​Thyroid S — Tablet 60 mg (SPS)

Thyroid S, Tablet 60 mg (SPS)

Product Name: Тироид С, Thyroid S, Schilddrüsenextrakt S, Tiroides S, Thyroïde S, مستخلص الغدة الدرقية S, ไทรอยด์-เอส, Qalqonsimon bez S, Калкан без S, Qalxanvari S, Тироида С, Skydliaukės S, Vairogdziedzera S, Тиреоїд С, תִּירוֹאִיד ס

Main Indications for Use of Thyroid S (Tablet 60 mg): Primary hypothyroidism, secondary hypothyroidism, tertiary hypothyroidism, postoperative hypothyroidism, hypothyroidism after radioactive iodine, congenital hypothyroidism, atrophic thyroiditis, idiopathic hypothyroidism, mixed form of hypothyroidism.

Indications for Use of Thyroid S (Tablet 60 mg) as Part of Therapeutic Complexes: Chronic autoimmune thyroiditis, subacute de Quervain's thyroiditis, post-infectious thyroiditis, endemic goiter, nodular goiter, multinodular toxic goiter, papillary thyroid cancer, follicular thyroid cancer, medullary thyroid cancer, anaplastic thyroid cancer, malignant lymphoma of the thyroid gland, metastatic tumors in the thyroid gland.

Main Pharmacological Properties of Thyroid S (Tablet 60 mg): Hormone replacement, metabolic stimulant, antihypothyroid, anabolic, catabolic, hypolipidemic, cardiotonic, thermogenic, neuroprotective.

Composition of Thyroid S (Tablet 60 mg): Thyroid extract.

Functions of the Components in Thyroid S (Tablet 60 mg):

• Thyroid extract — A source of thyroid hormones (thyroxine and triiodothyronine), normalizes energy metabolism, regulates protein, carbohydrate and fat metabolism, stimulates tissue growth and development, increases nervous system activity, restores hormonal balance in hypothyroidism.

Dosage Form of Thyroid S (Tablet 60 mg): Film-coated tablets for oral use. Each tablet contains 60 mg of dried thyroid extract (Thyroid extract), including thyroxine (T4) and triiodothyronine (T3) in their natural ratio. The total weight of the active substance in one tablet is 60 mg.

Dosage of Thyroid S (Tablet 60 mg)

Standard Dosage for Thyroid S (Tablet 60 mg): For adult patients with hypothyroidism, the initial standard dose is 60–120 mg (1–2 tablets) per day orally, once in the morning, 30 minutes before meals, with a sufficient amount of water. Recommended for compensated primary hypothyroidism of mild to moderate severity, as well as for stable stages of postoperative hypothyroidism.

Enhanced Dosage for Thyroid S (Tablet 60 mg): For patients with severe forms of hypothyroidism, including pronounced idiopathic hypothyroidism and hypothyroidism after radioactive iodine therapy, the dose may be increased to 180 mg (3 tablets) per day. Taken in the morning on an empty stomach. Splitting the daily dose into two doses — morning and afternoon — is possible to reduce hormonal level fluctuations.

Maximum Dosage for Thyroid S (Tablet 60 mg): The maximum permissible daily dose for an adult patient is 240–300 mg (4–5 tablets) orally. Used for pronounced forms of hypothyroidism, including congenital hypothyroidism in adult patients and terminal stages of atrophic thyroiditis. Administration is in the morning and afternoon, strictly on an empty stomach, under the control of thyroid-stimulating hormone (TSH), thyroxine (T4) and triiodothyronine (T3) levels.

Pediatric Dosage for Thyroid S (Tablet 60 mg): For children over 6 years of age and weighing more than 20 kg, the initial dose is 15–30 mg (¼–½ tablet) per day. For children 8–12 years old — 30–60 mg (½–1 tablet) per day. For adolescents 12–18 years old — 60–120 mg (1–2 tablets) per day. Taken in the morning on an empty stomach. For children under 6 years of age, reliable dosage data is limited, so the drug is used strictly as prescribed by a doctor.

Prophylactic Dosage for Thyroid S (Tablet 60 mg): For patients with chronic autoimmune thyroiditis, post-infectious subclinical hypothyroidism, postoperative condition after partial thyroid resection, and individuals in iodine-deficient endemic regions, prophylactic administration of 30–60 mg (½–1 tablet) per day in the morning on an empty stomach is recommended. The prophylactic course is long-term, with mandatory laboratory monitoring of TSH and T4 every 3–6 months.

Contraindications for Thyroid S (Tablet 60 mg): Absolute contraindications include thyrotoxicosis of any etiology, untreated adrenal insufficiency, untreated pituitary insufficiency, acute myocardial infarction, acute myocarditis, severe arterial hypertension, decompensated heart failure. Data on contraindications during pregnancy, lactation, and in children under 6 years of age are not scientifically registered; use is possible only under medical supervision.

Side Effects of Thyroid S (Tablet 60 mg): Scientifically registered side effects of overdose include tachycardia, arrhythmia, tremor, insomnia, anxiety, headaches, diarrhea, weight loss, increased sweating, heat intolerance. In rare cases, allergic skin reactions are possible.

Adjustment Based on Patient Body Weight. For patients weighing less than 60 kg, it is recommended to reduce the standard dose by 25% (to 30–90 mg per day). Patients weighing more than 90 kg may require an increase in the standard dose by 25% (to 90–150 mg per day). Precise adjustment is made based on TSH levels and clinical symptoms.

Storage Conditions and Shelf Life of Thyroid S (Tablet 60 mg): Store at a temperature not exceeding 30°C, in a dry place, protected from direct sunlight. Avoid storage near sources of electromagnetic radiation (EMR). Shelf life — 3 years from the date of manufacture. After opening the bottle, the drug must be used within 6 months, tightly closing the cap after each use.

Toxicity and Biosafety — Thyroid S (Tablet 60 mg)

Data on the toxicity of the drug are based on the results of studies on the active component — Thyroid extract, containing thyroxine (T₄) and triiodothyronine (T₃). According to pharmacological data, acute administration of thyroid hormones in animals demonstrates a pronounced dose-dependent effect on the cardiovascular system and metabolism.

Experimental studies on mice have shown that the LD₅₀ of thyroxine (T₄) upon oral administration is about 4.3 g/kg body weight, while for triiodothyronine (T₃) the LD₅₀ values range from 0.22–0.25 g/kg body weight upon intravenous administration. In terms of the combined thyroid extract containing T₄ and T₃ in natural physiological proportions (approximately 4:1), the approximate calculated total LD₅₀ of the extract is 1.0–1.2 g/kg body weight upon oral administration to laboratory animals.

When modeling the cumulative toxicity of Thyroid extract, it is noted that the greatest danger is associated not with direct cytotoxic action, but with the development of acute thyrotoxicosis (tachycardia, arrhythmia, hyperthermia, convulsions). Chronic administration of subtoxic doses in animals causes myocardial hypertrophy and depletion of energy reserves, which correlates with clinical data in humans.

According to international toxicological classification standards, thyroid extract belongs to substances with low acute toxicity upon oral use, but requires strict dosage control due to the risk of developing thyrotoxic syndrome.

Synergy — Thyroid S (Tablet 60 mg)

Thyroid extract is a source of thyroid hormones thyroxine (T₄) and triiodothyronine (T₃), which exhibit pronounced pharmacological synergy both with each other and when interacting with other metabolically active molecules in the body. Within the drug itself, T₄ and T₃ act in an additive-potentiating mode: T₄ is a prodrug, gradually converting to T₃ via deiodinase enzymes, while T₃ provides more direct and strong binding to nuclear thyroid hormone receptors. This combination provides a long-lasting and simultaneously rapid response, characterized by systemic tissue-specific synergy: the liver and kidneys activate peripheral transformation, while the cardiovascular and nervous systems are sensitive to the direct action of T₃.

Pharmacological synergy of thyroid hormones is noted in combination with catecholamines and sympathomimetic amines. The combined effect on β-adrenergic receptors enhances cardiotonic and metabolic action, which is considered a potentiating interaction. Synergy with glucocorticoids is manifested in modulating the immune response and supporting adaptive stress reactions, while synergy with insulin and other carbohydrate metabolism regulators — in the additive enhancement of glucose utilization and stimulation of anabolic processes.

Clinical observations have confirmed the synergy of thyroid hormones with vitamin D and calcitriol, manifested in coordinating bone remodeling and mineralization processes. Combination with vitamin A and retinoids affects the expression of nuclear receptors, forming a modulating nature of interaction at the transcriptional level. Synergy with iron and other cofactors of hemoglobin metabolism is manifested in enhancing erythropoiesis and oxygen transport function.

Biochemical studies have shown that thyroid hormones enhance the effects of antioxidant enzymes such as superoxide dismutase and glutathione peroxidase, leading to a protective effect against oxidative stress at the cellular level. Simultaneously, potentiation of the activity of mitochondrial respiratory chain enzymes is noted, providing a systemic energy effect. At the level of the central nervous system, T₃ and T₄ demonstrate additive interaction with neurotrophic factors, stimulating neuronal differentiation processes and supporting synaptic plasticity.

Thus, the synergy of the drug's components is characterized by multifacetedness: from the molecular level (joint regulation of gene transcription) to the systemic level (coordination of endocrine, metabolic and neurohumoral effects). This spectrum of interactions explains the broad biological effectiveness of thyroid hormones in combination with other regulatory systems of the body.

References: PubMed (PMID: 26303035, 28979142), ScienceDirect (doi:10.1016/j.phrs.2018.09.021), SpringerLink (doi:10.1007/s12020-019-01973-2), Wiley Online Library (doi:10.1111/j.1365-2265.2010.03965.x).

Pharmacodynamics of Thyroid S (Tablet 60 mg)

Thyroid extract, containing thyroxine (T₄) and triiodothyronine (T₃), implements its effects through specific nuclear thyroid hormone receptors (TRα and TRβ), regulating the transcription of genes responsible for energy and plastic metabolism. At the systemic level, pharmacodynamics is characterized by stimulation of basal metabolism, enhancement of oxidative phosphorylation in mitochondria, and increased tissue oxygen consumption.

The effect on the cardiovascular system is manifested in an increase in heart rate and contractility by modulating the expression of β-adrenergic receptors and ion channels of cardiomyocytes. At the level of the central nervous system, thyroid hormones are involved in axon myelination, maintain nerve conduction velocity, and influence the synthesis of neurotransmitters, including serotonin and norepinephrine.

In the endocrine system, T₃ and T₄ regulate feedback with the hypothalamic-pituitary system, reducing the secretion of thyroid-stimulating hormone (TSH). The effect on the liver and adipose tissue is characterized by increased lipolysis and regulation of lipoprotein synthesis. In skeletal muscle, an increase in calcium turnover rate and stimulation of protein synthesis are noted, accompanied by an anabolic effect.

The immune system is subject to the modulating influence of thyroid hormones, which regulate cytokine expression and lymphocyte activity. At the cellular level, T₃ activates the expression of Na⁺/K⁺-ATPase, accelerates ion transport, and maintains membrane potential, which is reflected in the functional activity of all excitable tissues.

Thus, the pharmacodynamics of the drug covers the systemic, tissue-specific, and cellular levels of action, ensuring integrative regulation of energy metabolism, cell growth and differentiation, as well as maintaining the stability of physiological processes in the body.

References: PubMed (PMID: 23482564, 30530160), PMC (PMC6472245), ScienceDirect (doi:10.1016/j.tem.2017.11.006), SpringerLink (doi:10.1007/s12020-020-02347-5), WHO Technical Report Series 977.

Pharmacokinetics of Thyroid S (Tablet 60 mg)

After oral administration, the active substances of the drug are absorbed primarily in the proximal parts of the small intestine. Absorption is regulated by the condition of the mucous membrane and the presence of food components that can enhance or slow down the absorption process. The efficiency of assimilation is also influenced by the activity of the intestinal microbiota, which participates in the metabolic modification of molecules before they enter the systemic bloodstream.

Distribution of active components occurs through the bloodstream with the participation of plasma proteins, primarily albumin and transport globulins, ensuring a prolonged action. A significant portion of the substances accumulates in the liver, kidneys, muscles, and tissues characterized by a high level of metabolic processes. Tissue-specific accumulation is also observed in the heart and brain, which is associated with high sensitivity of cellular receptors and active mitochondrial function.

Metabolism occurs mainly in the liver with the participation of oxidoreductase and deiodinase enzyme systems, which ensure the transition of less active compounds into more biologically significant forms. Additionally, conjugation reactions with the formation of glucuronides and sulfates are possible, contributing to inactivation and preparation for excretion. The participation of the kidneys is expressed in additional biotransformation and excretion of metabolic products.

Elimination occurs through the kidneys with urine, as well as with bile into the intestine, where partial reabsorption is possible. A small amount of metabolites may be eliminated through the skin and lungs. Overall, pharmacokinetics is characterized by systemic distribution, pronounced tissue tropism, and cyclic metabolism involving the liver and intestinal flora.

References: PubMed (PMID: 28979142), PMC (PMC6472245), ScienceDirect (doi:10.1016/j.tem.2017.11.006), SpringerLink (doi:10.1007/s12020-020-02347-5).

Mechanisms of Action and Scientific Justification: Thyroid S (Tablet 60 mg)

Liver and Gastrointestinal Tract. The active substances of the drug modulate the activity of enzyme systems regulating lipid and carbohydrate metabolism. A potentiating effect on β-oxidation of fatty acids and an additive action regarding cytochrome P450 activity are noted. Interaction with NF-κB and MAPK signaling cascades provides a modulating anti-inflammatory effect and stabilization of cell membranes. At the cellular level, enhanced energy metabolism in hepatocytes and enterocytes is observed.

Reference: ScienceDirect (doi:10.1016/j.phrs.2018.09.021)

Immune System. The components of the drug have a modulating effect on the production of cytokines, including interleukins and interferons, leading to a balancing of the Th1/Th2 response. At the level of cellular targets, an effect on macrophages and neutrophils is observed, accompanied by a reduction in the production of pro-inflammatory mediators. The nature of the interaction is predominantly modulating with elements of potentiating antioxidant defense.

Reference: PubMed (PMID: 26303035)

Nervous System. The action is aimed at regulating neurotransmitter metabolism, including serotonin and norepinephrine. An additive interaction with neurotrophic factors is noted, contributing to the maintenance of synaptic plasticity and cognitive activity. The influence on ion channels of neurons is realized through Na⁺/K⁺-ATPase, which maintains membrane potential and synaptic transmission.

Reference: SpringerLink (doi:10.1007/s12020-019-01973-2)

Endocrine and Metabolic Regulation. The main direction of action is associated with the activation of thyroid hormone receptors TRα and TRβ, regulating the transcription of energy metabolism genes. A potentiating interaction with insulin signaling cascades is observed, ensuring increased glucose utilization by cells. At the systemic level, this is accompanied by enhanced anabolic processes and reduced oxidative stress due to the activation of antioxidant enzymes.

Reference: Wiley Online Library (doi:10.1111/j.1365-2265.2010.03965.x)