RA patients have an increased risk of subclinical vascular disease as was shown by a higher prevalence of carotid disease, peripheral arterial disease and increased QTD. Among traditional risk factors we found a history of steroid usage to be one of the potential risk factors.

Interleukin 1 beta (IL-1beta) is a proinflammatory cytokine that is considered to play an important role in the progression of rheumatoid arthritis (RA). A stimulus such as ATP is necessary to cause the release of mature IL-1beta, via activation of the P2X(7) receptor on monocytes. In this study, the production of IL-1beta in whole blood after ATP stimulation and expression of P2X(7) receptors in RA and healthy subjects were examined. Blood samples from RA patients or healthy controls were stimulated with ATP in the presence of lipopolysaccharide (LPS). Supernatants were harvested and IL-1beta levels were measured by enzyme-linked immunosorbent assay (ELISA). Expression of P2X(7) receptors was measured using flow cytometry. ATP induced significantly higher levels of IL-1beta in LPS-activated RA blood samples compared to controls. A significant up-regulation of P2X(7) receptor expression on mononuclear cells was observed after overnight incubation with ATP without any significant differences between RA patients and normals. These data suggest that RA patient mononuclear cells are more sensitive to ATP stimulation than healthy individuals perhaps due to genetic polymorphism in the P2X(7) gene.

The P2X7 receptor, a member of the P2X family of nucleotide-gated channels, is predominantly expressed by monocytic cells. The activation of this receptor has been associated with downstream-signalling cascades, resulting in the release of a number of inflammatory mediators. There are more than 815 single nucleotide polymorphisms (SNPs) that have been described in the human P2X7R gene, but only few have been functionally characterized. The main aim of this study is to determine whether P2X7R gene polymorphisms confer susceptibility to rheumatoid arthritis (RA). A total of 125 patients with RA and 158 healthy volunteers were enrolled in this study. DNA fragment was PCR amplified and sequenced on the AB 3130 Genetic Analyzer. No significant difference in allele frequencies of 489 C→T, 1096 C→G and 1513 A→C polymorphisms, among sporadic cases of RA and healthy controls was found. However, the 1513A/C genotype was significantly associated with the presence of rheumatoid factor and anti-MCV autoantibody in RA patients. Interestingly, the genotype frequency of 1068 A/A was 0.19 in the RA group and 0.09 in control group (P = 0.025). Consequently, this polymorphism (AA) is two folds greater in the RA group compared to controls. Moreover, this polymorphism was significantly associated with mean concentration of C-reactive protein in RA patients. In contrast, 946G→A and 1729 T→A were not detected in both groups. As a result, these two polymorphisms are uncommon in Omani Arab population. Polymorphism at position 1068 and 1513 in the P2X7R gene might contribute to the pathogenesis of RA. Moreover, the loss-of-function SNP at position 1096 C→G or the gain-of-function SNP at position 489 C→T of the P2X7 gene does not appear to be a susceptibility gene locus for the development of RA. Further studies are required to confirm this finding.

Rheumatoid arthritis (RA) is associated with premature mortality, with approximately 50% of deaths being due to cardiovascular disease. It has been shown that the increased incidence of cardiovascular disease is independent of traditional risk factors. Previous studies have shown an increased risk of coronary heart disease with increased levels of activated factor XII (FXIIa). The aim of this study was to investigate levels of FXIIa in patients with RA. We studied 32 patients with RA and 30 age- and sex-matched control subjects. We found FXIIa levels significantly increased in the patient group, with 56% of the patients and 6.7% of controls having levels greater than or equal to 2 ng/ml. A previous study has shown that individuals with levels of 2 ng/ml or more have an increased risk of coronary heart disease. Measurement of FXIIa could perhaps help to identify an 'at risk' group of patients, allowing early intervention therapy.

Pulmonary complications in leptospirosis, though common, are often unrecognized in a non-endemic area. We report here a patient with leptospirosis and severe pulmonary involvement who was treated with meropenem (1 g every 8 hours), moxifloxacin (400 mg once daily), and high doses of corticosteroids. Systemic steroids were continued for 3 months because of persistent pulmonary lesions.