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Two Years of Modified Protocol with Cyclosporin A for Treatment of Acute Insulin Resistance Induced by Anti-Glutamic Acid Decarboxylase (GAD) Antibodies in Obese Type II Diabetics
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作者 Kamel El-Reshaid Shaikha Al-Bader 《Journal of Diabetes Mellitus》 2025年第1期52-58,共7页
Background: Diabetes mellitus (DM) is a disease characterized by hyperglycemia due to (a) insulin-insufficiency (type I DM), or (b) impaired glucose cell-entry (insulin resistance) due to the downregulation of insulin... Background: Diabetes mellitus (DM) is a disease characterized by hyperglycemia due to (a) insulin-insufficiency (type I DM), or (b) impaired glucose cell-entry (insulin resistance) due to the downregulation of insulin cell receptors (type II DM). Type I DM usually presents with florid manifestations contrary to a slowly-progressive type II. Patients and methods: Over the past 10 years, we encountered 9 obese patients with controlled insulin-requiring type II DM for years, at a dose of 62 ± 5 units/day, who developed sudden and severe insulin resistance (IR) that required 210 ± 25 units daily. All patients had very high levels of anti-Glutamic Acid Decarboxylase (GAD) antibodies. Despite a lack of previous testing for anti-GAD antibodies, they were treated, with Cyclosporin A (Cy), as an autoimmune disorder superimposed on their type II MD. Initially all patients were treated with 100 mg, of Cy, twice daily aiming at an initial trough level of 100 - 150 ng/ml. Three months later, the dose was reduced to 50 mg twice daily for a total of 2 years. Results: Amelioration of IR was achieved by 1 month with a reduction of daily insulin requirement to 123 ± 16 units that further decreased to 76 ± 11 by the end of the 3rd month. Such improvement persisted for 2 years and >1 year after Cy discontinuation. Moreover, a decline in insulin requirements was associated with a parallel decrease in anti-GAD antibody levels and an increase in C-peptide insulin without kidney disease. Conclusion: Anti-GAD antibodies can induce acute IR in type II DM, and this phenomenon can be treated safely and effectively with Cy. 展开更多
关键词 anti-gad Antibodies C-PEPTIDE Cyclosporin A Diabetes Mellitus HYPERGLYCEMIA Insulin Resistance Therapy
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槐果碱对神经病理性疼痛小鼠GABA信号通路的影响 被引量:16
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作者 金少举 任丽平 +3 位作者 马奔晖 郭留城 王雁梅 王文宝 《中药药理与临床》 CAS CSCD 北大核心 2016年第3期24-28,共5页
目的:研究槐果碱(Sohpocarpine,SC)对坐骨神经慢性缩窄性损伤神经病理性疼痛小鼠的镇痛作用,并探讨其GABA信号通路相关机制。方法:复制坐骨神经慢性缩窄性损伤神经病理性疼痛小鼠模型,采用Von Frey机械痛触觉阈测量系统、热刺痛仪及冷... 目的:研究槐果碱(Sohpocarpine,SC)对坐骨神经慢性缩窄性损伤神经病理性疼痛小鼠的镇痛作用,并探讨其GABA信号通路相关机制。方法:复制坐骨神经慢性缩窄性损伤神经病理性疼痛小鼠模型,采用Von Frey机械痛触觉阈测量系统、热刺痛仪及冷热板测痛仪测定槐果碱40、20、10 mg/kg对坐骨神经慢性缩窄性损伤小鼠的机械缩足反射阈值、热缩足反射潜伏期及冷缩足反射阈值的影响;用RT-PCR法检测槐果碱40、20、10 mg/kg对坐骨神经慢性缩窄性损伤小鼠脊髓组织GABA、GAD65及GAT1 mRNA表达的影响。结果 :与神经病理性疼痛坐骨神经慢性缩窄性损伤模型组小鼠比较,槐果碱40、20 mg/kg可提高坐骨神经慢性缩窄性损伤小鼠机械缩足反射阈值,延长热缩足反射潜伏期,降低冷缩足反射阈值;槐果碱40、20 mg/kg可上调坐骨神经慢性缩窄性损伤小鼠脊髓组织GABA、GAD65 mRNA表达水平,下调GAT1 mRNA表达。结论:槐果碱对坐骨神经慢性缩窄性损伤致神经病理性疼痛有较好的镇痛作用,其机制可能与其上调GABA、GAD65表达和下调GAT1表达有关。 展开更多
关键词 槐果碱 神经病理性疼痛 镇痛 GABA GAD GAT
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针刺对抑郁大鼠海马GAD65、GAD67调控作用研究 被引量:14
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作者 袁恺 张黎恒 +6 位作者 赵日霞 郭瑾 凌娴 段必双 陈兴华 何新芳 刘海静 《河北中医药学报》 2018年第1期5-8,共4页
目的:研究针刺治疗对抑郁模型大鼠海马谷氨酸脱羧酶65(GAD65)、谷氨酸脱羧酶67(GAD67)的蛋白表达水平,探讨针刺疗法的抗抑郁作用及其相关作用机制。方法:将100只大鼠随机分成5组,空白对照组、氟西汀组、针刺非穴组、针刺穴位组以及模型... 目的:研究针刺治疗对抑郁模型大鼠海马谷氨酸脱羧酶65(GAD65)、谷氨酸脱羧酶67(GAD67)的蛋白表达水平,探讨针刺疗法的抗抑郁作用及其相关作用机制。方法:将100只大鼠随机分成5组,空白对照组、氟西汀组、针刺非穴组、针刺穴位组以及模型组,各组均20只,采用慢性综合应激法建立抑郁模型,各组进行相应干预21 d,观察治疗前后大鼠行为学变化。并在实验结束后,从以上5组大鼠中,每组随机抽取8只,Western Blot法检测海马区GAD65、GAD67蛋白表达水平。结果:与空白组相比,实验21 d后,模型组、针刺组、非穴位针刺组的垂直运动次数明显减少,差异有非常显著性(P<0.01),模型组GAD65蛋白表达量降低,差异有显著性(P<0.05);与模型组相比,氟西汀组和针刺组体质量增幅较大、糖水摄入量明显增加、水平运动次数明显增加、垂直运动次数明显增加,差异有非常显著性(P<0.01),针刺穴位组GAD65蛋白表达量升高,差异有显著性(P<0.05);5组间GAD67蛋白表达水平差异无显著性(P>0.05)。结论:对慢性复合应激大鼠百会、三阴交以及内关等穴实施针刺,能够在一定程度上缓解其抑郁状态;穴位针刺的抗抑郁作用可能与增加GAD65合成、减少海马谷氨酸(Glu)含量、增加γ-氨基丁酸(GABA)含量有关。 展开更多
关键词 针刺疗法 抑郁症 谷氨酸脱羧酶65 抗抑郁 氟西汀胶囊
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Glutamic acid decarboxylase 65-positive autoimmune encephalitis presenting with gelastic seizure, responsive to steroid: A case report 被引量:1
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作者 Camerdy Yue Yang Sheng-Ta Tsai 《World Journal of Clinical Cases》 SCIE 2021年第19期5325-5331,共7页
BACKGROUND Anti-glutamic acid decarboxylase(GAD)antibody is known to cause several autoimmune-related situations.The most known relationship is that it may cause type I diabetes.In addition,it was also reported to res... BACKGROUND Anti-glutamic acid decarboxylase(GAD)antibody is known to cause several autoimmune-related situations.The most known relationship is that it may cause type I diabetes.In addition,it was also reported to result in several neurologic syndromes including stiff person syndrome,cerebellar ataxia,and autoimmune encephalitis.Decades ago,isolated epilepsy associated with anti-GAD antibody was first reported.Recently,the association between temporal lobe epilepsy and anti-GAD antibody has been discussed.Currently,with improvements in examination technique,many more autoimmune-related disorders can be diagnosed and treated easier than in the past.CASE SUMMARY A 44-year-old female Asian with a history of end-stage renal disease(without diabetes mellitus)under hemodialysis presented with diffuse abdominal pain.The initial diagnosis was peritonitis complicated with sepsis and paralytic ileus.Her peritonitis was treated and she recovered well,but seizure attack was noticed during hospitalization.The clinical impression was gelastic seizure with the presentation of frequent smiling,head turned to the right side,and eyes staring without focus;the duration was about 5–10 s.Temporal lobe epilepsy was recorded through electroencephalogram,and she was later diagnosed with anti-GAD65 antibody positive autoimmune encephalitis.Her seizure was treated initially with several anticonvulsants but with poor response.However,she showed excellent response to intravenous methylprednisolone pulse therapy.Her consciousness returned to normal,and no more seizures were recorded after 5 d of intravenous methylprednisolone treatment.CONCLUSION In any case presenting with new-onset epilepsy,in addition to performing routine brain imaging to exclude structural lesion and cerebrospinal fluid studies to exclude common etiologies of infection and inflammation,checking the autoimmune profile has to be considered.In the practice of modern medicine,autoimmune-related disorders are relatively treatable and should not be missed. 展开更多
关键词 anti-gad antibody GAD65 antibody Autoimmune encephalitis Gelastic seizure ELECTROENCEPHALOGRAM Case report
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抗谷氨酸脱羧酶65抗体相关性僵人综合征并自身免疫性多内分泌腺病综合征Ⅱ型1例并文献复习 被引量:5
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作者 朱凌 韩永升 +2 位作者 徐银 薛本春 王训 《中风与神经疾病杂志》 CAS 2023年第4期317-321,共5页
目的报告1例抗谷氨酸脱羧酶65抗体相关性僵人综合征(SPS)并发自身免疫性多内分泌腺病综合征Ⅱ型(APS-Ⅱ)的病例,旨在提高临床医师对该病的认识。方法回顾性分析2022年安徽省某神经病学研究所附院收治的1例51岁女性,临床以反复腰痛、腰... 目的报告1例抗谷氨酸脱羧酶65抗体相关性僵人综合征(SPS)并发自身免疫性多内分泌腺病综合征Ⅱ型(APS-Ⅱ)的病例,旨在提高临床医师对该病的认识。方法回顾性分析2022年安徽省某神经病学研究所附院收治的1例51岁女性,临床以反复腰痛、腰腹及双下肢僵硬伴无力为特点的病例资料,并复习相关文献。结果患者临床以反复腰痛、腰腹及双下肢僵硬伴无力为特点,早期误诊为分离转换障碍,后检查发现血清及脑脊液抗谷氨酸脱羧酶65抗体阳性,甲状腺球蛋白抗体及过氧化酶抗体滴度升高,空腹及餐后2 h血糖、糖化血红蛋白升高,神经电生理提示静息状态下以体轴肌为主的连续性运动单位电位发放,诊断为抗谷氨酸脱羧酶65抗体相关性SPS、APS-Ⅱ(桥本甲状腺炎、1型糖尿病),予免疫治疗和对症治疗后病情改善。结论抗谷氨酸脱羧酶65抗体相关性SPS并发APS-Ⅱ临床虽具有一定特异性,但由于临床罕见,易误诊、漏诊,尤其是病程早期。 展开更多
关键词 僵人综合征 自身免疫性多内分泌腺病综合征 GAD抗体谱系障碍 抗谷氨酸脱羧酶65抗体
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抗谷氨酸脱羧酶抗体相关脑炎九例临床特点分析 被引量:2
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作者 林鑫 陈鑫鑫 +5 位作者 张文琳 刘若雪 韩晓晨 赵辉 何俊瑛 卜晖 《中华医学杂志》 CAS CSCD 北大核心 2021年第33期2625-2628,共4页
本研究总结2018年4月至2020年10月就诊于河北医科大学第二医院神经内科的9例抗谷氨脱羧酶(GAD)抗体相关脑炎患者的临床特点。在9例患者中,7例以癫痫为首发症状,2例以记忆力减退为首发症状。4例患者合并其他自身免疫性疾病。4例患者头MR... 本研究总结2018年4月至2020年10月就诊于河北医科大学第二医院神经内科的9例抗谷氨脱羧酶(GAD)抗体相关脑炎患者的临床特点。在9例患者中,7例以癫痫为首发症状,2例以记忆力减退为首发症状。4例患者合并其他自身免疫性疾病。4例患者头MRI显示颞叶内侧结构的异常信号。6例患者的脑电图出现异常放电。8例患者经一线治疗后症状均较前缓解。抗GAD抗体相关脑炎以癫痫为主要临床表现,头颅MRI及脑电图检查对其诊断有指导意义。其中部分患者可合并自身免疫性疾病,因此对于可能患有此类疾病患者,必须进行自身免疫性抗体的检查。一旦确诊抗GAD抗体相关脑炎,应立即启动免疫治疗。 展开更多
关键词 脑炎 自身免疫性脑炎 抗谷氨脱羧酶抗体相关脑炎 癫痫
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