Abstracts For Dr. Plechner’s Clinical Articles on PubMed
Posted on May 28th, 2015I was reviewing some of my published clinical articles at PubMed recently and forgot how clearly these abstracts were written.
They were written by prominent MD and PHD Journals and I thought I’d share them with you.
Med Hypotheses. 2004; 62(4):575-81.
Cortisol abnormality as a cause of elevated estrogen and immune destabilization: insights for human medicine from a veterinary perspective.
Plechner, AJ
Abstract
For more than 35 years the author has treated multiple serious diseases in cats and dogs by correcting an unrecognized endocrine-immune imbalance originating with a deficiency or defect of cortisol. The cortisol abnormality creates a domino effect on feedback loops involving the hypothalamus-pituitary-adrenal axis. In this scenario, estrogen becomes elevated, thyroid hormone becomes bound, and B and T cells become deregulated. Diseases with this aberration as a primary etiological component range from allergies to severe cases of autoimmunity to cancer. The author has consistently identified excess estrogen or "estrogen dominance" as part of an endocrine-immune derangement present in many common diseases of dogs and cats. Ninety-percent of these cases involve spayed females and neutered or intact males, so the elevated estrogen cannot be attributed to ovarian activity. The author identifies the adrenal cortex as a source of the imbalance, which produces a variety of vital hormones. The author has developed an endocrine-immune blood test that measures cortisol, total estrogen, T3 and T4, and IgA, IgG, and IgM antibody levels. The protocol for corrective therapy involves the use of various cortisone medications, either standard pharmaceutical compounds or a natural bio-identical preparation made from an ultra extract of soy. The author's clinical success and the growing clinical applications of low-dosage cortisone therapy for humans strongly argue for sustained research into the nature, magnitude, and impact of cortisol defects, including an associated estrogen-immune problem, in the etiology of disease.
Med Hypotheses. 2003 Mar; 60(3):309-14.
An effective veterinary model may offer therapeutic promise for human conditions: roles of cortisol and thyroid hormones.
Plechner, AJ
Abstract
For nearly three decades, the author has treated multiple serious diseases of cats and dogs by correcting an unrecognized endocrine-immune imbalance originating with a deficiency or defect of cortisol. The cortisol abnormality creates a domino effect on feedback loops involving the hypothalamus-pituitary-adrenal axis. In this scenario estrogen becomes elevated, thyroid hormone becomes bound, and B and T cells become deregulated. Diseases with this aberration as a primary etiological component range from allergies and strange behavior to severe cases of autoimmunity and cancer. Successful treatment and control, even in critical cases, have been consistently achieved with a long-term physiologic (not pharmacologic) replacement with cortisone along with thyroid hormone (in dogs). The treatment represents a major healing modality for many seemingly unrelated chronic diseases of animals. In humans, this endocrine-immune dysfunction appears to exist and, as in veterinary medicine, has been overlooked by researchers and clinicians. Testing and treatment patterned after the animal model may offer significant clinical benefits for challenging human afflictions.
J Appl Toxicol. 2004 Jan-Feb; 24(1):53-8.
Adrenal toxicity in dogs and cats as a contributing cause of hormonal and immune destabilization.
Plechner, AJ
Abstract
The adrenal cortex is regarded as the organ most vulnerable to toxicity within the endocrine system. The production of cortisol, among the many steroidal hormones produced by the cortex, may suffer as a result. In a veterinary clinical practice, household dogs and cats with a wide variety of diseases ranging from allergies to cancer commonly have a cortisol deficiency or defect that triggers endocrine imbalances and immune system destabilization. The causes of deficient cortisol are linked primarily to genetics but also to acquired adrenal damage likely stemming from environmental toxins. An innovative blood test to determine relevant endocrine-immune imbalances in pets and a treatment method based on low-dosage steroidal medication, as a form of cortisol replacement therapy, are described. Despite a prevailing reluctance to use steroidal medications long term because of the fear of side effects, extended and even life-time usage of these medications at low, physiologic dosages has been applied successfully for decades and appears to be gaining wider acceptance. The validity of a combined testing and treatment method for humans based on the veterinary model deserves investigation as a tool with which to identify and correct toxic damage to adrenal function.
Copyright 2004 John Wiley & Sons, Ltd.
Mod Vet Pract. 1976 Nov; 57(11):917-21.
Canine immune complex diseases.
Plechner, AJ
Abstract
Though not conclusive, our primary findings indicate that a feature common to many of our tumor and ICD patients is depressed cortisol production. Additionally, the response to ACTH adrenal cortex stimulation tests, at 2-hour intervals between rest and stimulation, have ranged from negative to substantially less than would be expected in normal subjects. Peripheral plasma cortisol values for dogs, at rest and 2 hours after ACTH stimulation, respectively, have been reported as 2-10 and 25-30 mug/dl, 3-8 and 7.5-18 mug/dl, and 1-12.5 and 9.5-22 mug/dl. For representative patients, our resting values have been 1.2-5.2 mug/dl, vs 1.2-7.6 mug after ACTH stimulation (Table 2). Altogether we have studied 42 cases in detail, and we feel that a post-ACTH level of 8.0 mug/dl or less is a conservative indication of adrenocortical insufficiency; all levels have been between 1 and 8 mug/dl. We believe these low cortisol levels indicate either a genetically-induced adrenal cortical insufficiency (evident at 2 months to 1 year of age) or an immune complex adrenal cortical suppression (occurring after 1 year of age in association with other immunodeficiency disorders). Our studies demonstrate a need for biphasic therapy. We have found it necessary to not only initiate cortisone acetate therapy to support the deficient adrenal cortical secretion, but also use other immunosuppressive drugs to control the ICD. If the target organ has been suppressed or destroyed, the need for supplementation is obvious. However, other immune-injury moieties must be suppressed also, eg, ANA, anti-IgG antibodies, etc.
