THE ROLE OF NAILFOLD CAPILLAROSCOPY IN MONITORING LUNG INVOLVEMENT IN SYSTEMIC SCLEROSIS

The usefulness of capillaroscopy in the follow-up of scleroderma patients and the possible prognostic role for the appearance of visceral involvement is suggested by many authors but still under debate.The aim of this study was to assess the role of monitoring capillaroscopic abnormalities (qualitative and semiquantitative) in relation with parameters of interstitial lung involvement and pulmonary arterial hypertension(PAH). A strong correlation was identified between initial capillaroscopy scores and FVC (r=-.47, p=0.002), DLCO (r=- .51, p< 0.001) and sPAP (r=0.34, p<0.001). Active and late capillaroscopic pattern were correlated with diagnosis of lung fibrosis (χ2=14, p=0.007) and PAH at follow-up examinations (χ2=14,2, p=0.007). Progression of capillaroscopic pattern at follow-up evaluations was not correlated with significant worsening of lung volumes, DLCO, sPAP. Instead, progression of microangiopathy evolution score (>1) was asociated with worsening of FVC (r=0.32,p<0.001), DLCO(r=0.21,p=0.02) and new diagnosis of lung fibrosis on HRCT (r=0,19,p=0.035). Semiquantitative scoring, rather then qualitative capillaroscopic assessment can have a predictive role for new involvement or worsening of previous lung involvement (especially interstitial lung disease) in scleroderma patients, confirming the putative role of capillaroscopy as biomarker in SSc

Monitoring Drug and Antidrug Levels: A Rational Approach in Rheumatoid Arthritis Patients Treated with Biologic Agents Who Experience Inadequate Response While Being on a Stable Biologic Treatment

Clinical response in patients with rheumatoid arthritis (RA) treated with biologic agents can be influenced by their pharmacokinetics and immunogenicity. The present study evaluated the concordance between serum drug and antidrug levels as well as the clinical response in RA patients treated with biological agents who experience their first disease exacerbation while being on a stable biologic treatment. 154 RA patients treated with rituximab (RTX), infliximab (IFX), adalimumab (ADL), or etanercept (ETN) were included. DAS28, SDAI, and EULAR response were assessed at baseline and reevaluated at precise time intervals. At the time of their first sign of inadequate response, patients were tested for both serum drug level and antidrug antibodies level. At the next reevaluation, patients retreated with RTX that had detectable drug level had a better EULAR response (P=0.038) with lower DAS28 and SDAI scores (P=0.01 and P=0.03). The same tendency was observed in patients treated with IFX and ETN regarding EULAR response (P=0.002 and P=0.023), DAS28 score (P=0.002 and P=0.003), and SDAI score (P=0.001 and P=0.026). Detectable biologic drug levels correlated with a better clinical response in patients experiencing their first RA inadequate response while being on a stable biologic treatment with RTX, IFX, and ETN

GENERAL CHARACTERISTICS AND FAMILIAL AGGREGATION IN PATIENTS WITH SYSTEMIC LUPUS ERYTHEMATOSUS

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by the production of autoantibodies, which deposit within tissues and fix complement leading to systemic inflammation (1). Is a heterogeneous disease with a continuum of disease activity. Some patients can have predominant skin and joint involvement, whereas others can present with organ-threatening diseases such as nephritis, cardiac involvement or even neurologic manifestations. Relatives of patients with SLE appear to be at higher risk of SLE and other autoimmune diseases, but estimates of individual familial risks are largely unavailable or unreliable (2,3)

EVIDENCE FOR FAMILIAL AGGREGATION IN SIBLINGS WITH AUTOIMMUNE RHEUMATIC DISEASES

Autoimmune rheumatic disorders have a multifactorial determinism, caused by various environmental factors acting on the individual’s genetic susceptibility, destabilizing the systems which regulate the immune response. Epidemiological and genetic investigations are very important to demonstrate the contribution of genetic factors to the development of these autoimmune diseases. The contribution of genetic factors in causing autoimmune diseases has been demonstrated by familial aggregation. Moreover, it was also quantified by determining heritability, expressing the proportion of genetic factors in the etiology. It is now clear that common genes underlie multiple autoimmune disorders