Objectives Current knowledge of the cardiac manifestations of rheumatoid arthritis (RA) stems only from clinical and transthoracic echocardiography (TTE) studies. To determine the incidence and type of heart lesions in RA, we coupled TTE with transesophageal echocardiography (TEE), which is more sensitive and more accurate. Methods Thirty unselected RA patients (26 women and 4 men aged 27 to 84 years, with a mean age of 57.8 ± 15.1 years) free of known progressive heart disease underwent a chest radiograph, an electrocardiogram, laboratory tests, and TTE coupled with TEE. Results were compared with those in age‐ and sex‐matched patients who were free of rheumatic disease and who underwent TEE to investigate a neurologic or cardiologic disorder. Results Mitral regurgitation (MR) was evidenced in 24 cases (80%). Among the controls, only 11 (37%) had MR (P< 0.001). Aortic regurgitation was found in 10 cases (33%), versus 7 controls (not significant—NS). Seven cases (23%) versus only 2 controls (7%) had tricuspid valve abnormalities (NS). Pericarditis was found in 4 cases (13%) and in none of the controls. Eleven cases had evidence of cardiomyopathy (37%) and 12 (40%) had atheroma of the aorta, this last being missed by TTE in 10 patients. Echo‐generating nodules were seen on a mitral valve in 2 cases and on an aortic valve in 1. We found no correlations linking cardiac lesions to clinical or laboratory features of RA. Conclusion Our study demonstrated that cardiac involvement, particularly of the mitral valve, is extremely common in RA patients.
The aim of this study was to evaluate the prevalence of Raynaud's phenomenon in patients with rheumatoid arthritis (RA), and to relate this symptom to clinical, radiological and serological characteristics of the patients. All relevant information was retrospectively obtained from the standardized clinical records of 322 RA in-patients first admitted to the Rheumatology Unit of Brest University Medical School. Raynaud's phenomenon was found in 54 (17.2%) of 322 RA patients. There was no significant correlation between demographic, clinical or radiological characteristics. However, the subgroup of RA patients with Raynaud's phenomenon had a slightly higher prevalence of vasculitis than the subgroup without Raynaud's phenomenon. CRP level and C4 level were found to be lower in the former than in the latter group, whereas ESR and various serological findings (rheumatoid factor, antinuclear antibodies) were comparable in the two groups. We conclude that the prevalence of Raynaud's phenomenon is high in French RA in-patients, and that some clinical and biological abnormalities (vasculitis, low CRP level and low C4 level) suggest an association between Raynaud's phenomenon and vasculitis in a few cases, whereas this association might be fortuitous in the remainder.
Objectives. Current knowledge of the cardiac manifestations of rheumatoid arthritis (RA) stems only from clinical and transthoracic echocardiography (TTE) studies. To determine the incidence and type of heart lesions in RA, we coupled TTE with transesophageal echocardiography (TEE), which is more sensitive and more accurate. Methods. Thirty unselected RA patients (26 women and 4 men aged 27 to 84 years, with a mean age of 57.8 ؎ 15.1 years) free of known progressive heart disease underwent a chest radiograph, an electrocardiogram, laboratory tests, and TTE coupled with TEE. Results were compared with those in age-and sex-matched patients who were free of rheumatic disease and who underwent TEE to investigate a neurologic or cardiologic disorder. Results. Mitral regurgitation (MR) was evidenced in 24 cases (80%). Among the controls, only 11 (37%) had MR (P < 0.001). Aortic regurgitation was found in 10 cases (33%), versus 7 controls (not significant-NS). Seven cases (23%) versus only 2 controls (7%) had tricuspid valve abnormalities (NS). Pericarditis was found in 4 cases (13%) and in none of the controls. Eleven cases had evidence of cardiomyopathy (37%) and 12 (40%) had atheroma of the aorta, this last being missed by TTE in 10 patients. Echo-generating nodules were seen on a mitral valve in 2 cases and on an aortic valve in 1. We found no correlations linking cardiac lesions to clinical or laboratory features of RA. Conclusion. Our study demonstrated that cardiac involvement, particularly of the mitral valve, is extremely common in RA patients.
Matrix Gla protein (MGP) is a member of the vitamin K-dependent gamma carboxylase protein family expressed in cartilage. Insulin-like growth factor I (IGF1) stimulates chondrocyte differentiation, whereas basic fibroblast growth factor (FGF2) acts in an opposite manner. We explored the differential expression and regulation by IGF1 and FGF2 of the MGP gene during chondrocyte differentiation. We used a primary culture system of rabbit epiphyseal chondrocytes to show that MGP mRNA is mainly expressed during serum-induced proliferation. Much lower MGP mRNA content is observed in post-mitotic chondrocytes, which newly express alpha 1X procollagen mRNA, a marker of late-differentiated cells. From studies of a series of growth factors, it was shown that IGF1 decreased chondrocyte MGP transcripts, whereas FGF2 had the opposite effect. FGF2 stimulated chondrocyte MGP production in a dose- and time-dependent manner at the mRNA and protein levels. FGF2 acted in a dose- and time-dependent manner, reaching a maximum at 10 ng/ml at 20 h. The protein synthesis inhibitor cycloheximide did not modify FGF2 action, in agreement with a direct effect. Actinomycin D abolished FGF2-induced stimulation, strongly suggesting that FGF2 modulated MGP gene transcription. We transiently transfected chondrocytes with a construct containing the mouse MGP promoter from -5000 to -168 base pairs, relative to the transcription start site of the gene linked to the luciferase gene (MGP-Luc). In transfected cells, FGF2 stimulated luciferase activity up to sevenfold while IGF1 had no effect. Hence, FGF2 induces transcription of the MGP gene via the 5'-flanking region of the gene. Using a series of deleted MGP-Luc constructs, we identified a sequence of 748 base pairs which was sufficient for transcriptional activation by FGF2. These results led us to postulate that the inhibitory chondrogenic action of FGF2 involves a mechanism whereby MGP gene transcription and protein are induced.
Aims were to determine the prevalence of the HLA-B27 phenotype in a group of patients with RA, and to evaluate the clinical, radiological and, serological characteristics of RA in relation to this phenotype. All relevant information was obtained retrospectively from the standardized clinical records of 311 RA in-patients first admitted to the Rheumatology Unit of the Brest University Medical School. In the control population of Britanny, the frequency of HLA-B27 has been shown to be 12%, while HLA-B27 was present in 30 (9.6%) of the 311 RA patients. There was no significant association between demographic, clinical, biological, or radiological characteristics of the patients on the one hand, and the presence of the HLA-B27 allele on the other. The subgroup of RA patients with HLA-B27 had however a slightly higher IgA level than that without HLA-B27. Ankylosing spondylitis were found to coexist in three patients who all were HLA-B27 positive. We conclude (1) that the prevalence of HLA-B27 is not higher in French RA patients than in the normal controls, and (2) that HLA-B27 typing is not useful in RA. HLA-B27 does not confirm nor does it reject the diagnosis of associated ankylosing spondylitis.
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