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               本刊是中国科学技术协会主管、中国病理生理学会主办、暨南大学承办的国家级综合性病理生理学高级学术刊物。杂志刊登有关病理生理学理论研究(包括实验研究和临床研究)方面的论著、专题综述、教学研究、科研仪器和药品评价介绍等,注重介绍疾病发病机制和临床病理生理学研究。适合医药院校教学科研人员、研究生、临床医务工作者和高年级医学生阅读。                

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  • 杂志名称:中国病理生理杂志
  • 主管单位:中国科学技术协会
  • 主办单位:中国病理生理学会
  • 国际刊号:1000-4718
  • 国内刊号:44-1187/R
  • 出版周期:月刊
期刊荣誉:2008和2011年分别被评为第一届和第二届中国精品科技期刊;2008~2011年连续4次荣获“百种中国杰出学术期刊”奖;2011年被评为RCCSE(武汉大学中国科学评价研究中心)中国权威期刊;2010年荣获广东省期刊评选最高奖——品牌期刊奖;2011年荣获广东省优秀科技期刊一等奖。期刊收录:万方收录(中), JST 日本科学技术振兴机构数据库(日), 北大核心期刊(中国人文社会科学核心期刊), CA 化学文摘(美), 上海图书馆馆藏, 维普收录(中), 统计源核心期刊(中国科技论文核心期刊), 知网收录(中), CSCD 中国科学引文数据库来源期刊(含扩展版), 国家图书馆馆藏
中国病理生理杂志2001年第08期

关键词:glutamic acid decarboxylase
摘要:Antibodies to glutamic acid decarboxylase (GADab) is considered to be a marker for the autoimmune process against pancreatic β cells. Indeed, nearly 70% of patients with type 1 diabetes is repoted to be GAD ab+. A subgroup of patients diagnosed as type 2 diabetes has GADab. Therefore, it is questioned whether GADab+ patients with type 2 diabetes represent a late onset of type 1 diabetes or a unique disease entity. Fifty five GADab+ patients with type 2 diabetes were compared with 137 GADab- patients. They were admitted to Abe Diabetes Clinic for the control of diabetes. The age at onset of these patients was >30 years, and did not require insulin therapy for at least 6 months from the disease onset. The GADab+ patients had lower urinary C-peptide concentrations (uCPR) [(47.8±48.9) μg/d vs (58.1±49.9) μg/d, P=0.034] than the GADab- patients. The GAD+ patients were assigned insulin therapy more often (81.8% vs 56.3%, P=0.0038) and earlier [(8.5±7.5)years vs (10.1±7.3) years, P=3.3×10-12] than the GAD- patients. The levels of uCPR were associated with the titers of GADab (r=0.32, P=0.038). Among the susceptible HLA alleles for type 1 diabetes, the frequencies of B54 and DRB1* 0405 alleles, but not B61 and DRB1*0901 alleles, were increased among GADab+ patients. There data suggest that the GADab+ type 2 diabetes has an autoimmune nature, although the extent of insulin dependency and the distribution of HLA susceptible alleles are different from type 1 diabetes.