Calciferol (Ergocalciferol)

prevention and treatment of rickets and rickets-like diseases in children,

osteopathies of different origins,

in D-hypovitaminosis in pregnant women,

mineral metabolism disorders (osteoporosis) in women in the postmenopausal (menopause) period,

patients with orthopedic pathology or delayed consolidation of fractures.

prevention and treatment of rickets and rickets-like diseases in children,

osteopathies of different origins,

hypovitaminosis D₂ in pregnant women, patients with orthopedic pathology (osteoporosis) or delayed consolidation of fractures.

Inside, 1 time per day.

Pregnant women are recommended to take daily 400-500 ME/day starting from 30-32 weeks of pregnancy before delivery, if necessary, the daily dose can be increased to 1 thousand ME / day. IU / day.

Full-term children for the prevention of rickets are prescribed from 3 weeks of age for 400-500 ME of vitamin D₂ every day during the first year of life, except in the summer months. The course dose for a year on average is 100-150 thousand ME.

Preterm infants and children in unfavorable living conditions, vitamin D₂ prescribe from 8-10 days of age for 1000 ME daily for a year. The total dose is 200-250 thousand. ME per year.

In the treatment of rickets of the first degree, children are prescribed daily 2500-3000 ME of vitamin D₂ within 45-60 days. In total, 150-200 thousand ME are prescribed for the course of treatment.

In the treatment of rickets of II-III degree, 5-10 thousand ME/day of vitamin D is prescribed for the course of treatment₂ within 45-60 days. The course dose is 250-600 thousand ME.

In case of a relapse of rickets, a second course of treatment is recommended, but not earlier than 2 months after the end of the first course.

In rickets-like diseases, the selection of the therapeutic dose is carried out by the doctor individually for each patient. For the treatment of patients with osteoporosis and orthopedic pathology, it is recommended to take 3-5 thousand ME/day of vitamin D₂ within 30 days, a second course-after 3 months.

In other diseases, vitamin D₂ prescribe in accordance with the doctor's recommendations.

Inside.

Pregnant women are recommended to take the drug starting from 30-32 weeks of pregnancy before delivery daily at 700 ME/day (1 drop).

Full-term children for the prevention of rickets are prescribed from 3 weeks of age for 700 ME of vitamin D₂ (1 drop) every other day for the entire 1st year, except for the summer months. The course dose for a year on average is no more than 150 thousand ME.

Preterm infants and children in unfavorable living conditions, vitamin D₂ assign from 8-10 days of age to 700 ME (1 drop) daily for a year. The total dose — no more than 250-300 thousand. ME per year.

In the treatment of rickets of the first degree, children are given daily 2800 ME (4 drops) of vitamin D₂ within 45-60 days. In total, no more than 150-200 thousand are prescribed for the course of treatment. ME of vitamin D₂.

In the treatment of rickets of II-III degree, 4900-9800 ME (7-14 drops) of vitamin D are prescribed for the course of treatment₂ per day for 60 days. The course dose is no more than 300-600 thousand ME. In case of exacerbation or relapse of rickets, a second course of treatment is recommended, but not earlier than 2 months after the end of the first course.

In rickets-like diseases, the selection of the therapeutic dose is carried out by the doctor individually for each patient. For the treatment of patients with orthopedic pathology (osteoporosis), it is recommended to take 2800-4900 ME (4-7 drops) of vitamin D₂ a day for 30 days, a second course-after 3 months.

hypersensitivity to the components of the drug,

hypercalcemia,

hypervitaminosis D,

renal osteodystrophy with hyperphosphatemia.

With caution: atherosclerosis, old age, pulmonary tuberculosis (active form), sarcoidosis or other granulomatoses, chronic heart failure, hyperphosphatemia, phosphate nephrourolithiasis, chronic renal failure, pregnancy (in women over 35 years of age), lactation, childhood.

hypersensitivity to the components of the drug,

hypercalcemia,

hypervitaminosis D₂, renal osteodystrophy with hyperphosphatemia.

With caution: atherosclerosis, old age (may contribute to the development of atherosclerosis), pulmonary tuberculosis (active form), sarcoidosis or other granulomatosis, chronic heart failure, pregnancy (in women over 35 years of age), lactation, childhood.

Allergic reactions are possible.

Allergic reactions.

Symptoms hypervitaminosis D: early (due to hypercalcemia) — constipation or diarrhea, dryness of the oral mucosa, headache, thirst, pollakiuria, nycturia, polyuria, anorexia, metallic taste in the mouth, nausea, vomiting, extreme fatigue, asthenia, hypercalcemia, hypercalciuria, late — bone pain, turbidity of urine (appearance of hyaline cylinders in the urine, proteinuria, leukocyturia), increased blood pressure, itching, photosensitivity eye, conjunctival hyperemia, arrhythmia, drowsiness, myalgia, nausea, vomiting, pancreatitis, gastralgia, weight loss, rarely — changes in the psyche (up to the development of psychosis) and mood.

Symptoms chronic vitamin D intoxication (when taken for several weeks or months for adults in doses of 20-60 thousand mg). IU/day, children from 2 to 4 thousand IU / day): calcification of soft tissues, kidneys, lungs, blood vessels, arterial hypertension, renal and cardiovascular insufficiency up to a fatal outcome (these effects most often occur when hypercalcemia is associated with hyperphosphatemia), growth disorders in children (long-term administration at a dose of 1.8 thousand mg). IU/day).

Treatment: if signs of hypervitaminosis D appear, it is necessary to cancel the drug, limit the intake of calcium, and prescribe vitamins A, C, and B.

Symptoms hypervitaminosis D₂: early (due to hypercalcemia) - constipation or diarrhea, dryness of the oral mucosa, headache, thirst, pollakiuria, nycturia, polyuria, anorexia, metallic taste in the mouth, nausea, vomiting, unusual fatigue, asthenia, hypercalcemia, hypercalciuria, late — bone pain, turbidity of urine, (appearance of hyaline cylinders in the urine, proteinuria, leukocyturia), increased blood pressure, itching, photosensitivity of the eyes, conjunctival hyperemia, arrhythmia, drowsiness, myalgia, nausea, vomiting, pancreatitis, gastralgia, weight loss, rarely — changes in mood and psyche (up to the development of psychosis).

Symptoms chronic vitamin D intoxication₂ (when taken for several weeks or months for adults in doses of 20-60 thousand mg. IU/day, for children — 2-4 thousand. IU / day): calcification of soft tissues, kidneys, lungs, blood vessels, arterial hypertension, renal and cardiovascular insufficiency up to a fatal outcome (these effects most often occur when joining hypercalcemia/hyperphosphatemia), growth disorders in children (long-term use at a dose of 1.8 thousand mg). IU/day).

Treatment: if signs of hypervitaminosis D appear, it is necessary to cancel the drug, limit the intake of calcium, and prescribe vitamins A, C, and B.

Vitamin D₂ regulates the exchange of calcium and phosphorus in the body, accelerates the absorption of calcium in the intestine, improves the reabsorption of calcium and phosphorus in the kidneys, maintains the necessary level of these elements in the blood, promotes the formation of the bone skeleton in children, as well as the preservation of bone structure. Vitamin D₂ it is also necessary for the manifestation of the physiological action of a number of hormones (TSH and thyrocalcitonin). Vitamin D deficiency₂ in young children, it causes rickets.

Vitamin D₂ regulates the exchange of calcium and phosphorus in the body, accelerates the absorption of calcium in the intestine, improves the reabsorption of calcium and phosphorus in the kidneys, maintains the necessary level of these elements in the blood, promotes the formation of the bone skeleton in children, as well as the preservation of bone structure.

Vitamin D₂ is also necessary to demonstrate the physiological actions of several hormones (thyrotropin and thyrocalcitonin).

Vitamin D deficiency₂ in young children, it causes rickets.

Vitamin D₂ it has a cumulative property.

The toxic effect is weakened by vitamin A, tocopherol, ascorbic acid, pantothenic acid, thiamine, riboflavin, pyridoxine.

Thiazide diuretics, drugs containing calcium, increase the risk of hypercalcemia (require monitoring of the concentration of calcium in the blood).

In hypervitaminosis caused by Calciferol (Ergocalciferol)om, it is possible to increase the action of cardiac glycosides and increase the risk of arrhythmia due to the development of hypercalcemia (it is advisable to adjust the dose of cardiac glycoside). Under the influence of barbiturates (including phenobarbital), phenytoin and primidone, the need for Calciferol (Ergocalciferol)e can significantly increase, which is expressed in an increase in osteomalacia or the severity of rickets (due to the acceleration of the metabolism of Calciferol (Ergocalciferol)a to inactive metabolites due to the induction of microsomal enzymes).

Long-term therapy with the simultaneous use of antacids containing aluminum and magnesium increases their concentration in the blood and the risk of intoxication (especially in the presence of chronic renal failure).

Calcitonin derived etidronate and pamidronate acids, plicamycin, gallium nitrate and corticosteroids reduce the effect.

Colestyramine, colestipol and mineral oils reduce the absorption of fat-soluble vitamins in the gastrointestinal tract and require an increase in their dosage.

Increases the absorption of phosphorus-containing drugs and the risk of hyperphosphatemia.

Concomitant use with other vitamin D analogues increases the risk of hypervitaminosis.

The toxic effect is weakened by vitamin A, vitamin E, ascorbic acid, pantothenic acid, thiamine, riboflavin, pyridoxine.

Thiazide diuretics, drugs containing calcium, increase the risk of hypercalcemia (require monitoring of the concentration of calcium in the blood).

With hypervitaminosis caused by the use of ergocalciferol, it is possible to increase the action of cardiac glycosides and increase the risk of arrhythmia due to the development of hypercalcemia (it is advisable to adjust the dose of cardiac glycosides).

Under the influence of barbiturates (including phenobarbital), phenytoin, primidone, the need for ergocalciferol can significantly increase, which is expressed in an increase in osteomalacia or the severity of rickets (due to the acceleration of the metabolism of ergocalciferol into inactive metabolites due to the induction of microsomal enzymes).

Long-term therapy with the simultaneous use of antacids containing aluminum and magnesium ions increases their concentration in the blood and the risk of intoxication (especially in the presence of chronic renal failure).

Calcitonin derived etidronate and pamidronate acids, plicamycin, gallium nitrate and corticosteroids reduce the effect.

Colestyramine, colestipol and mineral oils reduce the absorption of fat-soluble vitamins in the gastrointestinal tract and require an increase in their dosage.

Increases the absorption of phosphorus-containing drugs and the risk of hyperphosphatemia.

Concomitant use with other vitamin D analogues₂ (especially calcifediol) increases the risk of hypervitaminosis.