Adrenal-thyroid-immune dysfunction as a cause of reproductive failure in pets: does a veterinary syndrome offer testing and treatment insights for infertility and miscarriages in humans?

Townsend Letter for Doctors and Patients, Dec, 2004 by Alfred J. Plechner

In dealing with a case of reproductive complications (and health disorders in general), I first draw blood for the endocrine-immune test I developed some 30 years ago. It measures cortisol, total estrogen, T3 and T4, and IgA, IgG, and IgM levels. Except for T4, the elements of this panel are not routinely tested for in veterinary medicine. I thus developed my own range of normal values based on continuing clinical experience (see table 1). Both males and females are tested. However, females are not tested when in heat to avoid the influence of ovarian estrogen.

In the syndrome of imbalance that I have identified, cortisol and thyroid hormones are bound to varying degrees, and their individual values in a blood test may or may not appear normal. For this reason I compare the relationships of hormone and antibody levels rather than relying on isolated single values. In my experience, the clear markers of cortisol-based imbalance are elevated estrogen and low IgA, IgG, and IgM.

Once the combination of clinical signs and testing determines the presence of imbalances, I initiate a correction process involving long-term, low-dosage synthetic cortisone or a natural cortisol hormone replacement made from soy. The exact type and amount of replacement depends on the weight and health status of a particular animal. I retest patients after two weeks into the therapy to determine if any modification of dosage is required. Decreased estrogen and increased antibodies indicate the effectiveness of this hormonal "re-regulating" approach.

During more than 30 years of practice, I have found that most imbalanced dogs also require T4 medication such as Soloxine. Steroid replacement promotes transference of T4 to T3. Initially I combined T3/T4 medication in dogs but found that TSH and natural T3 and T4 production were suppressed. I subsequently found that T4 alone was sufficient. Most imbalanced cats do not require thyroid replacement, unless they are outright hypothyroid or have a condition known as feline infectious peritonitis (FIP). Other than those exceptions, only cortisone/cortisol replacement is needed.

In my therapy program I give special attention to IgA level. I have found that IgA levels below 60 mg/dl reflect dysfunctional intestinal mucosa, meaning probable inflammation and malabsorption, including an inability to absorb medication. I find that low IgA is often the overlooked basis for inflammatory bowel disease. When IgA is moderately or substantially low I do not take a chance with oral medication, and instead utilize an intramuscular injection, including both immediate and long-acting steroids. This approach often returns the IgA level to near normal or normal within a few weeks, after which I am usually able to switch patients to an oral steroid. I treat each animal individually, using the lowest possible amount of cortisone to correct the deficiency and restore the missing equivalency of cortisol. In almost all cases, deficient animals need daily replacement for a lifetime.