Pharmacological properties of the drug Teraflex Advance
Chondroitin sulfate is a high molecular weight mucopolysaccharide that takes part in the construction of cartilage tissue. Reduces the activity of enzymes that destroy articular cartilage and stimulates the regeneration of the latter. In the early stages of the inflammatory process, chondroitin sulfate reduces its activity and thus slows down the degeneration of cartilage tissue. Eliminates pain, improves joint function, reduces the need for NSAIDs in patients with osteoarthritis of the knee and hip joints. Glucosamine sulfate has chondroprotective properties, reduces the deficiency of glycosamines in the body, and takes part in the biosynthesis of proteoglycans and hyaluronic acid. Having an affinity for cartilage tissue, glucosamine initiates the process of sulfur fixation during the synthesis of chondroitinsulfuric acid. Glucosamine sulfate selectively acts on articular cartilage, is a specific substrate and stimulator of the synthesis of hyaluronic acid and proteoglycans, inhibits the formation of superoxide radicals and enzymes that cause damage to cartilage tissue (collagenase and phospholipase); prevents disruption of glycosaminoglycan biosynthesis induced by NSAIDs and the destructive effect of glucocorticoids on chondrocytes. Ibuprofen has analgesic, anti-inflammatory, and antipyretic effects. The mechanism of action of ibuprofen occurs due to the selective blocking of cyclooxygenase (COX-1 and -2), the main enzyme in the metabolism of arachidonic acid, which leads to a decrease in the synthesis of prostaglandins. Reduces morning stiffness of joints, helps increase range of motion in joints and spine. Pharmacokinetics. Absorption: after a single oral dose of the drug in an average therapeutic dose, the maximum concentration of chondroitin sulfate in the blood plasma is achieved after 3-4 hours, in the synovial fluid - after 4-5 hours. Bioavailability of the drug is 13%. Excretion is carried out mainly by the kidneys within 24 hours. 90% of glucosamine taken enterally is absorbed in the intestine. Over 25% of the dose taken penetrates from the blood plasma into the cartilage tissue and synovial membranes of the joints. In the liver, part of the drug is metabolized to form urea, carbon dioxide and water. The bioavailability of glucosamine is 25% due to primary passage through the liver. The maximum concentration of glucosamine is determined in articular cartilage, liver and kidneys. About 30% of the dose taken persists for a long time in bone and muscle tissue. It is excreted primarily in urine unchanged, and partially in feces. The half-life is 68 hours. Ibuprofen, when administered orally, is almost completely absorbed from the gastrointestinal tract. Eating food at the same time slows down the rate of absorption. Metabolized in the liver (up to 90%). The half-life is 2–3 hours; 80% of the dose taken is excreted in the urine, mainly in the form of metabolites.
TERAFFLEX ADVANCE (capsules)
But now I can’t find it in the pharmacy, I regret that I didn’t immediately take several packages.
Who knew? Review: Cooling body gel-balm Flora-Pharm “Sabelnik” mint - Real relief. After many of my experiments, my son convinced me and insisted on taking the pills, especially since his friends had positive experiences. Initially, I wanted to buy Chondroxide, but as luck would have it, it was not available in nearby pharmacies. And on the advice of the pharmacy pharmacist, Teraflex, advertised on TV screens, was purchased, but with the addition of the word “Advance”.
For me, the drug was, of course, a little expensive, but my son’s wife convinced me that the same chondroitin sulfate was present in the composition and Teraflex Advance was purchased.
The rather large box with a bottle for capsules contained a lot of information. Everything was included here: from composition and indications for use to contraindications.
The drug Advance differs from the usual Theraflex in the presence of ibuprofen, which enhances the effect of the other two components of the drug and serves as a pain reliever.
The drug Teraflex Advance is a potent medicine used in special cases to relieve pain. And naturally, as a potent drug, it has a “heap” of contraindications.
The manufacturer, which is Sagmel, Inc., Chicago, USA, honestly warns about this in its instructions, which naturally were in the box.
It was especially vivid in my memory that this drug can only be used for ten days without consulting a doctor, and then only if there are no side effects from taking the medicine, and they are also described in detail in the instructions.
There is a protective film on the lid of the jar, and under the lid there is another protection made of glued thin cardboard with the drug logo.
Inside there are 60 blue-white gelatin soft capsules with the name of the drug.
The capsules are easy to swallow with a little water. They contain a light powder, almost no taste. I did not observe any side effects, so I drank all 60 capsules, after consulting with my doctor, two in the morning and in the evening. All this took fifteen days.
My doctor approved of my choice and explained to me that when taking the drug, there is no need to take other pain medications, since ibuprofen successfully copes with this task.
He also explained that after the first dose of the drug it is necessary to take a break. If necessary, you can repeat taking the drug after a month or two.
I was satisfied with the results of taking the drug.
I repeat that I had no side effects, all my organs peacefully accepted all the components of the drug and responded to them with gratitude. The debilitating, acute pain in my knees has stopped; I have already forgotten to fix my knee with an elastic bandage several times. Joint mobility has improved.
And if there are side effects and contraindications, the manufacturer claims that this drug can be taken by children from the age of twelve, since the drug is taken not only for osteochondrosis of the spine, arthrosis of large bones, but also for the purpose of rehabilitation after fractures or joint surgeries.
I don’t know about anyone, but the drug helped me and I will recommend it.
Special instructions for the use of the drug Teraflex Advance
Do not exceed the recommended dose and duration of use. There are no clinical data regarding the effectiveness and safety of the drug in children under 12 years of age, during pregnancy and lactation. In patients with concomitant liver or kidney diseases, monitoring of liver and kidney functions and hemograms is recommended at the beginning of treatment. Drinking alcohol is not recommended during treatment with Theraflex Advance. Taking the drug does not affect the ability to drive vehicles.
Teraflex Advance, 30 pcs., 250 mg+100 mg+200 mg, capsules
Inducers of microsomal oxidation (phenytoin, ethanol, barbiturates, rifampicin, phenylbutazone, tricyclic antidepressants) increase the production of hydroxylated active metabolites of ibuprofen, increasing the risk of severe hepatotoxic reactions.
Microsomal oxidation inhibitors reduce the risk of hepatotoxicity.
Reduces the hypotensive activity of vasodilators (including CCBs and ACE inhibitors), natriuretic and diuretic activity - furosemide and hydrochlorothiazide.
Reduces the effectiveness of uricosuric drugs, enhances the effect of indirect anticoagulants, antiplatelet agents, fibrinolytics (increasing the risk of hemorrhagic complications), ulcerogenic effect with bleeding of corticosteroids, NSAIDs, colchicine, estrogens, ethanol; enhances the effect of oral hypoglycemic drugs and insulin.
Antacids and cholestyramine reduce the absorption of ibuprofen.
Increases the blood concentration of digoxin, lithium and methotrexate.
Caffeine enhances the analgesic effect.
When administered simultaneously, ibuprofen reduces the anti-inflammatory and antiplatelet effect of acetylsalicylic acid (an increase in the incidence of acute coronary insufficiency in patients receiving small doses of acetylsalicylic acid as an antiplatelet agent is possible after starting ibuprofen).
The simultaneous use of drugs containing glucosamine and coumarin anticoagulants (for example, warfarin) can lead to an increase in INR and the risk of bleeding; it is necessary to monitor blood coagulation parameters.
When prescribed simultaneously with anticoagulant and thrombolytic drugs (alteplase, streptokinase, urokinase), the risk of bleeding increases.
Cefamandole, cefoperazone, cefotetan, valproic acid, plicamycin increase the incidence of hypoprothrombinemia.
Myelotoxic drugs increase the manifestations of hematotoxicity.
Cyclosporine and gold preparations enhance the effect of ibuprofen on the synthesis of PG in the kidneys, which is manifested by increased nephrotoxicity.
Ibuprofen increases the plasma concentration of cyclosporine and the likelihood of developing its hepatotoxic effects.
Drugs that block tubular secretion reduce excretion and increase plasma concentrations of ibuprofen.
Due to the glucosamine content in the drug, the effectiveness of hypoglycemic drugs, doxorubicin, teniposide, and etoposide may be reduced.
Glucosamine increases the absorption of tetracyclines and reduces the effect of semisynthetic penicillins and chloramphenicol.
Co-administration with potassium-sparing diuretics increases the risk of hyperkalemia.
NSAIDs may reduce the effect of mifepristone.
Concomitant use of NSAIDs and tacrolimus may increase the risk of nephrotoxicity.
Co-administration of zidovudine increases the risk of hematological toxicity of NSAIDs.
Concomitant use of quinolones and NSAIDs increases the risk of seizures.
The use of Teraflex in the complex therapy of osteoarthritis. A neurologist's view of the problem
According to modern concepts, OA is based on many endogenous and exogenous factors. The former respectively include age, gender, developmental defects, hereditary predisposition, and the latter – injuries, professional activity, sports activity and excess body weight. Since many risk factors are not modifiable, OA tends to progress to disease progression [1,4]. There are 2 main forms of OA: primary (localized or generalized) and secondary (post-traumatic, caused by congenital, metabolic, endocrine and a number of other diseases) [9,12]. The key pathogenetic mechanism of osteoarthritis is dystrophic changes in articular cartilage and its premature wear. Cartilage is a type of connective tissue and is a rigidly organized spatial structure of non-cellular matrix and cellular elements that covers the articular surfaces of the bones included in the articulation and provides their “soft” biomechanics due to shock absorption and smooth sliding relative to each other. This is one of the most vulnerable places of the musculoskeletal system (MSA). In the USA alone, about 40 million people are annually registered with diseases of the musculoskeletal system such as arthrosis, arthritis, tendovaginitis and bursitis. If we talk about osteoarthritis, its causes are dominated by severe simultaneous trauma with bruises, fractures, dislocations and/or damage to the ligamentous apparatus of the joint, or repeated microtrauma to the joint. Examples include arthrosis of the knee joints in miners and football players, elbow and shoulder joints in those working with jackhammers, ankle joints in ballerinas, and arm joints in boxers. OA has a significant prevalence, especially in older age groups, where its frequency exceeds 50% [20]. According to epidemiological data, 20 million adults in the United States have OA diagnosed by doctors [12]. The importance of the treatment of osteoarthritis is due not only to its high prevalence, but also to the social problems that the disease causes in the patient: a sharp decrease in physical activity leads to a pronounced decrease in the quality of life, social maladaptation, loss of ability to work, and in advanced cases, the ability to self-care. In addition, the trend of population aging leads to the fact that the number of patients with osteoarthritis is increasing year by year. Osteoarthritis after 60 years (as an age-related phenomenon) is found in every second person. However, metabolic and circulatory disorders in the extremities, endocrine disorders (for example, diabetes mellitus, thyroid diseases, menopause, genetic disorders) cause its appearance at a much earlier age. Visits to outpatient clinics for diseases of the musculoskeletal system account for up to 10% of all visits. The economic costs of it in Western countries are estimated at 1.5% of GDP. The noncellular matrix is rich in proteoglycans (glycosaminoglycans) glucosamine and chondroitin. In structure, cartilage is similar to a sponge, absorbing in a relaxed state and squeezing the proteoglycan phase of the matrix into the articular cavity under load. Under physiological conditions, renewal of matrix structures due to the absence of vessels in it is supported by active exchange with intra-articular synovial fluid, which contains all the components necessary for this. Intra-articular synovial fluid simultaneously acts as a “lubricant” for the moving parts of the joint. The ability of cartilage to withstand high dynamic and static loads is a function of the structure of the matrix and its high-quality self-renewal; in this case, the high concentration of proteoglycans in the matrix and synovial fluid plays an exceptional role. Any pathological phenomena in the joints is associated with dystrophic (in milder cases) and inflammatory (in more severe cases) changes in cartilage tissue and intra-articular synovial fluid, leading to degradation of the matrix. The cartilage loses its elasticity and continuity, thins unevenly, and deep cracks form in it. The growth of cartilage tissue along the edges, which do not bear physical load, causes joint deformation. As the process progresses, these phenomena intensify, and more and more new joints are involved. In the modern treatment regimen for osteoarthritis and other joint diseases, an important place is given to chondroprotectors. Along with nonsteroidal anti-inflammatory drugs (NSAIDs), they are the basis of the therapeutic approach in patients with osteoarthritis. The action of these drugs is based on an attempt to influence the composition of the synovial fluid. The fact is that with the development of osteoarthritis, clusters of pathological chondrocytes contribute to the production of inferior basic substance of cartilage tissue, which becomes partially depolymerized, with a reduced content of proteoglycans. The content of the latter determines the “lubricating” properties of the joint fluid, which is “squeezed out” from the cartilage matrix when the mechanical loads on the joint increase. Defective synovial fluid is no longer able to qualitatively support the participation of cartilage in articular biomechanics. Thus, the main link in the pathogenesis of degenerative changes in joints is a change in the quality and deficiency of proteoglycans, which consists in the depolymerization of protein-saccharide complexes with the formation of smaller compounds that leave the cartilage. At the same time, the function of chondrocytes is also impaired, they synthesize less stable proteoglycans, and a loss of physiological properties of cartilage develops, which is accompanied by the formation of erosions and cracks in the cartilage. At the same time, the amount of hyaluronic acid in the synovial fluid decreases, which is an important factor in chondroprotection. Drugs with chondroprotective properties are conventionally divided into three subgroups: drugs - mucopolysaccharides (a type of replacement therapy), stimulators of proteoglycan synthesis and others, including combination drugs. The main chondroprotectors are glucosamine and chondroitin sulfate. Natural components of articular cartilage, they are part of the proteoglycans of cartilage tissue. Glucosamine and chondroitin sulfate have been used in the treatment of osteoarthritis and related diseases since the 1980s. They are used as natural metabolites that can have a protective effect on cartilage and ensure the regeneration of the reparative capabilities of chondrocytes. Currently, a significant scientific base has been accumulated, represented by dozens of controlled studies with a high level of evidence 1A–1B, according to the American College of Rheumatology (ACR) 2000, 2005 [3,9]. Stimulators of proteoglycan synthesis are represented by glucosamine monosulfate. Glucosamine monosulfate is a substrate for the synthesis of proteoglycans by chondrocytes, participates in the synthesis of hyaluronic acid (a substance that ensures the viscosity of intra-articular fluid), and also inhibits the activity of metalloproteinases (collagenase, phospholipase). Thus, the drug has a double effect - anti-inflammatory and chondroprotective. According to available data obtained from randomized multicenter studies, 1500 mg of glucosamine sulfate per day improved the condition of patients during monotherapy, while in cases where the disease occurred with an unexpressed inflammatory component, the effectiveness of glucosamine sulfate was not inferior to that of NSAID therapy. Additionally, data have been obtained to support the presence of an additive effect with the combined use of glucosamine sulfate and NSAIDs. One of the factors determining additivity is the leveling of the adverse effects of NSAIDs on the structure of cartilage. Taking into account compliance with treatment, modern chondroprotective drugs taken enterally are certainly more preferable (glucosaminoglycans generally have high bioavailability and selectively accumulate in the synovial fluid). Taking into account the duration of use of chondroprotectors, enteral forms should be considered significantly more convenient than such “classical” drugs as rumalon and arteparon. Another feature of Rumalon that limits its use is the inappropriateness of prescribing this drug in the presence of an active inflammatory component - Rumalon can enhance the inflammatory response. Glucosamine is an aminomonosaccharide; in the body it is used by chondrocytes as a starting material for the synthesis of proteoglycans, glycosaminoglycans and hyaluronic acid. When taken orally, glucosamine is well absorbed (glucosamine sulfate up to 80%, glucosamine hydrochloride up to 95% due to better solubility); after passing through the liver, about 20–25% of the drug enters the blood. Radioisotope studies demonstrate a clear affinity of glucosamine for joint tissues. About 30% of the administered drug persists for a long time in the connective tissue. Numerous studies of the pharmacological effects of glucosamine have established a beneficial effect on cartilage metabolism - enhancing anabolic and weakening catabolic processes. Glucosamine stimulated the synthesis of proteoglycans and collagen, increased the production of extracellular matrix components, while the properties of glycosaminoglycans and proteoglycans (according to chromatographic analysis) were close to physiological. Glucosamine stimulated the incorporation of 35S4 (a marker of glycosaminoglycan synthesis) into chondrocytes and enhanced the synthesis of glycosaminoglycans in cell culture, and also stimulated in vitro and in vivo the uptake of 35S4 and 3H-proline by articular cartilage. An increase in the synthetic activity of chondrocytes was accompanied by inhibition of chondrolysis due to inhibition of the activity of chondrolytic proteinases (collagenases, etc.). The drug prevented the damaging effects of dexamethasone and some NSAIDs on chondrocytes and the matrix. In these cases, it had a chondroprotective and osteotropic effect, contributed to the normalization of the content of total chondroitin sulfates and alkaline phosphatase activity. Glucosamine exhibits moderate anti-inflammatory effects in various models of inflammation. It is not associated with suppression of prostaglandin synthesis, but is realized through antioxidant activity (by blocking the formation of superoxide radicals) and suppression of the activity of lysosomal enzymes. It has also been established that there is no toxicity or severe side effects of glucosamine, as well as clinical, biochemical or hematological changes with long-term use. Cases of mild side effects, often transient without stopping the drug, were at the placebo level and amounted to about 7% (1–16%) - mild nausea, dizziness, loose stools, etc. In most short-term (4-6 weeks) clinical studies, the effectiveness of glucosamine in doses of 800-1500 mg/day in patients with osteoarthritis exceeded that of placebo and was equivalent to the effectiveness of ibuprofen and diclofenac. Glucosamine was somewhat inferior to NSAIDs in terms of the speed of onset of analgesic and anti-inflammatory effects, but had a clear aftereffect. A noticeable improvement in clinical symptoms appeared 2–3 weeks after the start of treatment, with the effect maintaining for a month or more after discontinuation of treatment, which allows for intermittent courses of treatment. In long-term studies, when therapy with glucosamine at a dose of 1500 mg/day in patients with osteoarthritis continued for 1–3 years, good and excellent results were obtained in 50–60% of patients, satisfactory – in 25–30% of patients. It was noted that in order to clearly assess the results of treatment, glucosamine should be taken for at least 6–12 weeks, which is understandable given the characteristics of the blood supply to the joints and the rate of metabolism in the joint tissues. The group of mucopolysaccharide drugs includes chondroitin sulfate (CS). Chondroitin sulfate is formed in the body from glucosamine; its molecule is 100–200 times larger than its predecessor. The polyanionic molecule chondroitin sulfate is an integral part of the aggrecan structure and is responsible for the physicochemical properties of cartilage. In addition, chondroitin sulfate serves as the basis for the synthesis of hyaluronic acid, which provides lubrication necessary for the functioning of joints. In patients with osteoarthritis, the metabolism of chondroitin sulfate is impaired, the concentration of cholesterol in the synovial fluid is reduced, clusters of pathological chondrocytes produce defective basic substance of cartilage tissue. Pharmacokinetic studies have shown that when taken orally, the bioavailability of the drug is 13–15% (due to the significant size of the molecule). Other studies have found that both the complete form of the drug and its components formed as a result of degradation under the influence of intestinal digestive enzymes are present in the blood. In vivo and in vitro studies concerning the metabolism of externally administered chondroitin sulfate have shown that the drug penetrates the matrix of human chondrocytes without changing the quality of the proteoglycans they produce. Chondroitin sulfate stimulates the synthesis of hyaluronic acid and proteoglycans and inhibits the action of proteolytic enzymes, significantly reduces the activity of chondroitinase in synovial fluid. Chondroitin sulfate has a pronounced tropism for tissues rich in glycosaminoglycans and, in particular, for articular cartilage. It was noted that chondroitin sulfate is also involved in the process of bone mineralization, regulating calcium balance in vitro and promoting ossification processes. Studies on the pharmacological effects of chondroitin sulfate have established the presence of anti-inflammatory activity. An additional factor explaining the anti-inflammatory effect of chondroitin sulfate may be its antithrombotic effect. It has been shown that chondroitin sulfate can prevent the formation of fibrin thrombi in the synovial and subchondral microvasculature due to its structural proximity to heparin. Clinical studies have demonstrated the effectiveness of chondroitin sulfate in terms of its effect on pain and the functional state of joints. The majority of clinical studies that compared the effect of chondroitin sulfate and NSAIDs found that chondroitin sulfate at a dose of 1200 mg/day was as effective as diclofenac and ibuprofen at therapeutic doses, and more effective than placebo in reducing pain and increasing mobility. joints in patients with osteoarthritis. Although the effect of chondroitin sulfate occurred somewhat later (at 6–8 weeks of treatment) compared to the effect of NSAIDs (at 1–2 weeks of treatment), it lasted longer after cessation of treatment). An important advantage of the drug is its good tolerability, side effects when taking it are minor and infrequent - about 1-3% of cases, whereas when taking NSAIDs they are more serious (primarily gastrointestinal bleeding, ulceration, etc.) and occur in 30 –40% of persons. Generally, tolerability of chondroitin sulfate and placebo was similar. In vitro studies have shown that chondroitin sulfate has anti-inflammatory activity, stimulates the synthesis of hyaluronic acid and proteoglycans and inhibits the action of proteolytic enzymes. Clinical studies have demonstrated the effectiveness of cholesterol in influencing pain and the functional state of joints. The use of chondroitin sulfate in a dose of up to 1500 mg per day increases functional activity in patients with osteoarthritis and reduces local pain. Theoretical premises give reason to assume the presence of synergism between chondroitin sulfate and glucosamine in terms of chondroprotective effect. It consists of stimulating the metabolism of chondrocytes and synoviocytes, inhibiting the activity of enzymes that contribute to the degradation of the cartilage matrix, improving the microcirculation of the vascular bed of periarticular tissues (heparin-like effect of chondroitin sulfate). Studies with cell cultures and animal models support this hypothesis. Increased clinical efficacy in the treatment of osteoarthritis with the addition of chondroitin sulfate to glucosamine has been noted in several recent studies. In recent years, in connection with the widespread revision of the evaluation of drugs in accordance with the requirements of evidence-based medicine, a number of modern high-quality trials have been conducted regarding the clinical effectiveness of chondroprotectors. The data obtained indicate that chondroitin sulfate and glucosamine not only have a symptomatic effect, but are also able to have a beneficial effect on the metabolism of cartilage, restoring its structure and normalizing metabolism. Ultimately, these chondroprotectors really have a protective effect in relation to articular cartilage, impede its destruction and contribute (at least partially) its restoration. These data give reason to believe that chondroitin sulfate and glucosamine also have a pathogenetic effect and are able to have a modifying effect on the course of osteoarthrosis. This allows you to expand the range of therapeutic effect of these funds. According to many experts, chondroprotectors with a proven protective effect in relation to cartilage should become the basis of prolonged basic therapy of osteoarthrosis. Analyzing the clinical efficiency and tolerance of chondroprotective agents, the undoubted advantages of sulfate chondroitin and glucosamine should be distinguished as quite effective and safe drugs. Favorable clinical and pharmacological properties of glucosamine make it the drug of choice for basic therapy of osteoarthrosis. The average effective daily dose of the drug is at least 1500 mg per day. Glucosamine treatment makes it possible to get the effect after 2-4 weeks. The use of chondroitin sulfate (its daily dose on average is 1000–1500 mg) is especially indicated in elderly patients with concomitant atherosclerosis, obesity, lipid metabolism, metabolic syndrome, accompanying diabetes due to the presence of antitrobotic heparin -like effect and reduce the level of cholesterol and lipoprothems. Compared to glucosamine, the effect of chondroitin sulfate occurs a little later. Therefore, it is advisable to start therapy with the drug when the expected medical effect can be delayed; Or the pain syndrome should be stopped by the simultaneous reception of NSAIDs. In these cases, a smaller dose of NSAIDs is sufficient. The combined use of chondroitin sulfate and glucosamine provides faster saturation of the body with chondroprotectors compared to the action of one component, as well as a more pronounced clinical effect. Their joint purpose is shown if it is necessary to enhance the action when the effect of one drug is insufficient. This approach makes it possible to reduce the dose of each drug. In the foreground of the treatment of osteoarthritis (2–4 weeks), especially in the presence of pain syndrome, chondroprotectors should be combined with NSAIDs. Subsequently, the dose of NSAIDs can be reduced due to the growing effect of chondroprotectors or NSAIDs can even be canceled. This circumstance allows you to reduce the number of side effects and increase the safety of treatment. The duration of the reception of chondroprotectors, taking into account the features of their action, should be at least 12 weeks. At the same time, as clinical observations show, long (up to 3 years) therapy with chondroprotectors gives the best results. According to clinical indications, an intermittent treatment regimen for 12-16 weeks with a break of 8-10 weeks can be justified. Chondroitin sulfate and glucosamine, used as the basis of prolonged basic therapy of patients with osteoarthritis, can significantly change the course of the disease. Thus, the latest studies have made it possible to confirm all the requirements of evidence -based medicine to confirm the clinical significance of chondroprotectors in the treatment of osteoarthritis. One of the most commonly prescribed drugs of this class is teraflex. It is used for various pathologies of the ODA (supporting and engine apparatus) associated with degenerative changes in cartilage. The composition of the teraflex includes two active ingredients. The capsule includes: Glucosamine hydrochloride 500 mg and sodium chondroitin sulfate 400 mg. Both substances act synergically and directed. They take part in the production of structural elements of cartilage, thereby stimulating its restoration, which is especially important for such severe diseases as osteochondrosis and osteoarthrosis. Also, the components of the drug have a protective effect, preventing the negative effect of destructive factors of both endogenous and exogenous origin. In addition, the teraflex increases the mobility of the joints, reduces the severity of pain, and reduces the stiffness of movements. Teraflex is available in capsules for internal use, as well as in the form of a cream. In the first three weeks, adults and children of the eldest of 12 years are usually prescribed 1 capsule 3 times a day; In the following days - 1 tiraflex capsule 2 times a day. Capsules are taken orally with a small amount of water. The minimum duration of admission is 2 months (if necessary - for a longer time). Literature 1. Alekseeva L.I., Tsvetkova E.S. Osteoarthrosis: from the past to the future // Scientific and practical rheumatology. No. 2. 2009, application. S. 31–37. 2. Badokin V.V., Drezenko A.A., Korsakova Yu.L. Local therapy of osteoarthrosis // attending physician. No. 10. 2007. S. 2–4. 3. Belenky A.G. Hyaluronan preparations in the treatment of osteoarthritis of the knee and hip joints Textbook of GOU DPO RMAPO Roszdrava dated 04.23.2007. 4. Berglezov M.A., Andreeva T.M. Osteoarthrosis (etiology, pathogenesis) // Bulletin of traumatology and orthopedics named after N.N. Priorova. - 2006.– No. 4.– S. 79–86. 5. Vertkin A. L., Taliban O. B. Treatment of osteoarthrosis: the role of chondroprotectors. The attending physician, 09 (2000) 6. Vertkin A.L., Alekseeva L.I., Naumov A.V. et al. Osteoarthrosis in the practice of a therapist // RMG. 2008. T.16. No. 7. S. 478–480. 7. Goryachev D.V. The place of drugs of chondroitin sulfate in the arsenal of agents for the treatment of ostearthrosis // RMG. T.16. No. 10, 2008. S. 3-7. 8. Dzyak G.V. Non-steroidal anti-inflammatory drugs. Kyiv, Morion (1999) Clinical rheumatology. SPb., 2005. S. 386–388. 9. Clinical recommendations. Osteoarthritis. Diagnosis and conduct of patients with osteoarthritis of the knee and hip joints / Ed. O.M. Lesnyak. - M.: GEOTAR - Media, 2006. 176 p. 10. Nasonova V.A., Alekseeva L.I. Arkhangelskaya G.S. and others. The results of a multicenter clinical study of the drug Structure in Russia. New opportunities in the treatment of osteoarthritis and osteochondrosis. M., 2006. S. 5–7. 11. Nasonova V.A., Erdes Sh.F. On the World Decade of Bone Sustody Diseases 2000–2010 // Scientific and practical rheumatology. 2004. No. 4. S. 14–16. 12. National leadership. Rheumatology / Ed. E.L. Nasonova, V.A. Nasonova. - M.: GEOTAR - Media, 2008. S. 573–588. 13. Pavlova V.N., Kapyeva T.N., Slutsky L.I., Pavlov G.G. Cartilage. M.: Medicine, 1998.320 p. 14. Peshekhonova L.K., Peshekhonov D.V., Kuzovkina T.N. The clinical efficiency of chondroprotectors in the complex therapy of osteoarthrosis of the knee joints 1486 breast cancer 15. Rational pharmacotherapy of rheumatic diseases. M., 2003. T.3. S. 143-149. 16. Rudenko V.G. Chondroprotectors - the basis of constructive therapy of joint diseases 17. Chichasova N.V. The place of slow -acting drugs in the rational therapy of deforming osteoarthrosis // Consislium medicum. 2005. T.7. No. 8. S. 634–638. 18. Yabluchansky N.I. Chondroprotectors for all occasions to an article to patient 19. Hochberg MC, Altman RD, Brandt KD AT Al. Guidelines for the Medical Management of Osteoarthritis. Arthritis & Rheumatism, Vol. 38, N11 (1995) 20. Reginster Jy, Deroisy R, Rovati LC, et al. Long -Term Effects of Glucosamine Sulphate OstoArthritis ProgRESSION: A RANDOMISED, PLACEBO - Controlled Clinical Trial. Lancet 357 (2001)
