Serum IL-18 and IL-6 levels were elevated in patients with TA, especially in those with active disease. Serum IL-18 levels correlated well with disease activity of TA. These results suggest that IL-6 and IL-18 might contribute to the pathogenesis of TA and that IL-18 could be a useful marker for monitoring disease activity of TA.

The aim of this study was to investigate the prevalence and associated factors of glucocorticoid-induced diabetes mellitus (GDM) in patients with systemic lupus erythematosus (SLE) receiving high-dose glucocorticoid therapy. Patients with SLE who had received high-dose glucocorticoid therapy (prednisolone ≥1 mg/kg/day) at Yonsei University Medical Center, Seoul, Korea, were recruited between January 1999 and June 2009. In total 127 patients with SLE were evaluated. Sixteen (12.6%) of them developed GDM after high-dose glucocorticoid therapy (95% confidence interval, 6.8-18.4%). Univariate analysis showed that old age, family history of diabetes mellitus (DM), hypertension, higher body mass index, higher mean dose of prednisolone before high-dose glucocorticoid therapy, and concurrent use of mycophenolate mofetil (MMF) were factors that would increase the likelihood of GDM. Multivariate analysis determined that age, family history of DM, mean dose of prednisolone before high-dose glucocorticoid therapy and concurrent use of MMF were independent associated factors for GDM. In summary, GDM was developed among 12.6% of patients with SLE after high-dose glucocorticoid therapy. Old age, family history of DM, higher mean dose of prednisolone before high-dose glucocorticoid therapy and concurrent use of MMF were determined to be factors responsible for increasing the risk of developing GDM.

Alendronates seemed to decrease bone resorption but not to decrease bone formation. Empty lacunae were observed significantly more at later time points in implant sites compared to extraction sockets.

The prognostic nutritional index (PNI), which is calculated using serum albumin level and total lymphocyte count in the peripheral blood, is regarded as an index that reflects the immunonutritional status of patients. PNI was calculated in 217 systemic lupus erythematosus (SLE) patients according to the following formula: 10 × serum albumin value (g/dL) + 0.005 × peripheral lymphocyte count (/mm). Pearson's correlation analysis was used to elucidate the correlation between continuous variables. Linear and logistic regression analyses were performed to assess the correlation between laboratory variables and SLE Disease Activity Index-2000 (SLEDAI-2 K) and to differentiate between active and inactive SLE. Ninety-three patients were classified as active SLE (SLEDAI-2 K ≥ 5) and 124 as inactive SLE. Patients with active SLE exhibited lower median PNI than those with inactive SLE (39.0 vs. 49.1, p < 0.001). Multivariable logistic regression analysis revealed PNI as an independent predictor of active SLE. Multivariable linear regression analysis revealed that PNI was significantly correlated with laboratory variables of SLEDAI-2 K, erythrocyte sedimentation rate, C-reactive protein and SLEDAI-2 K. Furthermore, in patients who switched from active to inactive SLE after treatment ( n = 55), PNI increased as disease activity improved ( p < 0.001), which suggests that PNI may be useful for estimating SLE activity.

Serum LRG levels were increased in patients with AOSD and correlated well with disease activity measures. LRG may be a useful biomarker for distinguishing AOSD from RA and for monitoring the disease activity of AOSD.