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Lymphocytic thyroiditis is the underlying cause in many cases of primary hypothyroidism in dogs and the predisposition to its development is believed to be highly heritable. It is an immune mediated disorder characterized histologically by a diffuse infiltration of lymphocytes, plasma cells, and macrophages in the thyroid gland.
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In addition to testing for serum levels of total thyroxine (TT4), total tri-iodothyronine (TT3), and free thyroxine (FT4), 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, and FT4 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 75%) animals will have abnormally high cTSH levels.
In dogs, antibodies which cross-react with T4 and/or T3 are markers for lymphocytic thyroiditis. These antibodies are generated against T4 and T3 containing epitopes on the thyroglobulin molecule, i.e., they are subsets of TgAA. Positive values indicate thyroid gland pathology, and also tell us about the validity of the thyroid hormone results. T3AA and T4AA are present in around 35% and 14% of hypothyroid dogs respectively. In the MSU VDL Endocrinology Laboratory, T3 antibodies cause a false decrease in TT3. T4 antibodies falsely increase TT4 and may increase FT4 results in the standard thyroid profiles. In a hypothyroid dog with T4AA, T4 may be falsely elevated into the normal range and the true diagnosis masked. To obtain an accurate measure of T4 status in a T4AA positive animal, submit a sample for free T4 by equilibrium dialysis (FT4d) which is not affected by antibody. FT4d is included in Premium Thyroid Profiles. Although these antibodies have a large effect in the laboratory test tube, the clinical impression is that they do not interfere significantly with the availability of thyroid hormone in a thyroxine-treated hypothyroid dog.
The FT4 by dialysis test is indicated to better identify animals that are euthyroid but whose total- or standard free- T4 is falsely increased due to T4 antibodies or physiologically decreased due to general/systemic illness. A dialysis step first filters out the large antibodies and hormone binding proteins to provide a measurement technique unaffected by antibodies or by changes in T4-protein binding which can occur during non-thyroidal illness. FT4d is useful in cases were total- or standard free- T4 is borderline low and TSH is normal to assist in the differentiation of euthyroid but sick dogs from those 20-25% of hypothyroid dogs which could have a normal TSH result. FT4 by dialysis may rarely be increased in systemic illness due to decreased protein binding affinity for T4. FT4d is less commonly suppressed by non-thyroidal illness, but does occasionally fall below the reference range in some sick but euthyroid animals.
An important point to recognize is that results from both types of free T4 assays are highly correlated. Most samples that are normal in one assay will be normal in the other. Free T4 will be low with both assay methods in most hypothyroid dogs. There may be a slight improvement in diagnostic sensitivity for feline hyperthyroidism with free T4 by equilibrium dialysis, especially when seen in conjunction with a total T4 assay result. Situations in which measurement of free T4 by dialysis are likely to have an advantage over standard measures include:
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)
If T3AA is negative, consider the following: when comparisons are made between the performance characteristics of T4 and T3 in their ability to differentiate normal from hypothyroid dogs, the T4 assays generally perform better. In the absence of T4 cross-reacting antibodies, T4 results more directly reflect thyroid hormone production by the thyroid glands than T3, whose concentration is heavily based on modulation of peripheral de-iodinases responsible for T4 to T3 conversion. Such a finding may reflect a "low T3 state of medical illness" suggesting a significant non-thyroidal illness.
The opposite situation, of low T4 with normal T3 concentrations in the absence of antibodies, also occurs. In this case, the fact that T3 concentrations are being maintained makes it unlikely that the animal would have clinical signs of hypothyroidism. We often attribute a combination of low T4, normal T3 and normal TSH concentrations to a "low T4 state of medical illness". Whether there is any pattern to which dogs or which diseases are associated with Low-T4 or Low-T3 (or both) states of medical illness has not been determined.
Treating with corticosteroids might be desirable to decrease the immune/inflammatory components of this disease, but our laboratory does not advocate their use. There are no published studies evaluating this approach in dogs. There are more disadvantages to steroid use than advantages, because of their many side effects.
There have been anecdotal reports of hypothyroidism resulting in aggression and it may be that the effects of hypothyroidism can make dogs more irritable. However, an association of hypothyroidism with aggression has not been proven in any retrospective or prospective studies where large numbers of dogs have been evaluated. In one retrospective study performed here at Michigan State University, there was actually a negative correlation between a history of aggression and hypothyroidism. In other words, dogs with a history of aggression were actually less likely to be hypothyroid.
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The suggested initial dose is 0.5 to 3.0 mg levothyroxine sodium (T-4) per 100 pounds body weight (1 to 6 mg per 100 kg) once per day or in divided doses. The recommended daily dose is 1/2 to 2 1/2 level teaspoons for a 500 kg (1,100 lb) horse.
On a BID protocol we hope to achieve values at the top or slightly above the reference range at the expected time of peak concentration (approximately three hours post pill) and a value within the lower half of the reference range if sampled just prior to the administration of the next pill (trough concentration). The target range, necessarily, depends on the interval post-pill at which the sample was obtained. The variability in T4 half-lives in dogs is sufficiently narrow that in a BID case a thyroid monitoring result can be interpreted with confidence anytime after three hours post-pill as long as that interval is known. Another aim of adequate thyroid supplementation is to keep TSH suppressed within the lower half of the reference range. A high TSH indicates demand for T4, and inadequate supplementation.
The most common cause of failed T4 therapy is noncompliance by the owner or avoidance of therapy by the animal, where the dog never receives the prescribed level of medication. Diets with a high fiber or high mineral content also limit absorption of thyroid supplements. In addition, there are some dogs which absorb oral thyroid medication poorly in which no underlying problem can be identified.
2. Acetaminophen - When it comes to pain medications, acetaminophen (e.g., Tylenol) is popular. Even though this drug is safe for children, it is not safe for pets?especially cats. One regular strength tablet of acetaminophen may cause damage to a cat's red blood cells, limiting their ability to carry oxygen. In dogs, acetaminophen leads to liver failure and, in large doses, red blood cell damage.
5. Benzodiazepines and sleep aids (e.g., Xanax, Klonopin, Ambien, Lunesta) - These medications are designed to reduce anxiety and help people sleep better. However, in pets, they may have the opposite effect. About half of dogs that ingest sleep aids become agitated instead of sedate. In addition, these drugs may cause severe lethargy, incoordination (including walking "drunk"), and slowed breathing in pets. In cats, some forms of benzodiazepines can cause liver failure when ingested.
6. Birth control (e.g., estrogen, estradiol, progesterone) - Birth control pills often come in packages that dogs find irresistible. Thankfully, small ingestions of these medications typically do not cause trouble. However, large ingestions of estrogen and estradiol can cause bone marrow suppression, particularly in birds. Additionally, intact female pets are at an increased risk of side effects from estrogen poisoning.
9. Thyroid hormones (e.g., Armour desiccated thyroid, Synthroid) - Pets?especially dogs?get underactive thyroids too. Interestingly, the dose of thyroid hormone needed to treat dogs is much higher than a person's dose. Therefore, if dogs accidentally get into thyroid hormones at home, it rarely results in problems. However, large acute overdoses in cats and dogs can cause muscle tremors, nervousness, panting, a rapid heart rate, and aggression.
Total thyroxine (T4) concentrations are lower in healthy greyhounds compared to most other non-sighthound breeds. In humans, variations in the structure or concentration of the major thyroid hormone binding proteins are responsible for most reported differences between total T4 concentrations in healthy individuals from different ethnic groups or other subpopulations. The aim of this study was to determine if such variations are also responsible for the lower total T4 concentrations in greyhounds. The predicted protein sequences of thyroxine-binding globulin (TBG), transthyretin and albumin were determined in liver tissue from a euthyroid greyhound with decreased T4 concentration and a Jack Russell terrier using reverse-transcriptase PCR. Sequences were compared to each other and online reference sequences. Serum proteins from 21 greyhounds and 21 non-sighthound dogs were separated by denaturing electrophoresis and immunoblots probed with polyclonal antibodies to human TBG and transthyretin. Reactive bands were quantified by densitrometry, expressed relative to the mean of reference samples included in each gel. Serum albumin concentrations were measured using a commercially-available assay. Several SNPs were identified but none was thought likely to explain the lower total T4 concentrations in greyhounds. There was no significant difference between the quantity of any of the binding proteins in serum from greyhounds and non-sighthound dogs. However, total T4 and transthyretin concentrations were highly correlated in the greyhound group (r = 0.73, P = 0.0002). Variation in the sequence of thyroid hormone binding proteins is not responsible for low greyhound total T4 concentrations. Further evaluation of the role of transthyretin is warranted. 041b061a72