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OBJECTIVES: To investigate, in a population-based cohort of patients with juvenile chronic arthritis (JCA), onset characteristics, progression, outcome, and prognostic factors longitudinally for 5 years. METHODS: This cohort consisted of 132 incidence cases identified between 1984 and 1986 in southwestern Sweden followed for 5 years with annual reports of subgroup, joint assessment, disease activity, eye examinations, laboratory measurements, and medication. At the 5-year follow-up, the Childhood Health Assessment Questionnaire (Child-HAQ) was evaluated. European League Against Rheumatism (EULAR) criteria for diagnosis and disease activity were used. RESULTS: During the 5 years only four patients were lost to follow-up, 34% changed subgroup and 8% developed uveitis. At the 5-year follow-up the disease was active in 12% of the patients, stable in 28%, inactive in 25%, and in remission in 34%. Among those examined, 24% had radiological changes, of whom half had advanced changes. The Child-HAQ median score at the 5-year follow-up was 0.13 (range 0.0-1.9). The number of involved joints at inclusion correlated positively with active disease at the 5-year follow-up. Age at disease onset, the number of involved joints, and the number of joints with arthritis correlated positively with continuous disease and Child-HAQ score. CONCLUSION. Our study shows a diverse disease course during the first 5 years of JCA where one-third changed subgroup and two-thirds did not reach remission. Age of disease onset, the number of involved joints, and the number of joints with arthritis at inclusion were associated with poor outcome at the 5-year follow-up.

BACKGROUND: Tumour necrosis factor (TNF) antagonists have proved effective as treatment against rheumatoid arthritis (RA), but the unresolved issue of whether the use of anti-TNF therapy increases the already elevated risk of lymphoma in RA remains a concern. METHODS: Using the Swedish Biologics Register (ARTIS), the Swedish Cancer Register, pre-existing RA cohorts and cross-linkage with other national health and census registers, a national RA cohort (n = 67,743) was assembled and patients who started anti-TNF therapy between 1998 and July 2006 (n = 6604) were identified. A general population comparator (n = 471,024) was also assembled and the incidence of lymphomas from 1999 to 31 December 2006 was assessed and compared in these individuals. RESULTS: Among the 6604 anti-TNF-treated RA patients, 26 malignant lymphomas were observed during 26,981 person-years of follow-up, which corresponded to a relative risk (RR) of 1.35 (95% CI 0.82 to 2.11) versus anti-TNF-naive RA patients (336 lymphomas during 365,026 person-years) and 2.72 (95% CI 1.82 to 4.08) versus the general population comparator (1568 lymphomas during 3,355,849 person-years). RA patients starting anti-TNF therapy in 1998-2001 accounted for the entire increase in lymphoma risk versus the two comparators. By contrast, RR did not vary significantly by time since start of first treatment or with the accumulated duration of treatment, nor with the type of anti-TNF agent. CONCLUSION: Overall and as used in routine care against RA, TNF antagonists are not associated with any major further increase in the already elevated lymphoma occurrence in RA. Changes in the selection of patients for treatment may influence the observed risk.

Objectives: The degree to which treatment with tumour necrosis factor (TNF) antagonists may be associated with increased risks for serious infections is unclear. An observational cohort study was performed using prospectively collected data from the Swedish Biologics Register (ARTIS) and other national Swedish registers. Methods: First, in the ARTIS, all 4167 rheumatoid arthritis (RA) patients starting TNF antagonist treatment between 1999 and 2003 were identified. Secondly, in the Swedish Inpatient Register, all individuals hospitalised for any reason and who also carried a diagnosis of RA, between 1964 and 2003 (n = 44 946 of whom 2692 also occurred in ARTIS), were identified. Thirdly, in the Swedish Inpatient Register, all hospitalisations listing an infection between 1999 and 2003 were identified. By cross-referencing these three data sets, RRs for hospitalisation with infection associated with TNF antagonist treatment were calculated within the cohort of 44 946 RA patients, using Cox regression taking sex, age, geography, co-morbidity and use of inpatient care into account. Results: Among the 4167 patients treated with TNF antagonists, 367 hospitalisations with infections occurred during 7776 person-years. Within the cohort of 44 496 RA patients, the RR for infection associated with TNF antagonists was 1.43 (95% Cl 1.18 to 1.73) during the first year of treatment, 1.15 (95% Cl 0.88 to 1.51) during the second year of treatment, and 0.82 (95% Cl 0.62 to 1.08) for subjects remaining on their first TNF antagonist treatment after 2 years. Conclusion: Treatment with TNF antagonists may be associated with a small to moderate increase in risk of hospitalisation with infection, which disappears with increasing treatment duration.

70th Annual Scientific Meeting of the American-College-of-Rheumatology/41st Annual Scientific Meeting of the Association-of-Rheumatology-Health-Professionals, Washington, DC, NOV 10-15, 2006

70th Annual Scientific Meeting of the American-College-of-Rheumatology/41st Annual Scientific Meeting of the Association-of-Rheumatology-Health-Professionals, Washington, DC, NOV 10-15, 2006

Annual European Congress of Rheumatology, Vienna, AUSTRIA, JUN 08-11, 2005

Annual European Congress of Rheumatology, Vienna, AUSTRIA, JUN 08-11, 2005

Annual European Congress of Rheumatology, Vienna, AUSTRIA, JUN 08-11, 2005

Annual European Congress of Rheumatology, Vienna, AUSTRIA, JUN 08-11, 2005

Annual European Congress of Rheumatology (EULAR 2004), Berlin, GERMANY, JUN 09-12, 2004

Annual European Congress of Rheumatology (EULAR 2004), Berlin, GERMANY, JUN 09-12, 2004

Annual European Congress of Rheumatology (EULAR 2004), Berlin, GERMANY, JUN 09-12, 2004

Annual European Congress of Rheumatology (EULAR 2004), Berlin, GERMANY, JUN 09-12, 2004

Background: The polymorphic enzyme CYP2C19 is of importance for the metabolism and effects of omeprazole during short-term treatment. Aim: To investigate the relationship between CYP2C19 genotype and the effects of long-term omeprazole treatment. Material and methods: A total of 180 patients with acid related disorders were genotyped for wild type and mutated CYP2C19 alleles by allele-specific PCR amplification. Gastrin and chromogranin A were assessed by radioimmunoassays, and pepsinogen I and H. pylori serology were assessed by ELISA methods. Results: In 108 of the patients, who received a single dose of 20 mg omeprazole, there was no difference in gastrin and chromogranin A concentrations between the three CYP2C19 genotypes. In 72 patients on long-term treatment (> 1 year) with 20 mg omeprazole daily, serum gastrin as well as plasma chromogranin A concentrations (mean ▒ s.e.) were both about threefold higher in the wild type/mutated (52.1 ▒ 7.6 pM and 7.3 ▒ 1.3 nM (n = 19), respectively) compared to wild type/wild type (14.7 ▒ 0.9 pM and 2.5 ▒ 0.1 nM (n = 52), respectively, both comparisons P = 0.0001). In a single mutated/mutated patient on long-term treatment, both gastrin and chromogranin A were high (88 pM and 13.7 nM, respectively). Serum pepsinogen I concentration was significantly lower in wild type/mutated (n = 19) patients on long-term treatment, compared with the corresponding wild type/wild type (n = 49) group (147 ▒ 19 ╡g/L vs. 193 ▒ 12 ╡g/L, P = 0.04). Conclusion: Patients with one (and probably also with two) mutated CYP2C19 allele(s) on long-term treatment with omeprazole had significantly affected serum gastrin and pepsinogen I and plasma chromogranin A concentrations compared with patients with two normal alleles. This indicates that changes in gastric mucosal morphology during omeprazole treatment might be dependent upon the degree of the individual's capacity to metabolize omeprazole.