OR WAIT null SECS
In a 120-patient randomized trial, hydroxychloroquine was no better than placebo at relieving the dryness, pain, and fatigue of Sjögren syndrome.
Gottenberg J-E, Ravaud P, PuÃ©chal X. Effects of Hydroxychloroquine on Symptomatic Improvement in Primary SjÃ¶gren Syndrome: The JOQUER Randomized Clinical Trial. JAMA. (2014) 312:249-258. doi:10.1001/jama.2014.7682
This complete report from a European randomized trail of hydroxychloroquine in SjÃ¶gren syndrome, described at the 2013 annual meeting of EULAR (the European Union League Against Rheumatism), now appears in full. It found that hydroxychloroquine (400 mg/day) did not improve symptoms of patients with primary SjÃ¶gren syndrome during 24 or 48 weeks of treatment in 120 patients randomized to either the drug or placebo.
However, because hydroxychloroquine has a progressive action, and might be more efficacious used for longer than a year, the study had an open-label followup, in which all patients got hydrochloroquine.
Patients who were receiving stable doses of nonsteroidal anti-inflammatory drugs, oral corticosteroids, pilocarpine, tear substitutes, and topical cyclosporine were allowed to continue those treatments.
Because there is no consensus on the choice of primary outcome in clinical trials of primary SjÃ¶gren syndrome, the investigators used a “pragmatic” choice of the main symptoms of disease. The primary end point was the proportion of patients with a 30% or greater reduction by week 24 in scores on two of three numeric analog scales evaluating dryness, pain, and fatigue; 17.9% in the hydroxychloroquine group and 17.2% in the placebo group met that end point (p=0.98).
It is possible that hydroxychloroquine may have benefits over a longer time period, they wrote. There was a non-significant trend, of reduced pain (36% vs. 54% decreasing ≥1 point on the numeric analog scale), which might reach statistical significance in a longer study.
Hydroxychloroquine did lower the erythrocyte sedimentation rate. Previous research has shown that it inhibits the binding of pathogen- and damage-associated molecular patterns to toll-like receptors.