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Glucosamine Sulfate Use and Delay of Progression of Knee Osteoarthritis
 
A 3-Year, Randomized, Placebo-Controlled, Double-blind Study
 
 
Karel Pavelká, MD, PhD; Jindriska Gatterová, MD; Marta Olejarová, MD; Stanislav Machacek, MD; Giampaolo Giacovelli, PhD; Lucio C. Rovati, MD

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Background  Conventional symptomatic treatments for osteoarthritis do not favorably affect disease progression. The aim of this randomized, placebo-controlled trial was to determine whether long-term (3-year) treatment with glucosamine sulfate can modify the progression of joint structure and symptom changes in knee osteoarthritis, as previously suggested.

Methods  Two hundred two patients with knee osteoarthritis (using American College of Rheumatology criteria) were randomized to receive oral glucosamine sulfate, 1500 mg once a day, or placebo. Changes in radiographic minimum joint space width were measured in the medial compartment of the tibiofemoral joint, and symptoms were assessed using the algo-functional indexes of Lequesne and WOMAC (Western Ontario and McMaster Universities).

Results  Osteoarthritis was of mild to moderate severity at enrollment, with average joint space widths of slightly less than 4 mm and a Lequesne index score of less than 9 points. Progressive joint space narrowing with placebo use was -0.19 mm (95% confidence interval, -0.29 to -0.09 mm) after 3 years. Conversely, there was no average change with glucosamine sulfate use (0.04 mm; 95% confidence interval, -0.06 to 0.14 mm), with a significant difference between groups (P = .001). Fewer patients treated with glucosamine sulfate experienced predefined severe narrowings (>0.5 mm): 5% vs 14% (P = .05). Symptoms improved modestly with placebo use but as much as 20% to 25% with glucosamine sulfate use, with significant final differences on the Lequesne index and the WOMAC total index and pain, function, and stiffness subscales. Safety was good and without differences between groups.

Conclusion  Long-term treatment with glucosamine sulfate retarded the progression of knee osteoarthritis, possibly determining disease modification.

Arch Intern Med. 2002;162:2113-2123

Author/Article Information

 
From the Department of Medicine and Rheumatology, Charles University (Dr Pavelká), and the Institute of Rheumatology (Drs Pavelká, Gatterová, Olejarová, and Machacek), Prague, Czech Republic; and the Department of Clinical Pharmacology, Rotta Research Laboratorium, Monza, Italy (Drs Giacovelli and Rovati).
 
Corresponding author and reprints: Karel Pavelká, MD, PhD, Institute of Rheumatology, Na Slupi 4, 128 50 Praha 2, Czech Republic (e-mail: pavelka@revma.cz).

Accepted for publication February 13, 2002.This study was funded by the Rotta Research/Rottapharm Group.

This study was presented at the annual meeting of the American College of Rheumatology, Philadelphia, Pa, November 1, 2000, and at the annual meeting of the European Congress of Rheumatology, Prague, Czech Republic, June 14, 2001

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