Selesyn 100 mcg Sol.Inj

Selenium (as sodium selenite pentahydrate).

Colorless, transparent solution, contained in a transparent glass tube.
Each 2 mL ampoule of solution contains: Drug substance: Selenium (as sodium selenite pentahydrate) 100 mcg.
Excipients/Inactive Ingredients: Sodium chloride, hydrochloric acid 0.1M, water for injection.

Pharmacotherapeutic group: Mineral supplement. ATC code: A12CE02.
Pharmacology: Pharmacodynamics: Selenium is an essential trace element. To date, 20 selenoproteins have been identified in rodents. Glutathione peroxidase and a selenium-binding protein called selenoprotein P found in plasma have been detected or purified in humans. In both proteins, selenium is protein-bound in the form of the amino acid selenocysteine. In animals, 5'- deiodinase was recently characterized as a selenium enzyme, which catalyzes the conversion of tetraiodothyronine (T4) to the active thyroid hormone triiodothyronine (T3).
The selenium-containing glutathione peroxidase is part of the antioxidant protection system of the mammalian cell. In the presence of sufficient amounts of substrate, i.e. H. reduced glutathione, glutathione peroxidase converts a variety of different hydroperoxides into corresponding alcohols. In cellular or subcellular model systems it has been shown that the integrity of cellular and subcellular membranes crucially depend on the integrity of the glutathione peroxidase system. Synergistic action with vitamin E in various cell fractions is postulated but has not been conclusively proven.
Selenium as a component of glutathione peroxidase can reduce the rate of lipid peroxidation and the resulting membrane damage. Not all of the effects of selenium can be explained solely by the activity of glutathione peroxidase.
The pathophysiological relevance of the selenium-dependent reactions has been proven by observations of selenium deficiency in humans and animals: the selenium-containing glutathione peroxidase influences leukotriene, thromboxane, and prostacyclin metabolism.
Selenium deficiency activates and inhibits immune defense reactions, especially the non-specific, cell-bound and humoral reactions. Selenium deficiency affects the activity of some liver enzymes. Selenium deficiency potentiates oxidative or chemically induced liver damage as well as the toxicity of heavy metals such as mercury and cadmium.
Deficiency symptoms in humans: Keshan disease, an endemic cardiomyopathy, and the so-called Kaschin-Beck disease, an also endemic osteoarthropathy with severe deformation of the joints, have been described as selenium deficiency diseases. Clinically manifest selenium deficiency has also been observed as a result of long-term parenteral nutrition and balanced diets.
Cardiomyopathies and myopathies of the skeletal muscles in particular occurred.
Epidemiological studies indicate an inverse correlation between blood selenium levels and the incidence of cardiovascular diseases (cardiomyopathies, arteriosclerosis, myocardial infarction) as well as tumor diseases (especially of the digestive tract, breast and liver). Decreased plasma selenium levels may occur in patients with renal insufficiency and in gastrointestinal diseases. Suboptimal selenium intake leads to reduced glutathione peroxidase activity in humans and animals, but does not lead to any clinically tangible symptoms.
Selenium deficiency can be detected by reduced whole blood or plasma selenium levels and by reduced glutathione peroxidase activities in whole blood, plasma or platelets.
Pharmacokinetics: Sodium selenite is not incorporated directly into proteins. In the blood, selenite is mainly absorbed by erythrocytes and enzymatically reduced to hydrogen selenide. Hydrogen selenium serves as a central selenium pool for excretion and for targeted incorporation into selenoproteins. In this reduced form, selenium is bound to plasma proteins that travel to the liver and other organs.
The secondary plasmatic transport from the liver into the target tissue that synthesizes glutathione peroxidase probably occurs in the form of the P-Selenoprotein containing selenocysteine. The further metabolic course of selenoprotein biosynthesis is currently only known in prokaryotes. Selenocysteine is then specifically incorporated into the peptide chains of glutathione peroxidase during translation.
Excess hydrogen selenium is metabolized via methylselenol and dimethylselenide to trimethy|selenonium ion, the main excretion product.
After oral administration, selenite is primarily absorbed from the small intestine. Intestinal absorption of sodium selenite is not homeostatically regulated. Depending on the concentration and accompanying substances, it is between 44% and 89%, occasionally over 90%. The amino acid cysteine promotes the sodium selenite absorption.
The total amount of selenium in the human body is between 4 mg and 20 mg. Depending on the dose administered, selenium is excreted in humans via the faeces, urine or lungs. Selenium is primarily excreted renally in the form of the trimethylselenonium ion. Excretion depends on selenium status.
Selenium excretion after intravenous or oral administration occurs in three phases. When 10 mcg was administered orally in the form of [75Se] sodium selenite, 14-20% of the absorbed dose of selenium was excreted in the urine in the first two weeks, while practically no excretion via the lungs or skin was detected. Total body retention of selenium decreased triphasically with a half-life of 0.7-1.2 days in the 1st phase, 7-11 days in the 2nd phase and 96-144 days in the 3rd phase. Selenium concentrations decreased more rapidly in liver, heart, and plasma than in skeletal muscle or bone. Of an intravenously administered dose of [75Se] sodium selenite, 12% was excreted within the first 24 hours. An additional 40% was eliminated with a biological half-life of 20 days. The half-life of the third phase was determined to be 115 days.
In a direct comparison between oral and intravenous administration of a physiological dose of [74Se] sodium selenite, after intravenous administration of 82 mcg selenium in the form of sodium selenite, 18% of the dose was absorbed in the first 24 hours, and after peroral administration 12% of the absorbed Dose excreted in the urine together with metabolically exchanged body selenium. The excretion then proceeds in the same way for both types of application. Sodium selenite administered orally and parenterally is comparable in healthy subjects.

Proven selenium deficiency that cannot be corrected through nutrition. A selenium deficiency can occur at: Maldigestion and malabsorption states; Malnutrition and nutritional (e.g. total parenteral nutrition).

Method of administration: The drug is used by intramuscular or intravenous injection. The injection solution must be drawn under aseptic conditions.
The duration of use should be determined by the treating physician. When the drug is used as a supplement to total parenteral nutrition solutions, it is necessary to ensure that the correct dose of selenium is used, which is 100 mcg (equivalent to 1 ampoule) per day.
The drug can be mixed with common infusion solutions. For safety reasons, attention should be paid to the non-specific precipitation in all infusion solutions after mixing with the injectable drug selenium.
Posology: 100 mcg selenium daily, short term up to 300 mcg selenium/day (corresponding to 1 ampoule or up to 3 ampoules per injection).
Treatment should continue until the selenium status normalizes (selenium in plasma 80-120 µg/l, in whole blood 100-140 μg/l). Regular testing of the selenium level at appropriate intervals is recommended.
When treating extreme nutritional deficiencies such as systemic inflammatory response syndrome (SIRS)/sepsis can only be achieved by administering higher levels. Doses of selenium (up to 1000 mcg/day per injection, sometimes up to 2000 mcg/day, per injection) one normalization of the selenium status can be achieved (selenium in plasma 80-120 μg/l, in whole blood 100-140 μg/l). Close monitoring of selenium levels is recommended. If values are above normal, the dose should be reduced. The administration of higher doses should be limited to 14 days. The lower toxicity limit is 900 μg/l plasma or 1000 μg/l whole blood.

Symptom: Signs of acute overdose include garlic-like breath odor, tiredness, nausea, diarrhea, and abdominal pain. In chronic overdose, changes in nail and hair growth as well as peripheral polyneuropathies have been observed.
Treatment of overdose: Possible countermeasures include gastric lavage, forced diuresis, or high doses of vitamin C. In the event of an extreme overdose (1,000-10,000 times), the patient can try to eliminate the selenite through dialysis. The use of dimercaprol is not recommended as it increases the toxicity of selenium.

Patients with hypersensitivity to the active substance or to any ingredient of the drug.
Selenium intoxication.

The medicine contains less than 1 mmol sodium (23 mg) per mL ampoule, i.e. it is almost sodium-free.
Effects on Ability to Drive and Use Machines: None.

No restrictions if used as intended.

General disorders and administration site conditions: Frequency not known (frequency cannot be estimated from the available data): After intramuscular administration, pain may occur at the injection site.
"Any adverse drug reactions should be immediately reported to the physician or pharmacist".

When administered parenterally as an addition to infusion solutions, it must be ensured that no non-specific precipitation occurs. It is important to ensure that the pH value does not fall below 7.0 and that no mixture is mixed with reducing agents such as Vitamin C occurs since precipitation of elemental selenium cannot be ruled out. Elemental selenium is insoluble and not bioavailable in aqueous medium. For safety reasons, non-specific precipitation should be avoided after mixing the infusion solution with Selesyn 100 micrograms.

Store below 30°C.
Shelf-Life: 48 months from date of manufacture. Use immediately after opening.

Supplements & Adjuvant Therapy

A12CE02 - sodium selenite ; Belongs to the class of selenium-containing preparations. Used as dietary supplements.