Flare, persistently active disease, and serologically active clinically quiescent disease in systemic lupus erythematosus: a 2-year follow-up study.

OBJECTIVE: Several indices have been proposed to assess disease activity in patients with Systemic Lupus Erythematosus (SLE). Recent studies have showed a prevalence of flare between 28-35.3%, persistently active disease (PAD) between 46%-52% and serologically active clinically quiescent (SACQ) disease ranging from 6 to 15%. Our goal was to evaluate the flare, PAD and SACQ rate incidence in a cohort of SLE patients over a 2-year follow-up. METHODS: We evaluated 394 SLE patients. Flare was defined as an increase in SLEDAI-2K score of ≥4 from the previous visit; PAD was defined as a SLEDAI-2K score of ≥4, on >2 consecutive visits; SACQ was defined as at least a 2-year period without clinical activity and with persistent serologic activity. RESULTS: Among the 95 patients eligible for the analysis in 2009, 7 (7.3%) had ≥1 flare episode, whereas 9 (9.4%) had PAD. Similarly, among the 118 patients selected for the analysis in 2010, 6 (5%) had ≥1 flare episode, whereas 16 (13.5%) had PAD. Only 1/45 patient (2.2%) showed SACQ during the follow-up. CONCLUSION: We showed a low incidence of flare, PAD and SACQ in Italian SLE patients compared with previous studies which could be partly explained by ethnic differences.

Inflammation as "common soil" of the multifactorial diseases.

Inflammation is classically recognized as an essential step for the control of microbial invasion or tissue injury as well as for the maintenance of tissue homeostasis under a variety of noxious conditions. One of the most intriguing aspect of studying inflammation is the plurality of the inflammatory mediators that are continuously discovered (microRNAs, adipokines, inflammasomes and the danger signals, etc.) and their effects on target tissues. Several studies have demonstrated that inflammatory response represents the "common soil" of the multifactorial diseases, encompassing both chronic inflammatory rheumatic disorders and a wide variety of conditions including type 2 diabetes, cardiovascular and neurodegenerative diseases, obesity, cancer, asthma, and ageing. While the inflammatory response observed in the rheumatic disorders seems to be triggered by infection and injury, i.e. the main inducers of inflammation, in the other conditions mentioned it appears to be supported by tissue malfunction or homeostatic imbalance. In the present review, we discuss the data emerged from research on inflammatory mediators sustaining multifactorial diseases.