Allergic Dermatitis Case Reports in 3 Dogs

Allergic dermatitis has been of major concern for some time and seems to be increasing in incidence in our dog population.

Treating the effects will help but definitely will not stop the progression and development of an increase of allergic dermatitis in dogs.

This also relates to allied species like cats, horses and humans.

The cause must be identified and controlled while at the same time indicate how to identify the cause of allergic dermatitis in prospective dog parents and avoid breeding two parents that contain a similar cause for the development of allergic dermatitis which may be concentrated in their offspring.

This article is designed not only to make you think and ask questions but also designed to show you how to identify the cause of allergic dermatitis in dogs.

Did you ever wonder why steroids (cortisol) helped a dog with allergic dermatitis?

Did you realize a dog produces 30 to 35 units of natural cortisol every day from its middle layer adrenal cortex if the dog is to remain normal without developing an allergic dermatitis and many other disease maladies like autoimmunity and cancer?

Did you ever wonder if steroids (cortisol) helped a dog with an allergic dermatitis because the dog had a natural cortisol deficiency or imbalance?

Did you realize with all the concerns of high cholesterol, that cholesterol is the precursor of natural cortisol?

Furthermore, did you realize that it takes 5 separate enzyme cycles to turn cholesterol into cortisol and if any of the enzymatic cycles are damaged genetically or environmentally, an allergic dermatitis may occur including autoimmunity and cancer?

This affects your self also!

Even though normal, natural cortisol production is vital for maintaining good health in yourself and your dog, the use of cortisol was badly maligned in 1948 by a well-known medical facility giving human patients 100 mgs of a synthetic cortisol for arthritis which did work for a while until these large amounts caused side effects and cortisone acetate was labeled as the very harmful X Substance and should be avoided at all costs.

There appears to be some medical vectors that down the road are proven to be wrong.

The cause of allergic dermatitis occurs due to a natural cortisol
which is deficient, bound or defective.

What also is not realized yet, is that if there are normal or even elevated amounts of cortisol present, unless you compare them to their functions in the body, the body may not be able to use them.

Please remember with any measured hormone, without doing comparative testing along with that particular hormone, it may prove useless to the body.

The day will come when empirical hormone values mean very little while comparative values may suggest some answers.

The cause of allergic dermatitis begins with a deficient, bound or defective cortisol.

This leads to an in ability to fund the negative feedback from the middle layer adrenal cortex and the pituitary gland.

In other words, the pituitary gland releases its hormone ACTH when the cortisol level decreases due to its regulatory functions in the body.

When the ACTH release occurs, the middle layer adrenal cortex releases its cortisol and the ACTH production ceases until the cortisol level again declines.

This is called a negative feedback.

In a dog with allergic dermatitis, the cortisol is deficient, bound or defective and cannot fulfill its obligation to the negative feedback, so the pituitary gland keeps producing ACTH and the only other layer in the body that responds to this is the inner layer adrenal cortex.

This layer produces elevated amounts of adrenal estrogen and androgen.

The elevated adrenal estrogen deregulates the immune system so that the there is no B and T cell protection for the dog with the allergic dermatitis but also causes the B and T cell to no longer recognize self-tissue ad begin to make antiantibodies which often may cause a dog with an allergic dermatitis to develop autoimmunity and cancer.

The elevated adrenal estrogen apparently binds the receptor sites of the thyroid hormones. Note: I have found this to be true in animals clinically, but at this point it has only been proven in people through the development of testing for a reverse T3.

The last measurable effect that the elevated adrenal estrogen causes is with the B cell deficiency in producing protective antibodies.

This does open up the dog with allergic dermatitis to all kinds of bacterial infections plus an inability to produce protective antibodies to vaccines and in some cases develop diseases that the vaccines were supposed to protect the dog against.

When the B cell production of antibody is deficient, many medications and supplements will not work because they cannot be absorbed through the gut wall if the mucous membrane antibody called IgA is below 58 mgs. %.

This particularly applies to oral steroids.

This also applies to cats, horses and humans.

A prime example of this is if you or your pet are in the hospital on intravenous or intramuscular injections of a specific medication and when you are sent home to use the same medication orally, it did not work.

Often a different oral medication will be substituted and obviously that will not work because of the malabsorption in the gut due to the deficient IgA.

Hopefully the day may come when an IgA will be added to the standard blood tests that are routinely performed.

The standard treatment for the effects for a dog with allergic dermatitis besides, special bathes, lotions, supplements, immune modulators and ointments, is the use of antihistamines and antibiotics.

Antihistamines work better in humans than in dogs with allergic dermatitis.

The lethargy that usually accompanies the use of an antihistamine in a dog often will lessen the scratching because the dog is too lethargic to scratch.

The dog with an allergic dermatitis has a different type of allergic reaction that seems to make antihistamines less than satisfactory as far a stopping the actual inflammation of the skin.

Antibiotics will usually only give temporary relief and the reason for that is that with an immune deficiency the resident bacteria have an allergen in their wall called a mucopoly saccharide which by itself will cause an allergic reaction and when the antibiotic is used to kill the bacteria, that allergen is reduced and the itching and scratching improves.

However, because the cause of the immune deficiency remains, as the resident bacteria increase in their population so does their allergen which again causes an allergic reaction in the skin of a dog with allergic dermatitis.

Now let’s look at the cause of allergic dermatitis in a dog.

The following will be 3 different case reports to indicate that all 3 have the same cause with some variation of their hormone antibody level, but remember the basic cause for this imbalance begins with a deficient, bound or defective cortisol.

BLOOD TEST RESULTS FOR CASE # 1

This is a 2 years old male neutered Irish setter with an ongoing allergic dermatitis from birth which may indicate this is genetic and not acquired.

 Cortisol = .52 ug/dl

 1 to 2.5 ug/dl

 Total Estrogen = 25.13 pg/ml

 20 to 25 pg/ml

 T3 = 85 ng/dl

 100 to 200 ng/dl

 T4 = 1.4 ng/dl

 2 to 4.5 ng/dl

 IgA = 51 ng/dl

 70 to 170 ng/dl

 IgM = 75 ng/dl

 100 to 200 ng/dl

 IgG = 759 ng/dl

 1000 to 2000 ng/dl

Based upon the blood test results, it was clear to see that the cortisol was deficient, leading to the pituitary overstimulation of the inner layer adrenal cortex, allowing it to produce excess estrogen and causing a deregulation of the immune system, a binding of the thyroid hormones that were also deficient and a reduction in IgA below 58 which will cause maladsorption of oral steroids and many more supplements and medication.

Note: This may be the reason why many medications and supplements do not work because they never were properly absorbed.

In my experience, I recommended with an IgA of 51, 3 intramuscular injections of a combination steroid at 10 day intervals and 10 days after the last injection oral steroids can be given once daily.

A thyroid supplement should be started immediately twice daily.

A second hormone antibody blood test can be done at the time of the 3rd injection to make sure the IgA has reached 58 and if not a 4th injection may be indicated.

If after the 3rd injection, the patient is doing well, then repeat the blood test two weeks after the oral steroid has begun.

Those test levels will indicate if a hormone supplement modification is indicated or not.

If the hormone antibody levels are now within normal ranges and the allergic dermatitis continues then the dog has a food sensitivity and that can be easily handled by looking at the Food Elimination article on this website www.drplechner.com.

Before doing this blood test, if you are concerned about a food allergy or sensitivity, it is easy to have your veterinarian give your dog an injection of a steroid that lasts 5 to 7 days and if after the first three days there is no improvement, the dog is allergic to the food.

With this case, the food was fine and once the hormone antibody levels returned to normal, the allergic dermatitis subsided.

Supplemental blood test results

Cortisol = 1.2 ug/dl

1 to 2.5 ug/dl

Total Estrogen = 25.01 pg/ml

20 to 25 pg/ml

T3 = 130 ng/dl

100 to 200 ng/dl

T4 = 2.5 ng/dl

2.0 to 4.5 ng/dl

IgA = 72 ng/dl

70 to 170 ng/dl

IgM = 140 ng/dl

100 to 200 ng/dl

IgG = 1400 ng/dl

1000 to 2000 ng/dl

BLOOD TEST RESULTS FOR CASE # 2

This is a 8 year old female spayed Beagle with a severe allergic dermatitis.

It was first determined that she did not have a food sensitivity

 Cortisol = 4.6 ug/dl

 1 to 2.5 ug/dl

 Total Estrogen = 35.11 pg/ml

 30 to 35 pg/ml

 T3 = 140 ng/dl

 100 to 200 ng/dl

 T4 = 3.5 ng/dl

 2 to 4.5 ng/dl

 IgA = 56 ng/dl

 70 to 170 ng/dl

 IgM = 90 ng/dl

 100 to 200 ng/dl

 IgG = 905 ng/dl

 1000 to 2000 ng/dl

As the test indicates, her allergic dermatitis occurred because of a bound or defective cortisol which led to the over stimulation of the inner layer adrenal cortex by the pituitary gland.

The elevated adrenal estrogen binds the thyroid hormone site and reduces the IgA etc.

Thyroid hormone was immediately prescribed and taken orally twice daily.

Since the IgA was at 56 ng/dL, only one combination, intramuscular steroid injection was needed and oral steroids begun 10 days after the injection.

The dog returned to normal once the hormone antibody levels were supplemented properly.

Supplemental blood test results

Cortisol = 0.91 ug/dl

1 to 2.5 ug/dl

Total Estrogen = 34.97 pg/ml

20 to 25 pg/ml

T3 = 130 ng/dl

100 to 200 ng/dl

T4 = 3.0 ng/dl

2.0 to 4.5 ng/dl

IgA = 71 ng/dl

70 to 170 ng/dl

IgM = 150 ng/dl

100 to 200 ng/dl

IgG = 1300 ng/dl

1000 to 2000 ng/dl

BLOOD TEST RESULTS FOR CASE # 3

The 3rd case involved a 3years old neutered male, miniature Poodle that had suffered from food allergies his entire life including an allergic dermatitis.

The only problem was the foods were changed as soon as his allergies flared up and unfortunately without identifying this imbalance first, the day was coming when he could not tolerate any foods that were available.

Fortunately the Poodle had not quite reached this point and what needs to be realized is that once this imbalance has allowed a food allergy to develop, even after correcting the hormone antibody imbalance, the immune cells will still react to any foods they had become sensitive to before the imbalance had been identified and controlled.

The poodle also had allergic reactions to vaccines and stinging insects which is very common with an IgA deficiency.

 Cortisol = 0.36 ug/dl

 1 to 2.5 ug/dl

 Total Estrogen = 25.19 pg/ml

 20 to 25 pg/ml

 T3 = 95 ng/dl

 100 to 200 ng/dl

 T4 = 1.75 ng/dl

 2 to 4.5 ng/dl

 IgA = 50 ng/dl

 70 to 170 ng/dl

 IgM = 70 ng/dl

 100 to 200 ng/dl

 IgG = 780 ng/dl

 1000 to 2000 ng/dl

The allergic dermatitis in this dog occurred because of a deficiency in cortisol, high adrenal estrogen, bound thyroid receptor sites, decreased thyroid hormone and decreased immunoglobulins.

Thyroid hormone was initiated immediately, and because of the IgA at 50, 3 intramuscular injections of a combination steroid were needed to be given at a 10 day interval and 10 days later an oral steroid was begun.

The Poodle did return to normal but because of the deficient immunoglobulins, I had blood titers done on the dog and found because the immune deficiency was present at the time the vaccine program had been completed, the immune system had made no protective antibodies against Distemper or Parvo.

Since the imbalance was now corrected, the dog was revaccinated with no reaction and did develop protective antibodies to both Distemper and to Parvo.

Supplemental blood test results

Cortisol = 1.3 ug/dl

1 to 2.5 ug/dl

Total Estrogen = 25.01 pg/ml

20 to 25 pg/ml

T3 = 125 ng/dl

100 to 200 ng/dl

T4 = 3.2 ng/dl

2.0 to 4.5 ng/dl

IgA = 73 ng/dl

70 to 170 ng/dl

IgM = 121 ng/dl

100 to 200 ng/dl

IgG = 1120 ng/dl

1000 to 2000 ng/dl

These are just some of my thoughts that hopefully may also become part of your thoughts.

Sincerely,

Dr. AL Plechner