Glucosamine ineffective for low back pain
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Oral glucosamine did not reduce pain compared to placebo among patients with chronic low back pain and degenerative lumbar osteoarthritis (OA) after a six-month intervention or one year of follow-up.
A double-blind, randomized, placebo-controlled trial conducted at Oslo University Hospital Outpatient Clinic in Norway was performed with 250 patients older than 25 years of age who had chronic low back pain lasting more than six months and degenerative lumbar OA. The results appear in the July 7 Journal of the American Medical Association.
Patients were evenly randomized to 1,500 mg of oral glucosamine daily or placebo for six months, with assessment of effect after the intervention period and at one year. (In Norway, glucosamine is only available by prescription.) Patients could take their usual painkillers or nonsteroidal anti-inflammatory drugs, and continue their usual physical therapies.
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 from the quality-of-life EuroQol-5 Dimensions (EQ-5D) instrument.
At baseline, mean RMDQ scores were 9.2 (95% CI, 8.4 to 10.0) for glucosamine and 9.7 (95% CI, 8.9 to 10.5) for the placebo group (P=0.37). At six months, the mean RMDQ score was the same for the glucosamine and placebo groups (5.0; 95% CI, 4.2 to 5.8). At one year, the mean RMDQ scores were 4.8 (95% CI, 3.9 to 5.6) for glucosamine and 5.5 (95% CI, 4.7 to 6.4) for the placebo group.
No statistically significant difference in change between groups was found when assessed after the six-month intervention period and at one year using the assessments of RMDQ (P=0.72), low back pain at rest (P=0.91), low back pain during activity (P=0.97), and quality-of-life EQ-5D (P=0.20). Mild adverse events were reported in 40 patients in the glucosamine group and 46 in the placebo group (P=0.48).
Researchers commented that glucosamine may still work elsewhere in the body, a conclusion supported by other studies. For example, OA of the knee contains more of the proinflammatory target for glucosamine than OA of the hip.