Effects of glucosamine, chondroitin, or placebo in patients with osteoarthritis of hip or knee: network meta-analysis
Objective
To determine the effect of glucosamine, chondroitin, or the two in combination on joint pain and on radiological progression of disease in osteoarthritis of the hip or knee.
Design
Network meta-analysis. Direct comparisons within trials were combined with indirect evidence from other trials by using a Bayesian model that allowed the synthesis of multiple time points.
Main outcome measure
Pain intensity. Secondary outcome was change in minimal width of joint space. The minimal clinically important difference between preparations and placebo was prespecified at -0.9 cm on a 10 cm visual analogue scale.
Data sources
Electronic databases and conference proceedings from inception to June 2009, expert contact, relevant websites.
Eligibility criteria for selecting studies
Large scale randomised controlled trials in more than 200 patients with osteoarthritis of the knee or hip that compared glucosamine, chondroitin, or their combination with placebo or head to head.
Results
10 trials in 3803 patients were included. On a 10 cm visual analogue scale the overall difference in pain intensity compared with placebo was -0.4 cm (95% credible interval -0.7 to -0.1 cm) for glucosamine, -0.3 cm (-0.7 to 0.0 cm) for chondroitin, and -0.5 cm (-0.9 to 0.0 cm) for the combination. For none of the estimates did the 95% credible intervals cross the boundary of the minimal clinically important difference. Industry independent trials showed smaller effects than commercially funded trials (P=0.02 for interaction). The differences in changes in minimal width of joint space were all minute, with 95% credible intervals overlapping zero.
Conclusions
Compared with placebo, glucosamine, chondroitin, and their combination do not reduce joint pain or have an impact on narrowing of joint space. Health authorities and health insurers should not cover the costs of these preparations, and new prescriptions to patients who have not received treatment should be discouraged.
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BMJ 2010; 341:c4675
2010年9月23日 星期四
JAMA打破葡萄糖胺有效治療退化性關節炎的「神話」
Effect of glucosamine on pain-related disability in patients with chronic low back pain and degenerative lumbar osteoarthritis: a randomized controlled trial.
CONTEXT: Chronic low back pain (LBP) with degenerative lumbar osteoarthritis (OA) is widespread in the adult population. Although glucosamine is increasingly used by patients with chronic LBP, little is known about its effect in this setting. OBJECTIVE: To investigate the effect of glucosamine in patients with chronic LBP and degenerative lumbar OA. DESIGN, SETTING, AND PARTICIPANTS: A double-blind, randomized, placebo-controlled trial conducted at Oslo University Hospital Outpatient Clinic, Oslo, Norway, with 250 patients older than 25 years of age with chronic LBP (>6 months) and degenerative lumbar OA.
INTERVENTIONS: Daily intake of 1500 mg of oral glucosamine (n = 125) or placebo (n = 125) for 6 months, with assessment of effect after the 6-month intervention period and at 1 year (6 months postintervention).
MAIN OUTCOME MEASURES: The primary outcome was pain-related disability measured with the Roland Morris Disability Questionnaire (RMDQ). Secondary outcomes were numerical scores from pain-rating scales of patients at rest and during activity, and the quality-of-life EuroQol-5 Dimensions (EQ-5D) instrument. Data collection occurred during the intervention period at baseline, 6 weeks, 3 and 6 months, and again 6 months following the intervention at 1 year. Group differences were analyzed using linear mixed models analysis.
RESULTS: At baseline, mean RMDQ scores were 9.2 (95% confidence interval [CI], 8.4-10.0) for glucosamine and 9.7 (95% CI, 8.9-10.5) for the placebo group (P = .37). At 6 months, the mean RMDQ score was the same for the glucosamine and placebo groups (5.0; 95% CI, 4.2-5.8). At 1 year, the mean RMDQ scores were 4.8 (95% CI, 3.9-5.6) for glucosamine and 5.5 (95% CI, 4.7-6.4) for the placebo group. No statistically significant difference in change between groups was found when assessed after the 6-month intervention period and at 1 year: RMDQ (P = .72), LBP at rest (P = .91), LBP during activity (P = .97), and quality-of-life EQ-5D (P = .20). Mild adverse events were reported in 40 patients in the glucosamine group and 46 in the placebo group (P = .48).
CONCLUSIONS: Among patients with chronic LBP and degenerative lumbar OA, 6-month treatment with oral glucosamine compared with placebo did not result in reduced pain-related disability after the 6-month intervention and after 1-year follow-up.
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JAMA. 2010; 304(1):45-52 (ISSN: 1538-3598)
TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT00404079.
CONTEXT: Chronic low back pain (LBP) with degenerative lumbar osteoarthritis (OA) is widespread in the adult population. Although glucosamine is increasingly used by patients with chronic LBP, little is known about its effect in this setting. OBJECTIVE: To investigate the effect of glucosamine in patients with chronic LBP and degenerative lumbar OA. DESIGN, SETTING, AND PARTICIPANTS: A double-blind, randomized, placebo-controlled trial conducted at Oslo University Hospital Outpatient Clinic, Oslo, Norway, with 250 patients older than 25 years of age with chronic LBP (>6 months) and degenerative lumbar OA.
INTERVENTIONS: Daily intake of 1500 mg of oral glucosamine (n = 125) or placebo (n = 125) for 6 months, with assessment of effect after the 6-month intervention period and at 1 year (6 months postintervention).
MAIN OUTCOME MEASURES: The primary outcome was pain-related disability measured with the Roland Morris Disability Questionnaire (RMDQ). Secondary outcomes were numerical scores from pain-rating scales of patients at rest and during activity, and the quality-of-life EuroQol-5 Dimensions (EQ-5D) instrument. Data collection occurred during the intervention period at baseline, 6 weeks, 3 and 6 months, and again 6 months following the intervention at 1 year. Group differences were analyzed using linear mixed models analysis.
RESULTS: At baseline, mean RMDQ scores were 9.2 (95% confidence interval [CI], 8.4-10.0) for glucosamine and 9.7 (95% CI, 8.9-10.5) for the placebo group (P = .37). At 6 months, the mean RMDQ score was the same for the glucosamine and placebo groups (5.0; 95% CI, 4.2-5.8). At 1 year, the mean RMDQ scores were 4.8 (95% CI, 3.9-5.6) for glucosamine and 5.5 (95% CI, 4.7-6.4) for the placebo group. No statistically significant difference in change between groups was found when assessed after the 6-month intervention period and at 1 year: RMDQ (P = .72), LBP at rest (P = .91), LBP during activity (P = .97), and quality-of-life EQ-5D (P = .20). Mild adverse events were reported in 40 patients in the glucosamine group and 46 in the placebo group (P = .48).
CONCLUSIONS: Among patients with chronic LBP and degenerative lumbar OA, 6-month treatment with oral glucosamine compared with placebo did not result in reduced pain-related disability after the 6-month intervention and after 1-year follow-up.
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JAMA. 2010; 304(1):45-52 (ISSN: 1538-3598)
TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT00404079.
2010年9月22日 星期三
低溫治療 - Therapeutic Hypothermia
Targeted Temperature Management for Comatose Survivors of Cardiac Arrest
Targeted temperature management, also known as therapeutic hypothermia, is a therapeutic intervention that is intended to limit neurologic injury after a patient's resuscitation from cardiac arrest. Hypothermia causes a reduction in brain metabolism, including a reduction in oxygen utilization and ATP consumption.
What are the indications for therapeutic hypothermia?
Therapeutic hypothermia should be considered for adult patients successfully resuscitated from a witnessed out-of-hospital cardiac arrest of presumed cardiac cause, though patients after in-hospital cardiac arrest may also benefit. This measure should also be considered in patients who are comatose, and in patients with an initial rhythm of ventricular fibrillation or nonperfusing ventricular tachycardia (or other initial rhythms such as asystole or pulseless electrical activity).
How is therapeutic hypothermia achieved?
Several different cooling methods are available for use in therapeutic hypothermia. In the pivotal clinical trials, cooling was achieved by the application of numerous ice packs around the head, neck, torso, and limbs or with the use of a cold-air mattress covering the entire body. Other methods of surface cooling include the use of water-circulating cooling blankets or pads, refrigerated cooling pads, and thermal beds. Core cooling can be achieved with the use of intravascular cooling catheters (made of metal or containing balloons filled with cold saline) or by means of intravenous infusion of cold fluids. The objective is to reach a target temperature of 32 to 34°C and to maintain that temperature for 24 hours, if feasible.
What additional patient management is necessary before hypothermia is induced?
A. Before hypothermia is induced, sedation, analgesia, and paralysis should be initiated to prevent shivering (which can lead to increased oxygen consumption, excessively laborious breathing, increased heart rate, and a general stress-like response, in addition to impeding the cooling process) and to minimize the patient’s discomfort.
What metabolic disturbances are induced by therapeutic hypothermia?
A. Hypothermia can induce metabolic disturbances, including hypokalemia, hypomagnesemia, hypophosphatemia, and hyperglycemia. Therefore, regular measurement of electrolyte and glucose levels is necessary to guide the appropriate amount of electrolyte substitution and insulin therapy. Leukopenia and thrombocytopenia may occur but typically do not require intervention.
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TEACHING TOPICS from the NEJM
Targeted temperature management, also known as therapeutic hypothermia, is a therapeutic intervention that is intended to limit neurologic injury after a patient's resuscitation from cardiac arrest. Hypothermia causes a reduction in brain metabolism, including a reduction in oxygen utilization and ATP consumption.
What are the indications for therapeutic hypothermia?
Therapeutic hypothermia should be considered for adult patients successfully resuscitated from a witnessed out-of-hospital cardiac arrest of presumed cardiac cause, though patients after in-hospital cardiac arrest may also benefit. This measure should also be considered in patients who are comatose, and in patients with an initial rhythm of ventricular fibrillation or nonperfusing ventricular tachycardia (or other initial rhythms such as asystole or pulseless electrical activity).
How is therapeutic hypothermia achieved?
Several different cooling methods are available for use in therapeutic hypothermia. In the pivotal clinical trials, cooling was achieved by the application of numerous ice packs around the head, neck, torso, and limbs or with the use of a cold-air mattress covering the entire body. Other methods of surface cooling include the use of water-circulating cooling blankets or pads, refrigerated cooling pads, and thermal beds. Core cooling can be achieved with the use of intravascular cooling catheters (made of metal or containing balloons filled with cold saline) or by means of intravenous infusion of cold fluids. The objective is to reach a target temperature of 32 to 34°C and to maintain that temperature for 24 hours, if feasible.
What additional patient management is necessary before hypothermia is induced?
A. Before hypothermia is induced, sedation, analgesia, and paralysis should be initiated to prevent shivering (which can lead to increased oxygen consumption, excessively laborious breathing, increased heart rate, and a general stress-like response, in addition to impeding the cooling process) and to minimize the patient’s discomfort.
What metabolic disturbances are induced by therapeutic hypothermia?
A. Hypothermia can induce metabolic disturbances, including hypokalemia, hypomagnesemia, hypophosphatemia, and hyperglycemia. Therefore, regular measurement of electrolyte and glucose levels is necessary to guide the appropriate amount of electrolyte substitution and insulin therapy. Leukopenia and thrombocytopenia may occur but typically do not require intervention.
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TEACHING TOPICS from the NEJM
2010年9月14日 星期二
氧氣沒有想像中有幫助
Palliative Oxygen Offers No More Relief Than Intranasal Room Air
Simpler interventions might be preferable.
Intranasal oxygen is often used to relieve severe dyspnea in terminally ill patients, even when their PaO2 is not low enough to qualify for long-term oxygen therapy (i.e., below 55 mm Hg). But no clear evidence indicates that palliative oxygen has symptomatic benefits.
Investigators randomized 239 patients with life-limiting illness, refractory dyspnea, and PaO2 above 55 mm Hg to receive either oxygen or room air at 2L/minute via nasal cannula for at least 15 hours daily for 7 days. Beginning 2 days before the intervention started, patients were asked every morning and evening to rate their current dyspnea using a validated 10-point scale and to report secondary outcomes (e.g., quality of life).
No significant between-group differences were noted in reports of current dyspnea at any time. Both groups reported significant improvement during the course of the study (about 18% improvement in morning dyspnea and 9% improvement in evening dyspnea); the greatest decrease in both morning and evening dyspnea occurred within the first day of the intervention. Quality of life improved by about 12% in both groups.
Comment:
Evidence shows that air movement across the face (e.g., from a hand-held fan) helps relieve dyspnea, and intranasal gas (whether oxygen or room air) might have a similar effect. Oxygen use is costly, logistically demanding, and risky in some patients (e.g., smokers, those with hypercapnia). Except for patients with true hypoxia, simpler interventions may be preferable for relieving dyspnea at the end of life.
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Bruce Soloway, MD
Published in Journal Watch General Medicine September 14, 2010
Citation(s): Abernethy AP et al. Effect of palliative oxygen versus room air in relief of breathlessness in patients with refractory dyspnoea: A double-blind, randomised controlled trial. Lancet 2010 Sep 4; 376:784. (http://dx.doi.org/10.1016/S0140-6736(10)61115-4)
Simpler interventions might be preferable.
Intranasal oxygen is often used to relieve severe dyspnea in terminally ill patients, even when their PaO2 is not low enough to qualify for long-term oxygen therapy (i.e., below 55 mm Hg). But no clear evidence indicates that palliative oxygen has symptomatic benefits.
Investigators randomized 239 patients with life-limiting illness, refractory dyspnea, and PaO2 above 55 mm Hg to receive either oxygen or room air at 2L/minute via nasal cannula for at least 15 hours daily for 7 days. Beginning 2 days before the intervention started, patients were asked every morning and evening to rate their current dyspnea using a validated 10-point scale and to report secondary outcomes (e.g., quality of life).
No significant between-group differences were noted in reports of current dyspnea at any time. Both groups reported significant improvement during the course of the study (about 18% improvement in morning dyspnea and 9% improvement in evening dyspnea); the greatest decrease in both morning and evening dyspnea occurred within the first day of the intervention. Quality of life improved by about 12% in both groups.
Comment:
Evidence shows that air movement across the face (e.g., from a hand-held fan) helps relieve dyspnea, and intranasal gas (whether oxygen or room air) might have a similar effect. Oxygen use is costly, logistically demanding, and risky in some patients (e.g., smokers, those with hypercapnia). Except for patients with true hypoxia, simpler interventions may be preferable for relieving dyspnea at the end of life.
—
Bruce Soloway, MD
Published in Journal Watch General Medicine September 14, 2010
Citation(s): Abernethy AP et al. Effect of palliative oxygen versus room air in relief of breathlessness in patients with refractory dyspnoea: A double-blind, randomised controlled trial. Lancet 2010 Sep 4; 376:784. (http://dx.doi.org/10.1016/S0140-6736(10)61115-4)
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