$63 – $110
ANIMALS | Dogs |
---|---|
ACTIVE INGREDIENT | Levothyroxine |
FORM | Tablets |
Strenght | 200mcg, 400mcg, 600mcg, 800mcg |
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Levothyroxine For Dogs – FORTHYRON 250 Tablets
Forthyron flavoured tablets of 800 micrograms for dogs
Each tablet contains:
Active substance:
800 µg levothyroxine sodium in each tablet, which is equivalent to 778 µg levothyroxine
Excipients:
For the full list of excipients, see section 6.1.
Tablets.
A cream-coloured round tablet with brown spots is divided into four equal parts with markings on one side.
The tablets can be divided into halves and quarters.
4.1. Target species
Dogs.
4.2. Indications for use
For the treatment of hypothyroidism in dogs.
4.3. Contraindications
Do not use in dogs with uncorrected adrenal insufficiency. Do not use in cases of hypersensitivity to levothyroxine sodium or excipients.
4.4. Special precautions for use
Diagnosis of hypothyroidism should be confirmed through appropriate tests.
4.5. Special precautions for use
Special precautions for animals when using the product
The tablets are flavored. To avoid accidental ingestion, store the tablets in a place inaccessible to animals. The sudden increase in the need for oxygen supply to peripheral tissues, plus the chronotropic effects of levothyroxine sodium may subject poorly functioning hearts to unwanted stress. It may cause decompensation and signs of congestive heart failure. Dogs with hypothyroidism suffering from hypoadrenocorticism have a reduced capacity to metabolize levothyroxine sodium and are, therefore at an increased risk of thyrotoxicosis. Dogs with concurrent hypoadrenocorticism and hypothyroidism should be stabilized with glucocorticoid and mineralocorticoid therapy before initiating treatment with levothyroxine sodium to prevent the precipitation of a hypoadrenocortical crisis. Thyroid tests should then be repeated, gradually introducing levothyroxine therapy, starting with 25% of the normal dose and increasing gradually by 25% every two weeks until optimal stabilization is achieved, as recommended. The gradual introduction of therapy is also recommended for dogs with other concurrent diseases, particularly dogs with heart disease, diabetes mellitus, and renal or hepatic dysfunction.
Special precautions for persons administering veterinary medicinal products to animals
Wash hands after administering the tablets. Pregnant women should handle veterinary medicinal products with increased caution. In case of accidental ingestion, seek medical advice immediately, providing the package leaflet or product label to the doctor.
4.6. Adverse reactions (frequency and seriousness)
Resumption of physical activity may reveal or exacerbate other problems, such as osteoarthritis. Adverse reactions to thyroid hormones are usually associated with overdosing and correspond to symptoms of hyperthyroidism. See also section 4.10.
4.7. Use during pregnancy, lactation or lay
The safety of the veterinary medicinal product has not been established during pregnancy and lactation. However, levothyroxine is an endogenous substance, and thyroid hormones are crucial for fetal development, especially during the first gestational period. Hypothyroidism during pregnancy can lead to serious complications, such as fetal death and poor perinatal outcome. Therefore, pregnant female dogs should be regularly monitored from conception to several weeks after delivery.
4.8. Interaction with other veterinary medicinal products and other forms of interaction
Multiple products worsen plasma and tissue binding of thyroid hormones or alter thyroid hormone metabolism (e.g., barbiturates, antacids, anabolic steroids, diazepam, furosemide, mitotane, phenylbutazone, phenytoin, propranolol, high doses of salicylates and sulfonamides). When treating dogs receiving concomitant therapy, the properties of the products used should be taken into account. Estrogens can increase the need for thyroid hormones.
Ketamine can cause tachycardia and hypertension when applied to patients receiving thyroid hormones. The effect of catecholamines and sympathomimetics is enhanced by levothyroxine.
An increase in the dose of digitalis may be necessary for patients with pre-existing compensatory congestive heart failure who are also receiving thyroid hormone supplementation. Careful monitoring to control diabetes is recommended after treatment for hypothyroidism in dogs with concurrent diabetes. Most dogs on long-term high-dose daily glucocorticoid therapy will have very low or undetectable serum T4 concentrations and subnormal T3 values.
4.9 Dosage and method of administration
For oral administration.
The recommended initial dose for levothyroxine sodium is 10 µg/kg body weight orally every 12 hours. Due to variability in absorption and metabolism, dosage adjustments may be necessary before achieving a complete clinical response. The initial dose and frequency of administration are just starting points. Therapy should be highly individualized and adapted according to the needs of each dog. For dogs with a body weight below 5 kg, one-quarter of a 200 µg tablet should be taken once daily when initiating therapy. Such cases should be carefully monitored. In dogs, absorption of levothyroxine sodium may be affected by the presence of food. Therefore, the timing of treatment in relation to food intake should be consistent every day. Plasma T4 values (immediately before therapy) and peak values (approximately three hours after dosing) can be measured to monitor therapy correctly. In properly dosed dogs, peak plasma T4 concentration should be in the upper range of normal values (approximately 30 to 47 nmol/L), and the lowest values should be approximately above 19 nmol/L. If T4 levels are outside these limits, levothyroxine dose may be gradually adjusted by 50 to 200 µg until the patient becomes clinically euthyroid and serum T4 is within reference ranges. Plasma T4 levels can be checked again two weeks after dosage adjustment, but clinical improvement is no less important in determining individual dosing and typically takes four to eight weeks. After reaching the optimal replacement dose, clinical and biochemical indicators may be monitored every 6-12 months.
To properly and easily break the tablet, place the tablet with the marking facing up and press with a thumb.
Hold one half of the tablet down and press the other half down to break the tablet into two parts.
4.10 Overdose (symptoms, emergency measures, antidotes), if necessary
Thyrotoxicosis may occur following an overdose. Thyrotoxicosis as an adverse reaction to mild overdosing in replacement therapy is unusual in dogs because they can metabolize and excrete thyroid hormones. In cases of accidental ingestion of large amounts of VMP, absorption may be reduced by inducing vomiting followed by oral activated charcoal and magnesium sulfate administration.
Overdoses three to six times the recommended initial dose over four consecutive weeks in healthy euthyroid dogs have resulted in the absence of significant clinical signs attributable to therapy. A single overdose, up to three to six times the recommended dose maximum, poses no threat to the dog and requires no action. However, after prolonged replacement therapy overdosing, clinical signs of hyperthyroidism may theoretically occur, such as polydipsia, polyuria, dyspnea, weight loss without anorexia, as well as tachycardia and nervousness together or separately. The presence of these signs should prompt an assessment of serum T4 concentrations to confirm the diagnosis and immediately discontinue supplemental therapy. After subsidence of these signs (within days to weeks), the dosing of thyroid hormones should be reviewed. Once the animal is fully recovered, a lower dose may be introduced while closely monitoring the animal.
4.11 Withdrawal period
Not applicable.
5 PHARMACOLOGICAL PROPERTIES
Pharmacotherapeutic group: Synthetic thyroid hormones. Veterinary Anatomical-Therapeutic Chemical code: QH03AA01.
5.1 Pharmacodynamic properties
From a pharmacological perspective, levothyroxine is classified as a hormonal product that replaces deficient endogenous hormones.
Levothyroxine T4 is converted into triiodothyronine T3. T3 acts on cellular processes through specific ligand-receptor interactions with the nucleus, mitochondria, and plasma membrane. Interaction of T3 with binding sites leads to increased DNA transcription or modulation of RNA, thereby affecting protein synthesis and enzyme action.
Thyroid hormones act on many cellular processes. In animal and human development, they are crucial determinants for normal development and especially for the central nervous system. Thyroid replacement therapy enhances basal cell metabolism and oxygen uptake, practically affecting all organ systems’ functions.
5.2 Pharmacokinetic particulars
Some dogs consistently show better absorption of L-thyroxine and/or slower elimination compared to other dogs. Additionally, the extent of absorption and elimination is influenced by daily intake of levothyroxine sodium (high absorption/low elimination at low doses and vice versa at high doses). Variability in pharmacokinetic parameters between individual dogs is considerable and although food intake may influence absorption, it is considered to have a negligible effect on parameters overall. Absorption is relatively slow and incomplete: in most cases, Tmax is in the range of 1 to 5 hours after oral intake; Cmax varies over three times among individual dogs at equal doses. In inadequately dosed dogs, plasma peaks approach or slightly exceed upper plasma T4 levels; by the end of the 12-hour period following oral intake, plasma T4 levels usually drop to values lower than half normal limits. The rate of T4 elimination from plasma is delayed in hypothyroidism. Over 50% of produced daily T4 is lost through feces in dogs; extrathyroidal body T4 stores are eliminated and replaced within about 1 day; a large part of thyroxine is absorbed from the colon; L-thyroxine binds to plasma proteins and lipoproteins; part of thyroxine dose is metabolized into more potent triiodothyronine (T3) through deiodination; deiodination continues; these additionally deiodinated metabolites (other than T3 and T4) lack thyroid-mimetic activity; other pathways of thyroid hormone metabolism include conjugation to form soluble glucuronides and sulfates excreted through biliary and urinary pathways; as well as a breakdown of ether linkage on iodothyronine molecule.
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