8 results on '"Hadjivassiliou M"'
Search Results
2. MR spectroscopy and atrophy in Gluten, Friedreich's and SCA6 ataxias.
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Hadjivassiliou, M., Wallis, L. I., Hoggard, N., Grünewald, R. A., Griffiths, P. D., and Wilkinson, I. D.
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ATROPHY , *GLUTEN , *FRIEDREICH'S ataxia , *PROTON magnetic resonance spectroscopy , *CLINICAL trials , *STATISTICAL correlation , *BRAIN imaging - Abstract
Hadjivassiliou M, Wallis LI, Hoggard N, Grünewald RA, Griffiths PD, Wilkinson ID. MR spectroscopy and atrophy in Gluten, Friedreich's and SCA6 ataxias. Acta Neurol Scand: 2012: 126: 138-143. © 2011 John Wiley & Sons A/S. Background - Previous work using proton MR spectroscopy (1H-MRS) of the cerebellum in the ataxias suggested that 1H-MRS abnormalities and atrophy do not necessarily occur concurrently. Aims - To investigate the spectroscopic features of different types of ataxias. Methods - Using a clinical MR system operating at 1.5T, we performed 1H-MRS with a single voxel placed over the right dentate nucleus in 22 patients with gluten ataxia (GA), six patients with Friedreich's ataxia (FA), six patients with spinocerebellar ataxia type 6 (SCA6) and 21 healthy volunteers. Atrophy of the vermis and hemispheres on standard MRI was rated by a neuroradiologist. Any interaction between atrophy and 1H-MRS was analysed for the three groups of patients and controls. Results - Patients with GA had significant atrophy of the vermis and hemispheres as well as abnormal 1H-MRS. Patients with SCA6 had more severe overall atrophy of the vermis and hemispheres, but relatively preserved N-acetyl-aspartate/creatine (NAA/Cr). The FA group showed significant atrophy of only the superior vermis with normal 1H-MRS. Conclusions - This study suggests that 1H-MRS of the cerebellum in patients with ataxia provides information in addition to the presence of atrophy. There are significant 1H-MRS differences amongst different types of ataxia with interesting correlations between atrophy and NAA/Cr. [ABSTRACT FROM AUTHOR] more...
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- 2012
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3. GAD antibody-associated neurological illness and its relationship to gluten sensitivity.
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Hadjivassiliou, M., Aeschlimann, D., Grünewald, R. A., Sanders, D. S., Sharrack, B., and Woodroofe, N.
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GLUTAMATE decarboxylase , *IMMUNOGLOBULINS , *NEUROLOGICAL disorders , *GLUTEN , *SYNDROMES , *SEROLOGY , *GLUTEN-free diet - Abstract
Hadjivassiliou M, Aeschlimann D, Grünewald RA, Sanders DS, Sharrack B, Woodroofe N. GAD antibody associated neurological illness and its relationship to gluten sensitivity. Acta Neurol Scand: 2011: 123: 175-180. © 2010 The Authors Journal compilation © 2010 Blackwell Munksgaard. The high prevalence of gluten sensitivity in patients with stiff-person syndrome (SPS) lead us to investigate the relationship between gluten sensitivity and GAD-antibody-associated diseases. We used ELISA assays for anti-GAD and for serological markers of gluten sensitivity. Patients were recruited from clinics based at the Royal Hallamshire hospital, Sheffield, UK. Patients with gluten sensitivity were followed up after the introduction of a gluten-free diet and serological testing was repeated. Six of seven (86%) patients with SPS were positive for anti-GAD, mean titre 109 U/ml; This compared with 9/90 (11%) patients with idiopathic sporadic ataxia, mean titre 32 U/ml, 16/40 (40%) patients with gluten ataxia, mean titre 25 U/ml, and 6/10 patients with type 1 diabetes only, mean titre 8 U/ml. None of 32 patients with celiac disease only, and of 40 patients with genetic ataxia were positive for anti-GAD. The titre of anti-GAD reduced following the introduction of a gluten-free diet in patients with SPS who had serological evidence of gluten sensitivity. The same was observed in patients with gluten ataxia and anti-GAD antibodies. This was also associated with clinical improvement. These findings suggest a link between gluten sensitivity and GAD antibody-associated diseases. [ABSTRACT FROM AUTHOR] more...
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- 2011
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4. Neuropathy associated with gluten sensitivity.
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Hadjivassiliou, M., Grünewald, R. A., Kandler, R. H., Chattopadhyay, A. K., Jarratt, J. A., Sanders, D. S., Sharrack, B., Wharton, S. B., and Davies-Jones, G. A. B.
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NEUROPATHY , *ALTERNATIVE medicine , *IMMUNOGLOBULIN A , *IMMUNOGLOBULINS , *GLUTEN , *CELIAC disease , *MEDICAL research - Abstract
Objectives: To prospectively study the clinical, neurophysiological and neuropathological characteristics of axonal neuropathies associated with positive antigliadin antibodies and the prevalence of such neuropathies in a cohort of patients with sporadic axonal neuropathy. Methods: Prospective screening (using antigliadin, antiendomysium and tissue transglutaminase antibodies) of patients with peripheral neuropathy attending a neurology clinic. Results: 215 patients with axonal neuropathy were screened. 141 patients had symmetrical sensorimotor neuropathy, 47 had mononeuropathy multiplex, 17 had motor neuropathy and 10 had small-fibre neuropathy. Despite extensive investigations of the 215 patients, 140 had idiopathic neuropathy. Positive immunoglobulin (Ig)G with or without IgA antigliadin antibodies was found in 34% (47/140) of the patients with idiopathic neuropathy. This compares with 12% prevalence of these antibodies in the healthy controls. The prevalence of coeliac disease as shown by biopsy in the idiopathic group was at least 9% as compared with 1% in the controls. The clinical features of 100 patients (47 from the prevalence study and 53 referred from elsewhere) with gluten neuropathy included a mean age at onset of 55 (range 24–77) years and a mean duration of neuropathy of 9 (range 1–33) years. Gluten-sensitive enteropathy was present in 29% of patients. The human leucocyte antigen types associated with coeliac disease were found in 80% of patients. Conclusions: Gluten sensitivity may be aetiologically linked to a substantial number of idiopathic axonal neuropathies. [ABSTRACT FROM AUTHOR] more...
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- 2006
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5. Dietary treatment of gluten ataxia.
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Hadjivassiliou M, Davies-Jones G A B, Sanders D S, and Gr''newald R A
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GLUTEN , *ATAXIA , *IMMUNOLOGICAL deficiency syndromes - Abstract
BACKGROUND: Gluten ataxia is an immune mediated disease, part of the spectrum of gluten sensitivity, and accounts for up to 40% of cases of idiopathic sporadic ataxia. No systematic study of the effect of gluten-free diet on gluten ataxia has ever been undertaken. OBJECTIVE: To study the effect of gluten-free diet on patients presenting with ataxia caused by gluten sensitivity. METHODS: 43 patients with gluten ataxia were studied. All were offered a gluten-free diet and monitored every six months. All patients underwent a battery of tests to assess their ataxia at baseline and after one year on diet. Twenty six patients (treatment group) adhered to the gluten-free diet and had evidence of elimination of antigliadin antibodies by one year. Fourteen patients refused the diet (control group). Three patients had persistently raised antigliadin antibodies despite adherence to the diet and were therefore excluded from the analysis. RESULTS: After one year there was improvement in ataxia reflected in all of the ataxia tests in the treatment group. This was significant when compared with the control group. The diet associated improvement was apparent irrespective of the presence of an enteropathy. CONCLUSIONS: Gluten ataxia responds to a strict gluten-free diet even in the absence of an enteropathy. The diagnosis of gluten ataxia is vital as it is one of the very few treatable causes of sporadic ataxia. [ABSTRACT FROM AUTHOR] more...
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- 2003
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6. Diagnosis of Non-Celiac Gluten Sensitivity (NCGS): The Salerno Experts’ Criteria
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Luca Elli, Umberto Volta, Nicoletta Pellegrini, Gerd Bouma, Wolfgang Holtmeier, Daniel A. Leffler, Fernanda Cristofori, Carlo Catassi, Kamran Rostami, Ruggiero Francavilla, Jernej Dolinsek, Chris J. J. Mulder, David S Sanders, Detlef Schuppan, Victor F. Zevallos, Giuseppe Mazzarella, Antonio Carroccio, Ute Körner, Marianne Williams, Walburga Dieterich, Marios Hadjivassiliou, Alessio Fasano, Knut E.A. Lundin, Gemma Castillejo, Gry Irene Skodje, Yurdagül Zopf, Christophe Cellier, Laura de Magistris, Reiner Ullrich, Bruno Bonaz, Catassi, C., Elli, L., Bonaz, B., Bouma, G., Carroccio, A., Castillejo, G., Cellier, C., Cristofori, F., de Magistris, L., Dolinsek, J., Dieterich, W., Francavilla, R., Hadjivassiliou, M., Holtmeier, W., Körner, U., Leffler, D., Lundin, K., Mazzarella, G., Mulder, C., Pellegrini, N., Rostami, K., Sanders, D., Skodje, G., Schuppan, D., Ullrich, R., Volta, U., Williams, M., Zevallos, V., Zopf, Y., Fasano, A., Gastroenterology and hepatology, CCA - Disease profiling, Catassi, Carlo, Elli, Luca, Bonaz, Bruno, Bouma, Gerd, Carroccio, Antonio, Castillejo, Gemma, Cellier, Christophe, Cristofori, Fernanda, DE MAGISTRIS, Laura, Dolinsek, Jernej, Dieterich, Walburga, Francavilla, Ruggiero, Hadjivassiliou, Mario, Holtmeier, Wolfgang, Körner, Ute, Leffler, Dan A., Lundin, Knut E. A., Mazzarella, Giuseppe, Mulder, Chris J., Pellegrini, Nicoletta, Rostami, Kamran, Sanders, David, Skodje, Gry Irene, Schuppan, Detlef, Ullrich, Reiner, Volta, Umberto, Williams, Marianne, Zevallos, Victor F., Zopf, Yurdagül, and Fasano, Alessio more...
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Diagnosis ,Non-Celiac Gluten Sensitivity ,Pediatrics ,medicine.medical_specialty ,Settore MED/09 - Medicina Interna ,Glutens ,diagnosis ,lcsh:TX341-641 ,Disease ,Placebo ,Article ,Diet, Gluten-Free ,Double-Blind Method ,Rating scale ,Surveys and Questionnaires ,Humans ,Medicine ,Intestinal Mucosa ,Irritable bowel syndrome ,double-blind placebo-controlled challenge ,chemistry.chemical_classification ,irritable bowel syndrome ,Cross-Over Studies ,Nutrition and Dietetics ,business.industry ,non-celiac gluten sensitivity ,gastrointestinal symptom rating scale ,nutritional and metabolic diseases ,medicine.disease ,Gluten ,Crossover study ,Surgery ,chemistry ,Immunoglobulin G ,Biomarker (medicine) ,business ,lcsh:Nutrition. Foods and food supply ,Biomarkers ,Food Hypersensitivity ,Wheat allergy ,Food Science ,Diagnosi - Abstract
Non-Celiac Gluten Sensitivity (NCGS) is a syndrome characterized by intestinal and extra-intestinal symptoms related to the ingestion of gluten-containing food, in subjects that are not affected by either celiac disease or wheat allergy. Given the lack of a NCGS biomarker, there is the need for standardizing the procedure leading to the diagnosis confirmation. In this paper we report experts' recommendations on how the diagnostic protocol should be performed for the confirmation of NCGS. A full diagnostic procedure should assess the clinical response to the gluten-free diet (GFD) and measure the effect of a gluten challenge after a period of treatment with the GFD. The clinical evaluation is performed using a self-administered instrument incorporating a modified version of the Gastrointestinal Symptom Rating Scale. The patient identifies one to three main symptoms that are quantitatively assessed using a Numerical Rating Scale with a score ranging from 1 to 10. The double-blind placebo-controlled gluten challenge (8 g/day) includes a one-week challenge followed by a one-week washout of strict GFD and by the crossover to the second one-week challenge. The vehicle should contain cooked, homogeneously distributed gluten. At least a variation of 30% of one to three main symptoms between the gluten and the placebo challenge should be detected to discriminate a positive from a negative result. The guidelines provided in this paper will help the clinician to reach a firm and positive diagnosis of NCGS and facilitate the comparisons of different studies, if adopted internationally. more...
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- 2015
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7. The humoral response in the pathogenesis of gluten ataxia
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Tarcisio Not, C. A. Williamson, Enrico Tongiorgi, Sabrina Boscolo, David S Sanders, G. A.B. Davies-Jones, Julie E. Simpson, Richard A. Grünewald, Nicola Woodroofe, Marios Hadjivassiliou, Hadjivassiliou, M, Boscolo, Sabrina, DAVIES JONES, Gab, Grunewald, Ra, Not, Tarcisio, Sanders, D, Simpson, Je, Tongiorgi, Enrico, Williamson, Ca, and Woodroofe, Nm more...
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Male ,Calbindins ,Pathology ,medicine.medical_specialty ,Cerebellum ,Ataxia ,Glutens ,Gliadin ,Rats, Sprague-Dawley ,Central nervous system disease ,Purkinje Cells ,S100 Calcium Binding Protein G ,medicine ,Cerebellar Degeneration ,Animals ,Humans ,Aged ,chemistry.chemical_classification ,biology ,business.industry ,nutritional and metabolic diseases ,Middle Aged ,medicine.disease ,Immunohistochemistry ,Gluten ,digestive system diseases ,Rats ,Neurologic manifestation ,medicine.anatomical_structure ,chemistry ,Immunoglobulin G ,Antibody Formation ,Immunology ,biology.protein ,Female ,Neurology (clinical) ,Antibody ,medicine.symptom ,business - Abstract
Objective: To characterize humoral response to cerebellum in patients with gluten ataxia.Background: Gluten ataxia is a common neurologic manifestation of gluten sensitivity.Methods: The authors assessed the reactivity of sera from patients with gluten ataxia (13), newly diagnosed patients with celiac disease without neurologic dysfunction (24), patients with other causes of cerebellar degeneration (11), and healthy control subjects (17) using indirect immunocytochemistry on human cerebellar and rat CNS tissue. Cross-reactivity of a commercial IgG antigliadin antibody with human cerebellar tissue also was studied.Results: Sera from 12 of 13 patients with gluten ataxia stained Purkinje cells strongly. Less intense staining was seen in some but not all sera from patients with newly diagnosed celiac disease without neurologic dysfunction. At high dilutions (1:800) staining was seen only with sera from patients with gluten ataxia but not in control subjects. Sera from patients with gluten ataxia also stained some brainstem and cortical neurons in rat CNS tissue. Commercial anti-gliadin antibody stained human Purkinje cells in a similar manner. Adsorption of the antigliadin antibodies using crude gliadin abolished the staining in patients with celiac disease without neurologic dysfunction, but not in those with gluten ataxia.Conclusions: Patients with gluten ataxia have antibodies against Purkinje cells. Antigliadin antibodies cross-react with epitopes on Purkinje cells. more...
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- 2002
8. Anti Transglutaminase Antibodies Cause Ataxia in Mice
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Daniel Aeschlimann, Enrico Tongiorgi, Marios Hadjivassiliou, Fiorella Florian, Tarcisio Not, Daniele Sblattero, Sabrina Boscolo, Roberto Marzari, Alessandro Ventura, Andrea Lorenzon, Marco Stebel, Boscolo, Sabrina, Lorenzon, A., Sblattero, Daniele, Florian, Fiorella, Stebel, Marco, Marzari, Roberto, Not, Tarcisio, Aeschlimann, D., Ventura, Alessandro, Hadjivassiliou, M., and Tongiorgi, Enrico more...
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Male ,Tissue transglutaminase ,lcsh:Medicine ,medicine.disease_cause ,Cross-reactivity ,Gliadin ,Immunohistochemistry techniques ,Rats, Sprague-Dawley ,Mice ,Blood vessels ,Cerebellum ,Cytoplasmic staining ,Enzyme-linked immunoassays ,lcsh:Science ,Neurological Disorders/Movement Disorders ,Neurons ,Multidisciplinary ,biology ,Brain ,Middle Aged ,Isoenzymes ,Gastrointestinal disorder ,Motor Skills ,Anti-transglutaminase antibodies ,Immunohistochemistry ,Female ,medicine.symptom ,Antibody ,Research Article ,Biotechnology ,Adult ,Ataxia ,Immunology/Autoimmunity ,Antibodies ,Autoimmune Diseases ,medicine ,Animals ,Humans ,Protein Glutamine gamma Glutamyltransferase 2 ,Immunohistochemistry techniques,Enzyme-linked immunoassays, Ataxia,Neurons,Cytoplasmic staining, Blood vessels, Gluten, Cerebellum ,Transglutaminases ,business.industry ,lcsh:R ,Molecular biology ,Rats ,Mice, Inbred C57BL ,Celiac Disease ,Immunology ,biology.protein ,lcsh:Q ,business ,Gluten - Abstract
Background: Celiac disease (CD) is an autoimmune gastrointestinal disorder characterized by the presence of anti-transglutaminase 2 (TG2) and anti-gliadin antibodies. Amongst the neurological dysfunctions associated with CD, ataxia represents the most common one.\ud Methods: We analyzed by immunohistochemistry, the anti-neural reactivity of the serum from 20 CD patients. To determine the role of anti-TG2 antibodies in ataxia, two anti-TG2 single chain variable fragments (scFv), isolated from a phage-display IgA antibody library, were characterized by immunohistochemistry and ELISA, and injected in mice to study their effects on motor coordination. We found that 75% of the CD patient population without evidence of neurological involvement, has circulating anti-neural IgA and/or IgG antibodies. Two anti-TG2 scFvs, cloned from one CD patient, stained blood vessels but only one reacted with neurons. This anti-TG2 antibody showed cross reactivity with the transglutaminase isozymes TG3 and TG6. Intraventricular injection of the anti-TG2 or the anti-TG2/3/6 cross-reactive scFv provoked transient, equally intensive ataxia in mice.\ud Conclusion: The serum from CD patients contains anti-TG2, TG3 and TG6 antibodies that may potentially cause ataxia. more...
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- 2010
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