Forosa®
Take Forosa® tablets only with plain water, as other drinks (including mineral water, tea, coffee, fruit juices) impair the absorption of the drug. Taking alendronic acid before bed or in a horizontal position increases the risk of developing esophagitis.
If symptoms of esophageal irritation occur, such as dysphagia, chest pain, or new/worsening of existing heartburn, patients should consult a physician to evaluate the possibility of continuing therapy.
The risk of severe esophageal side effects is greater in patients who take alendronic acid not in accordance with these instructions and/or who continue to take it after symptoms suggestive of esophageal irritation have occurred. It is important to explain in detail to the patient the rules for taking the drug and make sure that he understands them. Patients should be aware of the increased risk of adverse events from the esophagus if they deviate from the instructions.
Before starting therapy with Forosa®, correction of hypocalcemia and other metabolic disorders (such as vitamin D deficiency) is necessary. Due to the increase in bone mineral density during alendronic acid therapy, a slight clinically asymptomatic decrease in serum calcium and phosphate levels is possible, especially in patients receiving
glucocorticosteroids, which may reduce calcium absorption. Therefore, it is important to ensure that sufficient amounts of calcium and vitamin D enter the body, which is especially important in patients receiving glucocorticosteroids.
Patients should be warned that if they accidentally miss a dose of the drug once a week, they should take 1 tablet in the morning of the next day (it is unacceptable to take 2 tablets in one day). In the future, you should continue to take 1 tablet on the day of the week that was chosen at the beginning of therapy.
There is also evidence of osteonecrosis of the jaw in patients with osteoporosis receiving oral bisphosphonates. Before initiating bisphosphonate therapy, patients with underlying risk factors (eg, cancer, chemotherapy, radiation therapy, corticosteroids, poor oral hygiene, anemia, coagulopathy, infection, gum disease) should undergo a dental examination with appropriate preventative dental treatment.
During treatment, these patients should avoid invasive dental procedures if possible. For patients who develop osteonecrosis of the jaw during bisphosphonate treatment, dental surgery may worsen the condition.
There are no data regarding the possible reduction in the risk of osteonecrosis of the jaw after discontinuation of bisphosphonates in patients requiring dental intervention.
Low-energy fractures (also known as stress fractures) of the proximal femoral shaft may occur in patients taking alendronic acid long-term. Fractures can occur after minimal or no trauma, and some patients may experience hip pain, often with outward signs of stress fractures weeks/months before a complete femur fracture occurs. Low-energy proximal femoral shaft fractures were often bilateral, so patients with a long-standing femoral shaft fracture taking bisphosphonates should have the contralateral hip evaluated. It is advisable to discontinue bisphosphonates in patients with stress fractures after assessing their condition based on an individual assessment of the risk/benefit ratio.
The decision to proceed with treatment must be made individually for each patient after a careful risk/benefit assessment, especially for patients with Barrett's esophagus.
Instructions for use FOROSA
Forosis can cause local irritation of the mucous membrane of the upper gastrointestinal tract. Because there is a risk of worsening concomitant diseases, caution should be exercised when prescribing Forosa to patients with upper gastrointestinal diseases such as dysphagia, esophageal disease, gastritis, duodenitis or ulcers, as well as to patients who have recently (within the last year) had a serious gastrointestinal disease ( for example, gastric ulcer, acute gastrointestinal bleeding) or surgery of the upper gastrointestinal tract, excluding pyloroplasty. In patients with Barrett's esophagus, the benefits and risks of treatment with alendronate should be individually assessed.
Esophageal side effects (in some cases severe and requiring hospitalization) such as esophagitis, ulcers or erosions of the esophagus, in rare cases complicated by stricture or perforation of the esophagus, have been described in patients treated with alendronate. Therefore, the physician should be alert for any sign or symptom of a possible esophageal reaction. Patients should be instructed to stop taking Forosa and seek medical attention if symptoms of esophageal irritation develop, such as dysphagia, pain when swallowing, chest pain, or new/worsening heartburn.
The risk of severe esophageal side effects increases in patients who misuse Forosa and/or continue to take the drug after developing symptoms indicating esophageal irritation. It is very important to give detailed instructions when prescribing and explain them to the patient. Patients should be advised that the risk of esophageal injury may increase if they do not follow these instructions.
There are post-marketing reports of rare cases of gastric and duodenal ulcers, some of them with severe course and complications. A causal relationship with the drug cannot be excluded.
Forosa is not recommended for use in patients with impaired renal function and GFR below 35 ml/min.
Before starting treatment with Forosa, hypocalcemia must be corrected. Before you start taking Forosa, it is also necessary to effectively compensate for other disorders of mineral metabolism (for example, vitamin D deficiency and hypoparathyroidism). In such patients, serum calcium levels and symptoms of hypocalcemia should be monitored during treatment with Forosa.
Due to the positive effects of Forosa on bone mineralization, a decrease in serum calcium and phosphorus levels may be observed. It is usually mild and asymptomatic. However, in rare cases, symptomatic hypocalcemia has been described, which is sometimes severe and occurs in patients with predisposing conditions (eg, hypoparathyroidism, vitamin D deficiency and cases of intestinal calcium malabsorption).
Therefore, it is especially important to ensure that a patient taking glucocorticoids gets enough calcium and vitamin D.
Osteonecrosis of the mandible, mainly associated with tooth extraction and/or local infection (including osteomyelitis), has been described in patients with cancer receiving IV bisphosphonates along with other treatment regimens. Many of these patients also received chemotherapy and corticosteroids. Osteonecrosis of the mandible has also been described in patients taking oral bisphosphonates.
In patients with underlying risk factors (eg, cancer, chemotherapy, radiation therapy, corticosteroids, poor oral hygiene, periodontitis), dental examination and appropriate prophylactic treatment should be performed prior to initiating bisphosphonate treatment.
These patients should avoid invasive dental procedures if possible during treatment. In patients with osteonecrosis of the mandible that develops during bisphosphonate treatment, surgery may aggravate the disease. There are no data suggesting a reduction in the risk of osteonecrosis of the mandible after discontinuation of bisphosphonate treatment in patients requiring dental procedures.
When developing a patient management plan, the physician must individually assess the benefits and risks of treatment.
Bone, joint and/or muscle pain has been reported in patients taking bisphosphonates. These symptoms were rare and/or rarely disabling. The time for symptoms to develop varied from one day to several months after the start of treatment. Most patients experienced improvement in symptoms after stopping treatment. Some have experienced a return of symptoms when they take the same drug or a different bisphosphonate again.
Stress fractures (also known as osteoporotic fractures) in the proximal femoral shaft have been reported with long-term use of alendronic acid (time to fracture ranged from 18 months to 10 years in most cases). These fractures occurred with minimal trauma or spontaneously. Some patients have complained of hip pain, often accompanied by radiographic evidence of a stress fracture, several weeks or months before a complete femur fracture. Such fractures were often bilateral, so when the femoral shaft is fractured during treatment with bisphosphonates, it is important to examine the contralateral limb. These fractures are characterized by poor healing. In such cases, discontinuation of bisphosphonates is recommended, depending on an individual assessment of the benefits and risks of such a decision.
If you miss a dose, take the pill the next morning after you remember to do so. You should not take two tablets on the same day. You must return to taking the pill on the originally chosen day of the week.
Forosa does not affect the ability to drive vehicles or operate machinery.
Forosa, 8 pcs., 70 mg, film-coated tablets
Take Forosa® tablets only with plain water, because other drinks (including mineral water, tea, coffee, fruit juices) impair the absorption of the drug. Taking alendronate before bed or in a horizontal position increases the risk of developing esophagitis.
If symptoms of esophageal irritation occur, such as dysphagia, chest pain, or new/worsening of existing heartburn, patients should consult a physician to evaluate the possibility of continuing therapy. The risk of severe esophageal side effects is greater in patients who take alendronic acid not in accordance with these instructions and/or who continue to take it after symptoms suggestive of esophageal irritation have occurred. It is important to explain in detail to the patient the rules for taking the drug and make sure that he understands them. Patients should be aware of the increased risk of adverse events from the esophagus if they deviate from the instructions.
Before starting therapy with Forosa®, correction of hypocalcemia and other metabolic disorders (such as vitamin D deficiency) is necessary. Due to the increase in bone mineral density during alendronate therapy, a slight clinically asymptomatic decrease in serum calcium and phosphate levels is possible, especially in patients receiving corticosteroids, in whom calcium absorption may be reduced. Therefore, ensuring that sufficient amounts of calcium and vitamin D enter the body is especially important in patients receiving corticosteroids.
Patients should be warned that if they accidentally miss a dose of the drug once a week, they should take 1 tablet. in the morning of the next day (it is unacceptable to take 2 tablets in one day). Subsequently, you should continue to take 1 tablet. on the day of the week that was chosen at the beginning of therapy.
There is also evidence of osteonecrosis of the jaw in patients with osteoporosis receiving oral bisphosphonates. Before prescribing bisphosphonate therapy, patients with associated risk factors (eg, cancer, chemotherapy, radiation therapy, corticosteroids, poor oral hygiene, anemia, coagulopathy, infection, gum disease) should undergo a dental examination with appropriate preventive dental treatment. During treatment, these patients should avoid invasive dental procedures if possible. For patients who develop osteonecrosis of the jaw during bisphosphonate treatment, dental surgery may worsen the condition.
There are no data regarding the possible reduction in the risk of osteonecrosis of the jaw after discontinuation of bisphosphonates in patients requiring dental intervention.
Low-energy fractures (also known as stress fractures) of the proximal femoral shaft may occur in patients taking alendronic acid long-term. Fractures can occur after minimal or no trauma, and some patients may experience hip pain, often with outward signs of stress fractures weeks/months before a complete femur fracture occurs.
Low-energy proximal femoral shaft fractures were often bilateral, so patients with a long-standing femoral shaft fracture taking bisphosphonates should have the contralateral hip evaluated. It is advisable to discontinue bisphosphonates in patients with stress fractures after assessing their condition based on an individual assessment of the risk/benefit ratio.
The decision to proceed with treatment must be made individually for each patient after a careful risk/benefit assessment, especially for patients with Barrett's esophagus.
Impact on the ability to drive vehicles and engage in other activities that require increased concentration and speed of psychomotor reactions.
Alendronic acid does not affect the ability to drive vehicles and engage in other activities that require increased concentration and speed of psychomotor reactions.
Special precautions when disposing of unused drug.
There is no need for special precautions when disposing of unused drug.
Treatment of osteoporosis: experience with alendronate
Using advanced, primarily radiological, research methods, the development and implementation of new methods of prevention and treatment, as well as active and purposeful educational activities of the International Osteoporosis Foundation (IOF) and its 186 national societies in 90 countries, including the Russian Association for Osteoporosis osteoporosis, the social and medical significance of the disease has increased significantly. Official registration of the incidence of AP began in the Russian Federation in 1999, and over the past 10 years (1999–2008) the total number of recorded cases of AP among adult residents of Russia increased almost 4 times (from 31,500 people in 1999 to 115,530 people . in 2008). An improvement in the technical basis for diagnosis, namely the supply of bone densitometers to medical institutions, which made it possible to measure bone mineral density (BMD) and make a diagnosis of AP, had a significant impact on the frequency of detection of the disease. In 2005, the Russian Association for AP developed clinical guidelines for the diagnosis, prevention and treatment of AP, including glucocorticoid AP, and in 2009 they were revised and supplemented. Recommendations are ranked according to a unified international system of levels of evidence. Despite general recommendations, treating AP in a particular patient is often a difficult task and depends both on the doctor’s interpretation of the patient’s condition and on the patient’s readiness for long-term therapy. There are two main types of AP – primary and secondary, with primary AP being the most common: the ratio of its frequency to the frequency of all possible forms of secondary AP reaches 4:1 [1]. Primary AP is conventionally divided into postmenopausal and senile. Postmenopausal AP is associated with accelerated bone loss in women after the cessation of the menstrual cycle, and is caused by estrogen deficiency. The main reasons for the development of senile AP in individuals of both sexes are a decrease in calcium intake, impaired absorption in the intestine and vitamin D deficiency, which can lead to secondary hyperparathyroidism and, as a result, accelerated bone remodeling. One of the factors influencing the development of senile AP is considered to be a decrease in physical activity in old age. It must be emphasized that during the aging process, the interaction of hormones with growth factors and other cytokines that influence the process of osteoblastogenesis undergoes significant changes, and the activity of many local factors decreases. AP develops gradually and is often clinically detected after fractures, which is the basis for calling it a “hidden epidemic.” It should be noted that the incidence of AP increases with age, therefore, the increase in life expectancy observed in recent decades in developed countries and the associated rapid increase in the number of elderly people, especially women, leads to an increase in the frequency of this disease, making it one of the most important health problems worldwide. world. Providing medical care to patients with primary AP is carried out on an outpatient basis, with the exception of cases requiring surgical treatment of complications of AP - fractures. Treatment and observation of the patient is long-term, over several years, and should be carried out by a primary care doctor - a local therapist or a general practitioner. If secondary causes of the possible development of AP are identified, the patient should be referred for consultation to a specialist (rheumatologist, endocrinologist, etc.). Among diagnostic measures, clinical examination methods come to the fore: studying the patient’s complaints and medical history in order to identify risk factors for AP and risk factors for falls, as well as clinical signs of bone fractures, including vertebral fractures. Identification of the presence of AP in a particular individual includes an assessment of the family history of AP, lifestyle (bad habits, physical activity, nutrition, etc.), the presence of fractures, reproductive history, the presence of diseases and drug therapy leading to the development of AP (Table 1). Falls are an independent risk factor for fractures because... most fractures of the proximal femur and distal forearm occur due to falls (Table 2). Physical examination of a patient with AP includes a general medical examination with measurement of height and weight. A decrease in height by 2.5 cm per year or by 4 cm or more compared to height at 25 years of age may indicate AP complicated by vertebral fractures. If the fracture was recent, local pain in the vertebral area may be noted, and progressive changes in posture may be accompanied by paravertebral pain on palpation and tension of the paravertebral muscles, and limited mobility in the spine. To diagnose AP, various instrumental methods are used: bone radiography and measurement of bone mineral density using bone densitometry. Bone radiography remains the only research method that allows one to evaluate the anatomical features of bones and the structure of bone tissue, as well as various skeletal injuries. One of the disadvantages of radiography in diagnosing AP is the low sensitivity of the method, which makes it possible to detect a decrease in bone mass when the degree of decrease in mineralization reaches 20–40%. Currently, radiography is used to detect or confirm bone fractures of any location. To diagnose osteoporotic fractures of the vertebral bodies, the method of X-ray morphometry of the spine in the lateral projection is used. X-ray morphometric analysis of the vertebral bodies includes measurement of the anterior, middle and posterior heights with the calculation of indices: anterior/posterior index - the ratio of the anterior height of the vertebral body to the posterior; middle/posterior index – the ratio of the average height of the vertebral body to the posterior; posterior/posterior index – the ratio of the posterior height of the body of the vertebra under study to the posterior heights of one or two overlying and underlying vertebrae. To assess deformations, the quantitative method of H. Genant is used [3]. Vertebral body indices of more than 0.8 (80%) indicate a normal configuration of the vertebra, with any index of 0.75–0.79 – a 1st degree of deformity, with 0.6–0.74 – a 2nd degree , and if 0.59 or less – a severe osteoporotic vertebral fracture of the 3rd degree. The OP of the spine is characterized by such types of deformities as anterior or posterior wedge-shaped, unilateral or biconcave deformities, as well as a compression fracture. Indications for referral of patients for X-ray examination include back pain and decreased height to detect osteoporotic vertebral fractures. Currently, the “gold standard” for diagnosis is the measurement of BMD using dual-energy X-ray absorptiometry (DXA), which estimates the amount of mineralized bone tissue in the scanned area (g /cm2). Standard testing methods include densitometry of the lumbar spine and proximal femur (femoral neck and total hip index), since the prevalence of fractures has been shown to correlate with BMD in these areas based on numerous assessment methods. The diagnosis of AP is made in postmenopausal women and men aged 50 years and older by comparing the obtained BMD data with the apparatus’s abstract database (the average value of “peak bone mass” in young healthy people according to the T-criterion) using the WHO recommendation [WHO, 1994] , according to which normal BMD values include indicators above -1SD from the reference base according to the T-criterion, values from -1SD to -2.5SD are classified as osteopenia, deviations below -2.5 SD - as OP, and with the additional presence of one and more fractures – as severe AP. If it is not possible to study the spine and hip, the results of measurements of the distal forearm can be used. Indications for referring patients for densitometry are the presence of risk factors for AP in patients under 65 years of age and to assess the effectiveness of pathogenetic treatment of AP. For the differential diagnosis of primary AP and metabolic diseases of the skeleton, as well as before prescribing antiresorptive therapy, a mandatory study of calcium, phosphorus and alkaline phosphatase in the blood, calcium in daily urine or the ratio of calcium to creatinine in morning urine is recommended. It should be remembered that in primary AP, the level of the above indicators in the blood is within normal limits, but hypercalciuria is possible, especially for the variant of AP with increased bone turnover. In addition, additional laboratory methods can be used, the purpose of which is to establish a diagnosis of the underlying disease, one of the symptoms of which is osteopenia (for example, thyroid-stimulating hormone, parathyroid hormone, 25-hydroxyvitamin D, etc.). To assess the rate of bone turnover, markers of bone formation (osteocalcin OS, carboxy- and aminoterminal propeptides of procollagen type I - PICP, PINP, bone isoenzyme of alkaline phosphatase - bALP), as well as markers of bone resorption (oxy- and deoxypyridinolines - PYR, DPYR, hydroxyproline - OHPr in urine, N- and C-telopeptides of type I collagen molecules cross-linked - NTX, CTX in blood serum or urine, as well as tartrate-resistant acid phosphatase - TRACP in blood plasma). However, at present there is no evidence of the importance of determining the level of bone markers for individual diagnosis of AP and for predicting the risk of fractures in individual patients in clinical practice; they can be used to assess the therapeutic effect of the drug (a decrease in their level by 30% or more when taking antiresorptive therapy is predicted good treatment effectiveness) and improved patient adherence to treatment. Treatment of AP includes both non-drug therapies and pharmacological interventions. Among the first, it should be noted educational programs, giving up bad habits (smoking, alcohol abuse, caffeine, heavy physical activity), physical education (walking, gymnastics, isometric exercises, swimming), fall prevention (vision correction, treatment of concomitant diseases, assessment and change home environment, movement pattern training, balance training), patients with vertebral fractures should be recommended to wear rigid or semi-rigid corsets for up to 4–6 hours during physical activity, because they reduce the severity of pain. With AP, such types of loads as jumping and strength exercises, sudden bends and rotations of the body should be excluded. Drug treatment of AP is a difficult task, since it is diagnosed quite late, when there may already be a history of fractures of various locations. Treatment must be long-term, since the effect may take many months to appear. In this regard, there is a constant search for highly effective and inexpensive drugs. The goal of therapy is to slow down and, if possible, stop bone loss, prevent bone fractures, improve the patient's condition, reduce pain, and improve his quality of life. Today, the range of drugs for the treatment and prevention of AP has expanded significantly; their use reduces the risk of fractures from 30 to 70%. The drugs of first choice for pathogenetic therapy are drugs of the bisphosphonate (BP) class and strontium ranelate. The action of BP is based on reducing the rate of bone turnover due to its effect on osteoclasts - cells that destroy old bone - while maintaining bone microarchitecture and increasing bone mineral density (BMD). One of the drugs in the BF class is alendronate, which has been widely used in clinical practice throughout the world for almost 15 years. When treated with alendronate, resorption processes by osteoclasts are suppressed and bone metabolism processes are restored to premenopausal levels and prevents microarchitectural disorders and bone loss. The processes of bone metabolism remain stable during long-term treatment with alendronate for 10 years, while the accumulation of the drug in the bone does not lead to excessive suppression of bone turnover, but, on the contrary, demonstrates that bone turnover remains at premenopausal levels, and bone quality remains normal throughout the treatment period . Data from pharmacokinetic studies have confirmed that the effectiveness of BP on bone mass and strength depends on the cumulative dose of these drugs. Thus, the same amount of alendronate is absorbed with a single dose of 70 mg once a week. or 10 mg 7 times/week. The effectiveness of alendronate in patients with AP has been proven in several randomized clinical double-blind placebo-controlled studies (RCTs) [4,5,6]. Taking alendronate showed high efficiency: it significantly reduced the incidence of vertebral fractures by 47%, hip fractures by 51–56%, and forearm fractures by 48% [5,7]. Currently, alendronate is the first drug that has a 10-year study duration that assessed the dynamics of BMD in groups of patients who took alendronate throughout this period or were switched to placebo after the first 5 years of active therapy. In women who continued to receive 10 mg/day. alendronate, there was a gradual increase in spine BMD to 13.7% (p<0.001), and hip BMD to 6.7% (p<0.001) relative to the initial level. As a result of alendronate administration, the level of bone turnover markers decreased to premenopausal levels, which remained stable over the entire 10-year period without signs of oversuppression. Compared with the study group, individuals who took placebo over the past 5 years showed a decrease in total hip BMD (–2.4%; 95% CI –2.9%; –1.8%; p<0.001) and lumbar spine (–3.7%; 95% CI –4.5%; –3.0%; p<0.001), however, mean BMD values remained above baseline at study entry. At 5 years, the overall risk of peripheral fracture was not significantly different between groups (RR 1.00; 95% CI 0.76, 1.32). Those who continued alendronate therapy had a significantly lower risk of clinically significant vertebral fractures: for example, in the placebo group they occurred in 5.3% of patients, and in the alendronate group – in 2.4% (OR 0.45; 95% CI 0.24; 0.85). For fractures detected by X-ray morphometry of the spine, such a pattern was not found (11.3 and 9.8%, respectively; RR 0.86; 95% CI 0.60, 1.22). A small number of iliac biopsies did not reveal any qualitative bone pathology. In summary, this study showed that stopping treatment after 5 years does not significantly increase the risk of fractures, but women at high risk of clinical vertebral fractures should continue treatment beyond 5 years [6]. When taking oral bisphosphonates, much attention is paid to adverse events (AEs) associated with damage to the gastrointestinal tract. It should be noted that during the studies, the frequency of all adverse events when taking 10 mg of alendronate per day did not exceed that in the placebo group [5]. Currently, all over the world, due to the problem of treatment compliance, preference is given to another dose of the drug 70 mg 1 time/week. RCTs have shown that this dosage of alendronate provides therapeutic equivalence to a daily dose of 10 mg of the drug, while at the same time better tolerability and ease of use [8–10]. Thus, the increase in BMD was 6.8 and 7.4%, respectively, in the spine, 4.1–4.3% in the hip. A two-year follow-up of patients receiving various doses of alendronate showed that the incidence of fractures in the 70 mg group once a week. was 7.3%, and in the group 10 mg/day. – 7.0% (p>0.05). There is clear evidence of a reduction in fracture risk with alendronate 10 mg daily, and the lack of difference in fracture incidence at both doses, comparable increases in BMD, and similar changes in bone turnover marker levels suggest a similar effect on fracture risk at these dosages. The biopsy material showed no signs of osteomalacia when taking both doses of the drug. In a comparative study, it was shown that the frequency of gastrointestinal AEs (esophagitis, erosion, hemorrhage, reflux, gastritis, stomach ulcer, etc.) in groups receiving different doses of alendronate was similar, i.e. an increase in a single dose of 7 times did not increase the risk of developing AEs [10,11]. The RI RAMS conducted a study of the effectiveness and safety of alendronate 70 mg/week. in an open-label, one-year controlled study [11]. After a year of therapy, a significant increase in BMD in the spine and femoral neck was obtained in patients receiving alendronate compared to the comparison group (p=0.00001 and p=0.030, respectively). When assessing the number of patients with a significant increase in the MPC in the spine and the proximal thigh department, it was revealed that in the group that received treatment with alendronate, 85.7% of patients had an increase in more than 2% in the spine and 42.8% of people - in the field of the hip neck, and 38.8% had a significant increase in both areas of measurement, which was significantly higher than in the comparison group (p = 0.01). At the same time, the increase in MPCT more than 6% in the spine was found in 53% of women who received alendronate, and in the neck of the thigh - an increase of more than 3% - in 30.6%. In addition, when taking alandronate, it was reliably more women who positively responded to treatment than women whose effect was absent (p <0.001). Our study showed high efficiency of alendronate at a dose of 70 mg 1 time/week. In the treatment of primary OP in women in postmenopausa: it had a positive effect on the MPC, reduced the pain syndrome and, as a result, reduced the restriction of the physical activity of patients. It is noted quite good tolerance of the drug, side effects in the treatment group were comparable to those in the comparison group. An analysis of the action of alendronate showed that it has a path for the 12 -month period after the end of treatment in relation to the MPC of the spine. Alendronate is effective in both men and women, for the prevention and treatment of glucocorticoid (Civil Code) OP both in relation to the increase in the IPC and a reduction in risk of fractures. The fundamental evidence of the effectiveness of the alendronate was obtained in a randomized clinical study with a placebo control, in which men and women (n = 477) with newly prescribed Civil Code (34% of patients) or with Civil Code of therapy that lasted more than 4 months. (66% of patients), were under observation of more than 48 weeks. Positive effects of treatment for 12 months. At the MPC, they were statistically reliable in the lumbar spine and the hip neck. It is noted that in the Alendronate group of new vertebral fractures during the observation period, there were less than the placebo group (2.3 and 3.7%, respectively, P> 0.05). Subsequently, observation of 208 patients showed the effectiveness of therapy with alendronate during the 2nd year and a significant decrease in the number of new vertebral fractures in the Alendronate group (0.7%) compared to the placebo group (6.8%; p = 0.026) [ 13]. Alendronate must be taken on an empty stomach immediately after lifting from bed, the tablet must be washed down with 1 cup (180–240 ml) of pure water, and after receiving you should be in an upright position (sitting or standing) for at least 30 minutes. BF can cause side effects associated with the defeat of the gastrointestinal tract, as well as headache, muscle pain and bones, a decrease in calcium and phosphorus in the blood serum, in rare cases - a rash and erythema. With an overdose of BF - hypocalcemia and hypophosphatemia, gastrointestinal tract disorders. Compliance with recommendations for taking the drug significantly reduces the risk of gastrointestinal nia. Contraindications to their purpose: hypersensitivity to the drug, stricture and esophagus ahalazia, severe renal failure (creatinine clearance below 35 ml/min.), Hypocalcemia, pregnancy and breastfeeding, children's age, severe hypoparastic, calcium malabsorption. It should be remembered that taking drugs affecting pathogenesis of the OP should take place against the background of sufficient intake of calcium and vitamin D with food or in the form of drugs. Active metabolites (alfacalcidol and calcitriol) can be used as a vitamin D donator, the combined use of them with BF leads to an increase in the MPC of the spine and the hips of the thigh, a decrease in the risk of falling and peripheral bones [14].
Literature 1. Guide to osteoporosis / Ed. Prof. L.I. Benevolenskaya. M.: BINOM, 2003. 524 p. 2. Clinical recommendations “Osteoporosis. Diagnostics, prevention and treatment / Ed. prof. L.I. Benevolenskaya and Prof. O.M. Lesnyak. M.: GEOTAR-Media, 2009; 272 pp. 3. Genant HK, Wu C, van Kuijk et al. Vertebral fracture assessment using a semiquantitative technique // JBMR 1993;9:1137–1148. 4. Pols HA, Felsenberg D, Hanley DA, et al. Multinational, placebo–controlled, randomized trial of the effects of alendronate on bone density and fracture risk in postmenopausal women with low bone mass: results of the FOSIT study. Fosamax International Trial Study Group. Osteoporos Int. 1999; 9:461–468. 5. Black DM, Thompson DE, Bauer DC and FIT research group. “Fracture risk reduction in women with osteoporosis: the Fracture Intervention Trial.” J Clin Endocrinol Metab 2000; 85:4118–24. 6. Black DM, Schwartz AV, Ensrud KE, Cauley JA, Levis S, Quandt SA, Satterfield S, Wallace RB, Bauer DC, Palermo L, Wehren LE, Lombardi A, Santora AC, Cummings SR; FLEX Research Group. Effects of continuing or stopping alendronate after 5 years of treatment: the Fracture Intervention Trial Long–term Extension (FLEX): a randomized trial. JAMA. 2006 Dec 27;296(24):2927–38. 7. Liberman UA, Weiss SR, Broll J, Minne HW, Quan H, Bell NH, et al. Effect of oral alendronate on bone mineral density and the incidence of fractures in postmenopausal osteoporosis. N Engl J Med 1995; 333:1437–43. 8. Schnitzer T., Bone H. G., Crepaldi G. et al. Therapeutic equivalence of alendronate 70 mg once–weekly and alendronate 10 mg daily in the treatment of osteoporosis. Aging Clin Exp Res 2000;12:1–12. 9. Rizzoli R, Greenspan SL, Bone G III et al. Two–Year Results of Once–Weekly Administration of Alendronate 70 mg for the Treatment of Postmenopausal Osteoporosis // J Bone Mineral Research, 2002, Nov 17(11):1988–96 10. Greenspan S, Field–Munves E, Tonino R, Smith M, Petruschke R, Wang L, Yates J, de Papp AE, Palmisano J. Tolerance of once–weekly alendronate in patients with osteoporosis: a randomized, double–blind, placebo–controlled study//.Mayo Clin Proc. 2002 Oct;77(10):1044–52. 11. Lanza F, Sahba B, Schwartz H, Winograd S, Torosis J, Quan H, Reyes R, Musliner T, Daifotis A, Leung A. The upper GI safety and tolerability of oral alendronate at a dose of 70 milligrams once weekly: a placebo–controlled endoscopy study//Am J Gastroenterol. 2002 Jan;97(1):58–64 12. Toroptsova N.V., Nikitinskaya O.A., Demin N.V., Benevolenskaya L.I. Results of a study of the effectiveness of weekly administration of alendronate (Fosamax®) in patients with primary osteoporosis // Osteoporosis and Osteopathy. 2006;1: 22–25. 13. Adachi JD, Saag KG, Delmas PD, Liberman UA, Emkey RD, Seeman E. Two–year effects of alendronate on bone mineral density and vertebral frac¬ture in patients receiving glucocorticoids: a randomized, double–blind, placebo–controlled extension trial. Arthritis Rheum 2001;44:202–211. 14. Ringe JD, Farahmand P, Schacht E, Rozehnal ASuperiority of a combined treatment of Alendronate and Alfacalcidol compared to the combination of Alendronate and plain vitamin D or Alfacalcidol alone in established postmenopausal or male osteoporosis (AAC–Trial). Rheumatol Int. 2007 Mar;27(5):425–34.
