Instructions for use redoxan
Indications for use
Hypo-and avitaminosis C, as well as conditions of increased demand for ascorbic acid – a period of artificial feeding and intensive growth, unbalanced diet, parenteral nutrition, hard work, a period of recuperation after severe illness, scurvy, alcoholism, burns, prolonged hypothermia, prolonged fever, hyperthyroidism, chronic infections, GI diseases (persistent diarrhea, small bowel resection, peptic ulcer, gastrectomy), smoking, prolonged stress, postoperative period, injuries, tuberculosis, pregnancy (especially multiple pregnancies, with nicotine or drug addiction), lactation.
Chronic intoxication with Fe drugs.
In laboratory practice: for erythrocyte labeling (together with sodium chromate Cr51).
Redoxan applies, drops for intravenous administration, lyophilisate for preparation of solution for intravenous and intramuscular injection, powder for preparation of solution for intravenous administration, solution for intravenous and intramuscular injection
Hypersensitivity. Diabetes mellitus, glucose-6-phosphate dehydrogenase deficiency, hemochromatosis, sideroblast anemia, thalassemia, hyperoxaluria, oxalosis, renal stone disease.
How to use: the dosage and course of treatment.
Inside, after a meal.
For prophylaxis of Hypovitaminosis C: to adults – 50-100 mg/day, to children – 25-75 mg/day, during pregnancy and lactation – 300 mg/day for 10-15 days; further 100 mg/day.
For therapeutic purposes: children – 50-100 mg 2-3 times a day, adults – 50-100 mg 3-5 times a day for 2 weeks.
Powder is used for making drinks – about 1 g (1/3 teaspoon) per 1 liter of water (juice).
The dose is 50-150 mg (1-3 ml of 5% solution) by injection, in case of poisoning – up to 3 g (60 ml); maximum single dose is 200 mg, daily dose – 1 g; for children – 50-100 mg/day.
Vitamin, has a metabolic effect, is not formed in the body, and comes only with food. Participates in the regulation of redox processes, carbohydrate metabolism, blood coagulation, tissue regeneration, increases the body’s resistance to infection, reduces vascular permeability, reduces the need for vitamins B1, B2, A, E, folic acid, pantothenic acid.
Participates in metabolism of phenylalanine, tyrosine, folic acid, norepinephrine, histamine, Fe, carbohydrate utilization, synthesis of lipids, proteins, carnitine, immune reactions, serotonin hydroxylation, increases absorption of non-hemin Fe.
It has anti-aggregant and pronounced antioxidant properties.
Regulates H+ transport in many biochemical reactions, improves glucose utilization in the tricarboxylic acid cycle, participates in tetrahydrofolic acid formation and tissue regeneration, synthesis of steroid hormones, collagen, procollagen.
Supports colloidal state of intercellular substance and normal capillary permeability (inhibits hyaluronidase).
Activates proteolytic enzymes, participates in the metabolism of aromatic amino acids, pigments and cholesterol, promotes the accumulation of glycogen in the liver. By activating respiratory enzymes in the liver, it enhances its detoxifying and protein-forming functions and increases the synthesis of prothrombin.
Improves bile secretion, restores external secretory function of the pancreas and thyroid hormone.
Regulates immunological responses (activates the synthesis of antibodies, C3 component of complement, interferon), promotes phagocytosis, increases the body’s resistance to infection.
It inhibits the release and accelerates the degradation of histamine, inhibits the formation of Pg and other mediators of inflammation and allergic reactions.
In low doses (150-250 mg/day orally) it improves complexing function of deferoxamine in chronic intoxication with Fe drugs, which leads to increased excretion of the latter.
CNS disorders: dizziness and fatigue when administered intravenously.
Digestive system: when administered orally – irritation of the gastrointestinal mucosa.
Allergic reactions: skin rash, skin hyperemia.
Laboratory parameters: thrombocytosis, hyperprothrombinemia, erythropenia, neutrophilic leukocytosis, hypokalemia.
Intensive consumption of chewable tablets or ingestion of oral forms may cause damage to dental enamel.Overdose. Symptoms: In long-term use of large doses (more than 1 g) – headache, increased CNS excitability, insomnia, nausea, vomiting, diarrhea, hyperacidic gastritis, ulceration of the mucosa of the gastrointestinal tract, inhibition of pancreatic insular apparatus function (hyperglycemia, glucosuria), hyperoxaluria, nephrolithiasis (from calcium oxalate), damage to the glomerular apparatus of the kidneys, moderate pollakiuria (when taking a dose over 600 mg/day).
Reduced capillary permeability (possible deterioration of tissue trophism, increased BP, hypercoagulation, development of microangiopathies.
When administered intravenously in high doses, there is a risk of abortion (due to estrogenemia) and erythrocyte hemolysis.
Foods rich in ascorbic acid: citrus fruits, herbs, vegetables (peppers, broccoli, cabbage, tomatoes, potatoes). During storage (including long-term freezing, drying, salting, pickling), cooking (especially in copper cookware), chopping vegetables and fruits in salads, making mashed potatoes is a partial destruction of ascorbic acid (at temperature treatment – up to 30-50%).
Due to the stimulating effect of ascorbic acid on the synthesis of corticosteroid hormones it is necessary to monitor renal function and BP.
Long-term use of high doses may suppress pancreatic insulatory apparatus function, so it should be regularly monitored during treatment.
In patients with elevated iron content in the body ascorbic acid should be used in minimal doses.
Currently considered unproven effectiveness of ascorbic acid for the prevention of cardiovascular diseases and some types of malignant tumors.
Ascorbic acid is not recommended for use in pyorrhea, infectious gum diseases, hemorrhagic phenomena, hematuria, hemorrhage in the retina, immune system disorders, depression not related to vitamin C deficiency.
The drug is considered ineffective in the treatment of anemia, vulgar acne, bronchial asthma, infertility, atherosclerosis, peptic ulcer, tuberculosis, schizophrenia, dysentery, collagenosis, skin ulcers, hay fever, fractures, drug intoxication, general hypothermia, to prevent thrombosis.
Prescribing ascorbic acid to patients with rapidly proliferating and intensely metastatic tumors may aggravate the course of the process.
As a reducing agent ascorbic acid can distort the results of various laboratory tests (blood glucose, bilirubin, activity of “liver” transaminases and LDH).
The minimum daily requirement of ascorbic acid in the II-III trimesters of pregnancy is about 60 mg. It should be borne in mind that the fetus can adapt to high doses of ascorbic acid taken by a pregnant woman, and then the newborn may develop a “withdrawal” syndrome.
The minimum daily requirement during lactation is 80 mg. A mother’s diet containing an adequate amount of ascorbic acid is sufficient to prevent deficiency in the infant. Theoretically there is a danger to the child when the mother uses high doses of ascorbic acid (it is recommended not to exceed the maximum daily requirement of ascorbic acid by the nursing mother).
Increases the blood concentration of benzylpenicillin and tetracyclines; at a dose of 1 g / day increases the bioavailability of ethinylestradiol (including those included in oral contraceptives).
Improves intestinal absorption of Fe preparations (converts trivalent iron to divalent iron); may increase iron excretion in concomitant use with deferoxamine.
Reduces the effectiveness of heparin and indirect anticoagulants.
Asc, oral contraceptives, fresh juices and alkaline drinking reduce absorption and assimilation.
When concomitant use with ASA, urinary excretion of ascorbic acid is increased and excretion of ASA is reduced.
ASA reduces absorption of ascorbic acid by about 30%.
Increases the risk of crystalluria during treatment with salicylates and short-acting sulfonamides, slows down renal excretion of acids, increases excretion of drugs that are alkaline (including alkaloids), reduces the blood concentration of oral contraceptives.
Increases total clearance of ethanol, which in turn reduces the concentration of ascorbic acid in the body.
Quinoline drugs, CaCl2, salicylates, GCS in long-term use deplete ascorbic acid.
With concomitant use reduces the chronotropic effect of isoprenaline.
Long-term use or use in high doses may disrupt disulfiram-ethanol interaction.
In high doses increases excretion of mexiletine by the kidneys.
Barbiturates and primidone increase urinary excretion of ascorbic acid.
Reduces the therapeutic effect of antipsychotic drugs (neuroleptics) – phenothiazine derivatives, channel reabsorption of amphetamine and tricyclic antidepressants.
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