<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Simonini, Gabriele</style></author><author><style face="normal" font="default" size="100%">Ferrara, Giovanna</style></author><author><style face="normal" font="default" size="100%">Pontikaki, Irene</style></author><author><style face="normal" font="default" size="100%">Scoccimarro, Erika</style></author><author><style face="normal" font="default" size="100%">Giani, Teresa</style></author><author><style face="normal" font="default" size="100%">Taddio, Andrea</style></author><author><style face="normal" font="default" size="100%">Meroni, Pier Luigi</style></author><author><style face="normal" font="default" size="100%">Cimaz, Rolando</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Flares After Withdrawal of Biologic Therapies in Juvenile Idiopathic Arthritis: Clinical and Laboratory Correlates of Remission Duration.</style></title><secondary-title><style face="normal" font="default" size="100%">Arthritis Care Res (Hoboken)</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Arthritis Care Res (Hoboken)</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2018</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2018 Jul</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">70</style></volume><pages><style face="normal" font="default" size="100%">1046-1051</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVE: &lt;/b&gt;To assess the time in remission after discontinuing biologic therapy in patients with juvenile idiopathic arthritis (JIA).&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;We enrolled 135 patients followed in 3 tertiary-care centers. The primary outcome was to assess, once remission was achieved, the time in remission up to the first flare after discontinuing treatment. Mann-Whitney U test, Wilcoxon's signed rank test for paired samples, chi-square tests, and Fisher's exact test were used to compare data. Pearson's and Spearman's correlation tests were used to determine correlation coefficients for different variables. To identify predictors of outcome, Cox regression model and Kaplan-Meier curves were constructed, each one at the mean of entered covariates.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;The majority of enrolled patients flared after stopping treatment with biologics (102 of 135, 75.6%) after a median followup time in remission off therapy of 6 months (range 3-109 months). A higher probability of maintaining remission after discontinuing treatment was present in systemic-onset disease compared to the rest of the JIA patients (Mantel-Cox χ = 8.31, P &lt; 0.004). In analysis limited to children with JIA with polyarticular and oligoarticular disease, patients who received biologics &gt;2 years after achieving remission had a higher probability of maintaining such remission off therapy (mean ± SD 18.64 ± 3.3 months versus 11.51 ± 2.7 months [P &lt; 0.009]; Mantel-Cox χ = 9.06, P &lt; 0.002). No other clinical variable was significantly associated with a long-lasting remission.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;Children with oligoarticular and polyarticular JIA who stop treatment before 2 years from remission have a higher chance of relapsing after biologic withdrawal.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">7</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28973842?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Taddio, Andrea</style></author><author><style face="normal" font="default" size="100%">Rossi, Eleonora Dei</style></author><author><style face="normal" font="default" size="100%">Monasta, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Pastore, Serena</style></author><author><style face="normal" font="default" size="100%">Tommasini, Alberto</style></author><author><style face="normal" font="default" size="100%">Lepore, Loredana</style></author><author><style face="normal" font="default" size="100%">Bronzetti, Gabriele</style></author><author><style face="normal" font="default" size="100%">Marrani, Edoardo</style></author><author><style face="normal" font="default" size="100%">Mottolese, Biancamaria D'Agata</style></author><author><style face="normal" font="default" size="100%">Simonini, Gabriele</style></author><author><style face="normal" font="default" size="100%">Cimaz, Rolando</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Describing Kawasaki shock syndrome: results from a retrospective study and literature review.</style></title><secondary-title><style face="normal" font="default" size="100%">Clin Rheumatol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Clin. Rheumatol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">C-Reactive Protein</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Echocardiography</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Heart Failure</style></keyword><keyword><style  face="normal" font="default" size="100%">Hemoglobins</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Immunoglobulins, Intravenous</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mucocutaneous Lymph Node Syndrome</style></keyword><keyword><style  face="normal" font="default" size="100%">Retrospective Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Shock</style></keyword><keyword><style  face="normal" font="default" size="100%">Syndrome</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 Jan</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">36</style></volume><pages><style face="normal" font="default" size="100%">223-228</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Kawasaki shock syndrome (KSS) is a rare manifestation of Kawasaki disease (KD) characterized by systolic hypotension or clinical signs of poor perfusion. The objectives of the study are to describe the main clinical presentation, echocardiographic, and laboratory findings, as well as the treatment options and clinical outcomes of KSS patients when compared with KD patients. This is a retrospective study. All children referred to two pediatric rheumatology units from January 1, 2012, to December 31, 2014, were enrolled. Patients were divided into patients with or without KSS. We compared the two groups according to the following variables: sex, age, type of KD (classic, with less frequent manifestations, or incomplete), clinical manifestations, cardiac involvement, laboratory findings, therapy administered, response to treatment, and outcome. Eighty-four patients with KD were enrolled. Of these, five (6 %) met the criteria for KSS. Patients with KSS had higher values of C-reactive protein (p = 0.005), lower hemoglobin levels (p = 0.003); more frequent hyponatremia (p = 0.004), hypoalbuminemia (p = 0.004), and coagulopathy (p = 0.003); and increase in cardiac troponins (p = 0.000). Among the KSS patients, three had a coronary artery involvement, but none developed a permanent aneurysm. Intravenous immunoglobulin resistance was more frequent in the KSS group, although not significantly so (3/5, 60 % vs. 23/79, 30 %, P = NS). None of the five cases was fatal, and all recovered without sequelae. KSS patients are more likely to have higher rates of cardiac involvement. However, most cardiovascular abnormalities resolved promptly with therapy.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27230223?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Simonini, Gabriele</style></author><author><style face="normal" font="default" size="100%">Bracaglia, Claudia</style></author><author><style face="normal" font="default" size="100%">Cattalini, Marco</style></author><author><style face="normal" font="default" size="100%">Taddio, Andrea</style></author><author><style face="normal" font="default" size="100%">Brambilla, Alice</style></author><author><style face="normal" font="default" size="100%">de Libero, Cinzia</style></author><author><style face="normal" font="default" size="100%">Pires Marafon, Denise</style></author><author><style face="normal" font="default" size="100%">Caputo, Roberto</style></author><author><style face="normal" font="default" size="100%">Cimaz, Rolando</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Predictors of Relapse after Discontinuing Systemic Treatment in Childhood Autoimmune Chronic Uveitis.</style></title><secondary-title><style face="normal" font="default" size="100%">J Rheumatol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Rheumatol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Antirheumatic Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Autoimmune Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Predictive Value of Tests</style></keyword><keyword><style  face="normal" font="default" size="100%">Recurrence</style></keyword><keyword><style  face="normal" font="default" size="100%">Retrospective Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Treatment Outcome</style></keyword><keyword><style  face="normal" font="default" size="100%">Uveitis</style></keyword><keyword><style  face="normal" font="default" size="100%">Withholding Treatment</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 06</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">44</style></volume><pages><style face="normal" font="default" size="100%">822-826</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVE: &lt;/b&gt;To identify clinical predictors of relapse in childhood autoimmune chronic uveitis after stopping systemic treatment.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;A retrospective, multicenter, cohort study.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Ninety-four children in remission, receiving no treatments and with at least a 6-month followup, were enrolled. A higher probability of maintaining remission after discontinuing treatment was shown in idiopathic compared with juvenile idiopathic arthritis uveitis (Mantel-Cox chi-square = 23.21) if inactivity had been obtained within 6 months from starting systemic treatment (Mantel-Cox chi-square = 24.17) and by antitumor necrosis factor-α treatment (Mantel-Cox chi-square = 6.43).&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;Type of disease, time, and type of systemic therapy to achieve inactivity predict different duration of uveitis remission after treatment withdrawal.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28365583?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Taddio, Andrea</style></author><author><style face="normal" font="default" size="100%">Zennaro, Floriana</style></author><author><style face="normal" font="default" size="100%">Pastore, Serena</style></author><author><style face="normal" font="default" size="100%">Cimaz, Rolando</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">An Update on the Pathogenesis and Treatment of Chronic Recurrent Multifocal Osteomyelitis in Children.</style></title><secondary-title><style face="normal" font="default" size="100%">Paediatr Drugs</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Paediatr Drugs</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adrenal Cortex Hormones</style></keyword><keyword><style  face="normal" font="default" size="100%">Anti-Inflammatory Agents, Non-Steroidal</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Chronic Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Diagnosis, Differential</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Osteomyelitis</style></keyword><keyword><style  face="normal" font="default" size="100%">Recurrence</style></keyword><keyword><style  face="normal" font="default" size="100%">Tumor Necrosis Factor-alpha</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 Jun</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">19</style></volume><pages><style face="normal" font="default" size="100%">165-172</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Chronic recurrent multifocal osteomyelitis (CRMO), also known as chronic non-bacterial osteomyelitis (CNO), is a rare inflammatory disorder that primarily affects children. It is characterized by pain, local bone expansion, and radiological findings suggestive of osteomyelitis, usually at multiple sites. CRMO predominantly affects the metaphyses of long bones, but involvement of the clavicle or mandible are suggestive of the diagnosis. CRMO is a diagnosis of exclusion, and its pathogenesis remains unknown. Differential diagnosis includes infection, malignancies, benign bone tumors, metabolic disorders, and other autoinflammatory disorders. Biopsy of the bone lesion is not often required but could be necessary in unclear cases, especially for differentiation from bone neoplasia. Non-steroidal anti-inflammatory drugs (NSAIDs) are the first-line treatment. Alternative therapies have been used, including corticosteroids, methotrexate, bisphosphonates, and tumor necrosis factor (TNF)-α inhibitors. No guidelines have been established regarding diagnosis and treatment options. This manuscript gives an overview of the most recent findings on the pathogenesis of CRMO and clinical approaches for patients with the condition.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28401420?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Taddio, Andrea</style></author><author><style face="normal" font="default" size="100%">Cattalini, Marco</style></author><author><style face="normal" font="default" size="100%">Simonini, Gabriele</style></author><author><style face="normal" font="default" size="100%">Cimaz, Rolando</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Recent advances in the use of Anti-TNFα therapy for the treatment of juvenile idiopathic arthritis.</style></title><secondary-title><style face="normal" font="default" size="100%">Expert Rev Clin Immunol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Expert Rev Clin Immunol</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 Jun</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">12</style></volume><pages><style face="normal" font="default" size="100%">641-9</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Juvenile Idiopathic Arthritis (JIA) encompasses a group of diseases of unknown etiology having in common arthritis in at least 1 joint that persists for 6 weeks and begins before 16 years of age, with other conditions excluded. With a prevalence of 1 per 1,000 children in the USA, JIA is the most common pediatric rheumatic illness and a major cause of acquired childhood disability. During the last 20 years, the advent of host immune response modifiers known as biologic agents, in particular the anti-TNFα agents (etanercept, infliximab, adalimumab), which directly inhibit the action of pro-inflammatory mediators, has revolutionized the treatment and the expected outcome of JIA. This article highlights treatment indications of anti-TNFα drugs and their more frequent side effects in JIA patients.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26809126?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Zannin, Maria E</style></author><author><style face="normal" font="default" size="100%">Birolo, Carolina</style></author><author><style face="normal" font="default" size="100%">Gerloni, Valeria M</style></author><author><style face="normal" font="default" size="100%">Miserocchi, Elisabetta</style></author><author><style face="normal" font="default" size="100%">Pontikaki, Irene</style></author><author><style face="normal" font="default" size="100%">Paroli, Maria P</style></author><author><style face="normal" font="default" size="100%">Bracaglia, Claudia</style></author><author><style face="normal" font="default" size="100%">Shardlow, Alison</style></author><author><style face="normal" font="default" size="100%">Parentin, Fulvio</style></author><author><style face="normal" font="default" size="100%">Cimaz, Rolando</style></author><author><style face="normal" font="default" size="100%">Simonini, Gabriele</style></author><author><style face="normal" font="default" size="100%">Falcini, Fernanda</style></author><author><style face="normal" font="default" size="100%">Corona, Fabrizia</style></author><author><style face="normal" font="default" size="100%">Viola, Stefania</style></author><author><style face="normal" font="default" size="100%">De Marco, Riccardo</style></author><author><style face="normal" font="default" size="100%">Breda, Luciana</style></author><author><style face="normal" font="default" size="100%">La Torre, Francesco</style></author><author><style face="normal" font="default" size="100%">Vittadello, Fabio</style></author><author><style face="normal" font="default" size="100%">Martini, Giorgia</style></author><author><style face="normal" font="default" size="100%">Zulian, Francesco</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Safety and efficacy of infliximab and adalimumab for refractory uveitis in juvenile idiopathic arthritis: 1-year followup data from the Italian Registry.</style></title><secondary-title><style face="normal" font="default" size="100%">J Rheumatol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Rheumatol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Antibodies, Monoclonal</style></keyword><keyword><style  face="normal" font="default" size="100%">Antibodies, Monoclonal, Humanized</style></keyword><keyword><style  face="normal" font="default" size="100%">Antirheumatic Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Arthritis, Juvenile</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Follow-Up Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant</style></keyword><keyword><style  face="normal" font="default" size="100%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Registries</style></keyword><keyword><style  face="normal" font="default" size="100%">Treatment Outcome</style></keyword><keyword><style  face="normal" font="default" size="100%">Tumor Necrosis Factor-alpha</style></keyword><keyword><style  face="normal" font="default" size="100%">Uveitis</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2013</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2013 Jan</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">40</style></volume><pages><style face="normal" font="default" size="100%">74-9</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVE: &lt;/b&gt;To evaluate safety and efficacy of adalimumab (ADA) and infliximab (IFX) for the treatment of juvenile idiopathic arthritis-related anterior uveitis (JIA-AU).&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;Starting January 2007, patients with JIA-AU treated with IFX and ADA were managed by a standard protocol and data were entered into the National Italian Registry (NIR). At baseline, all patients were refractory to standard immunosuppressive treatment and/or were corticosteroid-dependent. Data recorded every 3 months included uveitis course, number/type of ocular complications, drug-related adverse events (AE), treatment change or withdrawal, and laboratory measures. Data of patients treated for at least 1 year were retrieved from the NIR and analyzed using descriptive statistics. Treatment efficacy was based on change in uveitis course and in number of ocular complications.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Up to December 2009, data for 108 patients with JIA-AU treated with anti-tumor necrosis factor-α agents were recorded in the NIR and data from 91, with at least 12 months' followup, were included in the study. Forty-eight patients were treated with IFX, 43 with ADA. Forty-seven patients (55.3%) achieved remission of AU, 28 (32.9%) had recurrent AU, and 10 (11.8%) maintained a chronic course. A higher remission rate was observed with ADA (67.4% vs 42.8% with IFX; p = 0.025). Ocular complications decreased from 0.47 to 0.32 per subject. Five patients experienced resolution of structural complications. No patient reported serious AE; 8 (8.8%) experienced 11 minor AE (9 with IFX, 2 with ADA).&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;IFX and ADA appear to be effective and safe for treatment of refractory JIA-related uveitis, with a better performance of ADA in the medium-term period.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/23118110?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Taddio, Andrea</style></author><author><style face="normal" font="default" size="100%">Cimaz, Rolando</style></author><author><style face="normal" font="default" size="100%">Caputo, Roberto</style></author><author><style face="normal" font="default" size="100%">de Libero, Cinzia</style></author><author><style face="normal" font="default" size="100%">Di Grande, Laura</style></author><author><style face="normal" font="default" size="100%">Simonini, Gabriele</style></author><author><style face="normal" font="default" size="100%">Mori, Francesca</style></author><author><style face="normal" font="default" size="100%">Novembre, Elio</style></author><author><style face="normal" font="default" size="100%">Pucci, Neri</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Childhood chronic anterior uveitis associated with vernal keratoconjunctivitis (VKC): successful treatment with topical tacrolimus. Case series.</style></title><secondary-title><style face="normal" font="default" size="100%">Pediatr Rheumatol Online J</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Pediatr Rheumatol Online J</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">9</style></volume><pages><style face="normal" font="default" size="100%">34</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Uveitis treatment involves topical corticosteroids along with cycloplegic-mydriatics. Particularly severe cases may require systemic corticosteroids and immunosuppressive drugs. Vernal keratoconjunctivitis (VKC) treatment consists of a brief period of topical corticosteroids and/or cyclosporine. In patients refractory to traditional treatment, the use of 0.1% topical ophtalmic FK- 506 (tacrolimus) ointment has been occasionally reported.This is the first report of the coexistence of uveitis and VKC. The documented response to topical tacrolimus eyedrop of uveitis and VKC is also of interest, in particular since to our knowledge there are no published reports on its clinical use in uveitis.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22047067?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Taddio, Andrea</style></author><author><style face="normal" font="default" size="100%">Simonini, Gabriele</style></author><author><style face="normal" font="default" size="100%">Lionetti, Paolo</style></author><author><style face="normal" font="default" size="100%">Lepore, Loredana</style></author><author><style face="normal" font="default" size="100%">Martelossi, Stefano</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author><author><style face="normal" font="default" size="100%">Cimaz, Rolando</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Usefulness of wireless capsule endoscopy for detecting inflammatory bowel disease in children presenting with arthropathy.</style></title><secondary-title><style face="normal" font="default" size="100%">Eur J Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Eur. J. Pediatr.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Arthritis, Juvenile</style></keyword><keyword><style  face="normal" font="default" size="100%">Capsule Endoscopy</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Colitis, Ulcerative</style></keyword><keyword><style  face="normal" font="default" size="100%">Colon</style></keyword><keyword><style  face="normal" font="default" size="100%">Crohn Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Diagnosis, Differential</style></keyword><keyword><style  face="normal" font="default" size="100%">Follow-Up Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammatory Bowel Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Intestine, Small</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Predictive Value of Tests</style></keyword><keyword><style  face="normal" font="default" size="100%">Sensitivity and Specificity</style></keyword><keyword><style  face="normal" font="default" size="100%">Severity of Illness Index</style></keyword><keyword><style  face="normal" font="default" size="100%">Treatment Outcome</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011 Oct</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">170</style></volume><pages><style face="normal" font="default" size="100%">1343-7</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Inflammatory bowel disease (IBD) is a cause of chronic intestinal inflammation in children. In a subset of patients affected by IBD, arthropathy may be the leading presenting sign. In the past years, remarkable advances in gastrointestinal endoscopy techniques have been achieved; recently, the development of capsule endoscopy (CE) provided a non-invasive method for the complete endoscopic evaluation, including small bowel assessment. We report three children suffering from IBD but presenting with articular complaints in whom CE was a useful tool for detecting gut inflammation. Patients were investigated with the wireless CE: PillCam SB2 (Given Imaging, Yoqneam, Israel) capsule, the second-generation capsule, was used in our paediatric patients. Three patients were initially evaluated for arthropathy. Enteropathic arthritis was suspected for gastrointestinal symptoms and/or persistence of inflammatory markers elevation. In one of these children, conventional endoscopy was refused by parents, while in the other two children, CE was proposed as first-line diagnostic tool. In all patients, CE revealed to be safe and provided information that led to diagnosis. Paediatric rheumatologists should consider CE as a valid, non-invasive tool, eventually first level diagnostic approach in order to evaluate the presence of IBD in children presenting with chronic articular complaints.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">10</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/21643650?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Olivito, Biagio</style></author><author><style face="normal" font="default" size="100%">Taddio, Andrea</style></author><author><style face="normal" font="default" size="100%">Simonini, Gabriele</style></author><author><style face="normal" font="default" size="100%">Massai, Cristina</style></author><author><style face="normal" font="default" size="100%">Ciullini, Sara</style></author><author><style face="normal" font="default" size="100%">Gambineri, Eleonora</style></author><author><style face="normal" font="default" size="100%">de Martino, Maurizio</style></author><author><style face="normal" font="default" size="100%">Azzari, Chiara</style></author><author><style face="normal" font="default" size="100%">Cimaz, Rolando</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Defective FOXP3 expression in patients with acute Kawasaki disease and restoration by intravenous immunoglobulin therapy.</style></title><secondary-title><style face="normal" font="default" size="100%">Clin Exp Rheumatol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Clin. Exp. Rheumatol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Acute Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Flow Cytometry</style></keyword><keyword><style  face="normal" font="default" size="100%">Forkhead Transcription Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Genotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Immunoglobulins, Intravenous</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant</style></keyword><keyword><style  face="normal" font="default" size="100%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mucocutaneous Lymph Node Syndrome</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Single Nucleotide</style></keyword><keyword><style  face="normal" font="default" size="100%">Reverse Transcriptase Polymerase Chain Reaction</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA, Messenger</style></keyword><keyword><style  face="normal" font="default" size="100%">T-Lymphocytes, Regulatory</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2010 Jan-Feb</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">28</style></volume><pages><style face="normal" font="default" size="100%">93-7</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVES: &lt;/b&gt;The aims of this study were: 1) to investigate forkhead box P3 (FOXP3) expression in patients with Kawasaki disease (KD), exploring possible differences during the acute phase and after defervescence; 2) to evaluate a possible association of the FOXP3 single nucleotide polymorphism (SNP) 543 (SNP ID: rs2232367) with KD.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;FOXP3 expression was evaluated on 8 children with KD and 15 healthy children by flow cytometry and Real-Time polymerase chain reaction (RT-PCR). FOXP3 SNP 543 was genotyped by denaturing high-performance liquid chromatography (DHPLC) and sequencing on DNA samples from 58 additional children with KD and 114 healthy donors.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;The frequencies of CD4+CD25 +FOXP3+ regulatory T cells were significantly (p=0.0002) lower during the acute phase of KD than in sex- and age-matched healthy donors (median % + SD: 4.8+/-1.3 vs. 7.7+/-1.7) and a similar tendency was revealed for FOXP3 mRNA transcripts (p&lt;0.0001). FOXP3 expression increased significantly, at both protein and mRNA levels, after intravenous immunoglobulin (IVIG) therapy treatment and achieving complete remission of disease (at least 48 hrs; median 9.5 days, range 2-30). Of the 58 patients screened, only one female subject (1.7%) carried the presence of 543 SNP in heterozygosis (C&gt;T; for a total of 1 allele out of 88), with no difference between KD patients and controls (0.0%, 0/203 alleles).&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Our data reinforce the notion of an impaired immunoregulation in KD, suggesting also a role of IVIG treatment in modifying the Treg compartment. FOXP3 SNP 543 does not seem to be involved in susceptibility to KD in Italian children.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1 Suppl 57</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/20412712?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Ruperto, Nicolino</style></author><author><style face="normal" font="default" size="100%">Ozen, Seza</style></author><author><style face="normal" font="default" size="100%">Pistorio, Angela</style></author><author><style face="normal" font="default" size="100%">Dolezalova, Pavla</style></author><author><style face="normal" font="default" size="100%">Brogan, Paul</style></author><author><style face="normal" font="default" size="100%">Cabral, David A</style></author><author><style face="normal" font="default" size="100%">Cuttica, Ruben</style></author><author><style face="normal" font="default" size="100%">Khubchandani, Raju</style></author><author><style face="normal" font="default" size="100%">Lovell, Daniel J</style></author><author><style face="normal" font="default" size="100%">O'Neil, Kathleen M</style></author><author><style face="normal" font="default" size="100%">Quartier, Pierre</style></author><author><style face="normal" font="default" size="100%">Ravelli, Angelo</style></author><author><style face="normal" font="default" size="100%">Iusan, Silvia M</style></author><author><style face="normal" font="default" size="100%">Filocamo, Giovanni</style></author><author><style face="normal" font="default" size="100%">Magalhães, Claudia Saad</style></author><author><style face="normal" font="default" size="100%">Unsal, Erbil</style></author><author><style face="normal" font="default" size="100%">Oliveira, Sheila</style></author><author><style face="normal" font="default" size="100%">Bracaglia, Claudia</style></author><author><style face="normal" font="default" size="100%">Bagga, Arvind</style></author><author><style face="normal" font="default" size="100%">Stanevicha, Valda</style></author><author><style face="normal" font="default" size="100%">Manzoni, Silvia Magni</style></author><author><style face="normal" font="default" size="100%">Pratsidou, Polyxeni</style></author><author><style face="normal" font="default" size="100%">Lepore, Loredana</style></author><author><style face="normal" font="default" size="100%">Espada, Graciela</style></author><author><style face="normal" font="default" size="100%">Kone-Paut, Isabella</style></author><author><style face="normal" font="default" size="100%">Paut, Isabelle Kone</style></author><author><style face="normal" font="default" size="100%">Zulian, Francesco</style></author><author><style face="normal" font="default" size="100%">Barone, Patrizia</style></author><author><style face="normal" font="default" size="100%">Bircan, Zelal</style></author><author><style face="normal" font="default" size="100%">Maldonado, Maria del Rocio</style></author><author><style face="normal" font="default" size="100%">Russo, Ricardo</style></author><author><style face="normal" font="default" size="100%">Vilca, Iris</style></author><author><style face="normal" font="default" size="100%">Tullus, Kjell</style></author><author><style face="normal" font="default" size="100%">Cimaz, Rolando</style></author><author><style face="normal" font="default" size="100%">Horneff, Gerd</style></author><author><style face="normal" font="default" size="100%">Anton, Jordi</style></author><author><style face="normal" font="default" size="100%">Garay, Stella</style></author><author><style face="normal" font="default" size="100%">Nielsen, Susan</style></author><author><style face="normal" font="default" size="100%">Barbano, Giancarlo</style></author><author><style face="normal" font="default" size="100%">Martini, Alberto</style></author></authors><translated-authors><author><style face="normal" font="default" size="100%">Paediatric Rheumatology International Trials Organisation (PRINTO)</style></author></translated-authors></contributors><titles><title><style face="normal" font="default" size="100%">EULAR/PRINTO/PRES criteria for Henoch-Schönlein purpura, childhood polyarteritis nodosa, childhood Wegener granulomatosis and childhood Takayasu arteritis: Ankara 2008. Part I: Overall methodology and clinical characterisation.</style></title><secondary-title><style face="normal" font="default" size="100%">Ann Rheum Dis</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Ann. Rheum. Dis.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Biopsy</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Delphi Technique</style></keyword><keyword><style  face="normal" font="default" size="100%">Granulomatosis with Polyangiitis</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">International Cooperation</style></keyword><keyword><style  face="normal" font="default" size="100%">Internet</style></keyword><keyword><style  face="normal" font="default" size="100%">Polyarteritis Nodosa</style></keyword><keyword><style  face="normal" font="default" size="100%">Purpura, Schoenlein-Henoch</style></keyword><keyword><style  face="normal" font="default" size="100%">Reproducibility of Results</style></keyword><keyword><style  face="normal" font="default" size="100%">Takayasu Arteritis</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2010 May</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">69</style></volume><pages><style face="normal" font="default" size="100%">790-7</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVES: &lt;/b&gt;To report methodology and overall clinical, laboratory and radiographic characteristics for Henoch-Schönlein purpura (HSP), childhood polyarteritis nodosa (c-PAN), c-Wegener granulomatosis (c-WG) and c-Takayasu arteritis (c-TA) classification criteria.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;The preliminary Vienna 2005 consensus conference, which proposed preliminary criteria for paediatric vasculitides, was followed by a EULAR/PRINTO/PRES - supported validation project divided into three main steps. Step 1: retrospective/prospective web-data collection for HSP, c-PAN, c-WG and c-TA, with age at diagnosis &lt;or=18 years. Step 2: blinded classification by consensus panel of a subgroup of 280 cases (128 difficult cases, 152 randomly selected) enabling expert diagnostic verification. Step 3: Ankara 2008 Consensus Conference and statistical evaluation (sensitivity, specificity, area under the curve, kappa-agreement) using as 'gold standard' the final consensus classification or original treating physician diagnosis.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;A total of 1183/1398 (85%) samples collected were available for analysis: 827 HSP, 150 c-PAN, 60 c-WG, 87 c-TA and 59 c-other. Prevalence, signs/symptoms, laboratory, biopsy and imaging reports were consistent with the clinical picture of the four c-vasculitides. A representative subgroup of 280 patients was blinded to the treating physician diagnosis and classified by a consensus panel, with a kappa-agreement of 0.96 for HSP (95% CI 0.84 to 1), 0.88 for c-WG (95% CI 0.76 to 0.99), 0.84 for c-TA (95% CI 0.73 to 0.96) and 0.73 for c-PAN (95% CI 0.62 to 0.84), with an overall kappa of 0.79 (95% CI 0.73 to 0.84).&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;EULAR/PRINTO/PRES propose validated classification criteria for HSP, c-PAN, c-WG and c-TA, with substantial/almost perfect agreement with the final consensus classification or original treating physician diagnosis.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">5</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/20388738?dopt=Abstract</style></custom1></record></records></xml>