Furie discusses advances in SLE treatment

CHICAGO — At the American College of Rheumatology State-of-the-Art Clinical Symposium, Richard A. Furie, MD, compared lupus clinical trial results to the “curses” on the Chicago Cubs. The “wins” in research have been disappointingly few. “But, we have had some highlights,” Furie, an investigator at The Feinstein Institute for Medical Research and chief of the Division of Rheumatology at Northwell Health, said. “I think the introduction of mycophenolate mofetil has been great. It has now become pretty much the standard of care for patients with lupus nephritis.”

Furie reviewed data that supported the use of mycophenolate mofetil for lupus nephritis induction and maintenance therapies. Formerly, cyclophosphamide was used for induction therapy, and azathioprine was often used for maintenance.

Richard A. Furie

The approval of belimumab was a very important advance for the lupus community, and Furie also added that the widespread use of hydroxychloroquine was based on studies that demonstrated improved survival, effectiveness for many SLE patients with rash or arthritis, and reductions in lipid levels. “The dogma now is that every lupus patient should be on hydroxychloroquine,” Furie said.

Despite improvements in survival rates in lupus since the mid-1900’s, he argued, “We are not doing a good job if you look at data.” Response rates to new treatments are generally lower than 50%, according to Furie. “We were down in the single digits for one of the lupus nephritis studies,” Furie said. “So we have major unmet needs. I think the biggest need is for lupus nephritis. For those with severe renal disease, we need better drugs. We need safer drugs. We need more efficacious drugs.”

Organ damage prevention is key, he said, whether the damage is related to disease activity or side effects of the medication.

The pathogenesis of SLE, according to Furie, “starts with a genetically susceptible host, and there also has to be an environmental trigger.”

For some patients, the environmental trigger might be the sun, according to Furie, which can cause apoptosis of skin cells, the release of RNA and DNA, and activation of toll-like receptors-7 and -9. “The consequence of toll-like receptor signaling is the elaboration of a variety of cytokines, chief of which is interferon-alpha,” he said. Thereafter, many other components of the immune system are activated. It is this hyperactivity that needs to be controlled. There is currently unprecedented activity in the area of drug development in lupus. No doubt that there will be safer and more effective drugs in the future, which will translate into a brighter outlook for patients.

Reference:

Furie RA. Recent Advances in SLE Treatment. Presented at: American College of Rheumatology State-of-the-Art Clinical Symposium; April 9-10, 2016; Chicago.

Disclosures: Furie reports relationships with Pfizer, Amgen, Anthera, Biogenldec, BMS, Boehringer‐Ingelheim, Celgene, Dynavax, Eli Lilly, Exagen, Genetech/Roche, GlaxoSmithKline, Medimmune, Novartis, Pfizer, Mallinckrodt Pharmaceuticals, Sanofi, Takeda, UCB, Abbvie, Alnylam, Biogenldec, BMS, Boehringer‐Ingelheim , Celgene, Chugai, Eli Lilly, Estrela (Janssen), Exagen, Genetech/Roche, GlaxoSmithKline, Medimmune, Pfizer, Onyx, Mallinckrodt Pharmaceuticals, Regeneron, Sanofi, Takeda, UCB, Lupus Foundation of America, Lupus Alliance of America, SLE Foundation, Alliance for Lupus Research and The Lupus Academy.