No abstract

The aim of this study was to assess the efficacy and safety of tacrolimus for the treatment of lupus nephritis (LN). A systematic review of clinical trials on tacrolimus in LN was conducted. Seven studies met the review inclusion criteria. Two studies were case-control studies, and five studies were open-label trials. One randomized controlled trial (RCT) found that tacrolimus significantly improved lupus nephritis disease activity index (LNDAI) as compared with a placebo, but no difference was observed between these two groups in terms of treatment-related adverse events. The other case-control study compared tacrolimus with standard protocols of oral cyclophosphamide or azathioprine for the treatment of membranous LN and found that efficacies were similar. All five open-label prospective studies concluded that tacrolimus is safe and effective as an induction and maintenance therapy for LN or for the treatment of LN with persistent proteinuria that failed to respond to prednisolone and immunosuppressants. In conclusion, this systematic review shows that tacrolimus may be effective as an induction and maintenance therapy for LN or as a treatment for LN with persistent proteinuria despite gold standard treatment. However, further RCTs are needed to compare tacrolimus with standard regimens for the treatment of LN.

The aim of this study was to determine whether the functional interleukin-6 (IL-6) promoter -174 G/C and -572 G/C polymorphisms confer susceptibility to systemic lupus erythematosus (SLE) in ethnically different populations. Meta-analysis was conducted on the associations between the IL-6 polymorphisms and SLE using; 1) allele contrast, 2) the recessive model, 3) the dominant model, and 4) the additive model. A total of 11 studies were considered in this study, and ethnicity-specific meta-analysis was performed on European and Asian populations. Meta-analysis of the IL-6 -174 G/C polymorphism showed an association between SLE and the IL-6 -174 G allele in all study subjects (odds ratio (OR) = 1.344, 95% confidence interval (CI) = 1.052-1.718, p = 0.018). Furthermore, stratification by ethnicity indicated an association between the IL-6 -174 G allele and SLE in Europeans (OR = 1.264, 95% CI = 1.037-1.541, p = 0.020). Meta-analysis of the IL-6 -572 G/C polymorphism revealed that an association was found between SLE and the IL-6 -572 G/C polymorphism using the recessive model, but ethnicity-specific meta-analysis revealed no association between SLE and the IL-6 -572 G/C polymorphism in Asians. In conclusion, this meta-analysis demonstrates that the IL-6 -174 G/C polymorphism may confer susceptibility to SLE in Europeans, but that the IL-6 -572 G/C polymorphism is not associated with susceptibility to SLE in Asians.

We investigated the frequency of gut inflammation and the role of gut lesion in the pathogenesis of the ankylosing spondylitis (AS) in Korean patients. Ileocolonoscopy and biopsy of the colon and terminal ileum were performed on 24 Korean patients with AS. Endoscopic lesions were observed in 7 patients (29.2%). The lesions were found more often in the terminal ileum (6/7) than in the colon (1/7). Histologic signs of gut inflammation were detected in 14 patients (58.3%), acute lesions in 2 patients (8.3%) and chronic lesions in 12 patients (50%). Gut inflammation were as frequently found in Korean patients with AS as in Western patients. These findings suggest that gut inflammation may play a role in the pathogenesis of AS in Korean patients as it does in Western patients.

The aim of this study is to investigate whether the functional polymorphisms in the promoter of matrix metalloproteinase-1 (MMP-1) and in the regulatory region of the monocyte chemoattractant protein-1 (MCP-1) gene are associated with susceptibility to rheumatoid arthritis (RA) and its clinical features. The MMP-1 1G/2G polymorphism and the MCP-1 promoter A/G polymorphism were determined by polymerase chain reaction-restriction fragment length polymorphism in 117 RA patients and 97 healthy controls. The genotype distribution of the MMP-1 promoter did not differ between RA patients and control subjects. However, in the 2G/2G genotype, ESR and Plat were higher than the 1G/1G genotype. The genotype distribution of the MCP-1 promoter did not differ between the RA and control groups. Clinically there was no significant difference among RA patients according to the MCP-1 promoter genotypes. Our data show that the functional promoter polymorphism in the MMP-1 promoter may not play an important role in the susceptibility of RA, but the polymorphism may be related to clinical phenotypes.