The second clinical concept is the current international movement to incorporate treat-to-target (T2T) principles into management of people with lupus. “In my opinion,” she stated, “we need to do a better job [of treating patients]. That’s why we’re trying to introduce ‘treat to target.’ We should first treat to low level disease activity [LL-DAS, a concept introduced by the Asia Pacific League of Associations for Rheumatology and a EULAR committee] and then treat to prevent flares.” The goals of therapy should be to induce and maintain improvement, prevent damage and address pain, fatigue and depression, “which are major drivers of quality of life.” In conversation following the meeting, Dr. Hahn said she currently incorporates discussion of T2T in all her lupus talks and hopes that the U.S. rheumatology community will soon embrace the principles, which have been used successfully in rheumatoid arthritis.
Dr. Hahn described the SLE disease process, which begins with autoantibodies and immune complexes fixing to tissue and causing damage by activating the complement system (a component of the innate immune system). The resultant inflammatory response takes on “a domino effect.” Recent research has revealed that neutrophils in the process of netosis cast out nets of protein studded with DNA, which present to the immune system, activating additional inflammatory response. Dendritic cells also sense the neutrophil nets and react by releasing interferon alpha. “We never thought neutrophils were major players in SLE, but they are,” Dr. Hahn stated.
Researchers now know of 50–55 genes that predispose people to SLE; and environmental factors, such as Epstein-Barr virus and cigarette smoking, are now well validated as possible triggers for lupus. Female gender is also important. Dr. Hahn also noted, “If lupus begins when the patient is younger than 25, it’s far more severe.”