlife led him to the Big Horn Sheep Society of California as a research immunologist.

Dr. Plechner worked for years helping by consulting to both veterinarians and the pet owners on the ACEIS. He would generously give of his time to interpret and help people understand the endocrine problem. For hours he would share his cases and help tweak their care.

He had treated and consulted to over 100,000 humans and animals suffering with this immune endocrine imbalance. Through years of research and observation, he felt in his heart that there was a way to help prevent these allergic animals from becoming victims of cancer. He has written several books and tens of article on this topic and you can see them at his website www.drplechner.com.

Margo Roman, D.V.M. wrote the following on how she met Dr. Plecher, "Personally I had a client in 1997 who claimed that Dr. Plechner saved her dog in California, after she had gone to every referral hospital, including the veterinary school. She gave me a little pamphlet which I read and thought it crazy and discounted it. About four years later, I had a case of a client who had already spent $20,000 at Angell Memorial Hospital in Boston. Thirty-three year old male neutered Newfoundland had been diagnosed with Irritable Bowel at nine weeks of age, and had his cruciate repaired on the same leg three times, but it was not healed. He had been continuously on metronidazole and other drugs, and looked like a Mexican hairless. I asked to work on this case for six months, and was able to stop the IBS in one week; we corrected the cruciate in one month with acupuncture, homeopathy, ozone, chiropractic, herbs, nutrition and nutraceuticals. Four month later, I still had a hairless itchy dog that could not gain any weight. I suggested to the owner that the dog could have this endocrine imbalance I read about. He bought Dr. Plechner’s new book Pets At Risk, From Allergies to Cancer and he said “you read this and you test my dog and treat it exactly like Dr. Plechner says.” I had to read it two times to even begin to understand it and I still do not feel I completely understand it. But I did what the owner said and the dog healed and lived another seven years looking like a healthy Newfoundland. It was not my standard of care, but I was not getting results and could have declared this case an incurable case.

Since that first case, Dr. Plechner’s theories have helped me successfully treat hundreds of cases which might otherwise have been hopeless."

Dr. Alfred Plechner continued to feel rejection from many in academia, but he persisted as he had owner after owner and doctor after doctor seeing shifts in cases that no one else could help. He felt that some day he would be validated and started to consult to MDs to help humans having these life disrupting health issues.

Dr. Plechner is survived by his two sons, Jay and AJ, and four grandchildren, Cambria, Cassidy, Jayden and AJ.

09/28/2016

Last month Dr. P.'s patients received the sad news that he is forced to retire due to illness. Dr. P. is suffering from severe low back problems is no longer able to continue his private practice. This is very sad for someone who has dedicate his life to helping others and their pets. I hope he recovers quickly and can enjoy a pain-free retirement. Dr. P. is someone I personally hold very dear to my heart and know many others as well. He has sought out to fight the adverse reactions to his research regarding SARDS and Plechner Syndrome by mainstream veterinarians and medical doctors. I believe after 50 years, his research has finally been heard and others are starting to believe in his findings. Believe me, I completely understand how hard it is to take one person's word over everyone else's. When you're in a state of panic and you don't understand the first thing about animals and the endocrine system and you have people telling you that his protocol goes against everything they learned in Veterinary school, it's scary to think you're putting your pet and loved one who totally depends on you to make the right decision... to take a leap of faith and believe in one man's findings. But you don't have to take a leap of faith. You just have to take the time to read his work and it will begin to make sense. This is the problem. People are not taking the time to study it, learn about it, and really take it in. Vets are trying to help so many animals in their day-to-day and barely have the time to spend with their own families let alone spend all this time researching an illness that only effects a very small percentage of animals per year. But as this illness is becoming more common and more pet owners are unwilling to take the response from their vet that their is no known cause, no known treatment, and to read up on how to live with a blind dog... more vets are being forced to research this illness. And we are lucky they have Plechner to turn to even if they don't believe him at first. He's worked with many vets throughout the course of his career and more and more vets are starting to see the results of his work and following his protocol.

I found a post from Dr. Burlingame on Dr. P's website, found out where he practiced and made an appointment to drive Shasta up to see him in Washington. It was definitely worth the trip! He is very knowledgeable about SARDS, Plechner Syndrome, and he has a wealth of knowledge to offer from his own research. We had a great visit, had some bloodwork done and I'll be posting Shasta's results when I receive them later this week.

I realize it is not easy and in some cases impractical to take off work, get in the car and drive hundreds of miles to see a vet. But if you only had to do it once, and then were able to talk to your local vet about the incredible difference the treatment made in your dog/cat, they may be more inclined to treat the patient themselves. This is the only way will be able to reach more vets more quickly. We can't simply lay down and let vets, that do not know and do not understand this illness and treatment, passify our pets' health and lives. They depend on us.

07/28/2016

Great article by Dr. Plechner explaining his lifelong research and findings studying the endocrine system.

ENDOCRINE IMMUNE STUDIES BY DR. PLECHNER FROM THE PAST.
Pertaining to my clinical veterinary studies, this article was an attempt to share my thoughts with my veterinary profession. The California Veterinarian found my article to be interesting enough to publish it in their journal in January of 1979.
I also created this article titled The Theory of Endocrine Immune Surveillance which I would like to share with you almost 37 years later.
It has taken me all this time to use my theory to help thousands of patients including canines, felines, equines and humans, even though my theory was not accepted then and even now, when it has been proven.
This is the same studies that I have conducted, since the late 1960’s.
Today’s endocrine immune protocol and treatment plan began with this published theory.
What was true over 40 years ago, is still true today, but will not be considered by the veterinary profession.
Fortunately, The MD’s are beginning to realize the importance of this study, which is available on the internet with my name.
The article title is The Results of an International Convention of Integrative MD Oncologists, Regarding Dr. Plechner’s Findings, for Many Different Chronic Diseases.
For those of you that might be interested in reading more about my early clinical research articles from November of 1076, please go to ABOUT and Early Research.
I hope you enjoy the article.
Sincerely,
Dr. A. J. Plechner
Theory of Endocrine Immune Surveillance
Published in California Veterinarian – January 1979
Alfred J. Plechner, DVM – Los Angeles, California
(Editor’s Note: This theory is presented by Dr. Plechner to stimulate creative thinking and is based upon scientific facts and his own clinical research and observations.)
It is interesting to consider old diseases in modern times. One thinks of those many traditional bacteria, virus, and fungal infections. However, in present times, a clinician is forced to wonder about immunological diseases and ponder the immune system.
Many traditional diseases have been well documented. Detailed studies have carefully delineated the signs of clinical disease that an organism may cause. But in all actuality, does the organism really cause the disease, or does the organism as an antigenic agent elicit a specialized immune response which indeed may cause great damage to the host. Does the staphylococcus bacteria mediate a disease against the body or does the various antigenic compounds in the structure of the bacteria and its various toxins elicit a specific immune response that may destroy adjacent or involved host tissue. Then we are discussing the processing of foreign materials properly with immune conjugation with tolerance of foreign material without inflicting damage to the host while processing these materials. When treating a specific disease with a specific antibiotic, are you then destroying the bacteria which appears to be overwhelming the host response, or are you merely reducing the foreign antigen and removing its antigenicity and reducing the numbers of antigenic bacteria necessary to elicit this specific immune host tissue reaction.
It appears that it is of ultimate importance that the body remains in a state of immune homeostasis, therefore allowing for the proper processing of self antigens and foreign antigens. If this immune homeostasis is altered, then serious self-destructive diseases may occur. The immune system appears to be regulated by the endocrine system and its central point of organization may be mediated through the adrenal axis with central nervous system input through the pituitary, hypothalalmus, and cerebral cortex, etc. Whether agreed to or not, steroids have been as important to clinical veterinary practice as antibiotics. In practice, we all use steroids in various forms for a variety of diseases and generally achieve good results. No one admits to using these substances as frequently as most of us use them, because this is not a popular trend in today’s clinical veterinary medicine. But is this really true? I think not. The experts tell us steroids are usually contraindicated. However, if a practitioner is honest, it becomes quite apparent that steroids are very necessary. Ever since the 1940s when an “X” substance was found at the Mayo Clinic and this research effort sequelled because this substance was bad,” steroids have often remained in the realm of unacceptable therapy.
With the many uses of steroids and many lifesaving qualities produced by this drug, one wonders if this multipurpose hormone is not one of the most important substances in the body! I believe that cortisol is the mediator of endocrine immune surveillance. I have often wondered if we as practitioners, in giving a patient a steriod, might not merely be replacing in the body a synthetic hormone which acts as a replacement substance, which due to genetic defect or acquired damage does not occur in proper amounts.
A number of years ago, began looking at the adrenal gland for signs of clinical disease. By this time, veterinary pathologists had noted varying degrees of adrenal histopathology often not correlated with clinical disease. With the development and availability of more recent and more direct immunological methods and procedures, I have found good evidence that adrenal disorders exist clinically in veterinary practice and differ from the classic Addisonian and Cushing syndromes.
It is important to understand the anatomy of the adrenal cortex. The adrenal cortex is composed of three basic layers. The most superficial zone is the zona glomerulosa which produces aldosterone, which is necessary for the reabsorption of sodium and the excretion of potassium. The zone is primarily controlled by the reninangiotensin system. This zone is only slightly responsive to ACTH. In man it is suspicioned that ACTH may have a supportive effect on the zona glomerulosa, but chronic ACTH deficiency apparently does not alter the responsiveness of this layer.
The zona fasciculata produces cortisol for glucocorticoid action and I feel is involved clinically, at least in part, in endocrine immune surveillance. This zone is the target area for ACTH and proper cortisol production is necessary to activate the negative feedback mechanisms to the pituitary. The cortisol occurs in two major forms. Cortisol may be bound to albumen, which is biologically active and essential for activation of the anterior pituitary negative feedback system.
Cortisol may be bound to an alpha globulin as transcortin which is biologically inactive for the most part. Interestingly enough, of the total cortisol produced, 5% is in the biologically active state and 95% is in the bound form. Resting blood cortisol levels and ACTH stimulated blood cortisol levels are often measured by radioimmunoassay, which measures total cortisol (free and bound). Theoretically speaking, when resting and stimulated blood cortisol levels occur in proper amounts at the time of testing, are they really normal? The ratio between free and bound cortisol may be abnormal. Adrenal disease may be present therefore, even with normal test levels. With an incorrect ratio between active and bound cortisol, the negative feedback mechanism to the anterior pituitary gland is definitely damaged. It is important to remember that naturally occurring active steroids must have a hydroxyl group at the eleventh position to inhibit ACTH release. It may be necessary to collect 24 hour urine production from a patient to determine the ratio between bound cortisol and biologically active cortisol. The innermost layer of the adrenal cortex is the zona reticularis, which is under the control of ACTH and is responsible for the production of estrogens, androgens, and prostiglandins. In the human being, almost all androgen production in the female occurs in this layer. In the male, two-thirds of the androgen production occurs in the zona reticularis. If this is true in the canine, which I believe it is, then when a complete ovariohysterectomy is performed and a state of urinary incontinence occurs at a later time, there is certainly reason to suspect the zona reticularis is not producing sufficient amounts of the proper hormone. Cystic ovarian disease is certainly suspect and may be primarily or secondarily associated with this layer and may also have an influence or be associated with the zona fasciculata. With production of progesterone from the corpus luteum and concurrent production of estrogenic compounds from the zona reticularis, it becomes a little more apparent why pyometra complex might occur.
It is of utmost importance to understand some of the interrelationships of the adrenal cycles. The adrenal stimulation cycle may originate in the adrenal cortex due to diurnal factors or stress producing neural secretions (Figure 1). These and other secretions act upon the hypothalamus to release Corticotropic Releasing Factor (CRF). CRF acts upon the anterior pituitary to cause the release of ACTH. ACTH causes the release of cortisol from the zona fasciculata. If cortisol production is normal, and proper amounts of cortisol occur in the free state, then the negative feedback mechanism functions to stop further ACTH release (Figure 3). If, however, the zona fasciculata is malfunctioning and either the ratio of cortisol production between the active or bound state is incorrect, or the actual quantity of cortisol is depressed, then the negative feedback system is damaged and ACTH secretion continues (Figure 4). The ACTH then causes further secretion of estrogens, androgens, and prostiglandins from the zona reticularis. The significance of this phenomenon is that estrogens and prostiglandins cause biologically active cortisol to go into the bound state as transcortin and therefore cause further damage to the negative feedback system with the anterior pituitary. The estrogen and prostiglandins act then on a positive feedback system to the hypothalamus by causing secretion of CRF.
One can then begin to imagine, if active cortisol is necessary for the proper endocrine feedback schemes to function normally, then certain natural phenomenon may act to cause dysfunction.
If a female canine begins its estrus cycle, and has a genetically induced adrenal disorder, then the estrogens produced during the cycle may shift the active cortisol into transcortin, and then a certain degree of endocrine-immune surveillance is lost. Hypersensitivity diseases may occur due to a hyperactivity of the immune system because cortisol has been bound and is not as available.
A male canine might be stimulated by a female in estrus, and due to increased prostiglandin production, cause a transcortin shift with loss of surveillance and increased immune hypersensitivity. Any disease process, trauma, emotional stress, etc., that damages or fatigues the zona fasciculata can lead to a loss of endocrine-immune surveillance. (Note: Steroids occurring in low levels directly suppress or lyse T-Iymphocytes without effect on the B-lymphocytes, but in higher concentrations may cause suppression of both B and T lymphocytes. In many of the cases we have studied, B and T lymphocytes population are normal, however, the cortisol production is not. Therefore, one can begin to understand how a myriad of environmental conditions can change cortisol levels and concurrently alter the regulation of the populations of B and T lymphocytes. The overall process is certainly much more complex than the above, however, the basics are applicable.)
It is of ultimate importance to realize that estrogens and prostiglandins also cause a shift of certain thyroid compounds to a bound state and thereby may cause a change in the overall metabolic rate. This effect may explain why certain patients are less responsive or non-responsive to classic drug therapy. This may be part of the reason we find one-fourth to one-third of all hypothyroid canines with normal T3 and T4 levels, (Note: In man with subclinical adrenal damage, a state of hyperthermia may exist.) I have noted this same finding with our studies also.
The further one proceeds with this scheme of endocrine immune surveillance, the more it becomes apparent that this is a multisystem scheme of great complexity.
It appears that cortisol is necessary for catecholamine synthesis in the adrenal medulla, brain, spinal cord, and other nervous tissue (Figure 2). Synthesis of epinephrine at proper levels acts as a negative feedback mechanism involving Corticotrophic Releasing Factor and ACTH. Therefore, if the zona fasciculata is impaired, then cortisol levels are decreased. If catecholamine synthesis is reduced or inhibited then ACTH release is increased due to the damaged negative feedback system from epinephrine and cortisol (Figure 5). Resultant increased estrogen and prostiglandin then further reinforces the cyclic damage. The resultant effect again is the loss of endocrine-immune surveillance. (Note: One might then imagine that with people and animals undergoing great emotional stress, with persistent over-production and synthesis of epinephrine, the cortisol levels would be decreased due to a fatigue of the zona fasciculata with loss of endocrine-immune surveillance, with resultant production of disease.)
I believe that many diseases can be involved primarily or secondarily with adrenal gland disorders. It Is interesting to speculate that the difference between allergy and severe auto-immune diseases and tumors, at least in part, may be the difference of degrees of adrenal malfunction. A tumor, therefore, may merely be an end product due to loss of endocrine-immune surveillance mediated through a multisystem malfunction involving the adrenals, pituitary, thyroid, hypothalamus, cerebral cortex, immune system, and improperly processed foreign and/or self antigens. I further believe that generalized demodecosis, immune complex, or auto-immune diseases, certain endocrine diseases and tumors, have at least in part, one common denominator, which is a damaged adrenal cortex.
Summary
The actual theory of endocrine-immune surveillance indicates that cortisol, produced by the zona fasciculata is the mediator substance for endocrine-immune surveillance. This substance, through its production and modification, acts to regulate, control, and function as the link between the endocrine and immune systems. The other related layers of the adrenal cortex act to further modify the cortisol as a mediator substance and add further centralized regulatory functions for other related systems.
Concerning the theory and the diagrammed cycles, one may further understand that stress can cause increased epinephrine synthesis which may consume and fatigue cortisol production and damage the negative feedback system. The hypothalamic pituitary direct feedback cycles stimulate the zona reticularis which produces and releases estrogens and prostiglandins which further bind active cortisol into bound transcortin which further damages the endocrine-immune surveillance. Certain thyroid compounds are also bound by the estrogen, etc. An overall unresponsive state of immune hyperactivity may then exist with partial to total loss of endocrine-immune surveillance.
Many severe immune mediated diseases appear to be primarily or secondarily involved with the adrenal gland. Generalized demodecosis appears to be involved with an adrenal malfunction. Our own studies have shown a definite genetic transference of generalized demodecosis, at least in part, through a damaged adrenal cortex.
It is of major significance to realize that the degree of damage involving the adrenal cortex may be variable. There are specific disorders involving specific layers of the adrenal cortex. There are definitely a number of diseases that vary from those classic adrenal disorders that we are all familiar with at this time. Normal blood levels may still be produced and measured clinically with severe adrenal damage being present, if enough functional cells remain. Our histopathology and immunopathology studies definitely support this fact. Therefore, normal adrenal test levels do not rule out clinical disease of the gland. The disease may be inherited directly causing early manifestation or may be acquired and develop later in life due to immunological destruction of the adrenal tissue by the host’s own immune system and other diseases.
If cortisol then is the mediator of endocrine-immune surveillance, and varying degrees of adrenal mediated diseases are possible, it is interesting to speculate then that mild adrenal dysfunction might manifest itself as an allergy or hypersensitivity disorder and a more severe adrenal dysfunction might lead to a more serious endocrine immune complex malady resulting in auto-antibody disease and tumors.
Much more research is needed in this area, particularly involving the endocrine regulation and its influence of the endocrine system with its overall effect on the host.

Our annual road trip to see this famous guy! Dr. Al Plechner! Shasta has been seeing him for 3 yrs now and she is doing ...
06/25/2016

Our annual road trip to see this famous guy! Dr. Al Plechner! Shasta has been seeing him for 3 yrs now and she is doing great. She loves her uncle Al!

10/28/2015

If anyone has a dog or pet diagnosed with SARDS, or knows of anyone's dog suddenly losing their vision, please read this article and pass on to your friends. There are not many cases of this condition, but that is also why there is not much information regarding it either, other than Dr. Plechner's research and protocol.


------SUCCESSFUL RETURN OF VISION IN 10 CANINE SUDDEN ACQUIRED RETINAL DEGENERATION SYNDROME (SARDS) PATIENTS

Author:
Dr. A. J. Plechner DVM
Email: [email protected]

Abstract
33 cases were diagnosed, by board certified veterinary ophthalmologists with canine patients that have Sudden Acquired Retinal Degeneration Syndrome (SARDS).
Request was made, for the convenience of publication, to reduce the number of SARDS cases to only 10. I have listed those 10 cases but have also listed the other 23 cases that indicate the same endocrine immune imbalances and WHY canine SARDS happens.
Initial diagnosis of the 10 cases of canine SARDS, was followed by an endocrine immune blood panel. The study reflected High Total Estrogen in all 10 canines. Eight of the canines had high cortisol (defective or bound but often being diagnosed as Cushing’s syndrome) and low T3 and T4. IgA levels were initially below 58 in 9 canines, causing malabsorption of oral nutrients, supplements, vitamins and medication. IgG and IgM levels were low also in all 10 cases. Once endocrine immune replacement supplementation was begun, endocrine immune levels improved again in all 10 canine patients. Vision was restored to all 10 canines initially diagnosed with Sudden Acquired Retinal Degeneration Syndrome.
INTRODUCTION
At this time, the veterinary profession has not identified the cause of SARDS in canines.
However, veterinary researchers agree that SARDS is an autoimmune disease (2,3). Anti-retinal antibodies are not present, so the retinal destruction may be caused by a T- lymphocyte that is no longer regulated by an imbalanced endocrine immune system (2). This endocrine imbalance appears to allow the T- lymphocyte to lose recognition of self-tissue and cause cellular damage to the retinae.
An electroretinogram (ERG) is the diagnostic tool of choice once the canine develops a SARDS blindness (4,5).
The ERG is usually flat lined with a SARDS canine patient, however there are some very early non-verified reports that once vision has been reestablished in a SARDS canine patent, the repeat ERG may still remain flat lined.
If my research data is correct, then either one or more of the sight layers of the retina may be involved as well as the rods and cone, since vision can been restored (1).
My clinical studies indicate that the effects of canine SARDS comes from an imbalanced cortisol that is produced by the middle layer, zona fasciculata, of the adrenal cortex (5, 11-15, 18-22).
Research has led me to realize that the endocrine system regulates the immune system in canines.
My findings show that imbalanced cortisol not recognized by the hypothalamic-pituitary axis leads to a lack of funding of the negative feedback mechanism to the hypothalamic-pituitary axis.
When this occurs, the hypothalamus continues to release its corticotrophin hormone, which in turn stimulates the release of the pituitary adrenocorticotropic hormone (ACTH).
When the cortisol imbalance is due to a deficiency or due to the production of a defective cortisol, the negative feedback mechanism to the hypothalamic-pituitary axis does not function (23, 24).
The continued production of ACTH causes the inner layer adrenal cortex, zona reticularis, to respond as a positive feedback mechanism, which produces an excess amount of adrenal estrogen and adrenal androgen.
THIS PAPER DEALS SPECIFICALLY WITH THE INCREASED AMOUNTS OF ADRENAL ESTROGEN.
When damage to the production of cortisol occurs from the middle layer adrenal cortex, an elevated amount of adrenal estrogen is produced and I have found the following changes occur:
1) The elevated adrenal estrogen binds the receptor sites for Triiodothyronine (T3) and (Thyroxin) (T4) (6-11-15, 21).
2) The elevated adrenal estrogen deregulates the immune system (5, 6, 9).
The effect of which is the T-lymphocyte ceases to function in protecting the patient from viruses and fungi and a loss of recognition of self-tissue occurs, which may lead to autoimmunity, including canine SARDS.
The deregulated B-lymphocyte also loses its ability to protect the patient against bacteria and production of proper antibodies in response to vaccines. At the same time, the B-lymphocyte production of immunoglobulins is diminished and as the mucous membrane antibody Immunoglobulin A (IgA) falls below 58 mg/dL, malabsorption of oral nutrients, supplements, vitamins and medication, including steroids may additionally occur (8, 11-15, 18, 22).
Unless the IgA level is at 58 mg/dL or higher, replacement hormones will not be absorbed properly by the canine SARDS patient.
For the successful diagnosis and return of vision in all of my patients with canine SARDS, it appears to depend upon three events:
1) How well the canine deals with and hides their developing blindness.
2) How soon the owner of a SARDS canine realized that their pet was suffering from reduced vision.
3) How soon the canine SARDS was diagnosed and how soon I was able to correct the patients’ endocrine immune imbalance.
MATERIALS
I have found that an ERG and a simple blood test help diagnose canine SARDS, along with the other accompanying clinical signs.
The ERG was accomplished by referring my SARDS canine patients to veterinary ophthalmologists.
If the veterinary ophthalmologists confirmed SARDS, a simple blood serum test was indicated.
The blood serum test must include the following:
1) Total estrogen
2) Cortisol (no special time of day is needed to do this test)
3) Total T3 (Triiodothyronine)
4) Total T4 (Thyroxin)
5) Immunoglobulin A
6) Immunoglobulin M
7) Immunoglobulin G
METHODS
I followed these procedures, as instructed by the veterinary laboratory:
1) The blood sample was taken after fasting from food or medication for 3 to 4 hours.
2) If a repeat test was indicated at a later date, the blood sample was taken at the same time of day.
3) If alcohol was used at the blood draw site, it was made sure the blood draw site was dry before taking the blood sample, otherwise the alcohol would cause hemolysis of the erythrocytes. On a side note, the presence of alcohol with any blood draw will cause hemolysis of the serum sample.
4) Once the blood draw was been completed, the blood tube was laid on its side in a refrigerated unit for 15 minutes in order to help increase the surface area of the sample and enhance clotting.
5) Once this procedure was completed, the blood sample was centrifuged for 10 minutes and refrigerated immediately.
6) In the event the blood sample was not spun down, the sample was sent to the lab only refrigerated, not frozen.
7) In the event the blood sample was spun down and the serum was clear, the sample was frozen.
8) If the spun down serum was hemolyzed, the sample was only refrigerated, not frozen.
At this time, I have found only one veterinary laboratory in the United States that tests for total estrogen (a).
RESULTS
When hormonal therapy was administered to 10 SARDS canines, the endocrine immune values improved, as they regained their sight (Table 1).
Detailed information on the actual treatment for SARDS canines is available (b).
DISCUSSION
The diagnosis and successful treatment of the SARDS canines depended on how rapidly diagnosis was made and treatment plans were begin.
I have been involved with enough SARDS canines worldwide to realize that canine SARDS is an autoimmune disease that is caused by an imbalanced or deficient cortisol that is produced by the zona fasciculata of adrenal cortex which leads to the production of excessive adrenal estrogen from the zona reticularis of the adrenal cortex. This increase in the production of adrenal estrogen causes a binding of the receptor sites of the thyroid hormones and also deregulates the immune system.
I believe a true pivotal point in the development of canine SARDS comes from the use of monthly insect chemicals. This is not to say that the chemicals are primary in the development of SARDS, but it is to say, the monthly insect chemicals may be a trigger for the imbalance to occur.
Abnormal alteration of cortisol production may occur due to altered genetics; exposure to estrogen mimicking chemicals (xenoestrogens); exposure to plant estrogens (phytoestrogens); and exposure to chemical insect repellants, stress, vaccines, anesthetics, toxins, damaging heavy metals, radiation, poor nutrition, lack of exercise, and much more.
I personally believe that the Achilles tendon of the body is the middle layer adrenal cortex and its ability, or inability, to produce adequate amounts of active regulatory cortisol.
Many of the SARDS canines had elevated amounts of cortisol, but without comparing how the cortisol affects the negative feedback mechanism to the hypothalamic-pituitary axis, it was not determinable whether the measured cortisol level was active or inactive and was utilized by the canine SARDS patient (Figure 1).
Cushing’s syndrome produces excess active cortisol. Active cortisol is used to treat autoimmune diseases, including SARDS. Therefore, if a canine patient has Cushing’s syndrome, the patient will not have SARDS.
When I diagnosed a case of canine SARDS, there was no reason to perform an ACTH Stimulation or Dexamethasone Suppression Test for Cushing’s syndrome. If the amount of measured cortisol is elevated, and if the cortisol is in an inactive state, it cannot be used by the SARDS canine patient (Figure 2).
Once proper hormone therapy was provided, the endocrine immune regulation did return to normal and vision was restored to these 10 SARDS canine patients (Figure 3).
I refer to this canine syndrome as Atypical Cortisol Estrogen Imbalance Syndrome (ACEIS).


FOOTNOTES
a. National Veterinary Diagnostic Services, 26856 Clark Rd, Waller, TX 77484, http://national-vet.com, email: [email protected], phone: 281-661-4292
b. Atypical Cortisol Estrogen Imbalance Syndrome Protocol, http://drplechner.com/get-help-for-your-pet/test-procedures-info/atypical-cortisol-estrogen-imbalance-syndrome-protocol
* The sooner canine SARDS is diagnosed and treated, the better the chance that viable retinal tissue still remains. Because canine SARDS has been recognized as an autoimmune disease, even if sight does not return, proper replacement supplementation helps stop the development of other autoimmune diseases, including cancer.


REFERENCES
1. Miller P, Galbreath E, Kehren L, Steinberg H. Photoreceptor cell death by apoptosis in dog with sudden acquired retinal degeneration syndrome. Am. J. Vet Res 1998: 59: 149-152.
2. Keller R, Kania S, Dendrix D, Ward D. Evaluation of canine serum for the presence of anti-retinal autoantibodies in sudden acquired retinal degeneration syndrome. Vet Ophthalmol 2006: 9: 196-200.
3. Grozdanic, Sinisa, Harper, Mathew M, Kecova, Helga. Antibody-Mediated Retinopathies in Canine Patients – Mechanism and Treatment Modality. Veterinary Clinics of North America. Small Animal Practice. March 2008; 38; 361-387.
4. Electroretinography. U.S. National Library of Medicine. April 2006.
5. Brown M, Mamor M & Vaegan. ISCEV- Standard for Clinical Electro- Oculography (EOG) 2006 at Documenta Ophtlamologica 1133; 206-212.
6. Plechner AJ. Cortisol abnormality as a cause of elevated estrogen and immune destabilization: Insights for human medicine from a veterinary perspective. Medical Hypothesis 2004; 62: 575-581.
7. Plechner AJ. Reproductive Failure in Adrenal-Thyroid-Immune Dysfunction. Townsend Letter for Doctors and Patients. December 2008; 80-82
8. Plechner AJ. Importance of IgA. Townsend Letter for Doctors and Patients. November 2005; 268; 88-91
9. Plechner AJ. Do Adrenal-Immune Disturbances in Animals and Common Variable Immunodeficiency in Humans Have a Common Cause? Townsend Letter for Doctors and Patients. 239; 122-123.
10. Plechner AJ. An Innovative Cancer Therapy That Saves Animals, Can It help Save Humans as Well? Townsend Letter for Doctors and Patients. February 2004; 110-118.
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13. Plechner AJ. Unrecognized Endocrine Immune Defects in Multiple Diseases. Medical Hypothesis. March 2003.
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15. Plechner AJ. Theory of Endocrine Immune Surveillance. California Veterinarian. January 1979; 12-15.
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ILLUSTRATIONS

Figure 1: This diagram shows normal relationships and feedback activity between the adrenal cortex and the hypothalamus and pituitary, and in turn, a healthy regulatory influence on the immune system.

Figure 2: Genetic and toxicity factors can interfere with cortisol production, triggering excess ACTH and estrogen release. Cortisol deficiency is aggravated, thyroid function affected, and the immune system destabilized.

Figure 3: Correction of cortisol deficit with cortisol replacement therapy restores normal hypothalamus-pituitary-adrenal relationships and immune system integrity.


CLINICAL CASE STUDIES OF RETURNED SIGHT IN 10 SARDS CANINES
WITH EARLY ENDOCRINE IMMUNE REPLACEMENT SUPPLEMENTATION *
All Patients Began Treatment With Flat Line ERG’s
By Dr. A.J. Plechner, DVM
Case Breed S*x, DOB Collection Date Total Estrogen Cortisol T3 T4 IgA IgG IgM
Female (Normal Values)
Male ( Normal Values)
Units of Measurement 30-35
20-25
pg/ml 1-2.5
1-2.5
ug/dL 100-200
100-200
ng/dL 2-4.5
2-4.5
ng/dL 100-200
100-200
mg/ml 1000-2000
1000-2000
mg/ml 100-200
100-200
mg/ml
1 American Dingo Female 9/19/06 1/23/14 3/27/14 35.17 35.11 3.10 0.86 64.53 109.58 0.82 2.65 53 59 712 843 72 85
2 Maltese Male 10/15/03 10/27/14 12/19/14 25.19 25.15 4.63 0.68 108.11 86.99 2.39 1.64 51 55 716 768 70 76
3 Miniature Poodle Female S 3/15/93 2/01/09 4/18/09 35.29 35.13 7.51 1.74 89.94 134.72 1.22 4.65 48 58 816 941 83 96
4 Bearded Collie Male 7/03/03 10/17/14 10/18/14 11/21/14 12/18/14 1/22/15 2/05/15 25.21 25.19 25.13 25.11 25.12 25.09 4.29 4.01 0.82 0.94 0.82 0.72 56.84 77.15 143.94 77.68 88.57 107.14 0.73 1.27 4.70 0.98 1.53 2.33 50 51 57 59 58 61 712 720 802 842 832 868 70 71 79 83 83 87
5 Yorkshire Terrier Female 10/15/08 4/25/13 8/30/13 5/30/14 35.14 35.06 34.98 0.82 0.87 3.06 78.94 138.61 135.57 1.30 4.39 3.94 56 64 73 753 894 1082 74 90 105
6 Jack Russell Terrier Female S 1/28/04 6/07/13 7/26/13 8/23/13 12/4/14 35.17 35.13 35.14 35.11 6.15 0.83 0.87 0.85 84.94 95.24 72.97 168.94 1.55 1.92 1.03 5.69 53 57 56 59 768 803 782 832 75 79 77 81
7 Cocker Spaniel Male 4/16/05 4/01/14 5/09/14 6/20/14 25.21 25.18 24.17 6.38 0.77 0.58 47.31 53.74 54.05 0.51 0.58 0.59 49 52 53 684 736 740 68 72 73
8 Dachshund Male N 1/01/07 9/07/13 9/24/13 11/5/13 2/12/14 4/08/14 11/4/14 25.18 25.14 25.10 25.08 25.03 25.05 7.97 0.62 0.65 0.74 1.04 0.68 56.22 67.83 115.58 86.54 132.14 137.82 0.69 0.97 2.62 1.40 3.75 3.96 52 56 60
62
67
65 729 774 843 861 968 927 73 76 82 85 97 93
9 Wirehaired Dachshund Male N 4/01/06 5/02/14 5/16/14 25.07 25.04 1.83 1.35 98.43 133.92 2.03 3.85 63 66 901 942 89 93
10 Maltese Female 3/09/03 11/07/14 11/29/14 12/20/14 35.20 35.15 35.12 7.54 3.51 1.51 57.89 127.64 78.52 1.13 3.39 1.03 50 55 58 706 784 815 69 77 80


CLINICAL CASE STUDIES OF RETURNED SIGHT IN 33 SARDS CANINES
WITH EARLY ENDOCRINE IMMUNE REPLACEMENT SUPPLEMENTATION *
All Patients Began Treatment With Flat Line ERG’s
By Dr. A.J. Plechner, DVM
Total
Estrogen Cortisol T3 T4 IgA IgG IgM
Units of Measure pg/mL ug/dL ng/dL ug/dL mg/dL mg/dL mg/dL
Normal Values M Low 20.00 1.00 100.00 2.00 70 1000 100
High 25.00 2.50 200.00 4.50 170 2000 200
F Low 30.00 1.00 100.00 2.00 70 1000 100
High 35.00 2.50 200.00 4.50 170 2000 200
Breed S*x DOB Collection
Date Total
Estrogen Cortisol T3 T4 IgA IgG IgM
American Dingo F 9/19/2006 1/23/2014 35.17 3.10 64.53 0.82 53 712 72
3/27/2014 35.11 0.86 109.58 2.65 59 843 85

Maltese M 10/15/2003 10/27/2014 25.19 4.63 108.11 2.39 51 716 70
12/19/2014 25.15 0.68 86.99 1.64 55 768 76

Maltese F 1/21/2003 9/27/2012 35.15 3.03 162.11 5.61 55 783 77
10/17/2012 35.13 1.65 166.24 6.67 57 816 81
11/29/2012 35.09 1.81 150.16 4.63 61 861 86
1/18/2013 35.04 0.92 146.19 4.35 66 936 94
2/21/2013 35.03 0.98 141.58 4.21 67 958 96
3/21/2013 35.02 2.46 148.92 6.24 68 981 98
8/16/2013 35.02 1.96 159.82 7.34 68 987 99
10/18/2013 35.01 2.88 152.03 5.48 69 1002 99
3/20/2014 34.98 1.45 109.94 2.45 72 1061 107

Min Pin F 3/01/2003 3/14/2013 35.13 2.20 56.14 0.57 57 830 82
5/02/2013 35.10 0.82 60.13 0.78 60 864 85
11/15/2013 35.06 0.93 122.15 2.92 64 938 92
8/15/2014 35.03 2.35 139.68 6.97 67 952 95

Terrier Mix F 1/08/2009 4/29/2014 35.17 2.86 78.59 1.16 53 742 73
5/23/2014 35.14 0.59 82.57 1.32 56 779 78
6/05/2014 35.10 1.19 81.16 1.25 60 843 82
6/27/2014 35.06 2.68 126.42 2.99 64 931 92
7/18/2014 35.03 0.92 131.58 3.92 67 962 96
8/08/2014 35.01 1.10 152.16 6.07 69 989 99
8/29/2014 35.00 2.17 148.22 5.71 70 1013 100
9/19/2014 35.01 2.91 147.92 5.70 69 994 100
10/10/2014 35.00 2.35 145.16 4.97 70 1015 100
10/30/2014 35.01 0.74 136.84 3.57 69 989 100
11/20/2014 35.01 0.69 113.52 2.76 69 984 99
1/08/2015 35.02 0.86 107.25 2.29 68 984 99
2/05/2015 35.04 0.81 82.14 1.23 66 943 95

Min. Poodle S 3/15/1993 2/01/2009 35.29 7.51 89.94 1.22 48 816 83
4/18/2009 35.13 1.74 134.72 4.65 58 941 96

Maltese N 6/09/2006 1/27/2012 25.17 1.88 56.12 0.67 52 781 79
8/01/2012 25.13 1.43 66.27 0.89 57 884 87
8/06/2013 25.07 1.75 109.89 2.37 63 926 94
4/02/2014 25.09 1.77 78.91 1.26 61 882 87
1/10/2015 25.04 2.02 62.03 1.01 66 937 94
Total
Estrogen Cortisol T3 T4 IgA IgG IgM
Units of Measure pg/mL ug/dL ng/dL ug/dL mg/dL mg/dL mg/dL
Normal Values M Low 20.00 1.00 100.00 2.00 70 1000 100
High 25.00 2.50 200.00 4.50 170 2000 200
F Low 30.00 1.00 100.00 2.00 70 1000 100
High 35.00 2.50 200.00 4.50 170 2000 200
Breed S*x DOB Collection
Date Total
Estrogen Cortisol T3 T4 IgA IgG IgM
Greyhound M 6/01/2011 3/18/2014 25.20 6.20 51.22 0.47 49 694 70
4/04/2014 25.18 0.67 53.61 0.52 52 718 71
Greyhound N 6/01/2011 2/25/2014 25.18 2.62 51.12 0.48 51 731 72
3/18/2014 25.15 0.82 63.84 0.91 55 772 76
4/04/2014 25.14 0.86 58.67 0.73 56 788 77

Malamute/Shep S 6/21/2008 8/16/2013 35.13 1.97 86.24 1.66 57 784 77
9/11/2013 35.10 1.59 82.05 1.43 60 836 84
10/11/2013 35.09 0.88 126.84 3.36 61 868 87
1/31/2014 35.05 1.09 124.16 3.14 65 938 94
8/15/2014 35.03 3.20 132.91 3.93 67 972 96
11/21/2014 35.02 1.47 87.89 1.57 68 968 97

Yorkshire Terr. F 10/15/2008 4/25/2013 35.14 0.82 78.94 1.30 56 753 74
8/30/2013 35.06 0.87 138.61 4.39 64 894 90
5/30/2014 34.98 3.06 135.57 3.94 73 1082 105

Chow Mix N 8/25/2002 5/07/2013 25.17 0.53 128.94 2.99 53 741 73
8/02/2013 25.13 0.62 109.89 2.21 57 816 82
2/25/2014 25.06 0.78 143.22 5.24 64 921 93

Dachshund N 1/01/2006 4/05/2014 25.17 1.86 57.63 0.63 53 742 72
8/01/2014 25.13 0.68 110.64 2.80 57 773 78
2/05/2015 25.07 1.92 143.67 5.48 63 906 89

Dachshund S 1/14/2005 12/13/2014 35.18 5.38 84.62 1.54 52 736 73
1/27/2015 35.15 1.32 72.04 0.91 55 762 75
2/13/2015 35.11 0.96 94.27 1.83 59 843 85

Jack Russell
Terrier S 1/28/2004 6/07/2013 35.17 6.15 84.94 1.55 53 768 75
7/26/2013 35.13 0.83 95.24 1.92 57 803 79
8/23/2013 35.14 0.87 72.97 1.03 56 782 77
12/4/2014 35.11 0.85 168.94 5.69 59 832 81

Schnauzer N 4/16/2006 1/30/2014 25.19 0.60 64.91 0.87 51 726 72
9/09/2014 25.03 1.46 112.49 2.71 67 958 96

Bichon Frise S 6/18/2009 10/17/2014 35.18 6.12 137.94 4.00 51 723 71
11/11/2014 35.15 1.74 89.92 1.36 55 764 77

Wolf/Malamute
Mix M 5/01/2002 10/8/2008 25.37 1.45 56.92 1.58 43 712 56
11/1/2008 25.31 47
11/13/2008 25.19 60
1/17/2009 25.07 1.54 89.52 1.69 62 953 87
6/28/2009 25.03 3.01 142.13 4.67 66 994 97
8/19/2010 25.04 1.93 83.26 2.37 64 961 97
3/17/2011 24.98 1.33 113.92 2.38 71 1085 103
3/15/2012 25.04 0.79 109.97 2.41 66 972 98
3/14/2013 25.03 1.38 78.12 1.31 67 982 99
11/21/2014 25.02 0.82 101.03 2.01 68 984 98

Wirehaired
Dachshund N 4/01/2006 5/02/2014 25.07 1.83 98.43 2.03 63 901 89
5/16/2014 25.04 1.35 133.92 3.85 66 942 93
6/13/2014 1.33 72
Total
Estrogen Cortisol T3 T4 IgA IgG IgM
Units of Measure pg/mL ug/dL ng/dL ug/dL mg/dL mg/dL mg/dL
Normal Values M Low 20.00 1.00 100.00 2.00 70 1000 100
High 25.00 2.50 200.00 4.50 170 2000 200
F Low 30.00 1.00 100.00 2.00 70 1000 100
High 35.00 2.50 200.00 4.50 170 2000 200
Breed S*x DOB Collection
Date Total
Estrogen Cortisol T3 T4 IgA IgG IgM
Cocker Spaniel N 4/16/2005 4/01/2014 25.21 6.38 47.31 0.51 49 684 68
5/09/2014 25.18 0.77 53.74 0.58 52 736 72
6/20/2014 25.17 0.58 54.05 0.59 53 740 73

Maltese S 3/09/2003 11/7/2014 35.20 7.54 57.89 1.13 50 706 69
11/29/2014 35.15 3.51 127.64 3.39 55 784 77
12/20/2014 35.12 1.51 78.52 1.03 58 815 80

Bearded Collie M 7/03/2003 10/17/2014 25.21 4.29 56.84 0.73 50 712 70
10/18/2014 25.19 4.01 77.15 1.27 51 720 71
11/21/2014 25.13 0.82 143.94 4.70 57 802 79
12/18/2014 25.11 0.94 77.68 0.98 59 842 83
1/22/2015 25.12 0.82 88.57 1.53 58 832 83
2/05/2015 25.09 0.72 107.14 2.33 61 868 87

Westie S 5/13/2004 5/17/2013 35.17 0.56 58.93 0.92 52 731 72
7/24/2013 35.15 0.66 68.22 1.36 55 761 75
9/04/2013 35.14 0.73 68.37 1.38 56 767 76
10/25/2013 35.09 0.68 129.88 3.49 61 854 86
12/4/2013 35.10 0.62 135.12 4.08 60 831 82
2/07/2014 35.08 0.78 143.67 4.95 62 894 90
5/09/2014 35.03 2.01 108.99 2.47 67 943 93

Aruba Island Dog S 6/01/2003 7/03/2013 35.20 0.53 52.07 0.46 50 689 69
8/08/2013 35.16 0.62 117.58 2.76 54 761 75
8/28/2013 35.14 0.68 116.99 2.76 56 778 78
10/11/2013 35.12 0.67 136.64 4.43 58 804 79
11/27/2013 35.13 0.65 141.93 7.06 57 784 77
7/31/2014 35.06 2.65 68.68 1.09 64 889 87

Brussels Griffon N 7/25/2007 2/17/2014 25.15 3.12 87.62 1.72 55 743 73
3/07/2014 25.11 0.67 124.44 3.29 59 792 78
4/04/2014 25.13 0.64 101.89 2.03 57 771 76
4/25/2014 25.13 0.62 82.31 1.43 57 780 77
5/16/2014 25.11 0.65 100.84 1.99 59 789 78
5/30/2014 25.10 0.72 94.31 1.86 60 814 80
6/27/2014 25.06 0.91 152.94 6.39 64 924 93
7/25/2014 25.03 5.01 178.61 8.86 67 968 97
9/26/2014 25.01 2.81 153.61 4.81 69 984 99
12/5/2014 25.08 8.65 184.49 6.84 66 894 88
12/12/2014 25.04 2.36 173.22 6.73 67 952 95
12/31/2014 25.03 3.64 142.13 3.06 67 968 97

Chihuahua Mix S 1/01/2005 7/11/2013 35.13 2.77 94.64 1.92 57 791 77
10/17/2013 35.09 3.44 169.47 10.68 61 852 85
1/24/2014 35.06 2.62 162.14 10.03 64 922 91
4/11/2014 35.04 0.53 153.91 7.71 66 948 95
9/18/2014 35.02 1.08 154.05 7.34 68 978 98
Total
Estrogen Cortisol T3 T4 IgA IgG IgM
Units of Measure pg/mL ug/dL ng/dL ug/dL mg/dL mg/dL mg/dL
Normal Values M Low 20.00 1.00 100.00 2.00 70 1000 100
High 25.00 2.50 200.00 4.50 170 2000 200
F Low 30.00 1.00 100.00 2.00 70 1000 100
High 35.00 2.50 200.00 4.50 170 2000 200
Breed S*x DOB Collection
Date Total
Estrogen Cortisol T3 T4 IgA IgG IgM
Dachshund N 1/01/2007 9/07/2013 25.18 7.97 56.22 0.69 52 729 73
9/24/2013 25.14 0.62 67.83 0.97 56 774 76
11/5/2013 25.10 0.65 115.58 2.62 60 843 82
2/12/2014 25.08 0.74 86.54 1.40 62 861 85
4/08/2014 25.03 1.04 132.14 3.75 67 968 97
11/4/2014 25.05 0.68 137.82 3.96 65 927 93

Jack Russell Mix N 6/20/2005 3/12/2014 25.19 3.54 61.23 0.68 51 706 70
4/18/2014 25.15 0.80 82.14 1.49 55 768 77
6/11/2014 25.09 1.53 152.13 4.49 61 843 83
10/23/2014 25.03 1.80 104.64 2.20 67 971 96
1/27/2015 25.05 0.68 112.13 2.74 65 943 94

Maltese F 2/02/2006 7/24/2013 35.20 0.44 114.38 2.54 50 703 69
9/09/2013 35.22 0.98 129.94 3.30 52 731 72
9/12/2013 35.16 0.84 94.67 1.87 54 753 74
10/10/2013 59
1/16/2014 34.98 1.35 135.34 3.83 73 1105 109
6/07/2014 35.06 0.78 130.15 3.25 64 932 94

Maltese M 10/15/2003 10/27/2014 25.19 4.63 108.11 2.39 51 716 70
12/19/2014 25.15 0.68 86.99 1.64 55 768 76

Pug S 6/27/2005 1/21/2014 35.18 0.68 67.94 1.28 52 739 74
2/19/2014 35.16 0.73 77.86 1.51 54 761 75
3/25/2014 35.11 0.89 142.66 5.08 59 854 86

Shih Tzu F 7/11/2004 5/10/2014 35.19 2.52 66.84 0.83 51 739 72
6/13/2014 35.16 0.83 68.98 0.87 54 772 76

BviHany M 9/17/2006 9/19/2014 25.18 3.47 51.77 0.54 52 734 73
10/15/2014 25.15 0.87 82.13 1.42 55 772 76
11/7/2014 25.10 0.64 109.89 2.67 60 843 85
11/26/2014 25.06 0.75 138.96 4.65 64 928 92
1/09/2015 25.04 0.85 134.66 4.01 66 958 96

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