The purpose of this clinical update is to provide an overview of the fear of needles and needle phobia in children and adolescents including characteristics and diagnosis, prevalence and epidemiology, etiological factors, and treatment options. Needle-related fear and needle phobia present as significant needle-related distress and avoidance behavior. The etiology is biopsychosocial. These challenging conditions are more common in children and adolescents than in adults. The nurse–patient relationship enables the provision of suitable preparation before injection procedures. Nurses can use exposure-based interventions and incorporate coping strategies and teaching of parents and children. Nurses play a pivotal role in noticing the need for further treatment. Procedural needle-related distress is a complex phenomenon representing a continuum ranging from needle fear to more severe needle phobia. For patients with needle fear management and training methods used by nurses can possibly prevent a progression of the condition into needle phobia. In cases of needle phobia, a correct diagnosis made by a psychiatrist is necessary and enables referral to a psychotherapist with experience in treating children and adolescents with needle phobia.

Several studies have identified the PTPN22 allelic variant 1858 C/T that encodes the R620W amino-acid change as a putative susceptibility factor in autoimmune diseases. The current study was undertaken to examine a large cohort of Finnish rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA) subjects using both population control and, importantly, familybased association methods. The latter is particularly important when, as is the case for the 1858 C/T polymorphism, the frequency of the variant allele (T) differs in both major ancestral populations and in subpopulations. The analysis of rheumatoid factor-positive 1030 RA probands from Finland provides strong support for association of this variant in both population studies (allele specific odds ratio (OR) ¼ 1.47, 95% confidence interval (CI) ¼ 1.27-1.70, P ¼ 3 Â 10 À7 ) and in family studies (Po10 À6 ). In contrast, no allelic association was seen with JIA (230 probands) and only weak evidence for a genotypic effect of 1858T homozygotes was observed in this population. Genes and Immunity (2005) 6, 720-722.

BackgroundThe purpose of this study was to investigate the long-term effects of adalimumab, a tumor necrosis factor alpha antagonist, in the treatment of uveitis associated with juvenile idiopathic arthritis.MethodsAdalimumab was initiated in 94 patients with juvenile idiopathic arthritis to treat active arthritis and/or active associated uveitis. In 18 patients, therapy was discontinued after a short period because of inefficacy or side effects. The activity of uveitis (using Standardized Uveitis Nomenclature [SUN] criteria and clinical examination) and arthritis (number of swollen or active joints) was evaluated at the start and at end of the study.ResultsAt the end of the study, uveitis was under good clinical control in two thirds of 54 patients (31% did not need any local treatment and 35% used only 1–2 corticosteroid drops a day), and one third had active uveitis (at least three corticosteroid drops a day). According to SUN criteria, adalimumab treatment for uveitis showed improved activity (a two-fold decrease in uveitis activity) in 28% of patients, with a moderate response in 16 patients, no change in a further 16 patients, and worsening activity (a two-fold increase in uveitis activity) in 13% of patients. The overall proportion of patients with active arthritis decreased. At the beginning of the study, 69% of patients with uveitis had more than two active joints, and at the end of the study only 27% had active joint disease. In 27 patients with juvenile idiopathic arthritis without uveitis on adalimumab, the number of active joints decreased from 93% to 59%. Systemic corticosteroid treatment could be stopped in 22% of patients with uveitis and in 11% of those without uveitis. Most of the patients had received methotrexate, other immunosuppressive therapy, or other biological drugs before initiating adalimumab.ConclusionAdalimumab is a valuable option in the treatment of uveitis associated with active juvenile idiopathic arthritis.

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Objective. The SLC11A1 (formerly called NRAMP1) gene is important in natural resistance to a variety of intracellular infections mediated by macrophages and has been proposed as a candidate gene for autoimmune disease susceptibility. The aim of this study was to examine susceptibility in Finnish patients with persistent oligoarticular and polyarticular rheumatoid factor (RF)-negative juvenile idiopathic arthritis (JIA) due to the presence of the SLC11A1 locus on chromosome 2.Methods. A total of 234 Finnish JIA nuclear families and 639 elderly Finnish controls without a history of JIA were evaluated for association with JIA at 3 intragenic single-nucleotide polymorphisms: an intragenic insertion/deletion, a promoter microsatellite (NRAMP1), and a 3 microsatellite (D2S1471).Results. Analysis of marker haplotypes demonstrated a strong association of Finnish JIA with 6-marker, 4-marker, and 2-marker haplotypes. Most impressively, 1 of the 6-marker haplotypes showed an odds ratio (OR) of 4.0 (95% confidence interval [95% CI] 2.6-6.2) in all JIA patients, 3.5 (95% CI 1.9-6.5) in those with persistent oligoarticular JIA, and 4.1 (95% CI 2.5-6.7) in those with polyarticular RF-negative JIA. Stratification of the haplotype data suggested that susceptibility to JIA in the haplotype spanning the SLC11A1 locus is independent (P < 0.01) of an association with a DRB1 JIA shared epitope (DRB1*JIASE) that includes well-characterized strong susceptibility to DRB1*08 and *11 alleles. This SLC11A1 haplotype also had an additive effect with DRB1*JIASE in those with polyarticular, but not those with persistent oligoarticular, disease (P ‫؍‬ 0.06, OR 2.9 [95% CI 0.9-9.2] versus P ‫؍‬ 0.5, OR 1.6 [95% CI 0.4-6.0]).Conclusion. Taken together, these data provide support for the existence of a locus at or near SLC11A1 that is a strong susceptibility factor for JIA in Finnish patients.Aside from the T cell receptor (1-5) and several cytokine single-nucleotide polymorphisms (SNPs) (6-18), there are few published reports on genes outside the major histocompatibility complex (MHC) that have been examined for their contribution to genetic susceptibility in juvenile idiopathic arthritis (JIA). SLC11A1

This study used Finnish juvenile idiopathic arthritis (JIA) probands with pauciarticular and rheumatoid factor (RF) negative polyarticular subtypes of JIA to further define the genetic susceptibility to JIA. We examined 16 markers spanning an 18 cM region of chromosome 6 encompassing the MHC and surrounding genomic region in a set of 235 Finnish JIA nuclear families and 639 Finnish control individuals. Analysis by case/control association and transmission disequilibrium test (TDT) methods each demonstrated strong evidence for a susceptibility locus near the D6S2447 microsatellite (P<10(-6) for both methods) that is flanked by DQB1 and DRB1. Analysis of the DRB1 locus suggested that DRB1*0801 and DRB1*1101 rather than DQA1 or other HLA alleles may be responsible for conferring susceptibility to disease. These findings are consistent with the most compelling results of previous reports on HLA associations and suggest a JIA DRB1 shared epitope encompassing critical amino-acid residues in the third hypervariable region of this molecule. Most importantly, in pauciarticular patients, the strong association does not extend to proximal markers as it does in polyarticular patients (P<0.00001). Analysis strongly suggests that the difference is because of additional JIA susceptibility loci within the MHC being present in polyarticular RF negative patients.

Objective:To determine the prevalence of dry eye symptoms and signs in children with juvenile idiopathic arthritis (JIA).Patients and methods:A total of 192 children with JIA: 48 oligo-, 39 extended oligo-, 79 polyarthritis, and 26 with other types of arthritis (eight juvenile spondyloarthritis, five juvenile psoriatic arthritis, three mixed connective tissue diseases, two systemic onset arthritis, and eight undetermined arthritis) were interviewed for dry eye symptoms and tested with Schirmer test with anesthetic. Two thirds of the patients were female and the mean age of the patients was 13.1 years (range 10–16) and the mean duration of arthritis was six years (SD 4, 4). Thirty-one percent of the patients had a history of uveitis. Dry eye was defined as Schirmer test score ≤ 5 mm in five minutes. The type of arthritis, a history of uveitis, and the ocular and systemic medication used were evaluated for their correlation with dry eye symptoms and signs by using chi-square tests and the Mann–Whitney Monte Carlo analysis.Results:Altogether 17% of this cohort had decreased basal tear secretion. The most common symptoms of dry eye were discharge secretion, itching, and watering. The intensity of symptoms and signs did not correlate. The type of arthritis, a history or presence of uveitis, and the medication used did not correlate with the occurrence of dry eyes.Conclusion:Dry eye symptoms and signs are common in JIA, and Schirmer test with anesthetic is a useful tool in evaluating these patients.

The first patient entered the Rheumatism Foundation Hospital, Heinola, Finland in July 1951. From that point on, the hospital helped patients suffering from rheumatic disorders. Specialists in the hospital actively developed treatments and published a large number of scientific articles in international journals. The hospital was well known internationally among people working in the field. Progress in the development of disease-modifying medication (biological agents in particular) has dramatically improved the life of patients with rheumatic diseases, but all effective treatments may also have adverse effects. In this article, we briefly review the history of the Rheumatism Foundation Hospital, which was closed permanently in March 2010 due to bankruptcy. The economical difficulties were caused primarily by the progress made in disease-modifying therapy, which decreased the need of rehabilitation and operative treatment of patients with rheumatic diseases. It seems that a great success in biological agents can carry "serious adverse effects", which may kill hospitals. This is an important primary observation, which should be noticed when the future of specialised institutes is planned.