Furthermore, 10% of gout patients (16 out of 159 cases) had genotype combinations resulting in more than 75% reduction of ABCG2 function (odds ratio, 25.8).
Analysis of ABCG2 expression in the erythrocyte membranes of healthy volunteers and gout patients showed an enrichment of lower expression levels in the patients.
In this study, we found that the proportion of CD14-positive PBMCs was decreased in gout patients when compared with healthy controls and the serum sCD14 level was also considerably decreased in gout patients in comparison to healthy controls.
Results of the present study suggest that polymorphisms of the IL-1beta promoter and IL-1beta exon 5 are not related to gout patients in central Taiwan.
Although these 'evolutionary conserved' amino acids account for only 32% of the amino acids in the human hprt protein, they are involved in 76% of the missense mutations at the hprt locus in human T-lymphocytes, 67% in Lesch-Nyhan patients (with severe hprt-deficiency), but only 43% in gout patients (with partial hprt deficiency).
This study provides evidence for gout susceptibility genes, CLNK and ZNF518B, in a Chinese population, which may have potential as diagnostic and prognostic marker for gout patients.
To compare ultrasound-detected abnormalities, namely double contour sign (DCS) and hyperechoic aggregates (HAGs), at two sites (knee and first metatarsophalangeal [1st MTP] joints) versus six sites (knee joint, 1st MTP joint, radiocarpal joint, talar joint, patellar tendon and triceps tendon) in gout patients.
In the present study, we determined whether benzbromarone increases the serum level of adiponectin in gout patients and investigated the mechanism involved.
Furthermore, the IL-4 (promoter-590 and intron 3) and TNF-alpha genotypes were not found to be associated with the clinical and laboratory profiles in gout patients.
Correlation analysis indicated that the levels of Apo-A1 were negatively correlated with serum ESR and CRP (r = -0.475, P < .001; r = -0.380, P = .001, respectively) in the patients with GA. Taken together, this study gives us a better understanding of the relationships between serum lipid profile and inflammatory markers in gout patients.
In conclusion, our data provide clear evidences that the increased expression of IL-33 in the gout patients might be due to a cause of self-negative regulation, which inhibits the development of MSU-induced inflammation through expanding MDSCs.
Neither the polymorphisms -572C/G nor -373A(m)T(n) in the genotype or allele distributions showed a significant association related to clinical characteristics, biochemical markers, IL-6 levels or gout disease (all p>0.05).
Furthermore, the IL-4 (promoter-590 and intron 3) and TNF-alpha genotypes were not found to be associated with the clinical and laboratory profiles in gout patients.
Furthermore, the average number of days needed to achieve 100% resolution of gout symptoms in patients treated with ACTH was similar to those of the corticosteroid triamcinolone.
CC chemokine ligand 2 (CCL2), a chemokine involved in the recruitment and migration of monocytes/macrophages, has previously been shown to be increased in the plasma of gout patients.
To compare ultrasound-detected abnormalities, namely double contour sign (DCS) and hyperechoic aggregates (HAGs), at two sites (knee and first metatarsophalangeal [1st MTP] joints) versus six sites (knee joint, 1st MTP joint, radiocarpal joint, talar joint, patellar tendon and triceps tendon) in gout patients.