In patients with RA who do not fulfill the Boolean remission criteria, to avoid overtreatment, assessment of anxiety, fatigue, FM, and especially depression must be considered if PtGA scores and disease activity variables are significantly different.

Fatigue is common in clinically active BS patients compared with healthy controls and inactive BS patients. Depression, anxiety and physical dysfunction were significantly associated with fatigue.

The LupusQoL is a disease-specific health-related quality of life (HRQoL) measure for patients with lupus. We conducted this study to compare the efficiency of LupusQoL-TR (validated Turkish version of the LupusQoL questionnaire) with the 36-item Short-Form Health Survey (SF-36), a generic quality of life (QoL) scale, in Turkish patients with lupus. Both questionnaires were conducted at a single visit to the clinic. Disease activity was measured with the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI). Associations between the LupusQoL-TR and SF-36 domains were examined while also examining age, disease duration, and disease activity for each questionnaire. Descriptive statistics, Spearman's correlation coefficients, and Students t test were performed to analyze the data. A total of 113 consecutive patients with lupus (F/M 108:5, mean age 40.6 ± 11.9 years, mean disease duration 8.5 ± 7.0 years) were included, and 69 % of these were active. The median SLEDAI score was 2 (0-24), the mean global LupusQoL-TR score was 60.9 ± 23.3, and the mean SF-36 score was 41.2 ± 9.0. There was a significant correlation between LupusQoL-TR and SF-36 mean scores (r = 0.83; p < 0.001). QoL assessed by LupusQoL-TR and SF-36 did not correlate with disease activity (r = -0.11; p = 0.244 and r = -0.03; p = 0.721, respectively). LupusQoL-TR and SF-36 questionnaires were beneficial instruments in evaluating HRQoL in Turkish lupus patients. However, LupusQoL-TR and SF-36 were not associated with SLEDAI scores, which suggested that QoL might be affected by other factors besides disease activity, especially in clinically inactive or mildly active patients.

Due to the possible risk of infusion reactions of rituximab (RTX), a slow infusion rate (total infusion time, 255 min) is suggested for rheumatological use. However, especially in oncology field, accelerated infusion of RTX is reported to be well tolerated and safe. The aim of our study was to evaluate whether accelerated infusion rates of RTX would similarly be safe and tolerable in rheumatoid arthritis (RA) patients and other off-label rheumatological indications. All patients treated with RTX for RA and other autoimmune diseases between May 2011 and January 2012 were recruited to the study. Each treatment course consisted of two RTX 1,000 mg infusions, 2 weeks apart. Total time of the infusion for the first cycle was 255 min. Second and subsequent infusions were administered over 120 min as follows: 0-30 min, 100 mg; 30-60 min, 200 mg; 60-90 min, 300 mg; and 90-120 min, 400 mg. The Clinical Trials Classification of Adverse Events (CTCAE) version 4.3 was used to categorise side effects. The study population comprised 68 patients [F/M, 59:9; mean age, 52.4 (10.6) years]: 60 with RA, 4 with systemic lupus erythematosus (SLE), 1 with non-Hodgkin's lymphoma with SLE and 3 with vasculitis. A total of 77 fast infusions were administered. Eleven patients (16.2 %) had taken a fast infusion at the first course. A total of nine patients experienced at least one AE. Seven patients had a reaction on the first infusion (infusion-related reaction (IRR)), two patients on the second infusion and one patient on both infusions. When graded from 1 to 5 according to CTCAE v. 4.3, grade 1 IRRs were observed in a total of seven patients and grade 2 IRR in three patients. In this study of fast infusions, adverse events after RTX were mostly mild and seem to be well tolerated. Faster rituximab infusion times seem to be safe and might be incorporated into routine practice.

Carrier rate for the studied MEFV mutations was slightly lower in the SLE group, which is in agreement with previous observations that FMF may confer some protection from SLE. Exon 10 mutations were associated with SLE nephritis after the exclusion of the E148Q mutation. The significance of the E148Q as a disease-causing mutation is controversial, and whether E148Q substitution is a polymorphism generally affecting inflammatory pathways is not addressed in the current literature. In this regard, absence of the E148Q mutation in SLE nephritis may serve as a clue for further investigation into its role as a general modulatory polymorphism for inflammation. This clarification is necessary to conclude whether other more penetrant MEFV gene mutations confer susceptibility to nephritis in SLE.