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There is a history of clinical research done on glycosaminoglycans, especially glucosamine and chondroitin, for the treatment of arthritis. Since glucosamine is a precursor for glycosaminoglycans, and glycosaminoglycans are a major component of joint cartilage, some have hoped that supplemental glucosamine could beneficially influence cartilage structure, and alleviate arthritis. The effectiveness of glucosamine is controversial.〔(The effects of Glucosamine Sulphate on OA of the knee joint ). BestBets.〕 Most recent reviews found it to be equal to or only slight better than placebo. A difference may exist between glucosamine sulfate and glucosamine hydrochloride, with glucosamine sulfate showing a benefit and glucosamine hydrochloride not. The Osteoarthritis Research Society International recommends that glucosamine be discontinued if no effect is observed after six months and the National Institute of Clinical Excellence no longer recommends its use.〔 Despite the difficulty in determining the efficacy of glucosamine, it remains a viable treatment option. Similar trials have been done with chondroitin. ==History of trials== In general, the clinical trials of the mid-1990s that furnished positive results showing glucosamine efficacy were later deemed to be of poor quality due to shortcomings in their methods, including small size, short duration, poor analysis of drop-outs, and unclear procedures for blinding. At the same time, several independent studies did not detect any benefit of glucosamine supplementation on osteoarthritis. A Cochrane 2005 meta-analysis of glucosamine therapy for osteoarthritis found that only the Rotta brand of glucosamine appeared to be superior to placebo in the treatment of pain and functional impairment resulting from symptomatic osteoarthritis. However, when the low quality and older studies were discounted and only those using the highest-quality design were considered, there was no difference from placebo treatment. A second 2005 review of glucosamine clinical trials reached a different conclusion. Published in the ''Annals of Pharmacotherapy'', the authors of this review concluded that ″The available evidence suggests that glucosamine sulfate may be effective and safe in delaying the progression and improving the symptoms of knee OA.″ A systematic review in 2007 found that effect sizes from glucosamine supplementation were highest in industry-funded studies and lowest in independent studies. which may lead one to believe that bias is responsible for the heterogeneity of the clinical study findings regarding the efficacy of glucosamine. An alternative explanation may be that the two commonly available forms, sulfate and hydrochloride, while used interchangeably by the general public and even the medical community, appear to have different pharmacologic effects ''in vivo''. Another 2007 review of the available research concluded that there was ″compelling evidence″ that glucosamine sulfate (but not hydrochloride) slowed the progression of knee and hip osteoarthritis. This finding was confirmed by a 2013 meta-analysis of 19 glucosamine trials which concluded that while neither form of glucosamine appeared significantly more effective than placebo at symptom improvement, glucosamine sulfate alone showed efficacy in improving physical function in knee OA as measured by the Lequesne Index in trials lasting more than 24 months. In 2006, the U.S. National Institutes of Health (NIH) funded a 24 week, 12.5 million-dollar multicenter clinical trial (the GAIT trial) to study the effect of chondroitin sulfate, glucosamine hydrochloride, chondroitin/glucosamine in combination, and celecoxib as a treatment for knee-pain in two groups of patients with osteoarthritis of the knee: Patients with ''mild pain'' (n=1229), and patients with ''moderate to severe pain'' (n=354). When the data from both groups were pooled and analyzed, there was no statistically significant difference between groups taking glucosamine HCl, chondroitin sulfate, glucosamine/chondroitin; and those taking an inactive placebo or the positive control, the prescription analgesic celecoxib. The authors of the study analyzed the moderate-to-severe pain group and found that in this group, the combination of glucosamine and chondroitin was more effective at providing pain relief than the positive control with 79% of the glucosamine group reporting at least a 20% reduction in pain compared to 70% for celecoxib and only 54% reporting a similar reduction in the placebo group. However, the researchers caution that given the small size of the sub-group, these findings should be confirmed with further studies. Despite its size and design, the GAIT trial may have also had some important limitations, however. When considering the entire cohort, none of the treatments studied performed significantly better (or worse) than placebo in improving patient WOMAC pain and function scores. In other words, because of the inclusion of both a placebo and a positive control, and the fact that roughly 60% of each treatment group achieved the same level of improvement, it is difficult to conclude anything about the efficacy or non-efficacy of glucosamine in the treatment of knee OA from this study. In a follow-up study in 2008, 572 patients from the GAIT trial continued their supplementation for 2 years. After 2 years of supplementation with glucosamine and chondroitin sulfate, alone or in combination, there was no benefit in slowing the loss of cartilage, in terms of joint space width, when compared to a placebo or celecoxib. As in the original GAIT study, this follow up study was confounded by unexpected results that made if difficult to conclude anything definitive about the effect of glucosamine on slowing the progression of OA. Despite the fact that the glucosamine group showed less than one-tenth the joint narrowing (0.013 mm) as the placebo group (0.166 mm), none of the groups experienced joint space narrowing to the degree the researchers expected (0.4 mm) over the two year period based on earlier studies of OA disease progression. Thus, while the researchers rightly concluded that no treatment in this study was found to produce a ″a clinically important reduction″ in joint space width loss none of the participants experienced clinically important progression of their disease during the study period either. In another 2-year follow-up study involving 662 patients from the GAIT trial, published in 2010, there was neither significant pain reduction nor improved function when comparing glucosamine and/or chondroitin to a placebo although the positive control also failed to perform significantly better that the placebo in this study. 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「Clinical trials on glucosamine and chondroitin」の詳細全文を読む スポンサード リンク
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