After adjustment for microbial plaque, JIA is not a risk factor for periodontitis.

Objective-To study the eYcacy of combination therapy with etanercept and methotrexate in patients with refractory juvenile idiopathic arthritis. Methods-Seven children with active juvenile idiopathic arthritis refractory to at least combination therapy with methotrexate and sulfasalazine or cyclosporin A were studied. Concomitant treatment, consisting of non-steroidal drugs, corticosteroids, and methotrexate, remained unchanged. Results-Six patients continued the treatment for at least 24 weeks. In the child with systemic arthritis, etanercept was stopped because of persisting spiking fever, joint pain, and rash. In the remaining children an immediate significant decrease in joint pain (p<0.05), disappearance of morning stiVness, and regression of joint swelling (p<0.05) were observed. Improvement was apparent after two injections. An immediate significant (p<0.05) decrease in erythrocyte sedimentation rate, C reactive protein, and interleukin 6 was observed. Side eVects consisted of mild reactions at the injection site in two children. Conclusions-In this observational study, etanercept in combination with methotrexate was well tolerated and highly eVective in treating juvenile polyarthritis but not in the patient with systemic arthritis. Combination treatment appears to be feasible in terms of toxicity and may enhance eYciency. (Ann Rheum Dis 2001;60:410-412) The term juvenile idiopathic arthritis (JIA) was coined in 1996 and includes juvenile rheumatoid and chronic arthritis according to the earlier ARA and EULAR classification criteria.

Juvenile idiopathic arthritis (JIA) is the most common childhood autoimmune rheumatic disease and like rheumatoid arthritis (RA), it is characterized by inflammation and the progressive destruction of joints. In RA, cathepsins as proteinases play a major role in destroying synovial tissue and cartilage matrix. So far no data on cathepsin expression in pannus tissue of HA patients exist. The aim of this study was to characterize the expression levels of cathepsins B, D, H, and L in HA and to compare them with those in RA. Synovectomy tissue from 16 HA and 12 RA patients was investigated for cathepsin expression levels by Western blot analysis. Expression of cathepsins B, D and L was on comparable levels in the synovectomy tissue of HA and RA patients. The following graduation of expression was determined: cathepsin D > cathepsin L > cathepsin B. Cathepsin H was neither found to be expressed in HA nor in RA patients. The expression levels of cathepsins in pannus tissue showed no clear difference between patients with systemic JIA and patients with monoarticular JIA. In summary, the comparable expression of cathepsins B, D and L in RA and JIA synovectomy tissue suggests that they may play a similarly important role in destroying synovial tissue and cartilage matrix in the course of HA and RA.

Due to changing characteristics of infective endocarditis in the past two decades, we, retrospectively analysed 28 cases of infective endocarditis in children of age less than 15 years at Sher-i-Kashmir Institute of Medical Sciences, Soura, Srinagar from December, 1983 to November, 1993. The incidence of disease was observed as 1.5 cases/1000 children admitted with a M:F ratio of 2:1. Three patients were of age less than 2 years (group I) as 25 were above 2 years of age (group II). The two groups had significant difference in portal of entry of infection, infective microorganisms, echocardiography and prognosis. Congenital heart disease was the commonest underlying cardiac lesion in 24 (85.71%) patients. Portal of entry of infection was apparent in 35.71% only; dental route being more frequent in group II. Streptococcus viridans (in 9 cases) followed by staphylococcus aureus (in 4 cases) were the two common organisms isolated. Patients were treated, for a period of 4-6 weeks with a over all mortality rate of 25%. Factors associated with poor prognosis were age < 2 years, staphylococcal infection ad negative blood cultures. Heart failure resistant to medical therapy was a leading cause of death.

HLA-DRB3(*) could be a common putative risk indicator for juvenile idiopathic arthritis and chronic periodontitis among females.

The aim of this study was to investigate the p53 status in two autoimmune diseases; juvenile chronic arthritis (JCA) and rheumatoid arthritis (RA). In a PCR‐sequencing analysis of exons 4–9 of the p53 gene, no mutation was identified, except for the case of an RA synovectomy sample with two mutations of intron 7. p53 gene polymorphisms for codons 36, 47, and 213 were not detected. Codon 72 polymorphism showed an indication of an increased occurrence of the Pro/Pro allelotype in JCA. Expression of P53 protein was comparable for JCA and RA synovectomy samples. For all RA samples P53 protein was detectable, whereas one sample of a JCA patient failed to express P53 protein.

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