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author:("hukkanen, V")
1.  Impact of anti‐TNF treatment on growth in severe juvenile idiopathic arthritis 
Annals of the Rheumatic Diseases  2006;65(8):1044-1049.
Objectives
To evaluate the impact of anti‐tumour necrosis factor (TNF) treatment on growth and to identify the predictors for the change in growth in severe juvenile idiopathic arthritis (JIA).
Methods
Data from 71 JIA patients (43 on etanercept, 28 on infliximab) were reviewed two years before and two years on the anti‐TNF treatment. The patients had polyarticular disease course (48 polyarthritis, 19 extended oligoarthritis, two systemic arthritis, and two enthesitis related arthritis). At the initiation of the anti‐TNF treatment, their mean age was 9.6 years and the mean duration of JIA, 5.7 years.
Results
In the patients with delayed growth before anti‐TNF treatment (n = 53), the growth velocity, measured as the change in height standard deviation score, accelerated +0.45 (95% confidence interval, 0.33 to 0.56) (p<0.001) during the anti‐TNF treatment. In the patients with normal or accelerated growth before anti‐TNF treatment (n = 18), the change in growth velocity was +0.05 (0.07 to 0.16) (p = 0.39). At two years on anti‐TNF treatment, the growth velocity between these two groups was similar. No difference was found between the patients treated with etanercept or infliximab. A decelerating growth rate before the anti‐TNF treatment was the strongest predictor for the observed increase in the growth velocity. The change in the inflammatory activity remained a significant predictor of the growth velocity even after the decrease in glucocorticoid dose was taken into account.
Conclusions
In the treatment of polyarticular JIA, the anti‐TNF treatment not only suppresses inflammation but also restores growth velocity.
doi:10.1136/ard.2005.047225
PMCID: PMC1798245  PMID: 16449314
juvenile idiopathic arthritis; anti‐TNF treatment; growth
3.  Infliximab or etanercept in the treatment of children with refractory juvenile idiopathic arthritis: an open label study 
Annals of the Rheumatic Diseases  2003;62(3):245-247.
Methods: In a non-randomised, prospective, open label study, 24 patients (mean age 10.2 years, range 3.3–16.3) with polyarticular JIA were treated with either infliximab (n=14) or etanercept (n=10). The patients had had active polyarthritis for at least one year and standard treatment had failed. Anti-tumour necrosis factor (TNF) treatment was added to the current drug treatment. Infliximab (3–4 mg/kg) was given intravenously at weeks 0, 2, and 6, and thereafter at 4 to 8 week intervals. Etanercept (0.4 mg/kg) was given subcutaneously twice a week. Improvement of the patients was assessed at 3, 6, and 12 months according to established JIA response criteria.
Results: In intention to treat analyses, patients in both treatment groups improved significantly. ACR Paediatric 50 was achieved at 3, 6, and 12 months by 9/10 (90%), 8/9 (89%), and 8/9 (89%) patients with etanercept and by 8/12 (67%), 10/12 (83%), and 7/9 (78%) with infliximab, respectively. At 12 months, ACR Paediatric 75 was achieved by 67% of patients in both treatment groups. Five withdrawals due to adverse effects or lack of efficacy occurred in the infliximab group and one due to lack of compliance in the etanercept group.
Conclusion: In this open label clinical study of active JIA, both infliximab and etanercept provided a significant rapid and sustained reduction in disease activity. Adequately powered randomised controlled trials are needed to elucidate the long term safety and efficacy of TNF modulators in the treatment of JIA.
doi:10.1136/ard.62.3.245
PMCID: PMC1754468  PMID: 12594111
4.  Systemic lupus erythematosus patient guide: influence on knowledge of the disease. 
Annals of the Rheumatic Diseases  1991;50(12):900-902.
The knowledge of patients with systemic lupus erythematosus about their disease before and after reading a patient guide was tested. The scores for incorrect answers decreased from 28 to 24% after reading the guide, showing that it increased the patients' knowledge of the disease. The patients with an academic background had the best scores before reading the guide, but they did not improve their scores as much as patients with lower educational qualifications. The differences between the groups studied were not significant in a one way analysis of variance. Forty seven questions about the psychology and coping mechanisms of the patients were factorized. These factors, together with data on the duration and severity of SLE and the age of the patient, were used in multiple linear regression analysis, but had no significant predictive value for an improvement in knowledge. The scores in psychological tests were the same before and after reading the guide. It is concluded that the patient guide for SLE increases knowledge of the disease, but does not affect the psychological response of the patient. The improvement in knowledge cannot be predicted on the basis of various psychological and clinical factors or the social background of the patient.
PMCID: PMC1004577  PMID: 1768155
5.  Predictive clinical and laboratory parameters for serum zinc and copper in rheumatoid arthritis. 
Annals of the Rheumatic Diseases  1988;47(10):816-819.
Zinc and copper have important effects on T cell mediated immunity and on neutrophil function, but it is not known how the causes or effects, of low serum zinc and high serum copper relate to the clinical picture of rheumatoid arthritis (RA). In this study serum zinc and copper determined by flame atomic absorption spectrometry and 30 other clinical, immunological, and laboratory parameters in 60 patients with RA were analysed by stepwise multiple linear regression analysis. Joint score index, rheumatoid factor titre, seropositivity, haemoglobin, and C reactive protein (CRP) were among the nine independent variables which together predicted 73% of the serum zinc variation. This suggests that there is an association between the immune-inflammatory rheumatoid process and the serum zinc concentration. CRP alone had only a 3% independent predicting value for serum zinc, however. This suggests that metallothionein mediated sequestration in the liver, induced by interleukin 1, is not an important explanatory factor in a cross sectional study of chronic inflammation. Furthermore, serum zinc did not have any predictive value at all for serum copper concentration. This does not support the hypothesis suggesting that serum zinc deficiency leads to high serum copper by inducing gastrointestinal metallothionein and high caeruloplasmin.
PMCID: PMC1003609  PMID: 3196083

Results 1-5 (5)