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Error in the Abstract in the Article by Maldini et al (Arthritis Care Res [Hoboken], March 2014) 下载免费PDF全文
Carla Maldini Raphaèle Seror Olivier Fain Robin Dhote Zahir Amoura Michel De Bandt Jean‐Luc Delassus Géraldine Falgarone Loïc Guillevin Véronique Le Guern François Lhote Olivier Meyer Jacky Ramanoelina Karim Sacré Yurdagul Uzunhan Jean‐Louis Leroux Xavier Mariette Alfred Mahr 《Arthritis care & research》2014,66(5):794-794
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Sukru Uguz Gulsah Seydaoglu Cem Doğan Banu Yazgan Inanc Ebru Yurdagul Rasim Somer Diler 《Acta odontologica Scandinavica》2013,71(5):266-271
Objectives. The aims of this study were to determine the frequency of dental anxiety (DA) and dental phobia (DP) in panic disorder, and to follow the changes in DA levels during antidepressant treatment of panic disorder. Methods. Fifty-three controls and 102 panic disorder patients were assessed using the Structured Clinical Interview (SCID), the Panic-Agoraphobia Scale (PAS), and the Corah Dental Anxiety Scale (DAS). Oral health status was defined by the number of decayed, missing, and filled teeth (DMFT) index. The patients were classified into three groups: (1) those without dental anxiety (WDA), (2) those with dental anxiety (DA), and (3) those with dental phobia (DP). All patients were treated with antidepressants for 3 months and the response rates were assessed. Results. At baseline, DAS was significantly higher in both the DA and the DP groups than in the control group. Ten (9.8%) of the panic disorder patients fulfilled the diagnostic criteria for DP; 31 (30.4%) had severe DA. In the control group, none of the patients was diagnosed as DP, whereas 7 (13.5%) had severe DA. Panic disorder and DA both responded to the antidepressant treatment, but DAS scores remained significantly higher in the DP group than in the DA group and the control group at the end of the third month. Conclusions. Our data suggest that both DA and DP are more frequent in panic disorder than in healthy controls. Antidepressant treatment may have been helpful in decreasing DA levels in the DA group but not in the DP group. 相似文献
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Hours S Nunes H Kambouchner M Uzunhan Y Brauner MW Valeyre D Brillet PY 《Medicine》2008,87(3):142-151
Pulmonary cavitary lesions in the absence of concomitant comorbidities are an uncommon and often confusing manifestation of sarcoidosis. We retrospectively reviewed the clinical and high-resolution computed tomography (HRCT) characteristics and the natural history of a series of 23 patients with pulmonary cavitary lesions found on HRCT extracted from a large cohort of patients with pulmonary sarcoidosis. The estimated prevalence of cavitary sarcoidosis was 2.2%. Cavitary lesions developed in patients with severe and active sarcoidosis (serum angiotensin-converting enzyme [SACE] > or =2 times the upper limit of normal range: 63.6%). Twelve (52.2%) patients had evidence of radiographic stage IV, 9 of whom (75%) had persistently increased SACE. As found on HRCT, cavitary lesions were multiple in 21 patients (91.3%), including 5 patients with 10 or more cavities. The size of cavitary lesions was variable, with a median diameter of 20 mm (range, 11-100 mm). Follow-up was available for 20 patients with a median follow-up of 6.25 years (range, 6 months to 15 years). Seven patients (35%) experienced some type of complication related to cavitary lesions, including 6 episodes of hemoptysis in 5 patients and aspergilloma occurrence in 3 patients. As seen on HRCT, the evolution of the number and size of cavitary lesions was variable, with a complete resolution of the largest cavitary lesion in only 5 patients (25%). During follow-up, wall thickening was always associated with a further infectious complication. In summary, cavitary lesions are rare in pulmonary sarcoidosis and usually occur in active and severe sarcoidosis. Their evolution is unpredictable, and complications are frequent. 相似文献
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Edibe Pembegul Yildiz Dilek Gunes Gonca Bektas Tugce Aksu Uzunhan Burak Tatli Mine Caliskan Nur Aydinli Meral Ozmen 《Acta neurologica Belgica》2018,118(1):71-75
Population-based studies report that children with epilepsy have relatively better prognosis than those with an onset at infancy, though studies about this period are limited. We aimed to evaluate the etiology in infant epilepsy less than 2 years of age and foreseeable risk factors for anti-epileptic drug resistance. We evaluated the patients who were presented to the division of pediatric neurology in our university hospital with seizures when they were between 1 and 24 months of age and diagnosed as epilepsy. Two hundred and twenty-nine patients (110 male and 119 female) who were diagnosed between the ages of 1–24 months were included in the study. The etiologies were structural (n = 55;24%), genetic (n = 29;12.7%), metabolic (n = 27;11.7%), and infectious (n = 8;3.5%), and it was unknown in 110 patients (48%). One-hundred and forty (61%) patients met the criteria for drug-resistant epilepsy (DRE). Multivariate logistic regression analysis showed that developmental delay at onset (OR 3.9, 95% CI 1.22, 12.47, p = 0.021), multifocal epileptiform discharges (OR 2.8, 95% CI 1.1, 7.44, p = 0.031), and history of status epilepticus (OR 32.9, 95% CI 3.8, 285.35, p = 0.001) were strong predictive factors for DRE. The epilepsy in children under 2 years of age is highly resistant to the anti-epileptic drugs, which could be related to the history of status epilepticus, developmental delay at onset, and multifocal epileptiform discharges. 相似文献
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