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Antibodies to glutamic acid decarboxylase induced by interferon-alpha therapy for chronic viral hepatitis.

作者信息

Imagawa A, Itoh N, Hanafusa T, Waguri M, Kuwajima M, Matsuzawa Y

出版信息

Diabetologia. 1996 Jan;39(1):126. doi: 10.1007/BF00400426.

DOI:10.1007/BF00400426
PMID:8720616
Abstract
摘要

相似文献

1
Antibodies to glutamic acid decarboxylase induced by interferon-alpha therapy for chronic viral hepatitis.α-干扰素治疗慢性病毒性肝炎诱导产生的谷氨酸脱羧酶抗体
Diabetologia. 1996 Jan;39(1):126. doi: 10.1007/BF00400426.
2
[Pegylated-interferon-induced diabetes mellitus type 1 in two patients with chronic hepatitis C].[聚乙二醇干扰素诱发两名慢性丙型肝炎患者患1型糖尿病]
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3
Trajectories of anti-islet autoantibodies before development of type 1 diabetes in interferon-treated hepatitis C patients. Case reports and a literature review.干扰素治疗丙型肝炎患者发生 1 型糖尿病前胰岛自身抗体的变化轨迹:病例报告及文献复习。
Endocr J. 2010;57(11):947-51. doi: 10.1507/endocrj.k10e-207. Epub 2010 Aug 26.
4
Development of insulin-dependent diabetes mellitus in a patient with chronic hepatitis C during therapy with interferon-alpha.一名慢性丙型肝炎患者在接受α-干扰素治疗期间发生胰岛素依赖型糖尿病。
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Difference between islet cell antibodies and autoantibodies to glutamic acid decarboxylase-containing Purkinje cells in IDDM.胰岛素依赖型糖尿病中胰岛细胞抗体与含谷氨酸脱羧酶的浦肯野细胞自身抗体之间的差异。
Diabetes Care. 1992 Oct;15(10):1435-6. doi: 10.2337/diacare.15.10.1435b.
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Abrupt onset of diabetes during interferon-alpha therapy in patients with chronic hepatitis C.慢性丙型肝炎患者在接受α干扰素治疗期间突然发生糖尿病。
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A case of chronic hepatitis C developing insulin-dependent diabetes mellitus associated with various autoantibodies during interferon therapy.1例慢性丙型肝炎患者在干扰素治疗期间发生胰岛素依赖型糖尿病并伴有多种自身抗体。
Diabetes Res Clin Pract. 2000 Aug;49(2-3):101-6. doi: 10.1016/s0168-8227(00)00143-1.
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Interferon-alpha and IDDM: comment.
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[Prevalence and predictive value of islet cell autoantibodies and anti-glutamic acid decarboxylase in a family study in Lyons].
Journ Annu Diabetol Hotel Dieu. 1992:165-71.

引用本文的文献

1
Clinical associations and potential novel antigenic targets of autoantibodies directed against rods and rings in chronic hepatitis C infection.针对慢性丙型肝炎感染中杆状和环状抗体的临床关联和潜在新抗原靶点。
BMC Gastroenterol. 2013 Mar 19;13:50. doi: 10.1186/1471-230X-13-50.
2
Expression of endocrine autoantibodies in chronic hepatitis C, before and after interferon-alpha therapy.慢性丙型肝炎患者在干扰素-α治疗前后内分泌自身抗体的表达情况
J Endocrinol Invest. 2002 Dec;25(11):938-46. doi: 10.1007/BF03344065.
3
Induction of autoantibodies to the adrenal cortex and pancreatic islet cells by interferon alpha therapy for chronic hepatitis C.

本文引用的文献

1
Occurrence of IDDM during interferon therapy for chronic viral hepatitis.
Diabetes Res Clin Pract. 1994 Feb;23(1):33-6. doi: 10.1016/0168-8227(94)90124-4.
2
Evaluation of islet-specific autoantibodies in Japanese patients with insulin-dependent diabetes mellitus: a comparison between autoantibodies to glutamic acid decarboxylase, autoantibodies to 64 kDa islet cell protein and islet cell antibodies.日本胰岛素依赖型糖尿病患者胰岛特异性自身抗体的评估:谷氨酸脱羧酶自身抗体、64kDa胰岛细胞蛋白自身抗体与胰岛细胞抗体之间的比较
J Autoimmun. 1994 Dec;7(6):791-802. doi: 10.1006/jaut.1994.1062.
3
Interferon expression in the pancreases of patients with type I diabetes.I型糖尿病患者胰腺中的干扰素表达。
α干扰素治疗慢性丙型肝炎诱导产生针对肾上腺皮质和胰岛细胞的自身抗体。
Gut. 2001 Mar;48(3):378-83. doi: 10.1136/gut.48.3.378.
4
The role of interleukin-1 in the pathogenesis of IDDM.白细胞介素-1在胰岛素依赖型糖尿病发病机制中的作用。
Diabetologia. 1996 Sep;39(9):1005-29. doi: 10.1007/BF00400649.
Diabetes. 1995 Jun;44(6):658-64. doi: 10.2337/diab.44.6.658.
4
Immunoreactive alpha-interferon in insulin-secreting beta cells in type 1 diabetes mellitus.
Lancet. 1987 Dec 19;2(8573):1423-7. doi: 10.1016/s0140-6736(87)91128-7.
5
Two types of autoantibodies to adrenal medullary cells in type 1 (insulin-dependent) diabetic patients: prevalence, properties and implications.
J Autoimmun. 1991 Oct;4(5):807-18. doi: 10.1016/0896-8411(91)90175-c.
6
Development of thyroid disease during therapy of chronic viral hepatitis with interferon alfa.
Gastroenterology. 1992 Jun;102(6):2155-60. doi: 10.1016/0016-5085(92)90348-3.
7
Development of type 1 diabetes mellitus during interferon alfa therapy for chronic HCV hepatitis.
Lancet. 1992 Aug 29;340(8818):548. doi: 10.1016/0140-6736(92)91744-s.