Xidifon concentrate for the preparation of solution for oral administration 50 ml

Indications for use

As a means of regulating calcium metabolism in adults and children:

• for urolithiasis and other kidney diseases;
• with hypervitaminosis D;
• with hyperparathyroidism and concomitant interstitial nephritis;
• for the treatment and prevention of osteoporosis;
• as a means of preventing the development of osteopenia and osteoporosis during long-term immobilization of patients with rheumatoid arthritis, increasing bone mass in secondary osteoporosis.

To accelerate the removal from the body of excess heavy metals lead, tin, strontium, silicon and antimony.

In the complex therapy of mild and moderate bronchial asthma in adults with the aim of stabilizing the membranes of immunocompetent cells.

In complex therapy of hormone-dependent bronchial asthma in adults for the prevention of osteoporosis.

Analogues of Xydiphone

The medication does not have a large number of synonyms and substitutes , which is due to the characteristics of the effect of the active substance and its type.

When using analogues, you must first consult with your doctor, since various excipients may be used in medications. Against the background of this feature, some patients experienced serious side effects, and there was complete intolerance to the chosen drug.

Fosamax is prescribed for the treatment of osteoporosis Fosamax

Available in tablet form, it is often prescribed against the background of osteoporosis in women during menopause, and in men with any type of development of this disease. Included in combination therapy in the presence of a malignant tumor that interferes with calcium absorption. Dosages of the active substance are selected individually for each patient, taking into account the complexity of their condition.

Pleostat

A complete analogue of Xydiphon, it is also available in the form of a concentrate for the preparation of a solution for oral use. Pleostat is taken under the same conditions and has the same contraindications. When using both analogues, there is no noticeable significant difference in the occurrence of side effects and their severity.

Directions for use and doses

Xidifon is taken orally 30 minutes before meals, in the form of a solution diluted to 2%, which is prepared by adding 9 parts of distilled or boiled water to 1 part of a base 20% solution (for example, 450 ml of water is added to 50 ml of a 20% solution), the diluted solution is stored in a refrigerator.

Adults and children over 10 years of age are prescribed 300 mg (1 tablespoon) 2-3 times a day.

Children from 3 to 10 years old - 200 mg (1 dessert spoon) 2-3 times a day.

Children under 3 years old - at the rate of 10 mg/kg body weight (1 teaspoon) 2-3 times a day.

• The initial course of treatment is 14 days. In case of crystalluria and the presence of stones in the kidneys, 5-6 courses are carried out with three-week breaks for 1-2 years. To prevent recurrence of stone formation, the drug is prescribed for up to 2-6 months.
• For the treatment and prevention of osteoporosis, Xidifon is used at a dose of 5-7 mg/kg for 2-3 months, after 1-2 months the treatment courses are repeated.
• For trabecular osteoporosis and osteopenia in patients with rheumatoid arthritis, Xidifon is used for at least a year at a rate of 5-10 mg/kg body weight in 2 doses. At the same time, it is recommended to eat foods rich in calcium salts (equivalent to 500 ml of milk), or, if this is not possible for some reason, take calcium gluconate 1.5 g/day.
• In case of chronic intoxication with heavy metals and when living in environmental conditions unfavorable for heavy metals, it is recommended to use Xydiphone in a dose of 10 mg/kg body weight for 7-10 days every month.
• For bronchial asthma, Xidifon is used in complex therapy in adults over 16 years of age for no more than 30 days.

About the use of the drug Xidifon for calcium metabolism disorders

Currently, the need for the use of Xydifon has been proven in the complex treatment of diseases such as calcium nephrolithiasis and other kidney diseases with impaired calcium metabolism (dysmetabolic nephropathy, interstitial nephritis), hypervitaminosis D, hyperparathyroidism, as a means of preventing osteoporosis, immobilization, epilepsy, Recklinghausen's disease , Fahr's disease, dermatomyositis, progressive myositis ossificans and other myositis, with myofascial calcium deposits and atopic bronchial asthma. In addition, Xidifon has proven itself to be an accelerator of the elimination of heavy metal salts from the body in children [5]. The pharmacological properties of Xidifon have been studied in various pathological processes (including hypervitaminosis D and hyperparathyroidism) in humans and in animal experiments. The drug is eliminated from the body in the first 5–6 hours after a single oral dose. Over the next 6 hours, there is a gradual decrease in its excretion. A study of the pharmacokinetics of Xidifon revealed differences depending on the motor activity of patients, their age and the method of drug administration. It has been established that when Xydifon is taken orally, its concentration in the blood and urine increases sharply for a short time (within 1-2 hours), then gradually decreases and after 10-12 hours the drug is not detected in the urine. Absorption from the stomach averages 1–2% of the orally administered dose. Accordingly, a decrease in the concentration of the drug in the urine indicates its therapeutic effect. Xidifon reduces the concentration of ionized calcium and normalizes the level of total calcium in the blood [6]. From a clinical point of view, an extremely important property of Xydifon is its ability to stabilize cell membranes, the so-called membrane-protective properties with normalization of calcium homeostasis at the cellular level. It has been shown that Xidifon, like other diphosphonates, is fixed on the surface of cell membranes and is included in their structure, providing stability and resistance to spontaneous and enzymatic (phospholipase) hydrolysis of the phospholipid component of the membranes. It is the stabilization of membrane structures that is one of the main mechanisms for normalizing calcium homeostasis in cells [7,8]. In the process of searching for means of protection against mitochondrial pathology, an experiment was also conducted confirming the effect of Xydifon on smooth muscle mitochondria (bladder) and on their contractile ability. It has been shown that Xidifon potentiates the energy-dependent accumulation of calcium in mitochondrial fractions, which indicates its positive effect on calcium metabolism in mitochondria and on the contractile activity of smooth muscles [9,10]. As mentioned earlier, Xidifon has a wide range of applications in clinical practice. Let us take a closer look at some diseases in the pathophysiological treatment of which this drug is successfully used. Hyperparathyroidism is an endocrine disease characterized by increased production of the polypeptide hormone parathyrin or parathyroid hormone in the parathyroid glands. Parathyroid hormone is the main mediator of maintaining calcium homeostasis in the body. The secretion of parathyroid hormone is regulated directly by the plasma concentration of ionized calcium, and its action is aimed at increasing the concentration of plasma calcium. In developed countries, primary hyperparathyroidism is considered one of the main endocrinological problems along with diabetes mellitus and thyroid diseases. Since the early 70s of the 20th century, this pathology has ceased to be considered rare thanks to the introduction of systematic laboratory screening and the use of automatic analyzers for calcium levels in the blood [11]. Diffuse hyperplasia of all four glands occurs in 15–20% of patients, and in approximately half of them, as part of hereditary syndromes (in particular, multiple endocrine neoplasia syndrome type I or IIa). Typically, the disease is detected incidentally when hypercalcemia is detected in a patient in the absence of any symptoms [12]. Primary hyperparathyroidism is the most common cause of hypercalcemia. The disease occurs 2–4 times more often in women and affects 0.05–0.1% of the population, reaching 0.2% among hospitalized patients. Among women over 50 years of age, primary hyperparathyroidism is diagnosed in almost every second woman. The prevalence of primary hyperparathyroidism increases with age, but the disease can affect people of all ages, including children. In addition to primary, secondary and tertiary hyperparathyroidism are distinguished. Primary hyperparathyroidism is a disease initially caused by a tumor or hyperplastic change in one or more parathyroid glands, which leads to unregulated hypersecretion of parathyroid hormone and disruption of calcium homeostasis in the body. Secondary hyperparathyroidism is secondary hyperfunction and hyperplasia of the parathyroid glands, occurs with prolonged hypocalcemia (more often with chronic renal failure). Tertiary hyperparathyroidism is the occurrence of an autonomously functioning adenoma of the parathyroid glands against the background of long-existing secondary hyperparathyroidism. The etiology of the disease is unknown in most cases. The pathogenesis of clinical manifestations is multifaceted. It is based on the autonomization of parathyroid hormone production and the lack of feedback control in response to hypercalcemia [12]. The main targets of parathyroid hormone are bones and kidneys. The classic bone lesion observed in this pathology, osteitis fibrosa cystica, is now becoming less common. The most sensitive radiological sign of bone tissue damage is subperiosteal resorption of the middle phalanges of the fingers. An increased level of parathyroid hormone leads to constant resorption of calcium from the bones, which, in turn, can lead to osteopenia. Increased urinary calcium excretion also predisposes to the formation of nephrolithiasis. Other symptoms of hyperparathyroidism are associated with hypercalcemia itself and are not directly related to hyperparathyroidism. They may include muscle weakness, fatigue, hypovolemia, nausea, vomiting and, in extreme cases, lead to hyperosmolar hypercalcemic coma and death. Neuropsychiatric manifestations are the most common and may include depression, anxiety, memory impairment or very subtle disorders that often cannot be accurately characterized by patients. In severe cases, with calcemia exceeding 3 mmol/l, stuporous states and even coma are possible. Elevated calcium concentrations in the blood can increase gastric acid secretion, gastrin production, and contribute to the development of peptic ulcers. The development of gallstones and pancreatitis has also been associated with hyperparathyroidism in some patients. As a laboratory diagnosis, an increased level of intact parathyroid hormone is determined simultaneously with an increased concentration of ionized or total serum calcium, which confirms the diagnosis of hyperparathyroidism [11]. Determination of vitamin D and its metabolites is justified only if hyper- or hypovitaminosis is suspected. Drug therapy involves treating the hypercalcemia itself. The primary goal is to rehydrate patients, which can be achieved by drinking plenty of fluids in uncomplicated cases. In emergency situations, intravenous replenishment of the circulating plasma volume with sodium chloride and the administration of diuretics such as furosemide are used. For the purpose of pathophysiological treatment, the administration of diphosphonates (Xidifon) is used. Usually the effect occurs 4–5 days after the start of therapy. In the group of patients where a more rapid reduction in the level of calcemia is necessary, a synthetic salmon calcitonin preparation can be used. The effect occurs quickly, but after a few days complete refractoriness to this type of therapy develops. Glucocorticoids are also used as first-line drugs, especially in the case of paraneoplastic hypercalcemia, hypervitaminosis A and D. Experience with calcimimetics (a group of drugs that block calcium receptors on parathyroid cells) is promising, although it is not yet sufficient. The radical treatment for hyperparathyroidism is surgery [11]. Another, less common pathology, for the treatment of which Xydifon is successfully used, is hypervitaminosis D. This is a condition that occurs with an overdose of vitamin D or increased individual sensitivity, which is accompanied by the development of the symptom complex D–vitamin intoxication. Among the causes of this pathology are the use of large doses of vitamin D for treatment or prevention; usually the total dose is above 1 million IU. Sometimes hypervitaminosis is caused by small doses, which is explained by increased sensitivity to vitamin D. The pathogenesis is based on the toxic effect of vitamin D on cell membranes, metabolic disorders with the development of hypercalcemia and hypercalciuria, hyperphosphaturia, acidosis, calcification of tissues and internal organs. The clinical picture is characterized by lack of appetite, vomiting, combined with constipation, delayed physical development in children, thirst, and polyuria. The patient is excited, then becomes lethargic, convulsions, increased blood pressure, and slowed pulse may be observed. The leading biochemical signs are hypercalcemia, hypercalciuria. Differential diagnosis must be made with hyperparathyroidism and idiopathic calcinosis. The main treatment measure is to stop taking vitamin D, which leads to an improvement in the condition. In severe cases, especially in children in the first months of life, parenteral administration of an isotonic solution of sodium chloride and glucose, cardiovascular drugs, ascorbic acid and vitamins A, B is indicated; Prednisolone 1 mg/kg is also used for 5–7 days. It is necessary to carry out measures aimed at detoxification, restoration of impaired functions of internal organs, normalization of mineral metabolism and removal of calcium salts from the body. As mentioned above, the pathogenesis of hypervitaminosis D is based on the toxic effect of vitamin D on cell membranes, and therefore the use of the drug Xidifon leads to significant clinical improvement. The prognosis for this pathology depends on the degree of damage to internal organs. In case of intoxication with vitamin D and parathyroid hormone, morphological studies have shown that Xidifon helps accelerate the regeneration processes of damaged kidney tissue [13–15]. Not only the positive effect of the drug was noted, but also a general membrane-stabilizing and anti-inflammatory effect; normalization of serum calcium levels was also observed. A number of mechanisms for the positive action of Xydifon in cases of calcium metabolism disorders in soft tissues have been shown, one of which is the membrane-protective effect of Xydifon and indirect protection of soft tissues from calcification. In addition, in an experiment on animals that lasted for 3 years, the anticarcinogenic effect of Xydifon was confirmed, which since the 80s of the 20th century has been successfully used for malignant bone tumors (metastases) and breast cancer abroad [1,2,16 ]. In addition, Xidifon provides an additional positive effect in dysmetabolic nephropathy and interstitial nephritis, consisting of a moderate anti-inflammatory, analgesic and fibrinolytic effect, which is especially important when associated with infection or a tendency to stone formation [15,17]. As a membrane protector, Xidifon has a powerful inhibitory effect on the release of inflammatory and allergic mediators - leukotrienes and platelet activating factor, reduces the degree of basophil degranulation, increases the content of T-suppressors, reduces the level of immunoglobulin E in plasma and the transmembrane movement of calcium ions in stimulated leukocytes [18]. When treating bronchial asthma, Xidifon improves the ventilation function of the lungs [19]. Many other effects of diphosphonates, in particular Xydifone, have been described. Evidence has been obtained that in animal cells, diphosphonates significantly reduce the effect of mutagens [20–23]. The immunomodulatory effect of bisphosphonates has been sufficiently studied. It has been shown that they have a pronounced tropism for the tissues of the immune system. Under the influence of methylene diphosphonic acid in the immune cells of animals, the level of biosynthesis of DNA, RNA, protein, and the activity of some enzymes of adenosine and AMP metabolism change. On the other hand, methylene diphosphonic acid has virtually no effect on the uptake and metabolism of adenosine in immune cells. It has also been shown that bisphosphonates lead to inhibition of the biosynthesis of antibodies to T-dependent antigens and inhibition of cellular immune responses, which is due to their influence on the functional activity of T cells. It is believed that the biochemical basis of the immunomodulatory action of bisphosphonates is the inhibition of inorganic pyrophosphatase activity in the cell. Apparently, the immunomodulatory effect of Xidifon reflects the summation of their effect on biochemical reactions occurring with the participation of inorganic pyrophosphates in immunocompetent cells, and that this effect is based on the accumulation of diphosphonates in the immune system and the structural similarity between them and inorganic pyrophosphate. Using models of cellular immune response, it has been established that diphosphonates prevent the development of both systemic and local forms of delayed-type hypersensitivity reactions and do not have a cytotoxic effect on immune cells [24,25]. This is the basis for the use of Xydifon in atopic bronchial asthma, and this also partially explains the anti-inflammatory effect in kidney diseases. It has been shown that Xidifon, both in vivo and in vitro, significantly reduces the content of serum and intracellular cholesterol, the proliferative activity of cells, and normalizes the enzymatic spectrum of lysosomes in adipocytes and platelets. Recommendations for the use of Xydifon as an antiatherosclerotic agent are based on this action [26]. Also, in the process of clinical studies, it was proven that, together with the use of Xydifon, daily intake of vitamin E (in physiological doses) is necessary throughout the course of treatment. The initial course of treatment is 14 days. If long-term treatment with Xydifon is necessary, repeat courses are carried out after 1.5–2 months. for years (dermatomyositis, urolithiasis, intoxication with salts of heavy metals, etc.). Xidifon is currently used in the form of a 2% solution. Prescribed at the rate of 10 mg per 1 kg of body weight per dose 30 minutes before meals 1-2 times a day for 2 weeks to 3 months. Contraindications to the use of this drug are hypersensitivity, hypocalcemia, pregnancy, and lactation. It should be used with caution in chronic enterocolitis and renal failure. Thus, Xidifon is a unique drug that regulates calcium metabolism in the body, which currently occupies a strong place in the treatment of various pathologies. Literature 1. Arkhipova O.G., Yuryeva E.A., Dyatlova N.M. Prospects for the use of complexones in medicine. Journal of the All-Union Chemical Institute named after. DI. Mendeleeva 1984; 29:3:316–320. 2. Veltishchev Yu.E., Yuryeva E.A., Arkhipova O.G. Some prospects for the clinical study of the therapeutic use of phosphonic compounds. Vopr Med Chem 1975; 5:451–461. 3. Veltishchev Yu.E., Yuryeva E.A., Kudrin A.N. Biologically active phosphonic acids and their derivatives. Chem Pharm J. 1983; 17:3:282–290. 4. Fleisch H. Bisphosphonates in bone disease. New York, London 1997; 184. 5. Yuryeva E.A., Alekseeva N.V. Xidifon is a calcium-regulating drug. Russian Bulletin of Perinatology and Pediatrics, N4–1999, pp. 45–49. 6. Veltishchev Yu.E. (ed.) Xidifon is a new means of regulating calcium metabolism in the body in pathology. Dep. VNIIMI N 72–13–85 1985; 180. 7. Veltishchev Yu.E. Problems of membrane pathology in pediatrics. Vopro okhr mat i det 1981; 27:4:3–9. 8. Veltishchev Yu.E., Kapustyan A.M. Problems of childhood pathology in terms of disruption of the structure and function of biological membranes. Scientific review of VNIIMI. M 1982; 82. 9. Marchenko S.N., Burdyga F.V., Babich L.G., Yuryeva E.A. The effect of xydiphone and AMOC on Ca++ transport in subcellular fractions of smooth muscle and its contractility. In: Multiorgan membrane pathology. Ed. Yu.E. Veltishchev et al. M 1991; 181–191. 10. Yurieva EA, Osmanov JM, Raba GP, Matkovskaya TA Pharmacological characteristics of xydiphone. Bone 1996; 17: 6: 618. 11. Cherenko S.M. Primary hyperparathyroidism: modern view on prevalence, diagnosis and surgical treatment. Health of Ukraine 2007; 22/1; on pp. 50–53. 12. Zahrani AAI, Levine M. Primary hyperparathyroidism. Lancet 1997;349:1233–1238. 13. Yuryeva E.A., Simanina L.V., Alekseeva N.V., Vozdvizhenskaya E.S. Xidiphone as a means of pharmacological diagnosis in urolithiasis. In Sat.: a new helating agent - Xidiphone. Ed. Yu.E. Veltishchev et al. M 1990; 52–57. 14. Yuryeva E.A., Vozdvizhenskaya E.S., Alekseeva N.V., Simanina L.V. Clinical aspects of dimitabolic nephropathy, interstitial nephritis, urolithiasis in calcifilaxia. Pediatrics 1989; 1: 42–48. 15. Yuryeva E.A., Dunaeva I.P., Kulakova T.I., Korovina N.A. The effectiveness of xidiphone, depending on the method of its use in dispmetabolic nephropathy and interstitial nephritis. In Sat.: a new helating agent - Xidiphone. M 1990; 62–70. 16, Chalov MB, Arkhipova O.G., Krinitskaya L.V., Alekseeva N.V. The anticandine activity of xidiphone in experimental animals. In Sat.: a new helating agent - Xidiphone. Ed. Yu.E. Veltishchev et al. M 1990; 70–74. 17. Yuryeva E.A., Dunaeva I.P., Kulakova G.I., Korovina N.A. Dimitabolic nephropathy and interstitial nephritis combined with polyorgan membrane pathology in children. In Sat.: Polorgan membrane pathology. M 1991; 77–83. 18. Svyatkina O.P., Round B.I. A change in the release of leukotrienes in children with atopic bronchial asthma. Department VNIIMI AMN USSR. N 10328. M 1986; 2. 19. Svyatkina O.P. Leukotrienes are a new class of highly active biological substances. Successes of modern biology 1984; 99: 3: 413–425. 20. Veltishchev Yu.E., Seleznev Yu.S. Antimutagenic effect of xidiphone. Genetics 1978; 14: 1276–1278. 21. Veltishchev Yu.E., Yuryeva E.A., Dyatlova N.M. Helating agents in pharmacology, toxicology and therapy. In Sat.: a new helating agent - Xidiphone. Ed. Yu.E. Veltishchev. M 1990; 2–12. 22. Veltishchev Yu.E., Yuryeva E.A., Alekseeva N.V. Polyorgan membrane pathology as a result of oxidative stress in the body. In Sat.: Polorgan membrane pathology. Ed. Yu.E. Veltishchev. M 1990; 2–13. 23. Ablev S.K., Dyatlova N.M., Krinitskaya L.V., Chalov M.B. The antimutagenic activity of xidiphone in the experiment. In Sat.: a new helating agent - Xidiphone. Ed. Yu.E. Veltishchev et al. M 1990; 74–78. 24. Komissarenko S.V., Fomovskaya G.N., Penesina O.P., Borisova A.N. Bisphosphone complexes in immunjective molecules for diagnosing receptors on the surface of the cell. In Sat.: a new helating agent - Xidiphone. Ed. Yu.E. Veltishchev et al. M 1990; 28–29. 25. Fomovskaya G.N., Komissarenko S.V. The biochemical mechanisms of the immunotropic effects of methylenebospherfospherent acid. In Sat.: a new helating agent - Xidiphone. Ed. Yu.E. Veltishchev et al. M 1990; 24–28. 26. Knyazev Yu.A., Turkina T.I., Yuryeva Yu.A. The hypocholesterolemic effect of xidiphone. VOPR honey chem 1983; 29: 72–74.

How to replace the Xydiphone solution?

An analogue of a domestic drug should only be selected by a specialist. The following drugs have similar medicinal properties:

1. "Ostalon" (tablets).
2. Fosamax (tablets).
3. "Aclasta" (injection solution).
4. "Alendronic acid" (tablets).
5. "Alendronate" (tablets).
6. "Bonviva" (tablets and solution for intravenous administration).
7. "Zometa" (solution for infusion).

Most existing substitutes are expensive. However, you can choose more affordable medications to treat disorders of calcium absorption in the system.

"Xidifon": description

The drug "Xidifon" is available in the form of a concentrated solution for internal use. The main task of the medication is to regulate the process of calcium metabolism in the body. The solution not only prevents calcium deficiency, but also promotes the proper absorption of this substance.

The drug is a combination of potassium and sodium salts of etidronic acid, which can normalize the proper absorption of calcium by bone tissue. The substance also prevents the deposition of trace elements in soft tissues, which can lead to the development of severe pathologies.

100 ml of solution contains 20 mg of the active substance – etidronic acid. Purified water and sodium hydroxide are used as auxiliary components. The manufacturer produces the medicine in glass bottles of 50 and 100 ml. Finding a structural analogue of Xydiphone is quite difficult. Therefore, doctors prefer to prescribe medications to patients that have the same therapeutic effect and have similar indications for use.

Similar drugs:

• Vigantol Oral solution
• Videchol Substance-powder
• Veprena Nasal Spray

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** Attention! The information presented in this medication guide is intended for medical professionals and should not be used as a basis for self-medication. The description of the drug Xidifon is provided for informational purposes and is not intended for prescribing treatment without the participation of a doctor. Patients need to consult a specialist!

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