Safety of orally administered, USP-compliant levothyroxine sodium tablets in dogs.

The safety of synthetic levothyroxine sodium tablets (Thyro-Tabs® Canine; LLOYD, Inc.) in dogs was evaluated in a randomized, sham-dose controlled, parallel-group study. Young, healthy, euthyroid Beagle dogs were randomized into four groups (four females and four males per group) and received single daily doses of 0×, 2× (0.044 mg/kg), 6× (0.132 mg/kg), or 10× (0.22 mg/kg) the labeled starting dose of 0.022 mg kg-1  day-1 for 182 days. Every 2 weeks, physical examinations, electrocardiology examinations, and sample collections for thyroid panel, hematology, serum biochemistry, coagulation panel, and urinalysis were performed. At the end of the study, the dogs were euthanized and full necropsies performed. The most overt finding was the expected dose-dependent increase in serum concentrations of total and free thyroxine with dose-dependent suppression of the hypothalamic-pituitary-thyroid axis as evidenced by decreased serum thyroid-stimulating hormone concentrations, decreased thyroid+parathyroid/body weight ratios, and a trend for decreased pituitary weight/brain weight ratios. Clinical signs of thyrotoxicosis (excitation, tachypnea, tachycardia) in the treated dogs were sporadic with no dose-response relationship. Other findings statistically associated with levothyroxine treatment were generally mild and not clinically important. In summary, doses of levothyroxine sodium up to 10× the labeled starting dose were well tolerated in healthy dogs.

Thyrotoxicosis in a dog induced by the consumption of feces from a levothyroxine-supplemented housemate.

A 9-year-old golden retriever dog was evaluated for polyuria, polydipsia, weight loss, and elevated serum thyroxine. Targeted questioning revealed that the dog was coprophagic and routinely ingested the feces of a dog that was treated with twice-daily levothyroxine. Clinical signs resolved and serum thyroxine decreased to normal levels in the affected dog with prevention of coprophagy.

Thyrotoxicose chez un chien induite par la consommation de fèces d'un compagnon prenant des suppléments de lévothyroxine. Un chien Golden retriever âgé de 9 ans a été évalué pour la polyurie, la polydipsie, la perte de poids et la thyroxine sérique élevée. Des questions ciblées ont révélé que le chien était coprophage et ingérait régulièrement les fèces d'un chien qui était traité deux fois par jour à la lévothyroxine. Les signes cliniques se sont résorbés et la thyroxine sérique a baissé à des niveaux normaux chez le chien affecté avec la prévention de la coprophagie.(Traduit par Isabelle Vallières).

Pet Food-Associated Dietary Exogenous Thyrotoxicosis: Retrospective Study (2016-2018) and Clinical Considerations.

Dietary exogenous thyrotoxicosis is infrequently observed in pet food. A retrospective evaluation of pet food investigations (PFI) was conducted for 17 dogs, including review of medical records, dietary and environmental exposure interviews, food testing, and regulatory action. Five PFIs occurring between 2016 and 2018 involved 7 food products including 2 food types, jerky treats or canned food, made from beef or bison. The dogs' serum thyroid hormone concentrations were evaluated before and after diet change. The foods were tested for active thyroid hormones and hormone precursors using high performance liquid chromatography with inductively coupled plasma mass spectrometry detection. The foods were also examined microscopically. Serum thyroid hormone concentrations of thyroxine (T4) varied depending on the food type consumed. Dogs that consumed dried jerky containing greater T4 concentrations often had increased serum T4 concentrations, whereas dogs that consumed canned products containing greater and 3,4,5- and 3,5,3'-triiodothyronine (T3) concentrations often had decreased serum T4 concentrations. After the diets were changed, serum T4 and T3 concentrations normalized at 1 month. Seven foods containing beef or bison had iodine concentrations greater than 11 mg/kg, and iodine speciation identified variable concentrations of iodide, T4, T3, monoiodotyrosine (MIT), and di-iodotyrosine (DIT). Thyroid gland was found in microscopic sections from one finished food and one ingredient, gullet. FDA performed Health Hazard Evaluations to categorize the exposure risk, and 5 foods were recalled for which the product packaging had not been discarded. Dietary exogenous thyrotoxicosis should be considered in dogs exhibiting clinical signs compatible with hyperthyroidism, especially if consuming beef-based food. A thyroid panel that includes serum iodine, coupled with a thorough feeding history can aid in diagnosis. Thyrotoxicosis is typically reversible after removing the contaminated food from the diet.

[Alimentary thyrotoxcicosis in two dogs]. / Alimentäre Thyreotoxikose bei zwei Hunden.

Two dogs with increased thyroxin concentrations compatible with hyperthyroidism were referred for further examinations. One dog displayed clinical signs of hyperthyroidism. Based on history, clinical examination, laboratory evaluation and scintigraphy an alimentary thyrotoxicosis was identified. It was caused by feeding a BARF diet containing thyroidal tissue in one dog and by conventional dog food in the other patient. After changing the diet the clinical signs resolved in the affected dog. A control examination revealed thyroxin concentrations within the reference range in both dogs.

Thyrotoxicosis induced by excessive 3,5,3'-triiodothyronine in a dog.

CASE DESCRIPTION A 7-year-old castrated male Havanese was evaluated at a veterinary teaching hospital because of a 12-week history of hyperactivity, aggression, and progressive weight loss despite a healthy appetite. CLINICAL FINDINGS Tachycardia was the only remarkable finding during physical examination. Serum 3,5,3'-triiodothyronine (T3) and free T3 concentrations were markedly increased, and thyroxine (T4), free T4, and thyroid-stimulating hormone concentrations were at or decreased from the respective reference ranges. Thyroid scintigraphy revealed suppressed uptake of sodium pertechnetate Tc 99m by the thyroid gland but no ectopic thyroid tissue, which was indicative of thyrotoxicosis induced by an exogenous source of T3. TREATMENT AND OUTCOME The dog was hospitalized for 24 hours, and its diet was changed, after which the clinical signs rapidly resolved and serum T3 and free T3 concentrations returned to within the respective reference ranges. This raised suspicion of an exogenous source of T3 in the dog's home environment. Analysis of the commercial beef-based canned food the dog was being fed revealed a high concentration of T3 (1.39 µg/g) and an iodine (82.44 µg/g) concentration that exceeded industry recommendations. No other source of T3 was identified in the dog's environment. CLINICAL RELEVANCE To our knowledge, this is the first report of clinical thyrotoxicosis in a dog induced by exogenous T3, although the source of exogenous T3 was not identified. This case highlights the importance of measuring serum T3 and thyroid-stimulating hormone concentrations in addition to T4 and free T4 concentrations when there is incongruity between clinical findings and thyroid function test results.

Exogenous thyrotoxicosis in dogs attributable to consumption of all-meat commercial dog food or treats containing excessive thyroid hormone: 14 cases (2008-2013).

OBJECTIVE: To describe findings in dogs with exogenous thyrotoxicosis attributable to consumption of commercially available dog foods or treats containing high concentrations of thyroid hormone. DESIGN: Retrospective and prospective case series. ANIMALS: 14 dogs. PROCEDURES: Medical records were retrospectively searched to identify dogs with exogenous thyrotoxicosis attributable to dietary intake. One case was found, and subsequent cases were identified prospectively. Serum thyroid hormone concentrations were evaluated before and after feeding meat-based products suspected to contain excessive thyroid hormone was discontinued. Scintigraphy was performed to evaluate thyroid tissue in 13 of 14 dogs before and 1 of 13 dogs after discontinuation of suspect foods or treats. Seven samples of 5 commercially available products fed to 6 affected dogs were analyzed for thyroxine concentration; results were subjectively compared with findings for 10 other commercial foods and 6 beef muscle or liver samples. RESULTS: Total serum thyroxine concentrations were high (median, 8.8 µg/dL; range, 4.65 to 17.4 µg/dL) in all dogs at initial evaluation; scintigraphy revealed subjectively decreased thyroid gland radionuclide in 13 of 13 dogs examined. At ≥ 4 weeks after feeding of suspect food or treats was discontinued, total thyroxine concentrations were within the reference range for all dogs and signs associated with thyrotoxicosis, if present, had resolved. Analysis of tested food or treat samples revealed a median thyroxine concentration for suspect products of 1.52 µg of thyroxine/g, whereas that of unrelated commercial foods was 0.38 µg of thyroxine/g. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicated that thyrotoxicosis can occur secondary to consumption of meat-based products presumably contaminated by thyroid tissue, and can be reversed by identification and elimination of suspect products from the diet.

Serum thyroxine and triiodothyronine responses of hyperthyroid cats to thyrotropin.

OBJECTIVE: To document circulating total thyroxine (T4) and triiodothyronine (T3) responses after administration of thyrotropin (thyroid-stimulating hormone [TSH]) to hyperthyroid and healthy cats and assess the value of these responses as an additional diagnostic test for hyperthyroidism. DESIGN: Prospective case series. ANIMALS: 21 healthy and 40 hyperthyroid cats. PROCEDURES: Serum total T4 and T3 concentrations were measured by radioimmunoassay before and 6 hours after administration of 0.5 IU of bovine TSH/kg of body weight. RESULTS: In healthy cats, serum total T4 concentration increased after administration of TSH (mean +/- SD, 114.0 +/- 36.4 nmol/L) representing a mean increment 3 times baseline concentration (mean +/- SD, 33.7 +/- 7.6 nmol/L). In hyperthyroid cats, the relative increase in serum total T4 concentration was significantly (P < 0.001) different; baseline values (mean +/- SD, 236.2 +/- 146.0 nmol/L) increased minimally after TSH administration (mean +/- SD, 308.1 +/- 178.9 nmol/L) There was a significant negative correlation (rs = -0.366) between relative increase in serum total T4 concentration after TSH administration and baseline concentration in hyperthyroid cats. In 3 cats with equivocal baseline serum total T4 concentration, the T4 response to TSH administration was indistinguishable from that in healthy cats. Serum total T3 response to TSH administration was significantly (P < 0.001) lower in hyperthyroid, compared with healthy, cats but the T3 response in healthy cats was more variable than that for T4 CONCLUSIONS: Thyrotoxic cats with high baseline serum total T4 concentration have a limited T4 response to TSH stimulation. Hyperthyroid cats with equivocal baseline serum total T4 concentrations have T4 response after TSH stimulation similar to those of healthy cats. Measurement of serum total T3 concentration provides no additional information. CLINICAL RELEVANCE: The TSH response test is of limited value in diagnosing hyperthyroidism in cats.

Cardiovascular manifestations of iatrogenic hyperthyroidism in two dogs.

Two dogs were diagnosed with iatrogenic thyrotoxicosis (1 definitive, 1 presumptive). Both showed physical examination findings of agitation, tachypnea, and tachycardia. Sinus tachycardia with supraventricular ectopy was diagnosed in one case, and syncope and atrial flutter was present in the other. Both dogs had concurrent cardiac disease that might have contributed to the severity of their clinical signs. Excessive thyroid hormone supplementation in humans causes supraventricular arrhythmias including sinus tachycardia, supraventricular tachycardia, atrial fibrillation, and atrial flutter. Clinical signs and rhythm abnormalities resolved in both dogs with resolution of the thyrotoxicosis.

Determinação de desmineralização óssea em gatos após tirotoxicose experimental / Determination of bone demineralization in cats after experimental thyrotoxicosis

O hipertiroidismo é capaz de proporcionar efeitos sobre o metabolismo ósseo tanto em humanos como em animais. Para melhor avaliar este fato em gatos, em 16 animais foram induzidos a tirotoxicose a partir da administração oral de 150 μg/kg de levotiroxina sódica a cada 24 horas durante 42 dias. Os níveis hormonais foram avaliados por radioimunoensaio e a densidade mineral óssea da extremidade distal do rádio direito foi mensurada através de densitometria óptica radiográfica. Foi possível observar, a partir da primeira semana de experimento, significativa elevação sérica de T4 livre e T4 total acompanhada de desmineralização óssea do rádio.

Hyperthyroidism can result in serious effects on the bone metabolism in humans as well as animals. For a better characterization of thyrotoxicosis effects, 16 cats were induced into thyrotoxicosis by intaking a dose of 150 μg/kg of sodium L-thyroxine every 24 hours during 42 days. The hormonal levels were evaluated by radioimmunoassay technique and the bone mineral density of the right distal radius extremity was measured through the radiographic optical densitometry. Was verified significant bone demineralization seven days of hormonal intake as weel as radius demineralization.