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Introduction Anti-nuclear antibodies (ANA) are useful in the diagnosis of systemic autoimmune rheumatic diseases. Indirect immunofluorescence (IIF) on HEp-2 cell substrates is widely used to screen for ANA [ 1 ]. For identification of the specificity of the autoantibodies, solid-phase methods that use well characterized antigens are used (reviewed in [ 2 ]). Novel technologies such as fluorescent-enzyme immuno-assay and chemiluminescent immunoassay have been introduced and automated high throughput platforms have become available [ 2 ]. Moreover, multiplexed

BioMol Concepts, Vol. 2 (2011), pp. 149–157 • Copyright by Walter de Gruyter • Berlin • Boston. DOI 10.1515/BMC.2011.013 2010/038 Article in press - uncorrected proof Review Antineuronal autoantibodies in neurological disorders Katrin Bürk Department of Neurology, University of Marburg, D-35039 Marburg, Germany e-mail: Abstract Autoantibodies (abs) related to neurological disease are cur- rently classified into two large groups depending on the site of the respective target antigen: Group I encompasses abs that recognise intracellular

cell death with apoptotic features. Apoptosis 2000; 5:403–11. 20. Ferretti G, Bacchetti T, Moroni C, Vignini A, Nanetti L, Curatola GT. Effects of homocysteinylation on low density lipoprotein peroxidation of human endothelial cells. J Cell Biochem 2004, 92:351–60. 21. Undas A, Perła J, Łaciński M, Trzeciak W, Kaźmierski R, Jakubowski H. Autoantibodies against N-homocysteinylated proteins in humans: implications for atherosclerosis. Stroke 2004; 35:1299–304. 22. Perla J, Undas A, Twardowski T, Jakubowski H. Purification of antibodies against N



The aim of this report is to describe a case of GAD-65 autoantibody associated epilepcy, diagnosed long before the onset of autoimmune diabetes.

Case presentation

This report presents a 36-year-old female with type 1 diabetes, diagnosed at the age of 26, and a cryptogenic focal epilepsy with complex partial seizures, with duration of 2–3 min and frequency of 5–6 per month, diagnosed at 16 years of age. Electroencephalography revealed epileptiform abnormalities temporally and centro-parietally on the left and temporally on the right with forward propagation on both sides. Due to the drug refractory seizures, titers of GAD-65 autoantibodies were examined (19 years after the diagnosis of epilepsy and 9 years after the diagnosis of diabetes) and were found to be elevated in serum and cerebrospinal fluid, strongly supporting its autoimmune genesis. Insulin pump therapy was used in this patient with a beneficial effect on glycemia.


Autoimmune epilepsy is a clinical entity and should be taken into consideration in patients with other autoimmune diseases, especially diabetes, and with drug refractory seizures, even preceding the onset of diabetes. Achieving stable glycemic control, including the usage of the new technologies in type 1 diabetes treatment, is vital in these cases.

Introduction Antinuclear antibodies (ANA) are a heterogeneous group of autoantibodies [ 1 ] that can be detected in the sera of subjects with systemic autoimmune rheumatic diseases (SARD), such as systemic lupus erythematosus (SLE), Sjögren’s syndrome (SSj), systemic sclerosis (SS), rheumatoid arthritis (RA), idiopathic inflammatory myopathies (IIM) and systemic vasculitides (SV) [ 2 ], [ 3 ], [ 4 ]. Autoantibodies are very helpful in the diagnosis, prognosis assessment and monitoring of the clinical evolution of patients with SARD [ 2 ], [ 4 ], [ 5 ], [ 6

]. Folate deficiency in the mother can lead to pregnancy-related complications including neural tube defects (NTDs) in the fetus. Numerous studies have now established the benefits of folate supplementation in reducing the incidence of NTD pregnancy [5–7]. The benefits of folate supplementation in the absence of systemic folate deficiency or genetic abnormalities of folate pathways have not been adequately explained. The identification of FR autoantibodies (AuAbs) in women with a history of NTD pregnancy provides a mechanism by which the developing embryo could be

Introduction Autoimmune Addison’s disease (AD) is a rare condition that results from autoimmune destruction of the adrenal cortex and insufficient production of glucocorticoids, mineralocorticoids and androgens [ 1 ], [ 2 ], [ 3 ]. Autoimmune AD may present as isolated autoimmune AD or associated with other autoimmune conditions. The association of AD with different autoimmune conditions occurs in three principal combinations known as autoimmune polyglandular syndrome (APS) types 1, 2 and 4 [ 4 ], [ 5 ], [ 6 ]. Adrenal cortex autoantibodies (ACAs) measured by an

Review Autoantibodies Associated with Rheumatic Diseases Clin Chem Lab Med 2001; 39(3):189–208 © 2001 by Walter de Gruyter · Berlin · New York Andrea Griesmacher1 and Peter Peichl2 1 Institute of Laboratory Diagnostics, Kaiser-Franz-Josef-Hos- pital, Vienna, Austria 2 II. Department of Internal Medicine with Rheumatology and Osteology, Kaiser-Franz-Josef-Hospital, Vienna, Austria The identification of circulating autoantibodies con- tributes to the correct diagnosis as well as to the fol- low-up of rheumatic diseases. Some autoantibodies are even included in

Introduction Type 1A diabetes is an autoimmune disease caused by the destruction of the insulin-producing β-cells in the islets of Langerhans [ 1 ]. In the management of diabetes, differentiating type 1 from other types of diabetes is extremely critical in selecting the appropriate therapy, estimation of the disease prognosis, and identification of the risk of diabetes occurrence in relatives. Diabetes-associated autoantibodies are serological markers of β-cell autoimmunity. These markers are essential diagnostic tools to distinguish between type 1, type 2

Clin Chem Lab Med 2008;46(5):577–587 2008 by Walter de Gruyter • Berlin • New York. DOI 10.1515/CCLM.2008.138 2007/34 Article in press - uncorrected proof Review The diagnostic role of autoantibodies in the prediction of organ-specific autoimmune diseases Renato Tozzoli* Laboratorio di Chimica Clinica e Microbiologia, Ospedale Civile, Latisana, Udine, Italy Abstract Due to their pathogenetic role, many serum auto- antibodies can be detected a long time before the clin- ical onset and during the course of organ-specific autoimmune diseases. For these reasons