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.
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:
- The elevated adrenal estrogen binds the receptor sites for Triiodothyronine (T3) and (Thyroxin) (T4) (6-11-15, 21).
- 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:
- How well the canine deals with and hides their developing blindness.
- How soon the owner of a SARDS canine realized that their pet was suffering from reduced vision.
- How soon the canine SARDS was diagnosed and how soon I was able to correct the patients’ endocrine immune imbalance.
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:
- Total estrogen
- Cortisol (no special time of day is needed to do this test)
- Total T3 (Triiodothyronine)
- Total T4 (Thyroxin)
- Immunoglobulin A
- Immunoglobulin M
- Immunoglobulin G
I followed these procedures, as instructed by the veterinary laboratory:
- The blood sample was taken after fasting from food or medication for 3 to 4 hours.
- If a repeat test was indicated at a later date, the blood sample was taken at the same time of day.
- 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.
- 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.
- Once this procedure was completed, the blood sample was centrifuged for 10 minutes and refrigerated immediately.
- In the event the blood sample was not spun down, the sample was sent to the lab only refrigerated, not frozen.
- In the event the blood sample was spun down and the serum was clear, the sample was frozen.
- 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).
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).
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).
- National Veterinary Diagnostic Services, 26856 Clark Rd, Waller, TX 77484, http://national-vet.com, email: firstname.lastname@example.org, phone: 281-661-4292
- 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.
- 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.
- 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.
- 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.
- Electroretinography. U.S. National Library of Medicine. April 2006.
- Brown M, Mamor M & Vaegan. ISCEV- Standard for Clinical Electro- Oculography (EOG) 2006 at Documenta Ophtlamologica 1133; 206-212.
- 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.
- Plechner AJ. Reproductive Failure in Adrenal-Thyroid-Immune Dysfunction. Townsend Letter for Doctors and Patients. December 2008; 80-82
- Plechner AJ. Importance of IgA. Townsend Letter for Doctors and Patients. November 2005; 268; 88-91
- 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.
- 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.
- Plechner AJ. Treating Unrecognized Cortisol Based Imbalances Offers Major Healing Benefits for Multiple Disorders. American Holistic Veterinary Medical Association. 2004; 22 (4); 9-14.
- Plechner AJ. An Effective Veterinary Model May Offer Therapeutic Promises for Human Conditions. Medical Hypothesis. 2003; 60; 309-314.
- Plechner AJ. Unrecognized Endocrine Immune Defects in Multiple Diseases. Medical Hypothesis. March 2003.
- Plechner AJ. Preliminary Observations on Endocrine - Associated Immunodeficiency In Dogs - A Clinician Explores The Relationship of Immunodeficiency to Endocrinopathy. Modern Veterinary Practice. October 1979; 811-815.
- Plechner AJ. Theory of Endocrine Immune Surveillance. California Veterinarian. January 1979; 12-15.
- Plechner AJ, Shannon, Epstein, Goldstein & Howard. Endocrine Immune Surveillance. Pulse, June July 1978.
- Plechner AJ, Shannon M. Canine Immune Complex Diseases. Modern Veterinary Practice, November 1976; 917.
- Jeffries MK. Safe Uses of Cortisol Third Edition. Charles C. Thomas Publisher, Ltd. Springfield. 2004.
- Marik PE. Adrenal-exhaustion syndrome in patients with liver disease (abstract). Intensive Care Medicine 2006; 32: 275-280.
- Selye H. The Stress of Life Revised Edition. McGraw-Hill, Incorporated: New York. 1976.
- Hart JE. Endocrine pathology of estrogens: species differences (abstract). Pharmacology Therapeutics. 1990; 47: 203-218.
- Blum M, Zacharovich D, Pery J, Kitai E. Lowering effect of estrogen treatment on immunoglobulins in menopausal women (abstract). Revue française degynecologie et d’obstetrique. 1990; 4: 2078.
- Bayarri, VM, Sancho S, Campos R, Faus R, Simon JM, Porcar E, Tormo C, Hernandez A. The euthyroid sick syndrome in severe acute illness (abstract). Presse Medical. 2007; 36: 1550-1556.
- Cohen J, Ward G, Prins J, Jones, Venkatesh B. Variability of cortisol assays can confound the diagnosis of adrenal insufficiency in the critically ill population (abstract). Intensive Care Medicine. 32; 1901-1905.
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.
|Female (Normal Values)
Male ( Normal Values)
Units of Measurement
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
|Units of Measure||pg/mL||ug/dL||ng/dL||ug/dL||mg/dL||mg/dL||mg/dL|
|Breed||Sex||DOB||Collection Date||Total Estrogen||Cortisol||T3||T4||IgA||IgG||IgM|
|Jack Russell Terrier||S||1/28/04||6/7/13||35.17||6.15||84.94||1.55||53||768||75|
|Aruba Island Dog||S||6/1/03||7/3/13||35.2||0.53||52.07||0.46||50||689||69|
|Jack Russell Mix||N||6/20/05||3/12/14||25.19||3.54||61.23||0.68||51||706||70|