Higher frequencies of HLA DQB105:01 and anti-glycosphingolipid antibodies in a cluster of severe Guillain–Barré syndrome

Few regional and seasonal Guillain–Barré syndrome (GBS) clusters have been reported so far. It is unknown whether patients suffering from sporadic GBS differ from GBS clusters with respect to clinical and paraclinical parameters, HLA association and antibody response to glycosphingolipids and Campyl...

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Veröffentlicht in:Journal of neurology 2016-10, Vol.263 (10), p.2105-2113
Hauptverfasser: Schirmer, L., Worthington, V., Solloch, U., Loleit, V., Grummel, V., Lakdawala, N., Grant, D., Wassmuth, R., Schmidt, A. H., Gebhardt, F., Andlauer, T. F. M., Sauter, J., Berthele, A., Lunn, M. P., Hemmer, Bernhard
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container_end_page 2113
container_issue 10
container_start_page 2105
container_title Journal of neurology
container_volume 263
creator Schirmer, L.
Worthington, V.
Solloch, U.
Loleit, V.
Grummel, V.
Lakdawala, N.
Grant, D.
Wassmuth, R.
Schmidt, A. H.
Gebhardt, F.
Andlauer, T. F. M.
Sauter, J.
Berthele, A.
Lunn, M. P.
Hemmer, Bernhard
description Few regional and seasonal Guillain–Barré syndrome (GBS) clusters have been reported so far. It is unknown whether patients suffering from sporadic GBS differ from GBS clusters with respect to clinical and paraclinical parameters, HLA association and antibody response to glycosphingolipids and Campylobacter jejuni ( Cj ). We examined 40 consecutive patients with GBS from the greater Munich area in Germany with 14 of those admitted within a period of 3 months in fall 2010 defining a cluster of GBS. Sequencing-based HLA typing of the HLA genes DRB1 , DQB1 , and DPB1 was performed, and ELISA for anti-glycosphingolipid antibodies was carried out. Clinical and paraclinical findings ( Cj seroreactivity, cerebrospinal fluid parameters, and electrophysiology) were obtained and analyzed. GBS cluster patients were characterized by a more severe clinical phenotype with more patients requiring mechanical ventilation and higher frequencies of autoantibodies against sulfatide, GalC and certain ganglioside epitopes (54 %) as compared to sporadic GBS cases (13 %, p  = 0.017). Cj seropositivity tended to be higher within GBS cluster patients (69 %) as compared to sporadic cases (46 %, p  = 0.155). We noted higher frequencies of HLA class II allele DQB1*05:01 in the cluster cohort (23 %) as compared to sporadic GBS patients (3 %, p  = 0.019). Cluster of severe GBS was defined by higher frequencies of autoantibodies against glycosphingolipids. HLA class II allele DQB1*05:01 might contribute to clinical worsening in the cluster patients.
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Sequencing-based HLA typing of the HLA genes DRB1 , DQB1 , and DPB1 was performed, and ELISA for anti-glycosphingolipid antibodies was carried out. Clinical and paraclinical findings ( Cj seroreactivity, cerebrospinal fluid parameters, and electrophysiology) were obtained and analyzed. GBS cluster patients were characterized by a more severe clinical phenotype with more patients requiring mechanical ventilation and higher frequencies of autoantibodies against sulfatide, GalC and certain ganglioside epitopes (54 %) as compared to sporadic GBS cases (13 %, p  = 0.017). Cj seropositivity tended to be higher within GBS cluster patients (69 %) as compared to sporadic cases (46 %, p  = 0.155). We noted higher frequencies of HLA class II allele DQB1*05:01 in the cluster cohort (23 %) as compared to sporadic GBS patients (3 %, p  = 0.019). Cluster of severe GBS was defined by higher frequencies of autoantibodies against glycosphingolipids. 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We examined 40 consecutive patients with GBS from the greater Munich area in Germany with 14 of those admitted within a period of 3 months in fall 2010 defining a cluster of GBS. Sequencing-based HLA typing of the HLA genes DRB1 , DQB1 , and DPB1 was performed, and ELISA for anti-glycosphingolipid antibodies was carried out. Clinical and paraclinical findings ( Cj seroreactivity, cerebrospinal fluid parameters, and electrophysiology) were obtained and analyzed. GBS cluster patients were characterized by a more severe clinical phenotype with more patients requiring mechanical ventilation and higher frequencies of autoantibodies against sulfatide, GalC and certain ganglioside epitopes (54 %) as compared to sporadic GBS cases (13 %, p  = 0.017). Cj seropositivity tended to be higher within GBS cluster patients (69 %) as compared to sporadic cases (46 %, p  = 0.155). We noted higher frequencies of HLA class II allele DQB1*05:01 in the cluster cohort (23 %) as compared to sporadic GBS patients (3 %, p  = 0.019). Cluster of severe GBS was defined by higher frequencies of autoantibodies against glycosphingolipids. HLA class II allele DQB1*05:01 might contribute to clinical worsening in the cluster patients.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>27485170</pmid><doi>10.1007/s00415-016-8237-6</doi><tpages>9</tpages></addata></record>
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subjects Adolescent
Adult
Aged
Aged, 80 and over
Alleles
Antibodies
Autoantibodies - cerebrospinal fluid
Campylobacter
Campylobacter Infections - immunology
Campylobacter jejuni
Enzyme-Linked Immunosorbent Assay
Female
Follow-Up Studies
Gene Frequency
Genetic Predisposition to Disease - genetics
Germany
Glycosphingolipids - immunology
Guillain-Barre syndrome
Guillain-Barre Syndrome - cerebrospinal fluid
Guillain-Barre Syndrome - genetics
Guillain-Barre Syndrome - physiopathology
HLA-DQ beta-Chains - genetics
Hospitals
Humans
Infections
Male
Medicine
Medicine & Public Health
Middle Aged
Neural Conduction - genetics
Neurology
Neuromuscular diseases
Neuroradiology
Neurosciences
Original Communication
Severity of Illness Index
Young Adult
title Higher frequencies of HLA DQB105:01 and anti-glycosphingolipid antibodies in a cluster of severe Guillain–Barré syndrome
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