Comparison of the Effects of Different Doses of Glucocorticoids on Distinct Subtypes of Guillain-Barré Syndrome in Southern China

Comparison of the Effects of Different Doses of Glucocorticoids on Distinct Subtypes of Guillain-Barré Syndrome in Southern China | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Comparison of the Effects of Different Doses of Glucocorticoids on Distinct Subtypes of Guillain-Barré Syndrome in Southern China Linzhuo Ma, Shuping Liu, Zheman Xiao, Jingxia Guan, Yin Liu, Jiajia Yao, and 1 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-936464/v1 This work is licensed under a CC BY 4.0 License Status: Published Journal Publication published 05 Feb, 2022 Read the published version in BMC Neurology → Version 1 posted 10 You are reading this latest preprint version Abstract Background The effect of Glucocorticoids (GCs) on the treatment of Guillain-Barré syndrome (GBS) has been controversial. There is no information on whether specific subtypes of GBS respond differently to GCs. In this setting, we aimed to discuss whether GCs treating yield different effects in the distinct subtypes (acute inflammatory demyelinating polyneuropathy, AIDP; acute motor axonal neuropathy, AMAN). And further, we analyzed the impact of different doses on the outcome. Methods Medical records of patients with a diagnosis of GBS (AIDP & AMAN) admitted to 31 tertiary hospitals, located in 14 provinces of Southern China, from 1 January 2013 to 30 September 2016, were retrospectively collected. And those patients treated with GCs alone were reviewed and analyzed. Results Finally, 251 classic patients with available electromyographic data were collected, including AIDP (n=189) and AMAN (n=62). After GCs treatment, the Hughes score of AIDP patients was significantly lower than that of AMAN patients at discharge ( P =0.005) and 3 months after onset ( P =0.000). Further analysis revealed that among AIDP patients, the high-dose group had significantly shorter hospital stay ( P =0.023), lower Hughes score at nadir ( P =0.000), at discharge ( P =0.005), and 3 months after onset ( P =0.000), compared with the low-dose group. However, for AMAN patients, the outcome difference between groups was nonsignificant. Conclusion Our data suggest that the high doses of GCs may result, at least in part, from the side of the duration of hospital stay and short-term outcome, favorable outcomes in AIDP patients. Therefore, we cannot completely deny the priority of GCs in the treatment of GBS, because the effect of different doses of GCs varies in treating different subtypes. More studies are needed in the future to further validate this issue. Trial registration : ChiCTR-RRC-17014152. Registered 26 December 2017- Retrospectively registered. Neurobiology of Disease Guillain-Barré syndrome Glucocorticoids Southern China subtype Introduction Guillain-Barré syndrome (GBS) is an immune-mediated acute peripheral neuropathy involving mainly spinal nerve roots, peripheral nerves and cerebral nerves, and is currently the most common cause of acute flaccid paralysis worldwide. As an autoimmune disease (AID) with a high rate of mortality and disability, immunotherapy is essential [1,2]. Glucocorticoids (GCs) is considered as the most commonly used drug for the treatment of AID worldwide because of its cost-effectiveness and strong immunosuppressive effect [3]. Unfortunately, its use in GBS patients is controversial [4,5]. Clinical trials in Europe and North America did not observe significant efficacy of GCs alone in GBS, however, as it currently stands, the actual efficacy of GCs may be underestimated, because these above-mentioned studies did not discuss the efficacy of GCs in different subtypes in a categorical manner, and the use and dosage of GCs were not uniform [6-8]. Scholars such as Hughes have suggested that patients with GBS with conduction block respond well to GCs, while the use of GCs in patients with denervation delays the recovery of GBS, although the specific mechanism needs to be further explored [9]. According to neuroelectrophysiological studies, GBS consists of two major subtypes, acute inflammatory demyelinating polyneuropathy (AIDP), and acute motor axonal neuropathy (AMAN) [10]. AIDP is associated with macrophage and CD4 + T cell-mediated inflammation and peripheral nerve demyelination, whereas AMAN is mainly associated with the involvement of ganglioside autoantibodies and complement [11]. Given that these two major subtypes have different pathological characteristics and pathogenesis, and their epidemiology in Asia differs from foreign studies, it is necessary to explore the mechanism of action and effects of GCs based on different subtypes. Methods Patient ascertainment This is a retrospective multicenter study and the medical records of consecutive hospitalized patients with a diagnosis of GBS in 31 representative tertiary hospitals, located in 14 provinces in southern China, between 1 January 2013 and 30 September 2016, were collected. Patients who fulfilled the established clinical criteria of Asbury and Cornblath (1990) were enrolled [12]. In addition, the patients whose clinical presentation and ancillary data were typical of GBS except for preservation or exaggeration of reflexes were also included. Details regarding clinical data extraction and analysis, including inclusion and exclusion criteria, were described in our previous study [13]. Those patients with a diagnosis of AIDP or AMAN, including acute motor and sensory axonal neuropathy (AMSAN), and treated with GCs alone and symptomatic supportive treatment were analyzed. The study was approved by the ethics committee of the Renmin Hospital of Wuhan University, and the need for informed consent was waived. Treatment Grouping The high dose group patients received methylprednisolone (250–1,000 mg/d) for 3-5 days and then tapered as clinically indicated; while the low dose group received methylprednisolone (40–120 mg/d) for 3-5 days, or dexamethasone (10-20mg) for 5-7 days followed by a tapered dosage, or else oral prednisolone at 1 mg/kg/day for 1 week, tailed off over the next 2 months in a similar manner. Information Extraction Information on age, sex, preceding events, initial symptoms, concomitant symptoms, severity at admission, at nadir, at discharge, length of hospitalization, findings of electrodiagnosis (EDX), treatment regime, types and doses of GCs were extracted. The motor function deficits of included patients were assessed by the Hughes Functional Grading Scale, a widely accepted scale of disability for GBS (grade 6, dead; grade 5, requiring assisted respiration; grade 4, bed-bound; grade 3, able to walk with aid; grade 2, able to walk independently; grade 1, minimal signs and symptoms, able to run; grade 0, normal) [14]. Details regarding clinical data extraction were described in our previous study [13]. Statistical analysis Statistical analysis was performed using IBM SPSS 23.0 software. Categorical data were presented as proportions, and continuous data were presented as mean ± standard deviation (SD). Differences in proportions were tested by the χ2 tests. The continuous variables with a normal distribution were tested using the Student’s t-test or analysis of variance test, and the continuous variables with a skewed distribution were tested using the Mann-Whitney U test or the Kruskal-W allis analysis. For all statistical tests, P<0.05 was considered to be significant. Results Baseline clinical characteristics Finally, 251 patients with a diagnosis of GBS, including 189 (75.3%) cases with AIDP and 62 (24.7%) cases with AMAN, were analyzed. Among whom 157 (62.5%) were men and 94 (37.5%) were women, and 168 (66.9%) patients came from rural areas. The mean age was 49.6 years (age range 17–83 years). 133(53.0%) patients were treated with high-dose GCs, who received intravenous methylprednisolone (≥250 mg) for 3-5 days, followed by gradual reduction to oral prednisone. 118 (47.0%) patients were treated with low-dose GC, including dexamethasone, prednisone, and low-dose methylprednisolone (< 250 mg). Two patients died during their hospital stay. The common autonomic symptoms of our patients included hypertension, cardiac arrhythmia, hypotension, orthostatic hypotension, sweating, bowel and bladder incontinence or retention. Effects of GCs on the treatment of different subtypes (AIDP vs AMAN) There was no statistically significant difference between the two groups in terms of certain baseline characteristics, such as age, gender, urban-rural distribution, Hughes score on admission. As to complications and concomitant symptoms, autonomic dysfunctions and laboratory abnormality, for example, we found no significant difference between the two groups. However, facial/bulbar paralysis (45.5 vs 16.1, P =0.000) and paresthesia (49.2 vs 32.3, P =0.027) were more frequently observed in patients with AIDP, in whom hyperreflexia occurred less frequently (5.8 vs 19.3, P =0.004). With regard to clinical outcomes, AIDP patients had a significantly lower Hughes score at discharge (2.51±0.98 vs 2.84±0.73, P = 0.005) and 3 months after onset (2.06±1.14 vs 2.50±0.80, P =0.000), compared to that in AMAN patients. (Table 1 ) Table 1 Effects of GCs on the treatment of different subtypes Parameters AIDP(n=189) AMAN(n=62) P value (two-tailed) Age (years) 49.88±18.07 48.61±17.46 0.631 Male, n (%) 123(65.1) 34(54.9) 0.174 Rural area, n (%) 125(66.1) 43(69.4) 0.756 Hughes score on admission (g) 2.97±0.93 3.10±0.88 0.451 Hughes score at nadir (g) 3.50±0.89 3.71±0.69 0.155 Neurological symptoms, n (%) Facial/bulbar paralysis 86(45.5) 10(16.1) 0.000* Oculomotor paralysis 14(7.4) 3(4.8) 0.771 Paresthesia 93(49.2) 20(32.3) 0.027* Hyperreflexia 11(5.8) 12(19.3) 0.004* Complication, n (%) Autonomic dysfunction, n (%) Hypertension 38(20.1) 11(17.7) 0.854 Cardiac arrhythmia 13(6.9) 7(11.3) 0.283 Urinary retention 21(11.1) 12(19.4) 0.128 Deep venous thrombosis 7(3.7) 3(4.8) 0.712 Dyspnoea 49(25.9) 10(16.1) 0.124 Pulmonary infection 28(14.8) 8(12.9) 0.836 Diabetes 16(8.5) 4(6.5) 0.789 Laboratory abnormality, n (%) Hyponatraemia 53(28.0) 13(16.7) 0.320 Hypokalemia 42(22.2) 14(22.6) 1.000 Hospital stay (days) 14.18±8.10 15.35±7.29 0.221 Mechanical ventilation, n (%) 19(10.1) 7(11.3) 0.811 Death in hospital stay, n (%) 1(0.5) 1(1.6) 0.434 Hughes score at discharge (g) 2.51±0.98 2.84±0.73 0.005* Hughes score of 3 months after onset (g) 2.06±1.14 2.50±0.80 0.000* Values are mean ± standard deviation unless otherwise specified GCs Glucocorticoids, AIDP acute inflammatory demyelinating polyneuropathy, AMAN acute motor axonal neuropathy axonal neuropathy Effects of high-dose and low-dose GCs on the treatment of AIDP patients A total of 189 AIDP patients were enrolled in this study, 98 (51.9%) of them were treated with high-dose GCs and 91 (48.1%) patients received low-dose GCs. There was no statistically significant difference between the two groups in terms of age, gender, urban-rural distribution, and Hughes score on admission. Notably, patients that received low-dose GCs had a higher frequency of pulmonary infection (9.2 vs 20.9, P =0.026). Regarding to the clinical outcomes, patients in the high-dose group had a significantly shorter hospital stay (13.27±8.47 vs 15.16±7.62, P =0.023), lower Hughes score at nadir (3.28±0.88 vs 3.74±0.74, P =0.000), at discharge (2.36±1.03 vs 2.68±0.88, P =0.005) and 3 months after onset (1.83±1.30 vs 2.30±0.89, P =0.000), when compared with the low-dose group. During the hospitalization, one patient died. (Table 2 ) Table 2 Effects of high-dose and low-dose GCs on the treatment of AIDP Parameters High-dose(n=98) Low-dose(n=91) P value(two-tailed) Age (mean, years) 48.49±17.94 51.85±17.37 0.286 Male, n (%) 65(66.3) 58 (63.7) 0.761 Rural area, n (%) 62(63.3) 63(69.2) 0.443 Hughes score on admission (mean, g) 2.99±0.91 2.96±0.94 0.909 Hughes score at nadir (mean, g) 3.28±0.88 3.74±0.74 0.000* Neurological symptoms, n (%) Facial/bulbar paralysis 47(47.8) 39(42.9) 0.559 Oculomotor paralysis 6(6.1) 8(8.8) 0.583 Paresthesia 42(42.9) 51(56.0) 0.081 Hyperreflexia 6(6.1) 5(5.5) 1.000 Complication, n (%) Autonomic dysfunction Hypertension 17(17.3) 21(23.1) 0.413 Cardiac arrhythmia 6(6.1) 7(7.7) 0.777 Urinary retention 9(9.2) 12(13.2) 0.488 Deep venous thrombosis 3(3.1) 4(4.4) 0.713 Dyspnoea 28(28.6) 21(23.1) 0.411 Pulmonary infection 9(9.2) 19(20.9) 0.026* Diabetes 9(9.2) 7(7.7) 0.797 Laboratory abnormality, n (%) Hyponatraemia 22(22.4) 31(34.1) 0.105 Hypoalbuminaemia 19(19.4) 23(25.3) 0.383 Hospital stay (days) 13.27±8.47 15.16±7.62 0.023* Mechanical ventilation, n (%) 11(11.2) 8(8.8) 0.635 Death in hospital stay, n (%) 1(1.0) 0 - Hughes score at discharge (g) 2.36±1.03 2.68±0.88 0.005* Hughes score of 3 months after onset (g) 1.83±1.30 2.30±0.89 0.000* Values are mean ± standard deviation unless otherwise specified GCs Glucocorticoids, AIDP acute inflammatory demyelinating polyneuropathy * Significant difference between groups at p < 0.05 Effects of high-dose and low-dose GCs on the treatment of AMAN patients Totally, 62 patients with AMAN were enrolled in our study and received different treatment doses of GCs. No differences in baseline characteristics between groups were statistically significant. Concerning the short-term outcome, such as hospital stay ( P =0.943), Hughes score at nadir ( P =0.262), Hughes score at discharge ( P =0.591) and Hughes score at 3 months after onset ( P =0.386), the differences between the two groups were non-significant. (Table 3 ) Table 3 Effects of high-dose and low-dose GCs on the treatment of AMAN Parameters High-dose(n=35) Low-dose(n=27) P value (two-tailed) Age (years) 49.31±15.69 47.70±19.80 0.722 Male, n (%) 20(51.4) 14(51.9) 0.798 Rural area, n (%) 26 (74.3) 17(63.0) 0.805 Hughes score on admission (g) 3.11±0.93 3.07±0.83 0.940 Hughes score at nadir (mean, g) 3.63±0.69 3.81±0.68 0.262 Neurological symptoms, n (%) Facial/bulbar paralysis 4(11.4) 6(22.2) 0.308 Oculomotor paralysis 2(5.7) 1(3.7) 1.000 Paresthesia 12(34.3) 8(29.6) 0.788 Hyperreflexia 7(20.0) 5(18.5) 1.000 Complication, n (%) Autonomic dysfunction Hypertension 6(17.1) 5(18.5) 0.735 Cardiac arrhythmia 4(11.4) 3(11.1) 1.000 Urinary retention 5(14.3) 7(25.9) 0.335 Deep venous thrombosis 1(2.9) 2(7.4) 0.575 Dyspnoea 4(11.4) 6(22.2) 0.308 Pulmonary infection 3(8.6) 5(18.5) 0.279 Diabetes 3(8.6) 1(3.7) 0.626 Laboratory abnormality, n (%) Hyponatraemia 6(17.1) 7(25.9) 0.532 Hypoalbuminaemia 9(25.7) 5(18.5) 0.555 Hospital stay (days) 15.66±8.11 14.96±6.20 0.943 Mechanical ventilation, n (%) 3(8.6) 4(14.9) 0.689 Death in hospital stay, n (%) 0 1(5.00) - Hughes score at discharge (g) 2.80±0.76 2.89±0.70 0.591 Hughes score of 3 months after onset (g) 2.43±0.74 2.59±0.89 0.386 Values are mean ± standard deviation unless otherwise specified GCs Glucocorticoids, AMAN acute motor axonal neuropathy axonal neuropathy Discussion Our first multi-center study showed that the Hughes score at discharge and 3 months after onset were significantly lower in AIDP patients treated with GCs compared to that in AMAN patients. Further analysis found that among AIDP patients, the high-dose group had shorter hospitalization days and significantly lower Hughes score at nadir, at discharge and 3 months after onset than that in the low-dose group. However, among AMAN patients, according to our data, the short-term outcome in the high-dose group was not significantly different from that in the low-dose group. In regarding to complications, we found that, among AIDP patients, the incidence of pulmonary infections was higher in the low-dose group, which we speculated that the longer hospital stay of patients in the low-dose group may account. Because, as the length of hospital stay increases, says from some kind of significance, the effective activity of patients decreases and the risk of pathogenic bacteria infection greatly increases [ 15 ]. On the other side, studies have demonstrated that patients with refractory pulmonary treated with high-dose corticosteroid could achieve defervescence earlier and have a shorter hospitalization [ 16 ]. These data above suggest that we can’t dismiss wholesale the role of GCs in the treatment of GBS, subtyping to explore the effects of different doses of GCs on GBS treatment is necessary. After all, in China, especially in the 1990s, GCs were the drug of choice in the treatment of GBS because of their civilian price, and clinical observations found good results in many patients [ 17 ]. A study used a rabbit model of the axonal form of GBS initially explored the reasons for the ineffectiveness of GCs in treating AMAN, suggesting that MPS did not reduce complement C3 deposition and sodium (Nav) channel disruption, but significantly reduced macrophage infiltration in the ventral roots and thus delay the axonal regeneration [ 18 ]. Studies of pathophysiology about AMAN have shown that macrophages invasion was rare at the acute progressive phase but significantly more frequent at the site of inflammation mainly during the recovery phase, which suggested a role for macrophages in the clearance of damaged myelin and axon fragments and promoting nerve repair and regeneration [ 19 ]. Whereas, the classical experimental autoimmune neuritis (EAN) model, which highly replicates human AIDP in terms of clinical manifestations, immunology, histopathology, and electrophysiology [ 20 ], indicated that “Classically” activated (M1) macrophages mainly accumulated at the acute phase of EAN and promoted the inflammatory response, while during the recovery phase, macrophages could change their expression profile, M2 macrophages attenuated inflammation and promoted tissue repair [ 21 , 22 ]. Ultrastructural studies showed that macrophage-mediated nerve injury was a pathological hallmark of AIDP/EAN [ 21 – 23 ]. Macrophages (M1) were involved in this process by regulating cytokines, chemokines, adhesion molecules, NO and matrix metalloproteinases (MMPs), and as major antigen-presenting and effector cells, macrophages played a key role in EAN pathogenesis by expressing antigens and promoting Th1 and Th17 polarization [ 24 ]. In summary, we hypothesize that the different mechanisms of macrophages' role in the inflammatory response of AIDP and AMAN may lead to different effects of GCs therapy. We will further test our hypothesis through animal experiments. As a multicenter study, we derived relatively powerful results, but there exists inevitably some limitations. First, as a retrospective study, the long-term follow-up information was insufficient to further explore the prognosis of patients with different subtypes treated with different doses of GCs, further studies were anticipated; Second, the number of patients with AMAN subtypes in this study was relatively small; Third, because the study was a retrospective review of medical records and database, extracting bias was unavoidable. However, in order to reduce the bias as much as possible, a unified parameter standard in the analysis of NCS was adopted and data were extracted by our team members through strict training. Conclusion In conclusion, our data firstly provides information about whether the responses to GCs differ between the principal subtypes of GBS, and prompts recommendations about the design of future GBS trails. GCs induce different effects in specific GBS subtypes, among which high-dose GCs therapy has a better prognosis for patients with AIDP. The effects of GCs on GBS subtypes should be discussed separately in future clinical trials to explore its mechanism of action and provide more timely and effective treatment measures for GBS patients. Abbreviations GCs, Glucocorticoids; GBS, Guillain-Barré syndrome; AIDP, acute inflammatory demyelinating polyneuropathy; AMAN, acute motor axonal neuropathy; AMSAN, acute motor and sensory axonal neuropathy; AID, autoimmune disease; SD, standard deviation; EAN, experimental autoimmune neuritis; MMPS, matrix metalloproteinases. Declarations Ethics approval and consent to participate This retrospective study was approved by the ethics committee of the Renmin Hospital of Wuhan University and conducted in accordance with the principles of the Declaration of Helsinki. The requirement for informed consent was waived by the ethics committee of the Renmin Hospital of Wuhan University because the analysis was retrospective. Consent for publication Not applicable. Availability of data and materials The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request. Competing interests The authors declare that they have no competing interests. Funding This work was supported by grants from the Independent scientific research project of Wuhan University (2042020kf0053) and the National Natural Science Foundation of China (81971055). Authors' contributions ZX, JG and ZL took part in validating the diagnosis and information extraction; YL and JY involved in data collection and analysis, LM and SL contributed to the study design, data collection and analysis, and wrote the manuscript. All authors read and approved the final manuscript. Acknowledgements Not applicable. References van den Berg B, Walgaard C, Drenthen J, Fokke C, Jacobs BC, van Doorn PA. Guillain-Barré syndrome: pathogenesis, diagnosis, treatment and prognosis. Nat Rev Neurol 10(8):469–82. https://doi.org/10.1038/nrneurol.2014.121 Sipilä JOT, Soilu-Hänninen M, Ruuskanen JO, Rautava P, Kytö V. Epidemiology of Guillain-Barré syndrome in Finland 2004-2014. J Peripher Nerv Syst 22(4):440–445. https://doi.org/10.1111/jns.12239 Straub RH, Cutolo M. Glucocorticoids and chronic inflammation. Rheumatology (Oxford) 55(suppl 2):ii6-ii14. https:// doi.org/10.1093/rheumatology/kew348 Hughes RA. Treatment of Guillain-Barré syndrome with corticosteroids: lack of benefit? Lancet 363(9404):181–2 .https://doi.org/10.1016/S0140-6736(03)15367-6 Mastaglia FL. Neuromuscular disorders: molecular and therapeutic insights. Lancet Neurol 4(1):6–7. https://doi.org/10.1016/S1474-4422(04)00946-9 Walgaard C, Lingsma HF, Ruts L, van Doorn PA, Steyerberg EW, Jacobs BC. Early recognition of poor prognosis in Guillain-Barre syndrome. Neurology 76(11):968–75. https://doi.org/10.1212/WNL.0b013e3182104407 Double-blind trial of intravenous methylprednisolone in Guillain-Barré syndrome. Guillain-Barré Syndrome Steroid Trial Group. Lancet. 1993;341(8845):586–90. van Koningsveld R, Schmitz PI, Meché FG, Visser LH, Meulstee J, van Doorn PA; Dutch GBS study group. Effect of methylprednisolone when added to standard treatment with intravenous immunoglobulin for Guillain-Barré syndrome: randomized trial. Lancet 363(9404):192–6. https://doi.org/10.1016/s0140-6736(03)15324-x Hughes RA, Brassington R, Gunn AA, van Doorn PA. Corticosteroids for Guillain-Barré syndrome. Cochrane Database Syst Rev 10(10):CD001446. https://doi.org/10.1002/14651858.CD001446.pub5 Malek E, Salameh J. Guillain-Barre Syndrome. Semin Neurol 39(5):589–595. https://doi.org/10.1055/s-0039-1693005 Fan X, Zhang H, Cheng Y, Jiang X, Zhu J, Jin T. Double Roles of Macrophages in Human Neuroimmune Diseases and Their Animal Models. Mediators Inflamm 2016:8489251. https://doi.org/10.1155/2016/8489251 Asbury AK, Cornblath DR. Assessment of current diagnostic criteria for Guillain-Barré syndrome. Ann Neurol 27 Suppl: S21-4. https://doi.org/10.1002/ana.410270707 Liu S, Xiao Z, Lou M, Ji F, Shao B, Dai H, et al. Guillain-Barré syndrome in southern China: retrospective analysis of hospitalised patients from 14 provinces in the area south of the Huaihe River. J Neurol Neurosurg Psychiatry 89(6):618–626. https://doi.org/10.1136/jnnp-2017-316930 Hughes RA, Newsom-Davis JM, Perkin GD, Pierce JM. Controlled trial prednisolone in acute polyneuropathy. Lancet 2(8093):750–3. https://doi.org/10.1016/s0140-6736(78)92644-2 Kuderer NM, Dale DC, Crawford J, Cosler LE, Lyman GH. Mortality, morbidity, and cost associated with febrile neutropenia in adult cancer patients. Cancer 106(10):2258–66. https://doi.org/10.1002/cncr.21847 Okumura T, Kawada JI, Tanaka M, Narita K, Ishiguro T, Hirayama Y, et al. Comparison of high-dose and low-dose corticosteroid therapy for refractory Mycoplasma pneumoniae pneumonia in children. J Infect Chemother 25(5):346–350. https://doi.org/10.1016/j.jiac.2019.01.003 Cheng Q, Wang DS, Jiang GX, Han H, Zhang Y, Wang WZ, et al. Prospective study of clinical epidemiology of Guillain-Barré syndrome in Harbin, China. J Neurol Sci 215(1-2):63–9. https://doi.org/10.1016/s0022-510x(03)00187-4 Wang YZ, Lv H, Shi QG, Fan XT, Li L, Yi Wong AH, Hao YL, Si CP, Li CL, Yuki N. Action mechanism of corticosteroids to aggravate Guillain-Barré syndrome. Sci Rep 5:13931. https://doi.org/10.1038/srep13931 Susuki K, Rasband MN, Tohyama K, Koibuchi K, Okamoto S, Funakoshi K, Hirata K, Baba H, Yuki N. Anti-GM1 antibodies cause complement-mediated disruption of sodium channel clusters in peripheral motor nerve fibers. J Neurosci 27(15):3956–67. https://doi.org/10.1523/JNEUROSCI.4401-06.2007 Gonsalvez DG, Fletcher JL, Yoo SW, Wood RJ, Murray SS, Xiao J. A Simple Approach to Induce Experimental Autoimmune Neuritis in C57BL/6 Mice for Functional and Neuropathological Assessments. J Vis Exp (129): 56455. https://doi.org/10.3791/56455 Shen D, Chu F, Lang Y, Geng Y, Zheng X, Zhu J, Liu K. Beneficial or Harmful Role of Macrophages in Guillain-Barré Syndrome and Experimental Autoimmune Neuritis. Mediators Inflamm 2018:4286364. https://doi.org/10.1155/2018/4286364 Hartung HP, Schäfer B, Heininger K, Stoll G, Toyka KV. The role of macrophages and eicosanoids in the pathogenesis of experimental allergic neuritis. Serial clinical, electrophysiological, biochemical and morphological observations. Brain 111 (Pt 5):1039–59. https://doi.org/10.1093/brain/111.5.1039 Kiefer R, Kieseier BC, Stoll G, Hartung HP. The role of macrophages in immune-mediated damage to the peripheral nervous system. Prog Neurobiol 64(2):109–27. https://doi.org/10.1016/s0301-0082(00)00060-5 Han R, Xiao J, Zhai H, Hao J. Dimethyl fumarate attenuates experimental autoimmune neuritis through the nuclear factor erythroid-derived 2-related factor 2/hemoxygenase-1 pathway by altering the balance of M1/M2 macrophages. J Neuroinflammation 13(1):97. https://doi.org/10.1186/s12974-016-0559-x Additional Declarations No competing interests reported. Cite Share Download PDF Status: Published Journal Publication published 05 Feb, 2022 Read the published version in BMC Neurology → Version 1 posted Editorial decision: Major revision 16 Dec, 2021 Reviews received at journal 14 Dec, 2021 Reviewers agreed at journal 09 Dec, 2021 Reviews received at journal 31 Oct, 2021 Reviewers agreed at journal 29 Oct, 2021 Reviewers invited by journal 19 Oct, 2021 Editor assigned by journal 19 Oct, 2021 Editor invited by journal 18 Oct, 2021 Submission checks completed at journal 18 Oct, 2021 First submitted to journal 25 Sep, 2021 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-936464","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":57397796,"identity":"4d26651d-4a3c-4572-87ba-be5b87e958f1","order_by":0,"name":"Linzhuo Ma","email":"","orcid":"","institution":"Renmin Hospital of Wuhan University","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Linzhuo","middleName":"","lastName":"Ma","suffix":""},{"id":57397797,"identity":"86f09e57-2fee-41ad-922b-4233a1ca9856","order_by":1,"name":"Shuping Liu","email":"","orcid":"","institution":"Renmin Hospital of Wuhan University","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Shuping","middleName":"","lastName":"Liu","suffix":""},{"id":57397798,"identity":"d2d88684-5c74-4028-bcb9-6f55f79de93a","order_by":2,"name":"Zheman Xiao","email":"","orcid":"","institution":"Renmin Hospital of Wuhan University","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Zheman","middleName":"","lastName":"Xiao","suffix":""},{"id":57397799,"identity":"335b0fd0-7e37-4d72-857e-2ff04bcfd17c","order_by":3,"name":"Jingxia Guan","email":"","orcid":"","institution":"Renmin Hospital of Wuhan University","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Jingxia","middleName":"","lastName":"Guan","suffix":""},{"id":57397800,"identity":"5ccbee36-4f6c-43bd-b1ca-b7bd61d16b6e","order_by":4,"name":"Yin Liu","email":"","orcid":"","institution":"Renmin Hospital of Wuhan University","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Yin","middleName":"","lastName":"Liu","suffix":""},{"id":57397801,"identity":"51b6594c-2aa1-4bdd-ba84-fd1307a44fe0","order_by":5,"name":"Jiajia Yao","email":"","orcid":"","institution":"Renmin Hospital of Wuhan University","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Jiajia","middleName":"","lastName":"Yao","suffix":""},{"id":57397802,"identity":"4c642bb4-79f9-4aa7-ac64-be58bd355852","order_by":6,"name":"Zuneng Lu","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAArUlEQVRIiWNgGAWjYBACPgglJ8fG3n6AOC1sEMrYmI/nTAJpWhLnSTgYEKmF/+yxxxUVBultEgwJDD8qthFjy7l0wzNnDHLbpBsPMPacuU2EFsYeM8nGtj+5bTIHEpgZ24jRwswD0mKQziaRYECkFjaIlgQStPDwmBs2nDEwbAMG8kGi/MLPf8bsYUOFgbx8e/vBBz8qiNDCAI8aIDhAlHoULaNgFIyCUTAKsAIATMoyr3Fpg/IAAAAASUVORK5CYII=","orcid":"","institution":"Renmin Hospital of Wuhan University","correspondingAuthor":true,"submittingAuthor":false,"prefix":"","firstName":"Zuneng","middleName":"","lastName":"Lu","suffix":""}],"badges":[],"createdAt":"2021-09-25 06:29:04","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-936464/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-936464/v1","draftVersion":[],"editorialEvents":[{"content":"https://doi.org/10.1186/s12883-022-02567-8","type":"published","date":"2022-02-05T11:48:47+00:00"}],"editorialNote":"","failedWorkflow":false,"files":[{"id":17959841,"identity":"2e613e5a-33a1-48e5-ae5d-6bc3eb6636d1","added_by":"auto","created_at":"2022-02-05 11:48:49","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":430089,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-936464/v1/c72d16a5-0cf0-4897-a78e-58f4d963f838.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"\u003cp\u003eComparison of the Effects of Different Doses of Glucocorticoids on Distinct Subtypes of Guillain-Barré Syndrome in Southern China\u003c/p\u003e","fulltext":[{"header":"Introduction","content":"\u003cp\u003eGuillain-Barr\u0026eacute; syndrome (GBS) is an immune-mediated acute peripheral neuropathy involving mainly spinal nerve roots, peripheral nerves and cerebral nerves, and is currently the most common cause of acute flaccid paralysis worldwide.\u0026nbsp;As an\u0026nbsp;autoimmune disease\u0026nbsp;(AID) with a high rate of mortality and disability, immunotherapy is essential\u0026nbsp;[1,2].\u003c/p\u003e\n\u003cp\u003eGlucocorticoids\u0026nbsp;(GCs) is considered as the most commonly used drug for the treatment of AID worldwide because of its cost-effectiveness and strong immunosuppressive effect\u0026nbsp;[3]. Unfortunately, its use in GBS patients is controversial [4,5]. Clinical trials in Europe and North America did not observe significant efficacy of GCs alone in GBS, however, as it currently stands, the actual efficacy of GCs may be underestimated, because these above-mentioned studies did not discuss the efficacy of GCs in different subtypes in a categorical manner, and the use and dosage of GCs were not uniform [6-8]. Scholars such as Hughes have suggested that patients with GBS with conduction block respond well to GCs, while the use of GCs in patients with denervation delays the recovery of GBS, although the specific mechanism needs to be further explored [9].\u003c/p\u003e\n\u003cp\u003eAccording to neuroelectrophysiological studies, GBS consists of two major subtypes, acute inflammatory demyelinating polyneuropathy (AIDP), and acute motor axonal neuropathy (AMAN) [10]. AIDP is associated with macrophage and CD4\u003csup\u003e+\u003c/sup\u003e T cell-mediated inflammation and peripheral nerve demyelination, whereas AMAN is mainly associated with the involvement of ganglioside autoantibodies and complement [11]. Given that these two major subtypes have different pathological characteristics and pathogenesis, and their epidemiology in Asia differs from foreign studies, it is necessary to explore the mechanism of action and effects of GCs based on different subtypes.\u003c/p\u003e"},{"header":"Methods","content":"\u003ch2\u003ePatient ascertainment\u003c/h2\u003e\n\u003cp\u003eThis is a retrospective multicenter study\u0026nbsp;and the medical records of consecutive hospitalized patients with a diagnosis of GBS in 31 representative tertiary hospitals, located in 14 provinces in southern China, between 1 January 2013 and 30 September 2016, were collected. Patients who fulfilled the established clinical criteria of Asbury and Cornblath (1990) were enrolled [12]. In addition, the patients whose clinical presentation and ancillary data were typical of GBS except for preservation or exaggeration of reflexes were also included. Details regarding clinical data extraction and analysis, including inclusion and exclusion criteria, were described in our previous study [13]. Those patients with a diagnosis of AIDP or AMAN, including acute motor and sensory axonal neuropathy (AMSAN), and treated with GCs alone and symptomatic supportive treatment were analyzed. The study was approved by the ethics committee of the Renmin Hospital of Wuhan University, and the need for informed consent was waived.\u003c/p\u003e\n\u003ch2\u003eTreatment Grouping\u0026nbsp;\u003c/h2\u003e\n\u003cp\u003eThe high dose group patients received methylprednisolone (250\u0026ndash;1,000 mg/d) for 3-5 days and then tapered as clinically indicated; while the low dose group received methylprednisolone (40\u0026ndash;120 mg/d) for 3-5 days, or dexamethasone (10-20mg) for 5-7 days followed by a tapered dosage, or else oral prednisolone at 1 mg/kg/day for 1 week, tailed off over the next 2 months in a similar manner.\u003c/p\u003e\n\u003ch2\u003eInformation Extraction\u0026nbsp;\u003c/h2\u003e\n\u003cp\u003eInformation on age, sex, preceding events, initial symptoms, concomitant symptoms, severity at admission, at nadir, at discharge, length of hospitalization, findings of electrodiagnosis (EDX), treatment regime, types\u0026nbsp;and doses of GCs were extracted. The motor function deficits of included patients were assessed by the Hughes Functional Grading Scale, a widely accepted scale of disability for GBS (grade 6, dead; grade 5, requiring assisted respiration; grade 4, bed-bound; grade 3, able to walk with aid; grade 2, able to walk independently; grade 1, minimal signs and symptoms, able to run; grade 0, normal) [14]. Details regarding clinical data extraction were described in our previous study [13].\u003c/p\u003e\n\u003ch2\u003eStatistical analysis\u0026nbsp;\u003c/h2\u003e\n\u003cp\u003eStatistical analysis was performed using IBM SPSS 23.0 software. Categorical data were presented as proportions, and continuous data were presented as mean \u0026plusmn; standard deviation (SD). Differences in proportions were tested by the \u0026chi;2 tests. The continuous variables with a normal distribution were tested using the Student\u0026rsquo;s t-test or analysis of variance test, and the continuous variables with a skewed distribution were tested using the Mann-Whitney U test or the Kruskal-W allis analysis. For all statistical tests, P\u0026lt;0.05 was considered to be significant.\u003c/p\u003e"},{"header":"Results","content":"\u003ch2\u003eBaseline clinical characteristics\u003c/h2\u003e\n\u003cp\u003eFinally, 251 patients with a diagnosis of GBS, including 189 (75.3%) cases with AIDP and 62 (24.7%) cases with AMAN, were analyzed. Among whom 157 (62.5%) were men and 94 (37.5%) were women, and 168 (66.9%) patients came from rural areas. The mean age was 49.6 years (age range 17\u0026ndash;83 years). 133(53.0%) patients were treated with high-dose GCs, who received intravenous methylprednisolone (\u0026ge;250 mg) for 3-5 days, followed by gradual reduction to oral prednisone. 118 (47.0%) patients were treated with low-dose GC, including dexamethasone, prednisone, and low-dose methylprednisolone (\u0026lt; 250 mg). Two patients died during their hospital stay. The common autonomic symptoms of our patients included hypertension, cardiac arrhythmia, hypotension, orthostatic hypotension, sweating, bowel and bladder incontinence or retention.\u003c/p\u003e\n\u003ch2\u003e\u003cstrong\u003eEffects of GCs on the treatment of different subtypes (AIDP\u003c/strong\u003e \u003cspan class=\"BoldItalic\" name=\"Emphasis\" type=\"BoldItalic\"\u003evs\u003c/span\u003e \u003cstrong\u003eAMAN)\u003c/strong\u003e\u003c/h2\u003e\n\u003cp\u003eThere was no statistically significant difference between the two groups in terms of certain baseline characteristics, such as age, gender, urban-rural distribution, Hughes score on admission. As to complications and concomitant symptoms, autonomic dysfunctions and laboratory abnormality, for example, we found no significant difference between the two groups. However, facial/bulbar paralysis (45.5 \u003cem\u003evs\u003c/em\u003e 16.1, \u003cem\u003eP\u003c/em\u003e=0.000) and paresthesia (49.2 \u003cem\u003evs\u003c/em\u003e 32.3, \u003cem\u003eP\u003c/em\u003e=0.027) were more frequently observed in patients with AIDP, in whom hyperreflexia occurred less frequently (5.8 \u003cem\u003evs\u003c/em\u003e 19.3, \u003cem\u003eP\u003c/em\u003e=0.004). With regard to clinical outcomes, AIDP patients had a significantly lower Hughes score at discharge (2.51\u0026plusmn;0.98 \u003cem\u003evs\u003c/em\u003e 2.84\u0026plusmn;0.73, \u003cem\u003eP\u003c/em\u003e= 0.005) and 3 months after onset (2.06\u0026plusmn;1.14 \u003cem\u003evs\u003c/em\u003e 2.50\u0026plusmn;0.80, \u003cem\u003eP\u003c/em\u003e=0.000), compared to that in AMAN patients. (Table \u003cspan class=\"InternalRef\"\u003e1\u003c/span\u003e)\u0026nbsp;\u003c/p\u003e\u0026nbsp;\u003ctable border=\"1\" id=\"Tab1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e\n \u003cdiv class=\"CaptionContent\"\u003e\n \u003cp\u003eEffects of GCs on the treatment of different subtypes\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eParameters\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eAIDP(n=189)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eAMAN(n=62)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eP value (two-tailed)\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAge (years)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e49.88\u0026plusmn;18.07\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e48.61\u0026plusmn;17.46\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.631\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMale, n (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e123(65.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e34(54.9)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.174\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eRural area, n (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e125(66.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e43(69.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.756\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHughes score on admission (g)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.97\u0026plusmn;0.93\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3.10\u0026plusmn;0.88\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.451\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHughes score at nadir (g)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3.50\u0026plusmn;0.89\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3.71\u0026plusmn;0.69\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.155\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNeurological symptoms, n (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eFacial/bulbar paralysis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e86(45.5)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e10(16.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.000*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eOculomotor paralysis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e14(7.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3(4.8)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.771\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eParesthesia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e93(49.2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e20(32.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.027*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHyperreflexia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e11(5.8)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e12(19.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.004*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eComplication, n (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAutonomic dysfunction, n (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHypertension\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e38(20.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e11(17.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.854\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCardiac arrhythmia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e13(6.9)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7(11.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.283\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eUrinary retention\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e21(11.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e12(19.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.128\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eDeep venous thrombosis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7(3.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3(4.8)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.712\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eDyspnoea\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e49(25.9)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e10(16.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.124\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003ePulmonary infection\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e28(14.8)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e8(12.9)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.836\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eDiabetes\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e16(8.5)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e4(6.5)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.789\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eLaboratory abnormality, n (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHyponatraemia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e53(28.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e13(16.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.320\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHypokalemia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e42(22.2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e14(22.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e1.000\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHospital stay (days)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e14.18\u0026plusmn;8.10\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e15.35\u0026plusmn;7.29\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.221\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMechanical ventilation, n (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e19(10.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7(11.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.811\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eDeath in hospital stay, n (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1(0.5)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1(1.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.434\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHughes score at discharge (g)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.51\u0026plusmn;0.98\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.84\u0026plusmn;0.73\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.005*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHughes score of\u0026nbsp;3 months after onset (g)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.06\u0026plusmn;1.14\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.50\u0026plusmn;0.80\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.000*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003ctfoot\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"4\"\u003eValues are mean \u0026plusmn; standard deviation unless otherwise specified\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"4\"\u003eGCs Glucocorticoids, AIDP acute inflammatory demyelinating polyneuropathy, AMAN acute motor axonal neuropathy axonal neuropathy\u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tfoot\u003e\n\u003c/table\u003e\n\u003cp\u003e\u003c/p\u003e\n\u003cp\u003e\u003cbr\u003e\u003c/p\u003e\n\u003ch2\u003e\u003cstrong\u003eEffects of high-dose and low-dose GCs on the treatment of AIDP patients\u003c/strong\u003e\u003c/h2\u003e\n\u003cp\u003eA total of 189 AIDP patients were enrolled in this study, 98 (51.9%) of them were treated with high-dose GCs and 91 (48.1%) patients received low-dose GCs. There was no statistically significant difference between the two groups in terms of age, gender, urban-rural distribution, and Hughes score on admission. Notably, patients that received low-dose GCs had a higher frequency of pulmonary infection (9.2 \u003cem\u003evs\u003c/em\u003e 20.9, \u003cem\u003eP\u003c/em\u003e=0.026). Regarding to the clinical outcomes, patients in the high-dose group had a significantly shorter hospital stay (13.27\u0026plusmn;8.47 \u003cem\u003evs\u003c/em\u003e 15.16\u0026plusmn;7.62, \u003cem\u003eP\u003c/em\u003e=0.023), lower Hughes score at nadir (3.28\u0026plusmn;0.88 \u003cem\u003evs\u003c/em\u003e 3.74\u0026plusmn;0.74, \u003cem\u003eP\u003c/em\u003e=0.000), at discharge (2.36\u0026plusmn;1.03 \u003cem\u003evs\u003c/em\u003e 2.68\u0026plusmn;0.88, \u003cem\u003eP\u003c/em\u003e=0.005) and 3 months after onset (1.83\u0026plusmn;1.30 \u003cem\u003evs\u003c/em\u003e 2.30\u0026plusmn;0.89, \u003cem\u003eP\u003c/em\u003e=0.000), when compared with the low-dose group. During the hospitalization, one patient died. (Table \u003cspan class=\"InternalRef\"\u003e2\u003c/span\u003e)\u0026nbsp;\u003c/p\u003e\u0026nbsp;\u003ctable border=\"1\" id=\"Tab2\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv class=\"CaptionNumber\"\u003eTable 2\u003c/div\u003e\n \u003cdiv class=\"CaptionContent\"\u003e\n \u003cp\u003eEffects of high-dose and low-dose GCs on the treatment of AIDP\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eParameters\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eHigh-dose(n=98)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eLow-dose(n=91)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eP value(two-tailed)\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAge (mean, years)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e48.49\u0026plusmn;17.94\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e51.85\u0026plusmn;17.37\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.286\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMale, n (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e65(66.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e58 (63.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.761\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eRural area, n (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e62(63.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e63(69.2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.443\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHughes score on admission (mean, g)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.99\u0026plusmn;0.91\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.96\u0026plusmn;0.94\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.909\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHughes score at nadir (mean, g)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3.28\u0026plusmn;0.88\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3.74\u0026plusmn;0.74\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.000*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNeurological symptoms, n (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eFacial/bulbar paralysis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e47(47.8)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e39(42.9)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.559\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eOculomotor paralysis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e6(6.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e8(8.8)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.583\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eParesthesia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e42(42.9)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e51(56.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.081\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHyperreflexia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e6(6.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e5(5.5)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1.000\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eComplication, n (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAutonomic dysfunction\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHypertension\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e17(17.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e21(23.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.413\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCardiac arrhythmia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e6(6.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7(7.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.777\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eUrinary retention\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e9(9.2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e12(13.2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.488\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eDeep venous thrombosis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3(3.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e4(4.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.713\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eDyspnoea\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e28(28.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e21(23.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.411\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003ePulmonary infection\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e9(9.2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e19(20.9)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.026*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eDiabetes\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e9(9.2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7(7.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.797\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eLaboratory abnormality, n (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHyponatraemia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e22(22.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e31(34.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.105\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHypoalbuminaemia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e19(19.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e23(25.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.383\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHospital stay (days)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e13.27\u0026plusmn;8.47\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e15.16\u0026plusmn;7.62\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.023*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMechanical ventilation, n (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e11(11.2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e8(8.8)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.635\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eDeath in hospital stay, n (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1(1.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e-\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHughes score at discharge (g)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.36\u0026plusmn;1.03\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.68\u0026plusmn;0.88\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.005*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHughes score of\u0026nbsp;3 months after onset (g)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1.83\u0026plusmn;1.30\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.30\u0026plusmn;0.89\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.000*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003ctfoot\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"4\"\u003eValues are mean \u0026plusmn; standard deviation unless otherwise specified\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"4\"\u003eGCs Glucocorticoids, AIDP acute inflammatory demyelinating polyneuropathy\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"4\"\u003e* Significant difference between groups at p \u0026lt; 0.05\u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tfoot\u003e\n\u003c/table\u003e\n\u003cp\u003e\u003c/p\u003e\n\u003cp\u003e\u003cbr\u003e\u003c/p\u003e\n\u003ch2\u003e\u003cstrong\u003eEffects of high-dose and low-dose GCs on the treatment of AMAN patients\u003c/strong\u003e\u003c/h2\u003e\n\u003cp\u003eTotally, 62 patients with AMAN were enrolled in our study and received different treatment doses of GCs. No differences in baseline characteristics between groups were statistically significant. Concerning the short-term outcome, such as hospital stay (\u003cem\u003eP\u003c/em\u003e=0.943), Hughes score at nadir (\u003cem\u003eP\u003c/em\u003e=0.262), Hughes score at discharge (\u003cem\u003eP\u003c/em\u003e=0.591) and Hughes score at 3 months after onset (\u003cem\u003eP\u003c/em\u003e=0.386), the differences between the two groups were non-significant. (Table \u003cspan class=\"InternalRef\"\u003e3\u003c/span\u003e)\u003c/p\u003e\n\u003cdiv class=\"gridtable\"\u003e\u0026nbsp;\u003ctable border=\"1\" id=\"Tab3\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv class=\"CaptionNumber\"\u003eTable 3\u003c/div\u003e\n \u003cdiv class=\"CaptionContent\"\u003e\n \u003cp\u003eEffects of high-dose and low-dose GCs on the treatment of AMAN\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003ccolgroup cols=\"4\"\u003e\u003c/colgroup\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eParameters\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eHigh-dose(n=35)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eLow-dose(n=27)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eP value (two-tailed)\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAge (years)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e49.31\u0026plusmn;15.69\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e47.70\u0026plusmn;19.80\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.722\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMale, n (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e20(51.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e14(51.9)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.798\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eRural area, n (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e26 (74.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e17(63.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.805\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHughes score on admission (g)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3.11\u0026plusmn;0.93\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3.07\u0026plusmn;0.83\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.940\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHughes score at nadir (mean, g)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3.63\u0026plusmn;0.69\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3.81\u0026plusmn;0.68\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.262\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNeurological symptoms, n (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eFacial/bulbar paralysis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e4(11.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e6(22.2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.308\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eOculomotor paralysis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2(5.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1(3.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1.000\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eParesthesia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e12(34.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e8(29.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.788\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHyperreflexia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7(20.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e5(18.5)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1.000\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eComplication, n (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAutonomic dysfunction\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHypertension\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e6(17.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e5(18.5)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.735\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCardiac arrhythmia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e4(11.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3(11.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1.000\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eUrinary retention\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e5(14.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7(25.9)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.335\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eDeep venous thrombosis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1(2.9)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2(7.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.575\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eDyspnoea\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e4(11.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e6(22.2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.308\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003ePulmonary infection\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3(8.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e5(18.5)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.279\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eDiabetes\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3(8.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1(3.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.626\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eLaboratory abnormality, n (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHyponatraemia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e6(17.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7(25.9)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.532\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHypoalbuminaemia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e9(25.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e5(18.5)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.555\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHospital stay (days)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e15.66\u0026plusmn;8.11\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e14.96\u0026plusmn;6.20\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.943\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMechanical ventilation, n (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3(8.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e4(14.9)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.689\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eDeath in hospital stay, n (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1(5.00)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e-\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHughes score at discharge (g)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.80\u0026plusmn;0.76\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.89\u0026plusmn;0.70\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.591\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHughes score of\u0026nbsp;3 months after onset (g)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.43\u0026plusmn;0.74\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.59\u0026plusmn;0.89\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.386\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003ctfoot\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"4\"\u003eValues are mean \u0026plusmn; standard deviation unless otherwise specified\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"4\"\u003eGCs Glucocorticoids, AMAN acute motor axonal neuropathy axonal neuropathy\u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tfoot\u003e\n \u003c/table\u003e\n\u003c/div\u003e\n\u003cp\u003e\u003cbr\u003e\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eOur first multi-center study showed that the Hughes score at discharge and 3 months after onset were significantly lower in AIDP patients treated with GCs compared to that in AMAN patients. Further analysis found that among AIDP patients, the high-dose group had shorter hospitalization days and significantly lower Hughes score at nadir, at discharge and 3 months after onset than that in the low-dose group. However, among AMAN patients, according to our data, the short-term outcome in the high-dose group was not significantly different from that in the low-dose group.\u003c/p\u003e \u003cp\u003eIn regarding to complications, we found that, among AIDP patients, the incidence of pulmonary infections was higher in the low-dose group, which we speculated that the longer hospital stay of patients in the low-dose group may account. Because, as the length of hospital stay increases, says from some kind of significance, the effective activity of patients decreases and the risk of pathogenic bacteria infection greatly increases [\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e]. On the other side, studies have demonstrated that patients with refractory pulmonary treated with high-dose corticosteroid could achieve defervescence earlier and have a shorter hospitalization [\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eThese data above suggest that we can\u0026rsquo;t dismiss wholesale the role of GCs in the treatment of GBS, subtyping to explore the effects of different doses of GCs on GBS treatment is necessary. After all, in China, especially in the 1990s, GCs were the drug of choice in the treatment of GBS because of their civilian price, and clinical observations found good results in many patients [\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eA study used a rabbit model of the axonal form of GBS initially explored the reasons for the ineffectiveness of GCs in treating AMAN, suggesting that MPS did not reduce complement C3 deposition and sodium (Nav) channel disruption, but significantly reduced macrophage infiltration in the ventral roots and thus delay the axonal regeneration [\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e]. Studies of pathophysiology about AMAN have shown that macrophages invasion was rare at the acute progressive phase but significantly more frequent at the site of inflammation mainly during the recovery phase, which suggested a role for macrophages in the clearance of damaged myelin and axon fragments and promoting nerve repair and regeneration [\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e]. Whereas, the classical experimental autoimmune neuritis (EAN) model, which highly replicates human AIDP in terms of clinical manifestations, immunology, histopathology, and electrophysiology [\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e], indicated that \u0026ldquo;Classically\u0026rdquo; activated (M1) macrophages mainly accumulated at the acute phase of EAN and promoted the inflammatory response, while during the recovery phase, macrophages could change their expression profile, M2 macrophages attenuated inflammation and promoted tissue repair [\u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e, \u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e]. Ultrastructural studies showed that macrophage-mediated nerve injury was a pathological hallmark of AIDP/EAN [\u003cspan additionalcitationids=\"CR22\" citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e]. Macrophages (M1) were involved in this process by regulating cytokines, chemokines, adhesion molecules, NO and matrix metalloproteinases (MMPs), and as major antigen-presenting and effector cells, macrophages played a key role in EAN pathogenesis by expressing antigens and promoting Th1 and Th17 polarization [\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eIn summary, we hypothesize that the different mechanisms of macrophages' role in the inflammatory response of AIDP and AMAN may lead to different effects of GCs therapy. We will further test our hypothesis through animal experiments.\u003c/p\u003e \u003cp\u003eAs a multicenter study, we derived relatively powerful results, but there exists inevitably some limitations. First, as a retrospective study, the long-term follow-up information was insufficient to further explore the prognosis of patients with different subtypes treated with different doses of GCs, further studies were anticipated; Second, the number of patients with AMAN subtypes in this study was relatively small; Third, because the study was a retrospective review of medical records and database, extracting bias was unavoidable. However, in order to reduce the bias as much as possible, a unified parameter standard in the analysis of NCS was adopted and data were extracted by our team members through strict training.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eIn conclusion, our data firstly provides information about whether the responses to GCs differ between the principal subtypes of GBS, and prompts recommendations about the design of future GBS trails. GCs induce different effects in specific GBS subtypes, among which high-dose GCs therapy has a better prognosis for patients with AIDP. The effects of GCs on GBS subtypes should be discussed separately in future clinical trials to explore its mechanism of action and provide more timely and effective treatment measures for GBS patients.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003eGCs, Glucocorticoids; GBS, Guillain-Barr\u0026eacute; syndrome; AIDP, acute inflammatory demyelinating polyneuropathy; AMAN, acute motor axonal neuropathy; AMSAN, acute motor and sensory axonal neuropathy; AID, autoimmune disease; SD, standard deviation; EAN, experimental autoimmune neuritis; MMPS, matrix metalloproteinases.\u003c/p\u003e"},{"header":"Declarations","content":"\u003ch2\u003eEthics approval and consent to participate\u0026nbsp;\u003c/h2\u003e\n\u003cp\u003eThis retrospective study was approved by the ethics committee\u0026nbsp;of the Renmin Hospital of Wuhan University and conducted in accordance with the principles of the Declaration of Helsinki. The requirement for informed consent was waived by the ethics committee of the Renmin Hospital of Wuhan University because the analysis was retrospective.\u003c/p\u003e\n\u003ch2\u003eConsent for publication\u0026nbsp;\u003c/h2\u003e\n\u003ch2\u003eNot applicable.\u003c/h2\u003e\n\u003ch2\u003eAvailability of data and materials\u0026nbsp;\u003c/h2\u003e\n\u003cp\u003eThe datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.\u003c/p\u003e\n\u003ch2\u003eCompeting interests\u0026nbsp;\u003c/h2\u003e\n\u003cp\u003eThe authors declare that they have no competing interests.\u003c/p\u003e\n\u003ch2\u003eFunding\u0026nbsp;\u003c/h2\u003e\n\u003cp\u003eThis work was supported by grants from the Independent scientific research project of Wuhan University (2042020kf0053) and the National Natural Science Foundation of China (81971055).\u0026nbsp;\u003c/p\u003e\n\u003ch2\u003eAuthors\u0026apos; contributions\u0026nbsp;\u003c/h2\u003e\n\u003cp\u003eZX, JG and ZL took part in validating the diagnosis and information extraction; YL and JY involved in data collection and analysis, LM and SL contributed to the study design, data collection and analysis, and wrote the manuscript. All authors read and approved the final manuscript.\u003c/p\u003e\n\u003ch2\u003eAcknowledgements\u0026nbsp;\u003c/h2\u003e\n\u003cp\u003eNot applicable.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003evan den Berg B, Walgaard C, Drenthen J, Fokke C, Jacobs BC, van Doorn PA. Guillain-Barr\u0026eacute; syndrome: pathogenesis, diagnosis, treatment and prognosis. Nat Rev Neurol 10(8):469\u0026ndash;82. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1038/nrneurol.2014.121\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSipil\u0026auml; JOT, Soilu-H\u0026auml;nninen M, Ruuskanen JO, Rautava P, Kyt\u0026ouml; V. Epidemiology of Guillain-Barr\u0026eacute; syndrome in Finland 2004-2014. J Peripher Nerv Syst 22(4):440\u0026ndash;445. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1111/jns.12239\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eStraub RH, Cutolo M. Glucocorticoids and chronic inflammation. Rheumatology (Oxford) 55(suppl 2):ii6-ii14. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps:// doi.org/10.1093/rheumatology/kew348\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHughes RA. Treatment of Guillain-Barr\u0026eacute; syndrome with corticosteroids: lack of benefit? Lancet 363(9404):181\u0026ndash;2\u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e.https://doi.org/10.1016/S0140-6736(03)15367-6\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMastaglia FL. Neuromuscular disorders: molecular and therapeutic insights. Lancet Neurol 4(1):6\u0026ndash;7. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1016/S1474-4422(04)00946-9\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWalgaard C, Lingsma HF, Ruts L, van Doorn PA, Steyerberg EW, Jacobs BC. Early recognition of poor prognosis in Guillain-Barre syndrome. Neurology 76(11):968\u0026ndash;75. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1212/WNL.0b013e3182104407\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDouble-blind trial of intravenous methylprednisolone in Guillain-Barr\u0026eacute; syndrome. Guillain-Barr\u0026eacute; Syndrome Steroid Trial Group. Lancet. 1993;341(8845):586\u0026ndash;90.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003evan Koningsveld R, Schmitz PI, Mech\u0026eacute; FG, Visser LH, Meulstee J, van Doorn PA; Dutch GBS study group. Effect of methylprednisolone when added to standard treatment with intravenous immunoglobulin for Guillain-Barr\u0026eacute; syndrome: randomized trial. Lancet 363(9404):192\u0026ndash;6. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1016/s0140-6736(03)15324-x\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHughes RA, Brassington R, Gunn AA, van Doorn PA. Corticosteroids for Guillain-Barr\u0026eacute; syndrome. Cochrane Database Syst Rev 10(10):CD001446. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1002/14651858.CD001446.pub5\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMalek E, Salameh J. Guillain-Barre Syndrome. Semin Neurol 39(5):589\u0026ndash;595. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1055/s-0039-1693005\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eFan X, Zhang H, Cheng Y, Jiang X, Zhu J, Jin T. Double Roles of Macrophages in Human Neuroimmune Diseases and Their Animal Models. Mediators Inflamm 2016:8489251. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1155/2016/8489251\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eAsbury AK, Cornblath DR. Assessment of current diagnostic criteria for Guillain-Barr\u0026eacute; syndrome. Ann Neurol 27 Suppl: S21-4. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1002/ana.410270707\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLiu S, Xiao Z, Lou M, Ji F, Shao B, Dai H, et al. Guillain-Barr\u0026eacute; syndrome in southern China: retrospective analysis of hospitalised patients from 14 provinces in the area south of the Huaihe River. J Neurol Neurosurg Psychiatry 89(6):618\u0026ndash;626. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1136/jnnp-2017-316930\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHughes RA, Newsom-Davis JM, Perkin GD, Pierce JM. Controlled trial prednisolone in acute polyneuropathy. Lancet 2(8093):750\u0026ndash;3. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1016/s0140-6736(78)92644-2\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKuderer NM, Dale DC, Crawford J, Cosler LE, Lyman GH. Mortality, morbidity, and cost associated with febrile neutropenia in adult cancer patients. Cancer 106(10):2258\u0026ndash;66. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1002/cncr.21847\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eOkumura T, Kawada JI, Tanaka M, Narita K, Ishiguro T, Hirayama Y, et al. Comparison of high-dose and low-dose corticosteroid therapy for refractory Mycoplasma pneumoniae pneumonia in children. J Infect Chemother 25(5):346\u0026ndash;350. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1016/j.jiac.2019.01.003\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eCheng Q, Wang DS, Jiang GX, Han H, Zhang Y, Wang WZ, et al. Prospective study of clinical epidemiology of Guillain-Barr\u0026eacute; syndrome in Harbin, China. J Neurol Sci 215(1-2):63\u0026ndash;9. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1016/s0022-510x(03)00187-4\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWang YZ, Lv H, Shi QG, Fan XT, Li L, Yi Wong AH, Hao YL, Si CP, Li CL, Yuki N. Action mechanism of corticosteroids to aggravate Guillain-Barr\u0026eacute; syndrome. Sci Rep 5:13931. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1038/srep13931\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSusuki K, Rasband MN, Tohyama K, Koibuchi K, Okamoto S, Funakoshi K, Hirata K, Baba H, Yuki N. Anti-GM1 antibodies cause complement-mediated disruption of sodium channel clusters in peripheral motor nerve fibers. J Neurosci 27(15):3956\u0026ndash;67. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1523/JNEUROSCI.4401-06.2007\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGonsalvez DG, Fletcher JL, Yoo SW, Wood RJ, Murray SS, Xiao J. A Simple Approach to Induce Experimental Autoimmune Neuritis in C57BL/6 Mice for Functional and Neuropathological Assessments. J Vis Exp (129): 56455. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.3791/56455\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eShen D, Chu F, Lang Y, Geng Y, Zheng X, Zhu J, Liu K. Beneficial or Harmful Role of Macrophages in Guillain-Barr\u0026eacute; Syndrome and Experimental Autoimmune Neuritis. Mediators Inflamm 2018:4286364. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1155/2018/4286364\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHartung HP, Sch\u0026auml;fer B, Heininger K, Stoll G, Toyka KV. The role of macrophages and eicosanoids in the pathogenesis of experimental allergic neuritis. Serial clinical, electrophysiological, biochemical and morphological observations. Brain 111 (Pt 5):1039\u0026ndash;59. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1093/brain/111.5.1039\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKiefer R, Kieseier BC, Stoll G, Hartung HP. The role of macrophages in immune-mediated damage to the peripheral nervous system. Prog Neurobiol 64(2):109\u0026ndash;27. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1016/s0301-0082(00)00060-5\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHan R, Xiao J, Zhai H, Hao J. Dimethyl fumarate attenuates experimental autoimmune neuritis through the nuclear factor erythroid-derived 2-related factor 2/hemoxygenase-1 pathway by altering the balance of M1/M2 macrophages. J Neuroinflammation 13(1):97. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1186/s12974-016-0559-x\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-neurology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"nurl","sideBox":"Learn more about [BMC Neurology](http://bmcneurol.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/nurl","title":"BMC Neurology","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Guillain-Barré syndrome, Glucocorticoids, Southern China, subtype","lastPublishedDoi":"10.21203/rs.3.rs-936464/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-936464/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cstrong\u003eBackground\u003c/strong\u003e\u003c/p\u003e\u003cp\u003eThe effect of Glucocorticoids (GCs) on the treatment of Guillain-Barré syndrome (GBS) has been controversial. There is no information on whether specific subtypes of GBS respond differently to GCs. In this setting, we aimed to discuss whether GCs treating yield different effects in the distinct subtypes (acute inflammatory demyelinating polyneuropathy, AIDP; acute motor axonal neuropathy, AMAN). And further, we analyzed the impact of different doses on the outcome.\u003c/p\u003e\u003cp\u003e\u003cstrong\u003eMethods\u003c/strong\u003e\u003c/p\u003e\u003cp\u003eMedical records of patients with a diagnosis of GBS (AIDP \u0026amp; AMAN) admitted to 31 tertiary hospitals, located in 14 provinces of Southern China, from 1 January 2013 to 30 September 2016, were retrospectively collected. And those patients treated with GCs alone were reviewed and analyzed.\u003c/p\u003e\u003cp\u003e\u003cstrong\u003eResults\u003c/strong\u003e\u003c/p\u003e\u003cp\u003eFinally, 251 classic patients with available electromyographic data were collected, including AIDP (n=189) and AMAN (n=62). After GCs treatment, the Hughes score of AIDP patients was significantly lower than that of AMAN patients at discharge (\u003cem\u003eP\u003c/em\u003e=0.005) and 3 months after onset (\u003cem\u003eP\u003c/em\u003e=0.000). Further analysis revealed that among AIDP patients, the high-dose group had significantly shorter hospital stay (\u003cem\u003eP\u003c/em\u003e=0.023), lower Hughes score at nadir (\u003cem\u003eP\u003c/em\u003e=0.000), at discharge (\u003cem\u003eP\u003c/em\u003e=0.005), and 3 months after onset (\u003cem\u003eP\u003c/em\u003e=0.000), compared with the low-dose group. However, for AMAN patients, the outcome difference between groups was nonsignificant.\u003c/p\u003e\u003cp\u003e\u003cstrong\u003eConclusion\u003c/strong\u003e\u003c/p\u003e\u003cp\u003eOur data suggest that the high doses of GCs may result, at least in part, from the side of the duration of hospital stay and short-term outcome, favorable outcomes in AIDP patients. Therefore, we cannot completely deny the priority of GCs in the treatment of GBS, because the effect of different doses of GCs varies in treating different subtypes. More studies are needed in the future to further validate this issue.\u003c/p\u003e\u003cp\u003e\u003cstrong\u003eTrial registration\u003c/strong\u003e: ChiCTR-RRC-17014152. Registered 26 December 2017- Retrospectively registered.\u003c/p\u003e","manuscriptTitle":"Comparison of the Effects of Different Doses of Glucocorticoids on Distinct Subtypes of Guillain-Barré Syndrome in Southern China","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2021-10-20 16:22:24","doi":"10.21203/rs.3.rs-936464/v1","editorialEvents":[{"type":"communityComments","content":2},{"type":"decision","content":"Major revision","date":"2021-12-16T19:27:36+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2021-12-15T02:44:16+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"e851a24c-d539-49f5-a9da-e29721346731","date":"2021-12-10T01:41:55+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2021-11-01T00:29:39+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"96225901-e2c7-4674-bbc6-77e94fa6c078","date":"2021-10-29T21:04:29+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2021-10-19T07:52:00+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2021-10-19T07:01:33+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2021-10-18T15:48:25+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2021-10-18T15:31:04+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Neurology","date":"2021-09-25T06:15:29+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"bmc-neurology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"nurl","sideBox":"Learn more about [BMC Neurology](http://bmcneurol.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/nurl","title":"BMC Neurology","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"a0647cf9-6dea-4c20-8c1a-78ba61a86869","owner":[],"postedDate":"October 20th, 2021","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"published-in-journal","subjectAreas":[{"id":7982943,"name":"Neurobiology of Disease"}],"tags":[],"updatedAt":"2022-02-05T11:48:47+00:00","versionOfRecord":{"articleIdentity":"rs-936464","link":"https://doi.org/10.1186/s12883-022-02567-8","journal":{"identity":"bmc-neurology","isVorOnly":false,"title":"BMC Neurology"},"publishedOn":"2022-02-05 11:48:47","publishedOnDateReadable":"February 5th, 2022"},"versionCreatedAt":"2021-10-20 16:22:24","video":"","vorDoi":"10.1186/s12883-022-02567-8","vorDoiUrl":"https://doi.org/10.1186/s12883-022-02567-8","workflowStages":[]},"version":"v1","identity":"rs-936464","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-936464","identity":"rs-936464","version":["v1"]},"buildId":"7rjqhiLT3MXkJMwkYKINL","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}