Systemic and local factors are involved in the evolution of erosions in hand osteoarthritis.

OBJECTIVE: In order to gain insight in the pathogenesis of erosive hand osteoarthritis (OA), the evolution of erosions in hand OA and risk factors involved were investigated. METHODS: The 6-year evolution in radiographic Verbruggen-Veys anatomical phase was assessed in interphalangeal joints of 236 patients with hand OA (mean age 59 years, 83% women) from the GARP (for 'Genetics ARthrosis and Progression') sibling pair study. Erosive evolution comprised phase transitions from non-erosive to erosive phases and from active erosions to remodelling. Clustering of erosive evolution within patients was assessed using the χ² test. Familial aggregation was evaluated in sibling pairs by estimating ORs for siblings and probands sharing erosive evolution. Local baseline determinants and the effect of high sensitivity C reactive protein were assessed using generalised estimating equations. RESULTS: Erosive evolution took place in 181 of 4120 interphalangeal joints at risk (4.4%), corresponding to 60 patients (25.4% of study sample). Erosive evolution was found more often in multiple interphalangeal joints in one patient than would be expected by chance (χ² 373.0, p < 0.001). The adjusted OR (95% CI) for a sibling having erosive evolution if the proband had erosive evolution was 4.7 (1.4 to 15.8). Systemic inflammation was not associated with erosive activity. Independent local determinants were joint space narrowing (OR (95% CI) 8.9 (4.8 to 16.4)) and self-reported pain (OR (95%CI) 2.3 (1.1 to 4.7)). CONCLUSIONS: rosive evolution was clustered within patients and families. Local factors were also involved in the evolution. This increase in insight in the pathogenesis of erosive hand OA will contribute to the development of new treatments.

No increased risk of valvular heart disease in adult poststreptococcal reactive arthritis.

OBJECTIVE: Poststreptococcal reactive arthritis (ReA) is a (poly)arthritis presenting after a Streptococcus group A infection. Acute rheumatic fever (ARF), albeit caused by the same pathogen, has different risk characteristics and is considered to be a separate entity. Whereas ARF is known to cause carditis, the risk of carditis in adult poststreptococcal ReA is unknown. Consequently, the prevailing recommendations regarding long-term antibiotic prophylaxis in poststreptococcal ReA are imprecise and derived from the data on ARF. This study was undertaken to investigate the development of valvular heart disease in an unselected cohort of adult patients with poststreptococcal ReA who did not receive antibiotic prophylaxis and were followed up prospectively. METHODS: All patients presenting with early arthritis to an inception cohort of >2,000 white patients were evaluated. Patients presenting with poststreptococcal ReA (n = 75) were selected. After a median followup of 8.9 years, the occurrence of valvular heart disease was evaluated by transthoracic echocardiography in 60 patients. Controls were matched for age, sex, body surface area, and left ventricular function, with a patient-to-control ratio of 1:2. RESULTS: No differences were seen in left ventricular dimensions. Morphologic abnormalities of the mitral or aortic valves were not more prevalent among patients than among controls. Mild mitral regurgitation was present in 23% and 21% of patients and controls, respectively. Mild aortic regurgitation was present in 10% and 11%, and mild tricuspid regurgitation in 43% and 39%, respectively, revealing no significant differences. CONCLUSION: Our findings indicate that there is no increased risk of valvular heart disease in adult poststreptococcal ReA. Based on these data, routine long-term antibiotic prophylaxis is not recommended in adult poststreptococcal ReA.