Лечение деформирующего артроза коленного сустава

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Здравствуйте! Подскажите пожалуйста

Какое лечение нужно при заболевании деформирующий артроз коленного сустава?
 
Надежда, греша самоцитированием, предлагаю Вам посмотреть этот пост (http://forums./showpost.php?p=66533&postcount=2).

Если у Вас останутся вопросы, мы с коллегами постараемся на них ответить.
 
Надежда, греша самоцитированием, предлагаю Вам посмотреть этот пост (http://forums./showpost.php?p=66533&postcount=2).

Если у Вас останутся вопросы, мы с коллегами постараемся на них ответить.



спасибо за ответ



Диклофенак не помогает, терафлекс, милокс так же не помогают...



про Физиотерапию поподробнее напишие пожалуйста...
 
Надежда, физиотерапия - это как раз не самый эффективный метод лечения.

Кстати, в том сообщении я забыл упомянуть внутрисуставное введение препаратов гиалуроновой кислоты (остенил, синвикс) - т.н. в народе "искусственная смазка".



Но в каждом конкретном случае лечение назначает врач при очной консультации. Тактика лечения зависит от характера рентгенологических изменений, возраста пациента, сопутствующих заболеваний и некоторых других факторов.
 
Здравствуйте, Надежда !

информация на русском взята тут: http://64.233.183.104/search?q=cache:pIRF7ntMfKkJ:www.gaseta.com/gaseta/kontakt/article.php%3Fid%3D81%26type%3D2+orthokin&hl=ru&lr=lang_ru

Поищите в www.googe.ru, в русском инете, термин " ORTHOKIN "

В последнее время в терапии артрозов стали практиковаться новые методы. Йозеф Хойсен пользуется, например, ортокинным методом (Orthokin-Therapie), восстанавливающим естественные защитные функции организма. Причиной воспалений при артрозах и ревматизме служит, как известно, наша собственная иммунная система, вырабатывающая антитела для борьбы с возникшим недугом. Действие большинства лекарств основано на подавлении этой функции организма. Однако, подавляя иммунную систему, мы облегчаем задачу возбудителям других болезней. Ортокинный метод позволяет этого избежать. У больного берут кровь специальным шприцем, в котором находятся крошечные стеклянные шарики с особым покрытием. Взятая кровь под воздействием инородных тел сразу же начинает вырабатывать вещество против артроза, которое затем выделяется и изолируется в лаборатории биомедицинским способом. Полученный медикамент используется для инъекций: его впрыскивают в больной сустав. В течение считанных недель боли исчезают.

В 75 случаях из 100 новый метод помогает одолеть коварный артроз

Может и Вам поможет !!! Удачи !
 
У больного берут кровь специальным шприцем, в котором находятся крошечные стеклянные шарики с особым покрытием. Взятая кровь под воздействием инородных тел сразу же начинает вырабатывать вещество против артроза, которое затем выделяется и изолируется в лаборатории биомедицинским способом. Полученный медикамент используется для инъекций: его впрыскивают в больной сустав. В течение считанных недель боли исчезают.

"У, брат... это жулики" (с) :D

"Не прячьте ваши денежки по банкам и углам" (с) :D
 
Господин Радионов,

я просмотрел форум и понял, что термин Orthokin не очень знаком в России. Например тут, почти в конце топика http://forums./showthread.php?t=12089&page=2&pp=15 а поэтому могу понять скептический характер Вашей шутки ;) Незнание всегда порождает недоверие. Такова наша человеческая логика.

На самом деле всё не так просто.Стеклянные шарики, на самом деле сложный химический реагент. И никаких заклинаний при синтезе призносить не надо. Информации на русском языке практически нет, поэтому показал госпоже Надежда.Ж то , что нашлось. И, на мой взгляд, в доступной форме. Например в Германии, эта терапия широко распространена и достаточно эффективна. И уж если частные мед. страховые компании Германии признают и оплачивают пациентам эту терапию, то это уже о чём то говорит.

Если Вы понимаете немецкий, и есть желание, почитайте, например тут. http://www.orthogen.com/downloads/deutsch/orthokin_pm2.pdf или тут, на английскомhttp://www.orthogen.com/downloads/deutsch/inflammationresearch_orthokin_2003.pdf

Одобрившим Ваше сообщение, тоже рекомендую... ;)

И желаю удачи !
 
Господин systemshock, я просмотрел форум и понял, что русское имя РОдион (производное моей фамилии) знакомо далеко не всем :D



Но к делу!

Если Вы просмотрели форум внимательно, то, наверное обратили внимание, что говоря о новых методах лечения принято доказывать их КЛИНИЧЕСКУЮ эффективность.

Давайте посмотрим, что Вы нам предлагаете:



The production of antiinflammatory cytokines in whole blood

by physico-chemical induction



Abstract. Objective and design: Cytokines such as interleukin-

1 (IL-1) play an important role in degenerative musculo-

skeletal diseases, including osteoarthritis, and a multitude

of inflammatory disorders. Agents that inhibit the action

of such cytokines have a high therapeutic potential in such

diseases. Here we describe a new method for enhancing the

production of the interleukin-l-receptor antagonist (IL-1Ra)

and other anti-inflammatory cytokines in whole blood.

Material and methods: Human venous blood was incubated

in the presence of CrSO4-treated glass beads. Serum was

recovered and the concentrations of IL-1Ra and other relevant

cytokines were measured by ELISA. Так, понял... В человеческую венозную кровь помещали шарики, обработанные сульфатом хрома. Меряли интерлейкины.



Results: The interaction of the glass bead surface with cells

in whole blood increased production of IL-1Ra and antiinflammatory

cytokines. Removal of the beads and centrifugation

generated a serum preparation enriched in antiinflammatory

cytokines. This preparation may be of therapeutic

value in treating various inflammatory and degenerative

disorders.

МОЖЕТ БЫТЬ - ключевое слово..

Conclusions: The increased de novo production of antiinflammatory

cytokines by a direct physico-chemical induction

of whole blood is feasible and offers an alternative, novel

approach to treating mild to moderate OA and other

orthopaedic conditions such as degenerative spine diseases.



А вот откуда в выводах идея о возможности лечения ОА и еще mild to moderate - совершенно непонятно.



Написали бы честно - есть данные лабораторных исследований... возможно в перспективе... необходимы дальнейшие клинические исследования.



А вот рекомендовать совершенно КЛИНИЧЕСКИ не проверенный метод больным, да еще и брать за это деньги, как за "новейший беспрецедентный.. не имеющий аналогов.. не известный серым российским врачам.." - это, сорри, свинство.
 
Господин Родионов, (заметьте, исправленная версия :D )



Ну согласитесь, Вы повыхватывали часть информации, которая помогет Вам отстоять свою точку зрения. И это понятно. Но форум дискуссионный и мы дискутируем.

Я не беру деньги, а тем более не предоставляю услуги, а только дал информацию. Поэтому "свинство" и всё что там дальше Вами добавлено, о серости и т.д., пропускаю мимо ушей и обсуждать не желаю. ;) Это была цитата из статьи в российской газете. Остальное Вы сами добавили. Хотя... "Диклофенак не помогает, терафлекс, милокс так же не помогают..." Пациентка получила всё что можно с доказанным и обоснованным клиническим эффектом. И видимо, далеко не бесплатно. Так что о финансовой стороне мы помолчим. Конечно, медицина не всесильна и врачи не волшебники. Это всё понятно.

Согласитесь, что за Orthkin стоит серьёзная научная платформа. Статья, которую я навскидку тут показал датирована 2003 годом. На сегодняшний день есть статистические и клинические данные. Кстати, очень интересные. Таким образом, "...возможно в перспективе... совершенно КЛИНИЧЕСКИ не проверенный метод..." тут не уместно. Это уже сегодняшний день, повседневная практика. Может я не лучшую статью в спешке Вам показал? :)
 
Может я не лучшую статью в спешке Вам показал? :)



Кто же Вас знает. Что смогли - то и показали. Мало что показали. Что Антон Владимирович нашел - тоже продемонстрировал. Остальное - Ваше словоблудие.



Я вот вам продемонстрирую цитату из Harrison's Principles of Internal Medicine 16th Edition, а уж вы делайте выводы насчет "пациентка получила всё что можно с доказанным и обоснованным клиническим эффектом". Все же диклофенак и глюкозамин с хондроитином - далеко не все в лечении ОА.



Nonpharmacologic Measures* •* REDUCTION OF JOINT LOADING* OA1 may be caused or aggravated by poor body mechanics. Correction of poor posture and a support for excessive lumbar lordosis can be helpful. Excessive loading of the involved joint should be avoided. Patients with knee or hip OA should avoid prolonged standing, kneeling, and squatting. Obese patients should be counseled to lose weight. In patients with medial compartment knee OA, a wedged insole may decrease joint pain.



Rest periods during the day may be of benefit, but complete immobilization of the painful joint is rarely indicated, except in cases of hand OA. For DIP16 joint OA that is so painful that it interferes with hand function, a custom-molded thermoplastic splint that blocks flexion can reduce pain, improve overall hand function, and reduce muscle spasm. Splinting can also be very effective for trapeziometacarpal joint and pantrapezial OA. Rigid immobilization is not an acceptable long-term option for pain in the proximal interphalangeal joints, however, because it limits hand function and can result in shortening of the collateral ligaments. In patients with unilateral OA of the hip or knee, a cane, held in the contralateral hand, may reduce joint pain by reducing the joint contact forces. Bilateral disease may necessitate use of crutches or a walker.



PATELLAR TAPING* OA1 of the patellofemoral compartment can cause severe pain, especially with kneeling, squatting, or climbing stairs. Medial taping of the patella can significantly reduce pain in such cases. The taping procedure is simple and inexpensive and patients can learn to apply their own tape after minimal instruction. The prompt relief of symptoms that may be achieved by taping may be maintained by isometric exercises to strengthen the vastus medialis obliquus component of the quadriceps muscle, facilitating realignment of the patella on a long-term basis.



WEDGED INSOLES/ORTHOSES* In patients with medial compartment knee OA1, pain severity has been shown to be related to the magnitude of the external adduction moment (a measure of the varus torque on the knee during gait). Wedged insoles may be useful in conservative treatment of OA of the medial tibial femoral compartment. Their use may change the spatial position of the lower limb so that the mechanical axis becomes more nearly vertical and the calcaneal axis is shifted to a valgus position with respect to the tibiotalar joint, reducing excessive loading on the medial compartment of the knee and strain on the lateral collateral ligament. Use of lateral wedged insoles may result in a significant decrease in NSAID17 consumption by patients with knee OA. A polypropylene mesh insole is practical, inexpensive, and washable and may last about 2 years, i.e., approximately twice as long as a leather insole.



THERMAL MODALITIES* Application of heat to the OA1 joint may reduce pain and stiffness. A variety of modalities are available; often, the least expensive and most convenient is a hot shower or bath. Occasionally, better analgesia may be obtained with ice than with heat.



EXERCISE* Those who exercise regularly live longer and are healthier than those who are sedentary. Because OA1 of weight-bearing joints limits physical activity and the amount of exercise that an individual can perform, persons with this condition are at increased risk for hypertension, obesity, diabetes, and cardiovascular disease, i.e., diseases related to their inactivity. Only 24% of individuals with arthritis report a level of physical activity sufficient to achieve health; 75% do nothing or are not sufficiently active. Arthritis is the major reason that elderly individuals are not active or limit their activity and is a greater factor in limiting activity than heart disease, hypertension, blindness, or diabetes. Studies of cardiovascular health have shown that the aerobic capacity (cardiovascular fitness) of men with severe knee OA is >30% lower than that of controls who do not have OA. Even at slow speed, individuals with knee OA expend more energy (measured as oxygen consumption) in walking than age- and sex-matched controls.



Disability in patients with OA1 may have more to do with their ability to remain active and physically fit and maintain normal body weight than with pathologic changes in the OA joint. Even if we cannot cure OA, we can cure inactivity. Men in their forties who were not performing sufficient physical activity and had low scores on a treadmill test were found to have remarkably higher death rates than those who were fit. However, among those who were not fit at the outset but who became fit, the risk of mortality decreased by 44%.



The amount of aerobic conditioning (e.g., walking, cycling, aquatic exercise) necessary for cardiovascular fitness is not so great that it cannot be achieved by people with OA1. Patients with OA of lower extremity joints who are able to perform moderate to vigorous exercise at least 3 days per week (i.e., 70 to 85% of maximal heart rate) — an intensity that permits an individual to talk while exercising continuously for 20 to 60 min — improve their fitness and health without exacerbating their joint pain or increasing their need for analgesic drugs. Persons with OA who exercise consistently at this level report decreases in joint pain and disability while improving their cardiovascular muscular fitness (strength and endurance). They also report improvement in function and quality of life and exhibit improved gait and walking speed. Patients with hip or knee OA can participate safely in conditioning exercises to improve fitness and health without increasing their joint pain or need for analgesics or NSAIDs18.



Disuse of the OA1 joint because of pain will lead to muscle atrophy. Because periarticular muscles play a major role in protecting the articular cartilage from stress, strengthening exercises are important. In patients with knee OA, strengthening of the periarticular muscles may result, within weeks, in a decrease in joint pain as great as that seen with NSAIDs19. Most of the information available about the benefits of therapeutic exercise relates to strength training. However, the benefits of therapeutic exercise go far beyond muscle strengthening. In studies that employed 4 to 10 instructional sessions followed by self-directed home exercise in which patients initially exercised up to 5 days per week, with recommendations to decrease the frequency over the next 6 months to 2 days per week, compliance was excellent. The results showed that pain, anxiety, and depression decreased, while lower extremity strength, endurance, proprioception, and functional status improved and disability was reduced. With fairly minimal intervention and self-directed exercise, patients with OA can achieve and maintain important gains.



PATIENT EDUCATION* For effective management of many patients with OA1, encouragement, reassurance, advice about exercise, and recommendation of measures to unload the arthritic joint (such as a cane and proper footwear) may be all that is required. Patient education programs offer benefits beyond those that can be achieved with an NSAID20 in symptomatic treatment of patients with OA. Patient education interventions provide an additive benefit 20 to 30% as great as that of NSAID treatment alone. Relevant education for the patient with OA is not education about joint anatomy or the definition of an osteophyte but is education in self-management that emphasizes the central role of the patient in managing the disease; furthermore, it teaches the skills required to permit patients to manage medically and emotionally and to maintain their role in society.



A variety of self-management programs have been developed for patients with OA1, such as the Arthritis Self-Management Program that is sponsored in the United States by the Arthritis Foundation. Participation in a structured community-based education intervention, led by trained lay leaders, can result in significant decreases in pain, disability, and depression. Patients who participate in such programs report greater performance of self-management behaviors, e.g., taking their medication properly, communicating with their healthcare providers. Furthermore, the benefits may endure for years, even with no reinforcement of the intervention.



TIDAL IRRIGATION OF THE KNEE* Copious irrigation of the OA1 knee through a large-bore needle, flushing out fibrin, cartilage shards, and other debris, has been reported to provide months of comfort for some patient whose joint pain has been refractory to analgesics, NSAIDs21, and intraarticular glucocorticoid injections. However, results of a randomized controlled trial of patients with knee OA that included a sham-irrigation procedure led to the conclusion that the bulk of the benefit from this procedure is attributable to the placebo effect.
 
ARTHROSCOPIC DEBRIDEMENT AND LAVAGE* Arthroscopic surgery can be helpful in alleviating knee pain and improving function in the subgroup of patients with knee OA1 in whom loose bodies, flaps of cartilage, or disruption of the meniscus (e.g., a bucket handle tear) cause mechanical symptoms, such as locking, giving way of the limb, or catching. Although arthroscopic debridement, e.g., smoothing of the surface of fibrillated articular cartilage or meniscus, trimming of osteophytes, and removal of inflamed synovium, is employed widely in patients with symptomatic knee OA who do not have mechanical symptoms, but who have not benefited from pharmacologic therapy, this therapeutic modality appears to be of no greater symptomatic benefit than placebo in such patients.



Pharmacologic Therapy* •* NSAIDS22 AND ACETAMINOPHEN (N-ACETYL-P-AMINOPHENOL, APAP)* Drug therapy for OA1 today is palliative; no pharmacologic agent has been shown to prevent, delay the progression of, or reverse the pathologic changes of OA in humans. Although claims have been made that some NSAID23s slow the rate of cartilage damage, adequately controlled clinical trials in humans with OA to support this view are lacking.



In management of OA1 pain, pharmacologic agents should be used as adjuncts to nonpharmacologic measures, such as those described above. The latter are the keystone of OA treatment. Although NSAIDs24 often decrease joint pain and improve mobility in OA, the magnitude of improvement is generally modest — on average, about 30% reduction in pain and 15% improvement in function. Many patients taking a full therapeutic dose of NSAIDs continue to experience a significant level of residual joint pain. On the other hand, low (i.e., analgesic) doses of NSAIDs may be as effective as anti-inflammatory doses; 30 to 40% of patients with OA may find APAP25 — an analgesic recommended for treatment of mild-moderate pain — as effective as an NSAID. Even in patients with clinical signs of joint inflammation (synovial effusion, tenderness), relief of joint pain by APAP may be as effective as that achieved with an NSAID. Nonetheless, if simple analgesics are inadequate, it is reasonable to prescribe an NSAID for the patient with OA.



However, concern over the use of NSAIDs26 in OA1 has grown in recent years because of the adverse effects of these agents, especially those related to the gastrointestinal tract. Those at greatest risk for OA, i.e., the elderly, appear to be at greater risk than younger individuals for gastrointestinal symptoms, ulceration, hemorrhage, and death as a result of NSAID use. The annual rate of hospitalization for peptic ulcer disease among elderly current NSAID users was 16 per 1000, i.e., four times greater than that for persons not taking an NSAID. Among people age =65, as many as 30% of all hospitalizations and deaths related to peptic ulcer disease have been attributed to NSAID use. Risk factors for hemorrhage and other ulcer complications associated with NSAID use include, in addition to age, a history of peptic ulcer disease or of upper gastrointestinal bleeding, concomitant use of glucocorticoids or anticoagulants, and, possibly, smoking and alcohol consumption (Table 312-4).



SELECTIVE COX-2 INHIBITORS* In patients who carry risk factors for an NSAID27-associated gastrointestinal catastrophe, a cyclooxygenase (COX)-2 selective NSAID may be preferable to even a low dose of a nonselective COX inhibitor. In contrast to the nonselective NSAIDs, all of which inhibit COX-1 as well as COX-2, selective COX-2 inhibitors, e.g., celecoxib, rofecoxib, valdecoxib, are now available. These exhibit no greater efficacy than nonselective NSAIDs, but endoscopic studies show that they are associated with a lower incidence of gastroduodenal ulcer than nonselective NSAIDs. Of additional advantage with respect to the issue of upper gastrointestinal bleeding, selective COX-2 inhibitors do not have a clinically significant effect on platelet aggregation or bleeding time.



Results of two large-size gastrointestinal safety studies, the CLASS trial and VIGOR study, have been published (Table 312-5). Both were designed to ascertain whether treatment with celecoxib or rofecoxib, respectively, resulted in a lower incidence of clinically important NSAID28-associated ulcers and ulcer complications than that seen with nonselective NSAIDs. In the VIGOR trial, a clear reduction in the incidence of upper gastrointestinal events was apparent in the rofecoxib treatment arm, in comparison with the naproxen arm. The risk of all clinical upper gastrointestinal events was reduced by some 54% (p<. 01), of complicated upper gastrointestinal events by 57% (p =. 005), and of any gastrointestinal bleeding by 62% (p<. 01). In the CLASS study, the annualized incidence rates of ulcer complications (the primary outcome measure) with celecoxib was not significantly different from that and with the comparator nonselective NSAIDs after 6 months of treatment, although the difference for ulcer complications combined with symptomatic ulcers was significant (2.08% vs 3.54%, respectively, p =. 02). Although a significant reduction in ulcer complications was seen with celecoxib, use of low-dose aspirin for cardiovascular prophylaxis appeared to mitigate the gastroprotective effect of celecoxib. (Although only 22% of subjects in the CLASS study were taking low-dose aspirin, as many as 60% of patients with OA1 >60 years old may do so in clinical practice.) Furthermore, the superiority of celecoxib observed among nonaspirin users during the first 6 months was not sustained in patients treated for 12 months.



Unexpectedly, the incidence of myocardial infarction (MI) in the VIGOR study was fourfold greater among patients treated with rofecoxib than with naproxen. Although (1) the absolute number of MIs was small; (2) the study was not powered to compare the effects of the two treatments on MI; (3) the comparability of the treatment groups with respect to the prevalence of risk factors for MI (e.g., obesity, smoking, hypercholesterolemia, diabetes mellitus) was unknown; (4) the dose of rofecoxib was two to four times greater than that used for treatment of OA; and (5) the trial was conducted in patients with rheumatoid arthritis, in which the incidence of MI is about twice as great as that in OA1. The rofecoxib label contains a caveat about use of this drug in patients predisposed to ischemic heart disease.



GLUCOCORTICOID INJECTION* Systemic glucocorticoids have no place in the treatment of OA1. However, intra- or periarticular injection of a depot glucocorticoid preparation may provide marked symptomatic relief for weeks to months. Because studies in animal models have suggested that glucocorticoids may produce cartilage damage, and frequent injections of large amounts of steroids have been associated with joint breakdown in humans, the injection should generally not be repeated in a given joint more often than every 4 to 6 months.



INTRAARTICULAR INJECTION OF HYALURONAN* Intraarticular injection of hyaluronan has been approved for treatment of patients with knee OA1 who have failed a program of nonpharmacologic therapy and simple analgesics. Because the duration of benefit following treatment may exceed by many months the synovial half-life of exogenous hyaluronan, the mechanism of action is unclear. However, the placebo response to intraarticular injection of hyaluronan is often large and sustained. For example, the pivotal clinical trial of Hyalgan failed to demonstrate superiority of oral naproxen, 500 mg bid, over intraarticular injections of saline. Furthermore, intraarticular injection of a preparation of the high-molecular-weight hylan (Synvisc) which had been denatured to eliminate its viscoelasticity, was no less efficacious than injection of the intact hylan or non-cross-linked lower molecular weight hyaluronan. Consistent with this observation, no difference in efficacy was observed in a randomized placebo-controlled trial of Synvisc, a lower molecular weight hyaluronan formulation, and placebo.



OPIOIDS* Health professionals and patients hold concerns about tolerance and physical and psychological dependence, and many physicians hesitate to prescribe opioids for patients with nonmalignant chronic pain because of concerns about legal action by governmental regulatory authorities. However, the prevalence of narcotic abuse among older people is low: <1% of patients attending methadone maintenance programs are =60 years.



For acute flares of OA1 pain, when APAP29 or an NSAID30 does not provide adequate pain relief or is not well tolerated, a weak opioid, e.g., oral codeine, deserves consideration. Because codeine, when taken alone in a dose of 60 mg, is no more effective than 650 mg of aspirin or APAP, it is used in combination with these drugs to treat moderate or moderately severe OA pain.



Opioids may also be useful for chronic OA1 pain. The major problem associated with the use of chronic opioid therapy for OA pain is the side effects of these agents, e.g., nausea, vomiting, constipation, urinary retention, mental confusion, drowsiness, and respiratory depression. In the elderly, the central nervous system effects of opioids (e.g., dizziness) may have particularly serious consequences. Prescription of either codeine or propoxyphene may increase the risk of hip fracture by 60%. Concurrent use of these opioids and a psychotropic drug (e.g., sedative, antidepressant, antipsychotic) carries a fracture risk 2.6 times as high as that in nonusers of either drug class.
 
Tramadol hydrochloride is a centrally acting analgesic with a dual mechanism of action: the molecule is a u-opioid agonist and also inhibits reuptake of norepinephrine and serotonin. Although the affinity of binding to the u-opioid regimen is some 6000 times lower than that of morphine, the opioid and nonopioid activities are synergistic. In contrast to NSAIDs31, tramadol does not inhibit prostaglandin synthesis and has no adverse effects on the gastric mucosa, kidney, or platelet. It is a useful adjunct in patients with OA1 in whom APAP32 or a low dose of NSAID is ineffective or contraindications exist to the use of an NSAID. Improvement with tramadol, 200 to 400 mg/d, is comparable to that with ibuprofen, 1200 to 2400 mg/d, in patients with chronic joint pain. Because development of tolerance or dependence appears to be uncommon with long-term administration, tramadol has not been scheduled as a controlled substance. In general, its efficacy and adverse event profile are comparable to those of APAP/codeine. The latter, however, is considerably less expensive.



The frequency and severity of side effects of tramadol may be reduced considerably if treatment is initiated at a very low dose (e.g., 25 mg/d), which can then be increased gradually every few days. However, this "start low, go slow" approach limits the usefulness of the drug in management of acute pain. Because it inhibits the reuptake of serotonin and norepinephrine, tramadol should not generally be given to patients receiving a tricyclic antidepressant, selective serotonin reuptake inhibitor, or monoamine oxidase inhibitor. These combinations have been reported to cause convulsions. Even in the absence of concomitant therapy with the above agents, however, seizures may occasionally occur in some patients taking tramadol.



A combination of tramadol and APAP33 in a 37.5 mg/325 mg tablet (ULTRACET) has recently become available. It has a more rapid onset of action than tramadol alone and longer duration of action than APAP alone. In subjects with an acute flare of hip or knee OA1, who received 1 or 2 tablets of tramadol/APAP qid for 10 days in addition to their usual NSAID34 therapy, tramadol/APAP was significantly superior to placebo with respect to improvement in joint pain and global assessment by subjects and physicians. However, treatment-related adverse events (e.g., nausea, dizziness, vomiting) were reported in nearly 25% of the tramadol/APAP group, but in only 8% of the placebo group. Furthermore, the above figures may understate the true incidence of adverse events with this formulation, because subjects were excluded from the study if they had previously failed tramadol therapy or had discontinued tramadol because of an adverse event.



RUBEFACIENTS/CAPSAICIN* Because use of systemic analgesics and NSAIDs35 is often accompanied by adverse effects and older individuals with OA1 often require medication for comorbid conditions (e.g., hypertension, heart disease, diabetes mellitus) and are at increased the risk of serious drug interactions with NSAIDs, topical therapy for management of OA has appeal.



Application of topical irritants to painful joints and muscles and the local heat provided by rubefacients may be beneficial. However, although topical medications are widely used in the United States as over-the-counter preparations, they are not often prescribed for OA1 in this country, chiefly because evidence of their efficacy is limited. Except for formulations of salicylate, topical NSAIDs36 have not been approved for use in the United States. It is unclear whether the benefit attributed to their use is mediated through a pharmacologic action, placebo effect, or their action as a rubefacient. Capsaicin cream, which depletes local sensory nerve endings of substance P, may reduce joint pain and tenderness when applied topically by patients with hand or knee OA, even when used as monotherapy, i.e., without NSAIDs or systemic analgesics.



Glucosamine, Chondroitin Sulfate* Glucosamine and chondroitin sulfate have recently enjoyed striking popularity for treatment of OA1. They are sold widely in pharmacies, supermarkets, and health food stores but are not approved for use in OA by the U.S. Food and Drug Administration. Several studies have shown glucosamine to be superior to placebo and comparable to NSAIDs37 with respect to efficacy in patients with knee OA, and to have a better safety profile than NSAIDs. However, the efficacy of neither glucosamine nor chondroitin sulfate has been examined in large, well-designed placebo-controlled trials. In a meta-analysis of randomized, double-blind, placebo-controlled studies of glucosamine and chondroitin sulfate, moderate symptomatic benefit was demonstrated for both agents, relative to placebo. In studies of chondroitin sulfate, symptomatic improvement was apparent as long as 12 months after the onset of treatment. However, when only high-quality or large-size trials were considered, the effect sizes for glucosamine and chondroitin sulfate were diminished, i.e., the better the study design, the smaller the therapeutic benefit. In three recent randomized, double-blind trials in which the manufacturer did not have access to the raw data and was not involved in data analysis, glucosamine was no more effective than placebo.



The question arises whether glucosamine is "chondroprotective." Results of two recent randomized clinical trials have led to the suggestion that glucosamine not only improves joint pain in patients with knee OA1, but protects against articular cartilage damage, based upon analyses of changes in joint space width in the standing anteroposterior (AP) knee radiograph. However, concern has been expressed about the interpretation of the results of these studies because of limitations of the radiographic methods employed. A multicenter study supported by the National Institutes of Health, the Glucosamine Chondroitin Arthritis Intervention Trial (GAIT), is in progress which is comparing glucosamine, chondroitin sulfate, the combination, and celecoxib with placebo in patients with knee OA. Although the primary outcome measure is joint pain after 6 months of treatment, approximately 50% of the subjects will be maintained on treatment for 2 years and radiographs obtained at baseline will be compared with those obtained after 1 year and 2 years of treatment.



Orthopedic Surgery* Joint replacement surgery should be reserved for patients with advanced OA1 in whom aggressive medical management has failed. In such cases total joint arthroplasty may be remarkably effective in relieving pain and increasing mobility. Osteotomy, which is surgically more conservative than arthroplasty, can eliminate the concentration of peak dynamic loads and may provide effective pain relief in patients with hip or knee OA. It is of greatest benefit when the disease is only moderately advanced.



Cartilage Regeneration* Chondroplasty (abrasion arthroplasty) has enjoyed some popularity as treatment for OA1, but well-controlled studies of its efficacy are lacking and the fibrocartilage that resurfaces the abraded bone is inferior to normal hyaline cartilage in its ability to withstand mechanical loads. In one study, knee pain and function were not related to the extent of cartilage regeneration 2 years later in patients who had undergone tibial osteotomy for medial compartment knee OA. Autologous chondrocyte transplantation and attempts at cartilage repair using mesenchymal stem cells and autologous osteochondral plugs are currently being used experimentally for repair of focal chondral defects, but have not been proved to be effective in treatment of OA.
 
Уважаемый господин Dr. , ну тут вы погорячились... Зачем же так форум загружать...? Вопрос то был в конце концов у пациентки. Ей эта информация уж точно не понадобится. А если Вы меня хотели удивить, то послали бы всё это мне в личку. И тогда я бы удивился. :D Располагая таким шикарным списком на английском языке вы бы лучше совет дали госпоже < mila.ru > (топик ниже) Почему то там все молчат... А жаль.

Дааа... поле для экспериментов над пациенткой действительно впечатляет. Куда уж мне с моим скромным информационным советом... Только жизни нормального человека не хватит чтоб всё это попробовать.

Да и не об этом речь. Я дал информацию, а Вы на меня набросились. Причём голословно. Я что, купить его Вас заставляю? Или навязчиво продаю? Попробуйте обосновать неэффективность Orthokin. И не скрываясь при этом за фразами о "совершенно КЛИНИЧЕСКИ не проверенный метод". Метод проверен. Просто, видимо, Вам не известен.

Всё, на этом дискуссию прекращаю. Не интересно. :(

Удачи в испытаниях по вышеприведённому списку.
 
Ну согласитесь, Вы повыхватывали часть информации, которая помогет Вам отстоять свою точку зрения. Не соглашусь. Я процитировал абстракт ПОЛНОСТЬЮ, ничего из него не выхватывая. Лишь отметил ключевые позиции. Абстракт - это часть публикации, которая должна содержать ВСЮ ключевую информацию, достаточную для понимания.

Я что, купить его Вас заставляю? Или навязчиво продаю? Нас - нет, спасибо. Помимо явной рекламы существует еще и скрытая. Я сильно сомневаюсь, что немцы или кто другой вводит кровь, побывавшую в колбе с хромированными шариками, "безвозбезддо, то есть дадом" (с). Но это в сторону...

Попробуйте обосновать неэффективность Orthokin. НЕТ И ЕЩЕ РАЗ НЕТ!! Посыл ошибочный! Это Вы должны обосновать эффективность предлагаемого метода. Чувствуете разницу?

Метод проверен. Просто, видимо, Вам не известен. Докажите. Приведите ссылку на нормальное исследование с нормальным дизайном и нормальными конечными точками. Тогда и потолкуем.

Та ссылка на "не лучшую статью в спешке" доказательством клинической эффективности не является.

Всё, на этом дискуссию прекращаю. Не интересно.Как угодно, Вас никто за язык не тянул ;) А мне кажется, что всё только начинается :D
 
Господин Родионов,

исследования универститетских клиник Вам подойдёт, господа сомневающиеся и их поддерживающие? :) Уж больно вы консервативны, господа. Или мне кажется? :D Или это называется "сторонники классической медицины". Перед тем как обвинять в мошенничестве, неплохо бы хоть поверхностно в инете погулять. Медицина очень быстро развивается, а уж молекулярная биология и подавно... Orthokin применяется уже пару лет. Есть ещё его разновидности Orthogen, например. 75% успеха конечно очень оптимистично, но 50-60% успеха терапия запросто достигает. Это из реальной практики.



http://www.orthogen.com/downloads/english/pm_orthokin-trial%20oa_21072005.pdf



http://www.orthogen.com/downloads/english/PI221WSEnglisch.pdf



Да, есть ещё список литературы, ничем не уступающий по размерам и по смыслу списку господина Dr. Но я воздержусь... а то ещё забянят.

Не с кем и поспорить будет :p
 
Ссылки хороши :) , правда вторая ссылка - это пресс-релиз.

Но вот контрольные группы очень странные:

В первом исследовании: Ортокин-гиалуроновая кислота-плацебо

В пресс-релизе: Ортокин-5 мг кортизона в/с - 10 мг кортизона в/с



Кортизон в/с - не есть стандарт лечения остеоартроза (остеоартрита). Ну а гиалуронат тоже не ради прямого обезболивающего эффекта дается.
 

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