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1.
31例格林—巴利综合征病因学研究   总被引:1,自引:1,他引:0  
目的 检测急性感染性多发性神经根炎(GBS)病儿急性期、恢复期血清及脑脊液抗空肠弯曲菌(CJ)IgG抗体,探讨GBS的病因。方法 采用酶联免疫吸附试验方法研究31例GBS病儿急性期、恢复期血清及脑脊液中抗CJ IgG抗体,设立两组对照组,即非GBS神经系统疾病组和正常组。结果 GBS病儿急性期、恢复期血清抗CJ IgG抗体水平均高于两组对照组,脑脊液抗CJ IgG抗体水平高于对照组(P<0.01)。结论 东北地区空肠弯曲菌感染与GBS的发病有关,尤其是与GBS亚型急性运动轴索神经病(AMAN)发病密切相关。  相似文献   

2.
目的探索空肠弯曲菌(CJ)诱导周围神经损伤的关键抗原结构,为CJ诱发Guillain-Barré综合征的分子模拟理论提供免疫学证据。方法利用CJ亲代株(含脂寡糖及神经节苷脂结构)及waaF变异株(缺失脂寡糖及神经节苷脂结构)作为抗原,进行对照研究。将26只日本大耳兔随机分为CJ亲代株组(10只)、waaF变异株组(10只)、对照组(6只),分别用亲代株CJ、waaF变异株及免疫佐剂,对3组动物进行全身免疫。ELISA动态检测3组动物血清中神经节苷脂GM1-IgG抗体变化;于8周末,取动物坐骨神经进行免疫荧光检查,包括神经节苷脂(GM1)表达、GM1-IgG抗体及补体C3c的检查;对动物坐骨神经进行单纤维分离,检查病理形态学改变。结果①亲代株组动物免疫后2周,血清中抗GM1-IgG抗体滴度增高,4周进一步增高,6周达高峰,高于免疫前的4倍,持续到8周未见明显下降;waaF变异株和对照组免疫后未见抗GM1-IgG抗体增高。②免疫荧光检查显示3组动物坐骨神经均见GM1特异性配体-霍乱毒素B亚单位(CTB)在髓鞘及Ranvier结处不同程度染色。亲代株组4只动物坐骨神经Ranvier结处可见GM1-IgG抗体沉积及补...  相似文献   

3.
格林巴利综合征(GuillainBarreSyndrome,GBS)是一种常见的周围神经疾病,发病机制迄今未明。若干报道证明与感染后自身免疫反应有关。近年来某些类型空肠弯曲菌(CJ)感染后发生GBS的现象引起人们的密切关注。不少研究者认为:机体感染CJ后产生的特异性CJ抗体与具有相同表位的神经节苷脂发生抗原抗体反应而导致GBS,其中也有细胞免疫介导。此外可能还与GBS易患基因有关。本文将近年有关研究综述如下。  相似文献   

4.
目的 探讨空肠弯曲菌(CJ)脂寡糖结构是否为诱导周围神经传导阻滞的关键抗原结构,为cJ诱发Guillain-Barre综合征(GBS)的分子模拟理论提供证据.方法 利用CJ亲代株(含脂寡糖及神经节苷脂结构)及waaF变异株(缺失脂寡糖及神经节苷脂结构)作为抗原,进行对照研究.将26只日本大耳兔随机分为CJ亲代株组(10只)、waaF变异株组(10只)及对照组(6只),分别用亲代株CJ、waaF变异株及免疫佐剂,对3组动物进行全身免疫.ELISA动态检测3组动物血清神经节苷脂GMI-IgG抗体变化;于免疫前及免疫后4、8周进行神经电生理检查,包括坐骨神经复合肌肉动作电位(CMAP)、坐骨神经传导速度(MCV)、F波潜伏期及肌电图变化.结果 1.亲代株组动物免疫后2周,血清抗GMI-IgG抗体滴度增高,4周进一步增高,6周达高峰,高于免疫前的4倍,持续到8周未见明显下降;waaF变异株组免疫后未见增高.2.电生理检查显示:免疫前3组动物坐骨神经近、远端CMAP波幅无明显差异;免疫后4周,亲代株组动物坐骨神经近、远端CMAP波幅较免疫前明显降低,差异显著(Pa<0.05);8周时近、远端CMAP波幅较4周进一步下降,但差异不显著(Pa >0.05);变异株组坐骨神经近、远端CMAP波幅在4、8周时与免疫前无明显差异,与对照组各时段比较,波幅也无明显差异;3组动物坐骨神经MCV在免疫前、免疫后4、8周均无明显差异(Pa >0.05);3组动物坐骨神经F波潜伏期在免疫前后也无明显差异(Pa >0.05).3.肌电图显示:33.3%亲代株组动物4、8周时腓肠肌见纤颤电位和正尖波;变异株组及对照组未见明显异常波.结论 CJ外膜脂寡糖上神经节苷脂结构是诱导动物GMI抗体及轴索型周围神经传导阻滞的关键结构,支持CJ感染相关轴索型GBS的分子模拟发病理论.  相似文献   

5.
目的探讨空肠弯曲菌(CJ)脂多糖(LPS)中唾液酸(SA)基团参与q诱发周围神经病关键性抗原成分的重要地位,为CJ LPS与神经节苷脂间的分子模拟推论确立免疫病理学证据。方法构建唾液酸合成酶基因1(neuB1)失活、LPS外核寡糖缺乏SA基团的GBS相关CJ O:19变异株。分别以野生株和变异株LPS全身免疫豚鼠,ELISA法检测免疫血清中抗CJ LPS和抗神经节苷脂GM1 IgG抗体,取坐骨神经作病理学检查。再将免疫血清行坐骨神经外膜下注射并作病理学检查。结果(1)Pen O:19 CJ变异株的neuB1失活、LPS中SA基团缺失;(2)野生株LPS和变异株LPS全身免疫后,豚鼠均产生高滴度抗LPS特异性IgG;(3)全身免疫后第21、35天,野生株LPS免疫血清中检测到抗GM1 IgG抗体,而变异株LPS免疫血清中却测不到该抗体;(4)野生株LPS组中有17.3%的坐骨神经原纤维发生以轴索变性为主(占65.0%)的免疫性损伤,与变异株LPS组比较差异有统计学意义(X^2=125,P〈0.01)。而变异株LPS组病变率仅2.4%,与对照组比较差异没有统计学意义(P〉0.05);(5)野生株LPS免疫血清神经外膜下注射后,67.8%的豚鼠坐骨神经原纤维发生以轴索变性为主(占68.0%)的病变,而变异株LPS免疫血清注射后仅3.2%的神经原纤维发生病变,差异具有统计学意义(P〈0.01)。结论外核寡糖缺乏SA基团的GBS相关CJO:19变异株LPS不再能使实验动物血清中产生高滴度的抗GM1抗体,同时丧失对周围神经的免疫致病力,表明含SA基团的LPS寡糖侧链,是GJ诱发周围神经病的GM1样关键性抗原,从免疫病理学角度证实有关GJ诱发GBS的分子模拟推论。  相似文献   

6.
目的探索空肠弯曲菌(Campylobactejejuni,CJ)致外周神经损伤的关键结构,为CJ感染相关格林巴利综合征的分子模拟理论提供动物实验证据。方法将32只豚鼠随机分为亲代株组(10只)、变异株组(10只)、对照组(6只)、PBS组(6只),分别用亲代株及弗氏佐剂、galE变异株及弗氏佐剂、PBS及弗氏佐剂、单纯PBS进行全身免疫;动态检测血清细胞壁脂寡糖(LOS)IgG及神经节苷脂GM1IgG抗体水平;检查坐骨神经病理改变,包括单纤维分离、半薄切片光镜及电镜检查。结果①免疫后变异株组及亲代株组LOSIgG抗体水平均明显增高,两组间差异无统计学意义;②免疫后14、28d,亲代株组GM1IgG抗体滴度(0.661±0.290,0.984±0.025)明显高于变异株组(0.193±0.078,0.180±0.063),差异均有统计学意义;③变异株组坐骨神经单纤维病变率4.9%(98/2000),明显低于亲代株组(16%,320/2000),差异有统计学意义,后者主要为轴索变性;④亲代株组半薄切片显示以轴索变性为特征的病理改变;变异株组仅见极少数异常,两组间差异有统计学意义;⑤电镜检查证实光镜所见。结论与亲代株相比,galE变异株缺失神经节苷脂GM1样表位,不能诱导动物产生GM1抗体及周围神经损伤,支持CJ感染后格林巴利综合征发生的分子模拟理论。  相似文献   

7.
目的探讨合并血浆单唾液酸神经节苷脂(GM1)抗体阳性的急性脊髓炎(AM)患儿的临床特点及治疗。方法回顾分析2例患儿的临床资料,并随访3个月;同时复习相关文献。结果 2例AM患儿,男女各1例,均为5岁,均有脊髓炎表现并伴有影像学改变,血清GM1-IgM和甲状腺抗体均为阳性,同时血清幽门螺杆菌抗体IgG阳性,1例肺炎支原体IgM抗体阳性。大剂量激素及丙球治疗后均好转出院。院外继续口服泼尼松并康复治疗,随访3个月后1例恢复,1例可下肢承重。结论免疫损伤在伴有GM1抗体阳性的儿童急性脊髓炎发病中有重要作用,其临床治疗效果及预后较好。  相似文献   

8.
目的探讨合并血浆单唾液酸神经节苷脂(GM1)抗体阳性的急性脊髓炎(AM)患儿的临床特点及治疗。方法回顾分析2例患儿的临床资料,并随访3个月;同时复习相关文献。结果 2例AM患儿,男女各1例,均为5岁,均有脊髓炎表现并伴有影像学改变,血清GM1-IgM和甲状腺抗体均为阳性,同时血清幽门螺杆菌抗体IgG阳性,1例肺炎支原体IgM抗体阳性。大剂量激素及丙球治疗后均好转出院。院外继续口服泼尼松并康复治疗,随访3个月后1例恢复,1例可下肢承重。结论免疫损伤在伴有GM1抗体阳性的儿童急性脊髓炎发病中有重要作用,其临床治疗效果及预后较好。  相似文献   

9.
Liu C  Cai FC  Li Q  Li L  Yin P 《中华儿科杂志》2004,42(4):308-309
慢性炎症性脱髓鞘多发性神经病(chronic inflammatory demyelinating polyradjculoPathy,CIDP)是一种严重危害儿童健康的慢性周围神经病。其病因和发病机制尚不明了。1996年以来,我们在对四川川中地区急性感染性多发性神经根炎(CBS)的病因学研究中发现1例CIDP。患儿,经对其家庭成员和家禽家畜大便中空肠弯曲菌(camtpylobaeter JejuIIi,CJ)培养和质粒分析、  相似文献   

10.
急性感染性多发性神经根炎(AIP)至今仍无有效的特异性治疗方法,虽然激素疗法已应用于临床30多年,但对其疗效仍不能肯定。兹将我院儿科于1987年用大剂量甲基强的松龙冲击疗法治疗2例重症GBS报告如下。  相似文献   

11.
目的 探讨运动神经传导阻滞(CB)与儿童吉兰-巴雷综合征(GBS)不同亚型间的关系。方法 回顾性分析50例GBS患儿的临床资料和神经电生理资料,根据神经电生理结果分为2型:急性炎症性脱髓鞘性多发性神经根神经病(AIDP,n=29)和急性运动轴索型神经病(AMAN,n=21)。根据有无运动神经CB分为伴有运动神经CB的AMAN(n=10)、不伴有运动神经CB的AMAN(n=11)、伴有运动神经CB的AIDP(n=19)和不伴有运动神经CB的AIDP(n=10)。比较各组间患儿起病年龄、性别、疾病高峰期休斯功能分级量表(HFGS)评分、短期预后(起病1个月后HFGS评分)。结果 AMAN中,运动神经CB均为可逆性。伴有运动神经CB的AMAN的起病1个月后HFGS评分低于不伴有运动神经CB的AMAN(P < 0.05),伴有运动神经CB的AIDP的起病1个月后HFGS评分高于伴有运动神经CB的AMAN(P < 0.05)。结论 伴有可逆性运动神经CB的AMAN提示神经纤维病变轻微,短期预后较不伴有运动神经CB的AMAN和AIDP恢复快。  相似文献   

12.
Aim:   Guillain–Barré syndrome (GBS) is an acute inflammatory polyneuropathy commonly characterised by rapidly progressive, symmetric weakness and areflexia. This study is to assess the clinical characteristics of paediatric GBS, as well as its long-term functional prognosis.
Methods:   We retrospectively assessed the clinical manifestations, results of electrodiagnostic tests, functional status and prognosis of 56 children diagnosed with GBS. Based on clinical and electrophysiological findings, the patients were classified as having acute inflammatory demyelinating polyradiculoneuropathy ([AIDP] n  = 34), acute motor axonal neuropathy ([AMAN] n  = 14), acute motor and sensory axonal neuropathy ( n  = 1) and Miller Fisher syndrome ([MFS] n  = 7).
Results:   Upper respiratory infection was the most frequent preceding event, and limb weakness was the most frequent symptom at GBS onset. There was no significant difference in the mean time from the onset of illness to nadir between any of these groups. Both the AIDP and AMAN groups showed significantly poorer functional status, measured by the Hughes scale, than the MFS group. Two years after nadir, however, the three groups did not differ significantly. Functional status at nadir, as estimated by the Hughes scale, is a more important factor than electrophysiological types in predicting long-term outcome.
Conclusion:   The most common symptom at onset in paediatric GBS was limb weakness. Functional status at nadir in AMAN was not significantly different from that of AIDP, and both types achieved good functional outcome for ambulation after 2 years. Functional status at nadir was more important than the electrophysiological type in predicting long-term outcomes.  相似文献   

13.
目的 探讨不同类型儿童吉兰-巴雷综合征(GBS)的临床特点及丙种球蛋白(IVIG)的治疗效果.方法 回顾性分析了我科近5年住院诊治的108例GBS患儿,其中本组75例患儿均在急性期应用大剂量IVIG 400 mg/(kg·d)静点治疗5 d,收集患儿的临床、电生理资料和治疗效果,并对患儿病情恢复进行随访.结果 75例GBS患儿中急性运动性轴索型GBS(AMAN)34例(45.3%),急性炎症性脱髓鞘多发性神经病(AIDP)32例(42.7%),急性运动感觉性轴索型GBS(AMSAN)3例(4.0%),神经失电位型4例(5.3%),难以分类2例(2.7%).AIDP型起病达病情高峰时间明显比AMAN型长,差异有统计学意义(t=3.4042,P<0.01);病情高峰时Hughes功能障碍评分,AIDP和AMAN型差异无统计学意义(x2=1.5997,P>0.05).二者在呼吸肌麻痹、颅神经麻痹及植物神经症状方面差异无统计学意义;AIDP型患儿感觉障碍症状明显多于AMAN型,二者差异有统计学意义(x2=6.0475,P<0.05).经IVIG治疗后AIDP和AMAN型肌力开始改善平均时间分别为(5.59±3.63)、(7.21±4.68)d,二者经治疗肌力开始改善时间AIDP型较AMAN型短,但差异没有统计学意义(t=-1.5702,P>0.05);肌力提高1级所需时间AIDP和AMAN型分别为(8.88±4.39)、(12.67±8.35)d,二者经治疗肌力提高一级的时间AIDP型比AMAN短4 d左右,差异有统计学意义(t=-2.3689,P<0.05).本组无1例死亡,随访调查的病例中AIDP型和AMAN型治疗后完全恢复时间差异无统计学意义(t=0.2041,P>0.05).结论 AMAN型患儿临床进展速度较AIDP型快,除感觉神经受累方面AIDP型多于AMAN型患儿外,二者在肌无力严重程度、呼吸肌麻痹、颅神经麻痹及植物神经受累方面无明显差异.经IVIG治疗AIDP型临床恢复比AMAN型快,但AIDP和AMAN型长期预后无明显差异.
Abstract:
Objective To study the clinical characteristics and effects of immunoglobulin treatment hospitalized for GBS were retrospectively analyzed; 75 cases in this group were given acute high dose of gamma globulin(IVIG)400mg/(kg·d)intravenously for 5d.Clinical and electrophysiological data and information on treatment and recovery of the children were collected during the follow-up and were analyzed.Result According to the clinical and electrophysiologic findings, 32 patients manifested acute inflammatory demyelinating polyradiculoneuropathy( AIDP), 34 had acute motor axonal neuropathy( AMAN), 3 had acute motor and sensory axonal neuropathy (AMSAN), 4 were inexcitable, 2 were unclassified. The clinical progress of the AMAN was faster than the AIDP group. Except for sensory nerve involvement, there was no significant difference in the clinical feature and severity. The mean time of the muscle strength began to recover was (5.59 +3.63) days in the AIDP group and (7. 21 ±4.68) days in the AMAN group after IVIG treatment. The time of the AIDP group was shorter than the AMAN group, but the difference was not statistically significant ( t = - 1. 5702, P > 0. 05 ). The mean time of the muscle strength increased one grade was (8.88 ±4. 39) days in the AIDP group and ( 12. 67 ±8. 35) days in the AMAN group. The difference was statistically significant ( t = - 2. 3689, P < 0. 05 ). No patients in this group died. Follow-up data showed that the complete recovery time was not significantly different ( t = 0. 2041, P > 0. 05 ). Conclusion The clinical progress of the AMAN was faster than the AIDP group. Besides sensory nerve involvement,there was no significant difference in the clinical feature and severity. The AIDP group's clinical recovery was faster than AMAN's after the immunoglobulin treatment. The two groups were not significantly different in long-term prognosis.  相似文献   

14.
??Abstract??Objective??To study the epidemiology??clinical and electrophysiological characteristics of the children with Guillain-Barré syndrome. Methods??Retrospectively analyze the electrophysiological and clinical data of 77 children wtih GBS in our hospital. Results??According to clinical and electrophysiologic findings??32 patients manifested acute inflammatory demyelinating polyradiculoneuropathy??AIDP???? 34 had acute motor axonal neuropathy??AMAN????4 had acute motor and sensory axonal neuropathy??ASMAN???? 4 were inexcitable?? 2 were unclassified and 1 had Miller-Fisher syndrome. The 77 patients included 53 boys and 25 girls.There were 27 boys and 5 girls in AIDP group and 18 boys and 16 girls in AMAN group. The AMAN group wer clearly seasonal ??June 4 to August 28?? .The mean time from the onset of illness to nadir was 7.09±3.17 days in the AIDP group and 4.94±1.59 days in the AMAN group. The mean disability score at nadir by the Hughes scale of 12 cases in AIDP group and 9 cases in AMAN group was ≤3??and 20 cases in AIDP group and 25 cases in AMAN group was ≥4.The number of cases in the respiratory muscle paralysis?? cranial nerve palsy and autonomic symptoms in the AMAN was more than in the AIDP group??but there was no statistical significance. In the sensory nerve involvement?? the AIDP was obviously more severe than in the AMAN group. Conclusion??The incidence of the AMAN and the AIDP group is similar in north Chinese children.Compared with AIDP group??the AMAN group has seasonal characteristics and gender differences. Between the two groups?? besides sensory nerve involvement ??there was no significant difference in the clinical feature and severity. However?? the clinical progress of the AMAN is faster than the AIDP group.  相似文献   

15.
目的 探讨运动神经传导阻滞(CB)与儿童吉兰-巴雷综合征(GBS)不同亚型间的关系。方法 回顾性分析50例GBS患儿的临床资料和神经电生理资料,根据神经电生理结果分为2型:急性炎症性脱髓鞘性多发性神经根神经病(AIDP,n=29)和急性运动轴索型神经病(AMAN,n=21)。根据有无运动神经CB分为伴有运动神经CB的AMAN(n=10)、不伴有运动神经CB的AMAN(n=11)、伴有运动神经CB的AIDP(n=19)和不伴有运动神经CB的AIDP(n=10)。比较各组间患儿起病年龄、性别、疾病高峰期休斯功能分级量表(HFGS)评分、短期预后(起病1个月后HFGS评分)。结果 AMAN中,运动神经CB均为可逆性。伴有运动神经CB的AMAN的起病1个月后HFGS评分低于不伴有运动神经CB的AMAN(P < 0.05),伴有运动神经CB的AIDP的起病1个月后HFGS评分高于伴有运动神经CB的AMAN(P < 0.05)。结论 伴有可逆性运动神经CB的AMAN提示神经纤维病变轻微,短期预后较不伴有运动神经CB的AMAN和AIDP恢复快。  相似文献   

16.
目的 明确空肠弯曲菌(CJ)两种不同血清型(Pen19和Pen43)与格林-巴利综合征(GBS)的关系。方法 分别用CJ-Pen19和CJ-Pen43菌体灭活粗抗原加完全福氏佐剂并充分乳化后,经皮下多点注射反复致敏60只Wistar大鼠,对两种菌株空肠弯曲菌(Pen19和Pen43)进行分组对比研究。结果 (1)Pen19和Pen43免疫后,两组大鼠血清IgG类抗CJ抗体滴度均增高,并于3~4周后稳定于高峰水平;(2)Pen19组坐骨神经病变率(60.0%)及原纤维病变率(17.7%)均比Pen43组(分别为10.0%和0.5%)和生理盐水组(分别为5.0%和0.5%)明显增高(P<0.001),后两组间比较差异无显著意义(P>0.05);(3)Pen19组原纤维病变类型(轴索变性∶髓鞘脱失)比较,初期以轴索变性为主,比值为3.4%∶0.7%,后期则以髓鞘脱失占优势,比值为5.3%∶24.1%;(4)Pen19组大鼠血清IgG类特异性抗CJ抗体水平与神经轴索变性率呈正相关(r=0.801),而与脱髓鞘率关系不大(r=0.353),IgM的水平与轴索变性及髓鞘脱失的发生均无关(r分别为0.253和0.281)。结论 (1)CJ对周围神经免疫性损伤能力与其血清类型密切相关;(2)CJ-Pen19所诱发的实验性周围神经病变病理类型初期以轴索变性为主,后期髓鞘脱失占优势;(3)特异性IgG类抗CJ抗体在轴索变性的发生中可能起重要作用。  相似文献   

17.
BACKGROUND: Antiganglioside antibodies have been reported to play a part in the pathophysiology of Guillain-Barré syndrome (GBS). AIMS: To investigate the prevalence and correlation of anti-ganglioside antibodies with clinical data in children with GBS in a multicentre clinical trial. METHODS: Immunoglobin (Ig)G and IgM to GM1, GM1b, GD1a, GalNAc-GD1a, GD1b, GT1a, and GQ1b were measured by ELISA in sera obtained before treatment. In addition, serological testing for Campylobacter jejuni was carried out. In parallel, a group of adults with GBS and a control group of children without GBS or other inflammatory diseases were evaluated. RESULTS: Sera from 63 children with GBS, 36 adults with GBS and 41 children without GBS were evaluated. Four of the children with GBS showed positive IgG to GM1, in one case combined with anti-GalNAc-GD1a and in one with anti-GD1b. Two others showed isolated positive IgG to GD1b and GT1a. One showed increased anti-GalNAc-GD1a IgM. In 5 of the 63 children, serological evidence of a recent infection with C jejuni was found, and this correlated significantly with the raised antibodies (p = 0.001). In the control group without GBS, no child showed positive IgG, but one showed anti-GalNAc-GD1a IgM. Compared with the adults with GBS, the frequency of antibodies in children was insignificantly lower. In our study, patients with positive antibodies did not show a more severe GBS course or worse outcome than those who were seronegative, and we could not show an increased incidence of axonal dysfunction. CONCLUSIONS: In some children with GBS, one can detect raised IgG against various gangliosides, similar to that in adults. A recent infection with C jejuni is markedly associated with the presence of these antibodies. However, in contrast with what has been reported in adults, in this study we were unable to show a negative effect of these findings on the clinical course.  相似文献   

18.
We describe the case of a 10-year-old child with the acute motor axonal neuropathy (AMAN) form of Guillain-Barré syndrome (GBS) with preserved tendon reflexes, 6 days after a bout of gastroenteritis. The child quickly showed weakness of the distal muscles of his four limbs, with preserved tendon reflexes and a raised CSF protein concentration with no cells. Nerve conduction studies showing motor axonal degeneration confirmed the diagnosis of GBS in spite of preserved tendon reflexes. The serum was positive for IgG antibodies to gangliosides GM1 and GD1b. The child received intravenous immunoglobulins, which resulted in a favorable progression. This case proves that GBS with normal tendon reflexes exists. The other cases of SGB with preserved tendon reflexes already described in the literature were the AMANs form with antibodies to gangliosides in the serum and only adults were affected.  相似文献   

19.
目的 探讨外周血淋巴细胞亚群和脑脊液蛋白对评估急性期吉兰-巴雷综合征(GBS)早期疾病严重程度的意义.方法 回顾分析2011年11月至2020年3月住院确诊的60例GBS患儿的临床资料.根据入院时病情、Hughes量表评分将患儿分为轻症组和重症组,比较两组患儿的年龄、性别、有无前驱感染以及外周血淋巴细胞亚群、脑脊液蛋白...  相似文献   

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