Chronic, systemic inflammatory disorder that primarily affects joints.
It may result in deformed and painful joints, which can lead to loss of function. The disease may also have signs and symptoms in organs other than joints.
The cause of RA is not completely understood.
Patients hospitalized in the Osaka Rosai Hospital for acute ischemic cerebrovascular disease from August 2002 to February 2018 were divided into two groups at February 2010.
Hashimoto et al., retrospectively identified patients with rheumatoid arthritis (RA). The incidence of RA, occurrence of acute exacerbation of inflammation due to causes other than synovitis preceding ischemic cerebrovascular disease (iCVD) (non-synovitis AEI), and serum C reactive protein (CRP) were compared.
In the first and second periods, 23/1203 patients (1.9%) and 22/1094 patients (2.0%) with acute iCVD had RA, respectively. Non-synovitis AEI was significantly less frequent in the second period (5%, n=1) than the first period (35%, n=8) (p <0.05). CRP was significantly lower at iCVD onset in the second period (median and interquartile range: 2.72 [0.89-4.5] vs. 0.34 [0.12-1.19 mg/dl], p<0.01). Excluding 9 patients with non-synovitis AEI, CRP was still lower in the second period (1.21 [0.47-2.72] vs. 0.33 [0.11-0.98 mg/dl], p <0.01). CRP levels before both iCVD and non-synovitis AEI tended to be lower in the second period (1.53 [0.3-2.78] vs. 0.69 [0.06-1.28 mg/dl], p=0.059). Two patients using tocilizumab developed iCVD despite persistently low CRP levels.
With progress in treatment, RA-related inflammation was better suppressed and CRP decreased, but the prevalence of RA among acute iCVD patients was unchanged. Strategies for tighter control of inflammation are needed, and a new biomarker may be required in patients using tocilizumab 1).
A total of 201 patients with RA who had been followed up at the outpatient clinic of the authors' institution were enrolled in this study. retro-odontoid soft-tissue (ROST) thickness was evaluated on midsagittal T1-weighted MRI. The correlations between ROST thickness and radiographic findings or clinical data on RA were examined. The independent factors related to ROST thickness were analyzed using stepwise multiple regression analysis.
The average thickness of ROST was 3.0 ± 1.4 mm. ROST thickness showed an inverse correlation with disease duration (r = -0.329, p < 0.01), Steinbrocker stage (r = -0.284, p < 0.01), the atlantodental interval (ADI) in the neutral position (r = -0.326, p < 0.01), the ADI in the flexion position (r = -0.383, p < 0.01), and the ADI in the extension position (r = -0.240, p < 0.01). On stepwise multiple regression analysis, ADI in the flexion position and Steinbrocker stage were independent factors associated with ROST thickness.
Although the correlations were not strong, ROST thickness in patients with RA was inversely correlated with ADI and Steinbrocker stage. In other words, ROST thickness tends to be smaller as atlantoaxial instability and peripheral joint destruction worsen. Clinical trial registration no.: UMIN000000980 (UMIN Clinical Trials Registry) 2).