Objective-To investigate the association of interleukin 10 (IL10) promoter polymorphisms and neuropsychiatric manifestations of systemic lupus erythematosus (SLE). Methods-IL10 haplotypes of 11 healthy volunteers were cloned to confirm that in the Dutch population, only the three common haplotypes (-1082/-819/-592) GCC, ACC and ATA exist. The IL10 promoter polymorphisms of 92 SLE patients and 162 healthy controls were determined. The medical records of the SLE patients were screened for the presence of neuropsychiatric involvement. Results-All cloned haplotypes were either GCC, ACC or ATA. Forty two SLE patients had suVered from neuropsychiatric manifestations (NP-SLE). In NP-SLE patients, the frequency of the ATA haplotype is 30% versus 18% in the controls and 17% in the non-NP-SLE group (odds ratios 1.9, p=0.02, and 2.1, p=0.04, respectively), whereas the GCC haplotype frequency is lower in the NP-SLE group compared with controls and non-NP-SLE patients (40% versus 55% and 61%, odds ratios 0.6, p=0.02 and 0.4 p=0.006). The odds ratio for the presence of NP-SLE is inversely proportional to the number of GCC haplotypes per genotype when the NP-SLE group is compared with non-NP-SLE patients. Conclusions-The IL10 locus is associated with neuropsychiatric manifestations in SLE. This suggests that IL10 is implicated in the immunopathogenesis of neuropsychiatric manifestations in SLE. (Ann Rheum Dis 1999;58:85-89) Genetic factors play an important part in the aetiopathogenesis of systemic lupus erythematosus (SLE). This is illustrated by the 50-60% concordance rate of SLE beween monozygotic twins.1 Furthermore, several susceptibility loci have been identified, including HLA class I and II, C4A complement null alleles, tumour necrosis factor (TNF), and Fc--RIIIa polymorphisms. [2][3][4][5][6]

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Our pilot data suggest that MMF appears to be an effective therapy for patients with naive or refractory CIDP, and further controlled studies are warranted for their confirmation.

Background: Diabetic kidney disease is a leading cause of end-stage kidney disease worldwide, its incidence is still increasing and the precise mechanism is not yet fully understood.This study aimed to investigate the possible association of miR-30a and its potential target gene, SNAI1, polymorphisms with diabetic kidney disease in patients with type 2 diabetes mellitus. Methods: This case-control is study included 240 type 2 diabetes mellitus patients with diabetic kidney disease and 280 patients without diabetic kidney disease. Genotyping of miR-30a and SNAI1 polymorphisms were performed by allelic discrimination assay with Taq-Man-MGB probes. Result: The results demonstrated that the CC genotype of rs2222722 in miR-30a was associated with an increased risk of diabetic kidney disease in Chinese type 2 diabetes mellitus patients (OR = 2.81, 95% CI 1.58-4.97, p < 0.001). Stratified analyses revealed that the miR-30a CC genotype was strongly associated with an increased risk of diabetic kidney disease in subjects who were young (< 65 years), male, and had a low body mass index, as well as those with poor glycemic control. What’s more, CC genotype carriers were more likely to exhibit decreased estimated glomerular filtration rate levels and urinary protein production. In addition, the GG genotype of SNAI1 was also associated with the development of diabetic kidney disease, and the risk was 1.73 times higher than that in AA+AG genotype carriers (95% CI 1.01-2.96, p = 0.046). Multiple logistic regression analysis showed that the miR-30a CC and SNAI1 GG genotypes were indispensable and dangerous contributing factors to the development of diabetic kidney disease. Conclusion: The CC genotype of miR-30a rs2222722 and GG genotype of SNAI1 rs1543442 might be associated with diabetic kidney disease risk in Chinese type 2 diabetes mellitus patients.