UNASSIGNED: Machine learning (ML) is increasingly used in medical predictive modeling, but there are no studies applying ML to predict prognosis in Guillain-Barré syndrome (GBS).
UNASSIGNED: The medical records of 223 patients with GBS were analyzed to construct predictive models that affect patient prognosis. Least Absolute Shrinkage and Selection Operator (LASSO) was used to filter the variables. Decision Trees (DT), Random Forest (RF), Extreme Gradient Boosting (XGBoost), k-nearest Neighbour (KNN), Naive Bayes (NB), Neural Network (NN). Light Gradient Boosting Machine (LGBM) and Logistic Regression (LR) were used to construct predictive models. Clinical data from 55 GBS patients were used to validate the model. SHapley additive explanation (SHAP) analysis was used to explain the model. Single sample gene set enrichment analysis (ssGSEA) was used for immune cell infiltration analysis.
UNASSIGNED: The AUCs (area under the curves) of the 8 ML algorithms including DT, RF, XGBoost, KNN, NB, NN, LGBM and LR were as follows: 0.75, 0.896 0.874, 0.666, 0.742, 0.765, 0.869 and 0.744. The accuracy of XGBoost (0.852) was the highest, followed by LGBM (0.803) and RF (0.758), with F1 index of 0.832, 0.794, and 0.667, respectively. The results of the validation set data analysis showed AUCs of 0.839, 0.919, and 0.733 for RF, XGBoost, and LGBM, respectively. SHAP analysis showed that the SHAP values of blood neutrophil/lymphocyte ratio (NLR), age, mechanical ventilation, hyporeflexia and abnormal glossopharyngeal vagus nerve were 0.821, 0.645, 0.517, 0.401 and 0.109, respectively.
UNASSIGNED: The combination of NLR, age, mechanical ventilation, hyporeflexia and abnormal glossopharyngeal vagus used to predict short-term prognosis in patients with GBS has a good predictive value.

Glutamic acid decarboxylase (GAD) antibodies are frequently measured in diabetes care as islet-associated autoantibodies that are useful in the diagnosis of type 1 diabetes. However, GAD antibodies derived from other persons may contaminate immunoglobulin preparations, and there have been cases of transiently positive GAD antibodies after intravenous immunoglobulin (IVIg) in patients who were originally negative for GAD antibodies. Clinicians may be unaware of such contamination and misdiagnose some cases as type 1 instead of type 2 diabetes mellitus based on positivity for GAD antibodies. Herein, we present a case of type 2 diabetes mellitus that revealed transiently positive GAD antibodies following immunoglobulin administrations. A 68-year-old woman with a medical history of diabetes mellitus was admitted to our hospital for the treatment of Guillain-Barré syndrome, and IVIg was started on the day of admission. Blood tests on admission revealed negative for GAD antibodies but showed weak positivity on day one after IVIg. Afterward, GAD antibodies turned negative on day 72. Immunoglobulin preparations were revealed to have a high concentration of GAD antibodies. Based on changes in GAD antibody titers and all negativity for anti-insulinoma-associated antigen-2 (IA-2), insulin, and zinc transporter 8 (ZnT8) antibodies, the patient was diagnosed with type 2 diabetes mellitus rather than slowly progressive type 1 diabetes mellitus (SPIDDM). This case demonstrates that it is important for the medical clinician to be aware of the possible presence of GAD antibodies in immunoglobulin preparations and to measure antibody titers before and after their use for diagnosing the type of diabetes mellitus.

Gullain-Barré syndrome (GBS) is an acute peripheral neuropathy often preceded by respiratory or gastrointestinal infections, though molecular testing of cerebrospinal fluid (CSF) is often inconclusive. In a recent case of severe pediatric GBS in British Columbia, Canada, we detected CSF antibodies against enterovirus D (EV-D) to link GBS with prior EV-D68 respiratory infection.

OBJECTIVE: Guillain-Barré syndrome (GBS) is a rare autoimmune disorder that affects the peripheral nervous system. The purpose of our study was to evaluate maternal and fetal/neonatal outcomes among pregnancies complicated by GBS.
METHODS: We performed a retrospective cohort study using the Healthcare Cost and Utilization Project - National Inpatient Sample from the United States. ICD-9 codes were used to identify all pregnant women who delivered between 1999 and 2015 and had a diagnosis of GBS. The remaining women without GBS who delivered during that time period constituted the comparison group. The associations between maternal GBS and obstetrical and fetal/neonatal outcomes were evaluated using multivariate logistic regression, while adjusting for the confounding effects of maternal characteristics.
RESULTS: Of 13,792,544 births included in our study, 291 were to women with GBS, for an overall incidence of 2.1/100,000 births. A steady increase in maternal GBS was observed over the study period (from 1.26 to 3.8/100,000 births, p=0.02). Further, women with GBS were more likely to have pregnancies complicated by preeclampsia, OR 1.69 (95 % CI 1.06-2.69), sepsis, 9.30 (2.33-37.17), postpartum hemorrhage, 1.83 (1.07-3.14), and to require a transfusion, 4.39 (2.39-8.05). They were also at greater risk of caesarean delivery, 2.07 (1.58-2.72) and increased length of hospital stay, 4.48 (3.00-6.69). Newborns of women with GBS were more likely to be growth restricted, 2.50 (1.48-4.23).
CONCLUSIONS: GBS in pregnancy is associated with maternal and newborn adverse outcomes. These patients would benefit from close follow-up throughout their pregnancy and in the postpartum period.

暂无摘要。

UNASSIGNED: Guillain-Barré syndrome (GBS) is a polyradiculoneuropathy mediated by the immune system and is the primary reason for acute flaccid paralysis. Intravenous immunoglobulin (IVIg) is a recognized immunotherapeutic drug that can accelerate recovery from GBS. Limited literature exists concerning cerebral infarction complications with IVIg following its use in the treatment of GBS.
UNASSIGNED: A patient was diagnosed with the acute inflammatory demyelinating polyradiculoneuropathy subtype of GBS, while another patient was diagnosed with the acute bulbar palsy variant of GBS 2 years prior and experienced a relapse of GBS. Both patients received immunoglobulin therapy, during which multiple acute cerebral infarctions were detected using magnetic resonance imaging. Both patients had a history of coronary artery atherosclerotic heart disease and vertebral artery stenosis, and D-dimer and fibrinogen degradation products were significantly elevated after immunoglobulin therapy.
UNASSIGNED: The risk of cerebral infarction associated with IVIg is generally low in patients with different GBS variants. Nevertheless, the occurrence of cerebral infarction associated with IVIg might not be insignificant in older patients with vascular risk factors and should be carefully monitored.

The objective is to characterize differentially expressed proteins (DEPs) in Guillain-Barré Syndrome (GBS) and Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) through high-throughput analysis. Sera from 11 healthy controls (HCs), 21 GBS and 19 CIDP patients were subjected to Olink Proteomics Analysis. In the comparison between CIDP and GBS groups, up-regulation of ITM2A and down-regulation of NTF4 were observed. Comparing GBS with HCs revealed 18 up-regulated and 4 down-regulated proteins. Comparing CIDP with the HCs identified 15 up-regulated and 4 down-regulated proteins. Additionally, the correlation between clinical characteristics and DEPs were uncovered. In conclusion, the DEPs have significant potential to advance our understanding of the pathogenesis in these debilitating neurological disorders.

The complete genome sequence of Edwardsiella tarda strain GBS0709, isolated from an 81-year-old Japanese patient with the acute motor axonal neuropathy subtype of Guillain-Barré syndrome, was determined. It comprised a 3,632,068 bp circular chromosome and a 5,386 bp plasmid. The overall guanine and cytosine content was 57.3%.

UNASSIGNED: Chronic inflammatory demyelinating polyneuropathy (CIDP) is an acquired immune-mediated neuropathy defined by clinical progression for more than 2 months. 16-20% of CIDP patients may present with rapidly progressive weakness that resembles GBS, known as acute-onset CIDP (A-CIDP). However, it is challenging to distinguish from GBS-TRF because of their similar clinical symptom and features. In this case review, we report a patient with A-CIDP with the detection of anti-GM3 and anti-sulfatides antibodies, which rarely have been in A-CIDP and may account for her progressive and recurrent symptoms.
UNASSIGNED: We analyzed existing medical literature and described a clinical case of A-CIDP with antibodies positive.
UNASSIGNED: We reported a 56-year-old female presented with bilateral lower extremity weakness and distal numbness. She experienced similar symptoms four times and responded well to the IVIg therapy. Lumbar puncture demonstrated albumin-cytologic dissociation and EDX examination revealed multiple peripheral nerve damage. After ruling out other demyelination diseases, a diagnosis of A-CIDP was made.
UNASSIGNED: The antiganglioside and anti-sulfatide antibodies are involved in CIDP pathogenesis and can help to distinguish A-CIDP and other variants. To prevent secondary damage, it is important to monitor relapse and remission symptoms along the treatment line. A rare case of A-CIDP is discussed concerning the detection of anti-GM3 and anti-sulfatides antibodies, thus making a retrospective comparison of antibodies in some literature to understand A-CIDP better.

Zika virus (ZIKV), a mosquito-borne flavivirus, is prominently associated with microcephaly in babies born to infected mothers as well as Guillain-Barré Syndrome in adults. Each cell type infected by ZIKV-neuronal cells (radial glial cells, neuronal progenitor cells, astrocytes, microglia cells, and glioblastoma stem cells) and non-neuronal cells (primary fibroblasts, epidermal keratinocytes, dendritic cells, monocytes, macrophages, and Sertoli cells)-displays its own characteristic changes to their cell physiology and has various impacts on disease. Here, we provide an in-depth review of the ZIKV life cycle and its cellular targets, and discuss the current knowledge of how infections cause neuropathologies, as well as what approaches researchers are currently taking to further advance such knowledge. A key aspect of ZIKV neuropathogenesis is virus-induced neuronal apoptosis via numerous mechanisms including cell cycle dysregulation, mitochondrial fragmentation, ER stress, and the unfolded protein response. These, in turn, result in the activation of p53-mediated intrinsic cell death pathways. A full spectrum of infection models including stem cells and co-cultures, transwells to simulate blood-tissue barriers, brain-region-specific organoids, and animal models have been developed for ZIKV research.