Medical records were centralised. Patients were selleck kinase inhibitor compared with 60 controls with sarcoidosis.\n\nClinical examination showed more frequent crackles in patients than controls (45% versus 1.7%, respectively; p<0.001). On thoracic computed tomography scans, nodules (often multiple and with smooth margins), air bronchograms and halo signs were more frequent in patients than controls (80% versus 42%, respectively; p=0.004) as well as bronchiectasis (65% versus

23%, respectively; p<0.001). The micronodule distribution was perilymphatic in 100% of controls and in 42% of patients (p<0.001). Bronchoalveolar lavage analysis showed lower T-cell CD4/CD8 ratios in patients than in controls (mean +/- SD 1.6 +/- 1.1 versus 5.3 +/- 4, respectively; p<0.01). On pathological analysis, nodules and consolidations corresponded to granulomatous lesions with or without lymphocytic disorders in most cases. Mortality was higher in patients than controls (30% versus 0%, respectively) and resulted from common variable immunodeficiency complications.\n\nILD in CVID/GD presents a specific clinical picture and evolution that are markedly different from those of sarcoidosis.”
“Background: The loss of neurological function is closely related to axonal damage. Neurofilament subunits are concentrated in neurons and axons and have emerged as promising

biomarkers for neurodegeneration. Electrochemiluminescence (ECL) based assays are known to be of superior sensitivity Ulixertinib and require less sample volume than conventional ELISAs.\n\nMethods: We developed an ECL based solid-phase sandwich immunoassay to measure the neurofilament heavy chain protein (NfH(SMI35)) in CSF. We employed commercially available Liproxstatin-1 molecular weight antibodies as previously used in a conventional ELISA (Petzold et al., 2003; Petzold and Shaw, 2007). The optimised and validated assay was applied in a reference cohort and defined patient groups.\n\nResults: Analytical sensitivity (background plus three SD) of our assay was 2.4 pg/ml. The

mean intra-assay coefficient of variation (CV) was 4.8% and the inter-assay CV 8.4%. All measured control and patient samples produced signals well above background. Patients with multiple sclerosis (MS) (median 46.2 pg/ml, n = 95), amyotrophic lateral sclerosis (ALS) (160.1 pg/ml, n = 50), mild cognitive impairment/Alzheimer’s disease (MCI/AD) (65.6 pg/ml, n = 20), Guillain Barre syndrome (GBS) (91.0 pg/ml, n = 20) or subarachnoid hemorrhage (SAH) (345.0 pg/ml, n = 20) had higher CSF NfH(SM135) values than the reference cohort (27.1 pg/ml, n = 73, p <0.0001 for each comparison).\n\nConclusion: The new ECL based assay for NfH(SM135) in CSF is superior in terms of sensitivity, precision and accuracy to previously published methods (Petzold et al., 2003; Shaw et al., 2005; Teunissen et al., 2009).