Clinical Trials

Study Findings: Glucosamine Sulfate Significantly Reduces Progression Of Knee Osteoarthritis Over 3 Years: A Large, Randomised, Placebo-Controlled, Double-Blind, Prospective Trial. J Y Reginster, R Deroisy, I Paul, R L Lee, Y Henrotin, G Giacovelli, J Dacre, L C Rovati, C Gosset.

Background. Results of clinical trials like, the one above, support a role for glucosamine sulfate as a Symptom Modifying Drug in osteoarthritis (OA). This study was designed to test the long-term effects of the drug on the progression of knee OA joint structural changes and symptoms.

Specifics: 212 patients with knee OA (ACR criteria) were randomly assigned, in a double-blind fashion, to the continuous treatment with oral glucosamine sulfate 1500 mg once-a-day or placebo for 3 years. Weight-bearing, antero-posterior radiographs of each knee were taken at enrolment and after 1 and 3 years standardising patient positioning and radiographic procedure. Total mean joint space width (JSW) of the medial compartment of the tibio-femoral joint was assessed by digital image analysis by a validated computerised algorithm, with the narrowest medial joint space at enrollment being taken for the primary evaluation (signal joint). Symptoms were scored at each 4-month visit by the (total) WOMAC index, VA3.0 version. Data were analysed separately according to a per-protocol (PP) approach on 3-year completers, or on an intention-to-treat (ITT) basis including all randomised patients by the last-observation-carried-forward. Results. The two groups of 106 patients each were comparable for demographic and disease characteristics. Placebo-treated patients had an average joint space narrowing (JSN) of approximately 0.08-0.1 mm/year, while no JSN occurred in the glucosamine sulfate group. A slight worsening in symptoms was evident at the end of treatment with placebo, compared to the improvement observed after glucosamine sulfate.

Conclusions:. Combined Structure and Symptom Modifying effects suggest that glucosamine sulfate may be a possible Disease Modifying agent in OA.

Disclosure: Work reported in this abstract was supported by the Rotta Research Group

Source:American College of Rheumatology 1999 Annual Meeting, Boston, MA Presentation Date: Wednesday, November 17, 1999 ACR Plenary Abstract.