Objective To investigate the clinic features and risk factors for central nervous system (CNS) infection in patients with systemic lupus erythematosus. Methods Clinical data of 18 cases of hospitalized lupus patients with CNS infection were analyzed retrospectively.Thirty-three lupus patients without CNS infection were selected as control. Results There were significant differences between the CNS infection group and control group in the dosage of corticosteroid used for pulse therapy (22% vs 3%, P<0.05), the aver-age dosage of corticosteroid used within one year (35±18 vs 24±17, P<0.05), peripheral blood leukocyte count (4.4±3.4 vs 6.7±2.9, P<0.05) and lymphocyte count (0.7±0.6 vs 1.5±0.7, P<0.01), and clinical outcome (mortality rate was 22% vs 0, P<0.05). Conclusion The clinical manifestations of CNS infection may be atypical. Large-dosage corticosteroid therapy, higher daily dosage of corticosteroid used, decreased peripheral lymphocytes and leucocytes counts are risk factors of central nervous system infection in lupus patients.

Objective To investigate the clinical significance of anti-β2 glycoprotein Ⅰ(anti-β2GP Ⅰ)antibodies in patients with systemic lupus erythematosus(SLE)and to assess their association with lupus thrombocytopenia.Methods Anti-β2GP Ⅰ antibodies were tested in 108 SLE patients(including 37thrombocytopenia patients),30 patients with rheumatoid arthritis(RA)and 30 healthy individuals by enzyme-linked immunosorbent assay(ELISA).The clinical features and laboratory findings were collected,and the associations of anti-β2GP Ⅰ antibody with laboratory findings and disease activity were analyzed.Results Sensitivities of anti-β2GP Ⅰ antibody were 19.44%(21/108)in SLE and 10%(3/30)in RA,respectively.The specificity of anti-β2GP Ⅰ antibody was 95.0% in SLE.The anti-β2GP Ⅰ antibody titers of the SLE group were significantly higher than normal group(P ＜ 0.05).There was no significant correlation between anti-β2GP Ⅰ antibodies and thrombocytopenia(r =-0.028,P ＞0.05).Anti-β2GP Ⅰ antibody was positively correlated to anticardiolipin antibody(r = 0.566,P ＜ 0.01).No associations were found between anti-β2GP Ⅰ antibody and other clinical and laboratory features.There was no statistical correlation between the level of anti-β2GP Ⅰ antibody and SLEDAI scores.Conclusions Anti-β2GP Ⅰ antibody had high specificity in SLE.There was no significant correlation between anti-β2GP Ⅰ antibodies and lupus thrombocytopenia.

Objective To investigate the release and intracellular localization of high mobility group box chromosomal protein 1(HMGBl)in the peripheral blood monocytes of rheumatoid arthritis(RA) patients and the inhibitive effect of thaiidomide.Methods 19 RA patients and 20 healthy controls were included in the study.Monocytes were separated from peripheral blood with Ficoll density gradient centrifugation.Monocytes were treated with 100 ng/ml tumor necrosis factor α(TNFa)or 100 ng/ml TNFα plus 40 μg/ml thalidomide and grown in an incubator at 37℃ with 5%CO,for 24 hours.The cuIture supernatants of the monocytes were collected.HMGB1 level in the culture medium was detected with Western blot.In addition,the intraceUular localization of HMGB1 in the fflonocytes was investigated with immunocytochemical analysis. Results Without stimulation. the release of HMGBl protein was significantly increased in the culture supernatants of peripheral blood monocytes from RA patients as compared with that from healthy controls(P<0.05).TNFα(100 ng/ml)did not further increase the release of HMGBl in the monocytes from the patients with RA.Thalidomide(40 μg/ml)could inhibit the release of HMGB1 in the monocytes from RA patients stimulated with TNFα(P<0.05).In the monocytes from RA patients,HMGBl was mainly localized in the nucleus.Treatment with TNFOL(100 ng/ml)for 24 hour resulted in a cytoplasmic translocation of HMGB1,which was inhibited significantly by thalidomide. Conclusion TNFα induces the release and cytoplasmic translocation of HMGBI in the peTipheral blood monocytes of RA patients and thalidomide inhibits the release and translocation of HMGB1.

Objective To determine the safety, pregnancy outcome and the affect on neonates in pregnant patients with systemic lupus erythematosus(SLE).Methods Sixty-two pregnant patients with SLE were evaluated retrospectively from 1999 to 2009 in our hospital. These patients were divided into two groups:selective pregnancy group and nonselective pregnancy group. The pregnancy outcomes, fetal outcomes, and lupus activity during pregnancy were compared between the two groups. The children of the SLE patients were followed up. Results There were 43 patients in the selective pregnancies group and 19 patients in nonselective pregnancies group. In the selective pregnancies group, lupus flare occurred in 10 pregnancies(23%), 35(81%)had a live birth, 7 had low birth weight infants and 7 had premature delivery; however, in the nonselective pregnancies group, lupus flare occurred in 16 pregnancies(84%), 13(68%) had abortion,6 had a live birth, but all neonates were low birth weight infants. The rates of lupus flare and pregnancy loss in the nonselective pregnancy group were higher than those of the selective pregnancy group(P＜0.05). None of the 22 children had SLE during the follow-up period. Conclusion Both selective and nonselective pregnancy may adversely affectmaternal and fetal outcomes, but patients with selective pregnancy have better outcomes either in lupus flare or maternal and fetal outcomes compared with those of the nonselective pregnancy.

Objective To understand the diagnostic values of procalcitonin (PCT),C-reactive protein (CRP),erythrocyte sedimentation rate (ESR),white blood cell (WBC) and neutmphilic granulocyte ratio (NE％) in distinguishing concurrent bacterial infection from idiopathic inflammatory myopathy (ⅡM).Methods Clinical data and laboratory examinations of 118 ⅡM patients were collected.The ⅡM patients were assigned to the bacterial infection group (n=66) or the non-infection group (n=52).The levels of PCT,CRP,ESR,WBC and NE％ were compared by the Mann-Whitney U tests between the two groups and receiver operating characteristic curves were generated in order to evaluate the diagnostic value.Results The levels of PCT (0.06 ng/ml,0.03 ng/ml,U=2.637,P＜0.01);CRP (15.80 mg/L,4.40 mg/L,U=5.944,P＜0.01);ESR (43.50 mm/1 h,27.00 mm/1 h,U=2.266,P＜0.05);WBC (9.85×109/L,7.70×109/L,U=2.675,P＜0.01) and NE％ (80.70％,75.75％,U=2.344,P＜0.01) were significantly higher in the ⅡM patient group with concurrent infection than in the noninfection ⅡM patient group.CRP showed the highest diagnostic value with sensitivity,specificity,positive predictive value and negative predictive value of 72.7％,82.7％,84.2％ and 70.5％,respectively.Conclusion The inflammatory biomarkers PCT,CRP,ESR,WBC and NE％ offer diagnostic accuracy in detecting bacterial infection in ⅡM patients.Particularly,CRP is the most sensitive and specific biomarker indetecting bacterial infection in ⅡM patients.

Objective To investigate the effect of high mobility group box chromosomal protein 1 (HMGB-1) on the proliferation and inflammatory phenotype of human fibroblast like synoviocytes (FLS).Methods FLSs were isolated from the synovial tissues of rheumatoid arthritis (RA) patients undergoing joint replacement surgery.All the experiments described here utilize the FLSs between the third and sixth passages.FLS were incubated with HMGB1 at (100,500,2 000 ng/ml) or interleukin (IL)-1β (0.5 ng/ml) or lipopolysaccharide (LPS) (100 ng/ml) alone or HMGB1/IL-1β complexes or HMGB1/LPS complexes.Cell proliferation assay were used by CCK-8,IL-6,IL-8 and matrix metalloproteinase-3 (MMP-3) in culture supernatants were measured using enzyme-linked immunosorbent assays.The measurement data were compared with single factor analysis of variance.Results Stimulation with all concentrations of HMGB1,IL-1β and LPS alone did not affect the cell proliferation of FLS.HMGB1/IL-1β complexes and HMGB1/LPS complexes did not affect the cell proliferation of FLS,neither (F=0.415.P=0.915).Except high concentration of HMGB1 (2 000 ng/ml) could significantly stimulate the secretion of IL-6 from FLS [(23.0±1.1) ng/ml],HMGB1,IL-1β and LPS alone did not affect the production of IL-6,IL-8 and MMP-3.However,HMGB1/IL-1β complexes and HMGB1/LPS complexes increased IL-6,IL-8 and MMP-3 production from FLS (F=97.804,117.383,70.179,P=0.000).Conclusion Neither HMGB1,IL-1β,LPS alone nor HMGB1/IL-1β complexes or HMGB1/LPS complexes affect the cell proliferation of FLS.HMGB1 in complex with LPS or IL-1β boost IL-6,IL-8 and MMP-3 production in synovial fibroblasts from RA patients.