Antimalarial Medication Can Reduce Inflammation in SLE Patients, Study Shows

Hydroxychloroquine, an antimalarial medication, can help normalize levels of an immune molecule that promotes inflammation in patients with systemic lupus erythematosus, a study shows.

The study, “Efficacy analysis of hydroxychloroquine therapy in systemic lupus erythematosus: a study on disease activity and immunological biomarkers,” was published in the journal  Inflammopharmacology.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease associated with high levels of pro-inflammatory cytokines — the immune molecule linked to inflammation.  These are especially high in SLE patients during the active phase of lupus, suggesting that they play a direct role in disease activity.

Some studies have demonstrated that antimalarials such as hydroxychloroquine (HCQ) can suppress the production of pro-inflammatory cytokines.

While HCQ therapy has been shown to display anti-inflammatory properties in patients with rheumatic diseases, much of the evidence for its use in SLE originates from observational studies and not prospective clinical trials.

Researchers investigated the effectiveness of HCQ therapy in combination with a limited dose of the corticosteroid prednisolone in patients with SLE.

They focused on levels of pro-inflammatory cytokines and their association with clinical parameters during a two-month course of treatment.

Researchers studied 41 newly diagnosed SLE patients who were given 400 mg of HCQ per day over the course of the study. Levels of cytokines were compared to 41 age-matched healthy controls.

Outcome measures were assessed before starting the HCQ therapy, and at follow-up visits one and two months afterward.

Researchers found that, at baseline, the median levels of the pro-inflammatory cytokine IL-1β, IL-6, and TNF-α were significantly higher compared to controls.

Conversely, the median level of CH50, a type of complement protein, was significantly lower in SLE patients compared with controls. Low levels of complement proteins are known markers of autoimmune diseases such as SLE.

After two months of treatment with HCQ, scores for SLEDAI-2K — a measure of SLE disease activity — significantly decreased. Levels of anti-dsDNA, an autoantibody that contributes to autoimmunity in lupus, were also significantly lower at two months.

Levels of IL-1β, IL-6, and TNF-α were significantly reduced at two months with a concurrent increase in CH50 levels.

The reductions in SLEDAI-2K and levels of IL-1β and TNF-α were significantly greater in the first month compared with the second.

“This somehow shows that the logarithmic phase of HCQ effect occurs in the first month and at the end of the second month it perhaps starts reaching the plateau,” investigators said.

“HCQ therapy is effective on clinical improvement of SLE patients through interfering with inflammatory signaling pathways, reducing anti-DNA autoantibodies and normalizing the complement activity,” they concluded.