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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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. |
doi_str_mv | 10.1007/s00415-016-8237-6 |
format | Article |
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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.</description><identifier>ISSN: 0340-5354</identifier><identifier>EISSN: 1432-1459</identifier><identifier>DOI: 10.1007/s00415-016-8237-6</identifier><identifier>PMID: 27485170</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>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</subject><ispartof>Journal of neurology, 2016-10, Vol.263 (10), p.2105-2113</ispartof><rights>Springer-Verlag Berlin Heidelberg 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3206-169c82c0d84cf5b5e7b135b06889ad48ca4b821ed9d209fccc3d8a20efcedfd03</citedby><cites>FETCH-LOGICAL-c3206-169c82c0d84cf5b5e7b135b06889ad48ca4b821ed9d209fccc3d8a20efcedfd03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00415-016-8237-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00415-016-8237-6$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27485170$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schirmer, L.</creatorcontrib><creatorcontrib>Worthington, V.</creatorcontrib><creatorcontrib>Solloch, U.</creatorcontrib><creatorcontrib>Loleit, V.</creatorcontrib><creatorcontrib>Grummel, V.</creatorcontrib><creatorcontrib>Lakdawala, N.</creatorcontrib><creatorcontrib>Grant, D.</creatorcontrib><creatorcontrib>Wassmuth, R.</creatorcontrib><creatorcontrib>Schmidt, A. H.</creatorcontrib><creatorcontrib>Gebhardt, F.</creatorcontrib><creatorcontrib>Andlauer, T. F. M.</creatorcontrib><creatorcontrib>Sauter, J.</creatorcontrib><creatorcontrib>Berthele, A.</creatorcontrib><creatorcontrib>Lunn, M. P.</creatorcontrib><creatorcontrib>Hemmer, Bernhard</creatorcontrib><title>Higher frequencies of HLA DQB105:01 and anti-glycosphingolipid antibodies in a cluster of severe Guillain–Barré syndrome</title><title>Journal of neurology</title><addtitle>J Neurol</addtitle><addtitle>J Neurol</addtitle><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.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Alleles</subject><subject>Antibodies</subject><subject>Autoantibodies - cerebrospinal fluid</subject><subject>Campylobacter</subject><subject>Campylobacter Infections - immunology</subject><subject>Campylobacter jejuni</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Gene Frequency</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Germany</subject><subject>Glycosphingolipids - immunology</subject><subject>Guillain-Barre syndrome</subject><subject>Guillain-Barre Syndrome - cerebrospinal fluid</subject><subject>Guillain-Barre Syndrome - genetics</subject><subject>Guillain-Barre Syndrome - physiopathology</subject><subject>HLA-DQ beta-Chains - genetics</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Infections</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Neural Conduction - genetics</subject><subject>Neurology</subject><subject>Neuromuscular diseases</subject><subject>Neuroradiology</subject><subject>Neurosciences</subject><subject>Original Communication</subject><subject>Severity of Illness Index</subject><subject>Young Adult</subject><issn>0340-5354</issn><issn>1432-1459</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqNkd9qFDEUxoNY7Fp9AG8k4I030ZN_Mxnv2qpdYUEEvQ6ZJLNNmU3WZKeweOM7-BQ-R9-kT2KWqVIEwYsQyPl93zknH0LPKLyiAO3rAiCoJEAbohhvSfMALajgjFAhu4doAVwAkVyKY_S4lCsAULXwCB2zVihJW1igb8uwvvQZD9l_nXy0wRecBrxcneK3n84oyDdAsYmunl0g63FvU9lehrhOY9iG-blP7iALERtsx6nsql_1KP7aZ48vpjCOJsTb7z_OTM43P3HZR5fTxj9BR4MZi396d5-gL-_ffT5fktXHiw_npytiOYOG0KazillwSthB9tK3PeWyh0apzjihrBG9YtS7zjHoBmstd8ow8IP1bnDAT9DL2XebU12y7PQmFOvrVNGnqWiqWNtR3qj_QgVj9UdlRV_8hV6lKce6yIHivJEdaytFZ8rmVEr2g97msDF5rynoQ4h6DlHXEPUhRN1UzfM756nfePdH8Tu1CrAZKLUU1z7fa_1P1197-qg3</recordid><startdate>20161001</startdate><enddate>20161001</enddate><creator>Schirmer, L.</creator><creator>Worthington, V.</creator><creator>Solloch, U.</creator><creator>Loleit, V.</creator><creator>Grummel, V.</creator><creator>Lakdawala, N.</creator><creator>Grant, D.</creator><creator>Wassmuth, R.</creator><creator>Schmidt, A. H.</creator><creator>Gebhardt, F.</creator><creator>Andlauer, T. F. M.</creator><creator>Sauter, J.</creator><creator>Berthele, A.</creator><creator>Lunn, M. P.</creator><creator>Hemmer, Bernhard</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20161001</creationdate><title>Higher frequencies of HLA DQB105:01 and anti-glycosphingolipid antibodies in a cluster of severe Guillain–Barré syndrome</title><author>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</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3206-169c82c0d84cf5b5e7b135b06889ad48ca4b821ed9d209fccc3d8a20efcedfd03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Alleles</topic><topic>Antibodies</topic><topic>Autoantibodies - cerebrospinal fluid</topic><topic>Campylobacter</topic><topic>Campylobacter Infections - immunology</topic><topic>Campylobacter jejuni</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Gene Frequency</topic><topic>Genetic Predisposition to Disease - genetics</topic><topic>Germany</topic><topic>Glycosphingolipids - immunology</topic><topic>Guillain-Barre syndrome</topic><topic>Guillain-Barre Syndrome - cerebrospinal fluid</topic><topic>Guillain-Barre Syndrome - genetics</topic><topic>Guillain-Barre Syndrome - physiopathology</topic><topic>HLA-DQ beta-Chains - genetics</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Infections</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Neural Conduction - genetics</topic><topic>Neurology</topic><topic>Neuromuscular diseases</topic><topic>Neuroradiology</topic><topic>Neurosciences</topic><topic>Original Communication</topic><topic>Severity of Illness Index</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schirmer, L.</creatorcontrib><creatorcontrib>Worthington, V.</creatorcontrib><creatorcontrib>Solloch, U.</creatorcontrib><creatorcontrib>Loleit, V.</creatorcontrib><creatorcontrib>Grummel, V.</creatorcontrib><creatorcontrib>Lakdawala, N.</creatorcontrib><creatorcontrib>Grant, D.</creatorcontrib><creatorcontrib>Wassmuth, R.</creatorcontrib><creatorcontrib>Schmidt, A. H.</creatorcontrib><creatorcontrib>Gebhardt, F.</creatorcontrib><creatorcontrib>Andlauer, T. F. M.</creatorcontrib><creatorcontrib>Sauter, J.</creatorcontrib><creatorcontrib>Berthele, A.</creatorcontrib><creatorcontrib>Lunn, M. P.</creatorcontrib><creatorcontrib>Hemmer, Bernhard</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schirmer, L.</au><au>Worthington, V.</au><au>Solloch, U.</au><au>Loleit, V.</au><au>Grummel, V.</au><au>Lakdawala, N.</au><au>Grant, D.</au><au>Wassmuth, R.</au><au>Schmidt, A. H.</au><au>Gebhardt, F.</au><au>Andlauer, T. F. M.</au><au>Sauter, J.</au><au>Berthele, A.</au><au>Lunn, M. P.</au><au>Hemmer, Bernhard</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Higher frequencies of HLA DQB105:01 and anti-glycosphingolipid antibodies in a cluster of severe Guillain–Barré syndrome</atitle><jtitle>Journal of neurology</jtitle><stitle>J Neurol</stitle><addtitle>J Neurol</addtitle><date>2016-10-01</date><risdate>2016</risdate><volume>263</volume><issue>10</issue><spage>2105</spage><epage>2113</epage><pages>2105-2113</pages><issn>0340-5354</issn><eissn>1432-1459</eissn><abstract>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.</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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language | eng |
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source | MEDLINE; SpringerNature Journals |
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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