Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2020
Glutamic acid decarboxylase antibodies in neurocritical patients: a culprit or a bystander?
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Wang Dongmei, Huang Kaibin, Lin Zhenzhou, Zhang Yongfang, Liu Guanghui, Wu Yongming, Wang Shengnan
Аннотация
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.
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.