Cargando…
Glutamic acid decarboxylase antibodies in neurocritical patients: a culprit or a bystander?
BACKGROUND: Glutamic acid decarboxylase (GAD) is an intracellular enzyme, which is widely expressed in central nervous system (CNS), pancreas, and other organs. GAD antibodies (GAD-Abs) are linked to various neurological disorders. However, the significance of GAD-Abs in neurocritical patients is un...
Autores principales: | , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer International Publishing
2020
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7278224/ https://www.ncbi.nlm.nih.gov/pubmed/32514855 http://dx.doi.org/10.1007/s10072-020-04466-7 |
_version_ | 1783543290837073920 |
---|---|
author | Wang, Dongmei Huang, Kaibin Lin, Zhenzhou Zhang, Yongfang Liu, Guanghui Wu, Yongming Wang, Shengnan |
author_facet | Wang, Dongmei Huang, Kaibin Lin, Zhenzhou Zhang, Yongfang Liu, Guanghui Wu, Yongming Wang, Shengnan |
author_sort | Wang, Dongmei |
collection | PubMed |
description | BACKGROUND: Glutamic acid decarboxylase (GAD) is an intracellular enzyme, which is widely expressed in central nervous system (CNS), pancreas, and other organs. GAD antibodies (GAD-Abs) are linked to various neurological disorders. However, the significance of GAD-Abs in neurocritical patients is undetermined. MATERIALS AND METHODS: Patients with serologically positive GAD-Abs and requiring neurocritical care were included. The clinical, laboratory, and outcome data were retrospectively collected. RESULTS: We included 9 patients with serologically positive GAD-Abs. Clinical manifestations involved both CNS and peripheral nervous system (PNS). Six (66.7%) patients had other specific autoimmune antibodies. Non-specific autoimmune responses were observed in 8 (88.9%) patients. All patients clinically responded well to immunotherapy. The titers of GAD-Abs decreased in 7 (77.8%) patients but remained unchanged in the other 2 patients. One (11.1%) patient awoke before the negative conversion of GAD-Abs, and 3 (33.3%) patients remained unconscious and/or under mechanical ventilation for several weeks after the vanishing of GAD-Abs. CONCLUSIONS: Most neurocritical patients with serologically positive GAD-Abs had other specific autoimmune antibodies. All patients responded well to immunotherapy, but not parallel to the titers of GAD-Abs. These results indicated that GAD-Abs might be more a bystander than a culprit in neurocritical patients, suggesting that an underlying autoimmune disease should be explored. |
format | Online Article Text |
id | pubmed-7278224 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Springer International Publishing |
record_format | MEDLINE/PubMed |
spelling | pubmed-72782242020-06-09 Glutamic acid decarboxylase antibodies in neurocritical patients: a culprit or a bystander? Wang, Dongmei Huang, Kaibin Lin, Zhenzhou Zhang, Yongfang Liu, Guanghui Wu, Yongming Wang, Shengnan Neurol Sci Original Article BACKGROUND: Glutamic acid decarboxylase (GAD) is an intracellular enzyme, which is widely expressed in central nervous system (CNS), pancreas, and other organs. GAD antibodies (GAD-Abs) are linked to various neurological disorders. However, the significance of GAD-Abs in neurocritical patients is undetermined. MATERIALS AND METHODS: Patients with serologically positive GAD-Abs and requiring neurocritical care were included. The clinical, laboratory, and outcome data were retrospectively collected. RESULTS: We included 9 patients with serologically positive GAD-Abs. Clinical manifestations involved both CNS and peripheral nervous system (PNS). Six (66.7%) patients had other specific autoimmune antibodies. Non-specific autoimmune responses were observed in 8 (88.9%) patients. All patients clinically responded well to immunotherapy. The titers of GAD-Abs decreased in 7 (77.8%) patients but remained unchanged in the other 2 patients. One (11.1%) patient awoke before the negative conversion of GAD-Abs, and 3 (33.3%) patients remained unconscious and/or under mechanical ventilation for several weeks after the vanishing of GAD-Abs. CONCLUSIONS: Most neurocritical patients with serologically positive GAD-Abs had other specific autoimmune antibodies. All patients responded well to immunotherapy, but not parallel to the titers of GAD-Abs. These results indicated that GAD-Abs might be more a bystander than a culprit in neurocritical patients, suggesting that an underlying autoimmune disease should be explored. Springer International Publishing 2020-06-08 2020 /pmc/articles/PMC7278224/ /pubmed/32514855 http://dx.doi.org/10.1007/s10072-020-04466-7 Text en © Fondazione Società Italiana di Neurologia 2020 This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic. |
spellingShingle | Original Article Wang, Dongmei Huang, Kaibin Lin, Zhenzhou Zhang, Yongfang Liu, Guanghui Wu, Yongming Wang, Shengnan Glutamic acid decarboxylase antibodies in neurocritical patients: a culprit or a bystander? |
title | Glutamic acid decarboxylase antibodies in neurocritical patients: a culprit or a bystander? |
title_full | Glutamic acid decarboxylase antibodies in neurocritical patients: a culprit or a bystander? |
title_fullStr | Glutamic acid decarboxylase antibodies in neurocritical patients: a culprit or a bystander? |
title_full_unstemmed | Glutamic acid decarboxylase antibodies in neurocritical patients: a culprit or a bystander? |
title_short | Glutamic acid decarboxylase antibodies in neurocritical patients: a culprit or a bystander? |
title_sort | glutamic acid decarboxylase antibodies in neurocritical patients: a culprit or a bystander? |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7278224/ https://www.ncbi.nlm.nih.gov/pubmed/32514855 http://dx.doi.org/10.1007/s10072-020-04466-7 |
work_keys_str_mv | AT wangdongmei glutamicaciddecarboxylaseantibodiesinneurocriticalpatientsaculpritorabystander AT huangkaibin glutamicaciddecarboxylaseantibodiesinneurocriticalpatientsaculpritorabystander AT linzhenzhou glutamicaciddecarboxylaseantibodiesinneurocriticalpatientsaculpritorabystander AT zhangyongfang glutamicaciddecarboxylaseantibodiesinneurocriticalpatientsaculpritorabystander AT liuguanghui glutamicaciddecarboxylaseantibodiesinneurocriticalpatientsaculpritorabystander AT wuyongming glutamicaciddecarboxylaseantibodiesinneurocriticalpatientsaculpritorabystander AT wangshengnan glutamicaciddecarboxylaseantibodiesinneurocriticalpatientsaculpritorabystander |