How do I interpret MSU's thyroid profile?
In addition to testing for serum levels of total thyroxine (TT4), total tri-iodothyronine (TT3), free thyroxine (FT4), and free tri-iodothyronine (FT3), this profile tests for T4 antibodies (T4AA), T3 antibodies (T3AA), canine thyrotropin (cTSH; thyroid stimulating hormone), and thyroglobulin antibodies (TgAA). The cTSH test provides much needed information in any attempt to diagnose hypothyroidism. Many non-thyroidal factors can cause decreases of TT4, TT3, FT4, and FT3 into the hypothyroid range in a dog with normal thyroid function making it difficult to differentiate sick-but-euthyroid animals from those with hypothyroidism. When thyroid hormone levels are low due to primary hypothyroidism, most (around 85%) animals will have abnormally high cTSH levels...
Non-thyroidal illness (sick euthyroid). It is well known that thyroid hormone concentrations can decrease as part of a metabolic response to non-thyroidal illness. This decrease occurs in part from changes in thyroid hormone production, characteristics of serum binding, and metabolism of thyroid hormones. In these circumstances, measurement of free T4 in the direct-serum analog assay (standard profile) may underestimate the true circulating concentration of free T4 and give a falsely low result. Free T4 by equilibrium dialysis gives a more accurate result and so will more correctly identify normal free T4 concentrations in sick animals, allowing for better identification of animals that are not hypothyroid...
My patient has low thyroid hormone concentrations, but thyroid stimulating hormone is not elevated. What does this mean?
Depending on the clinical presentation, one of two main possibilities is likely.
The more common explanation is that T4 values often decline in animals with non-thyroidal illness and in animals receiving certain drug therapies (some glucocorticoids or anticonvulsants). Non-thyroidal illness may suppress TSH release from the pituitary via glucocorticoid-mediated inhibition or lower T4 concentrations by altering serum protein binding affinities...
With this pattern of test results, a trial with T4 supplementation is suggested only if there is a strong clinical presentation consistent with hypothyroidism and if no non-thyroidal illness can be detected. An objective case review should be conducted after 6-8 weeks of therapy for evidence of clinical improvement. Thyroid supplementation can be discontinued if no improvement has occurred in that time, and the diagnosis reconsidered. A therapeutic monitoring sample taken during treatment should help confirm whether adequate amounts of thyroid medication were being absorbed. Even when there is clinical improvement, strictly speaking, therapy should be discontinued to see if the original clinical signs return in the absence of medication. Admittedly, this latter protocol is rarely followed in clinical practice.
While the administration of thyroid hormone to animals which do not have hypothyroidism is generally considered to have minimal risk, large scale studies in human medicine have shown detrimental effects of such treatment in patients that have decreases in serum thyroid hormone concentrations due to non thyroidal illness. (Brent GA and Hershman JM. Thyroxine therapy in patients with severe non-thyroidal illness and low serum thyroxine concentrations. J Clin Endocrinology and Metabolism. 1986, 63:1)