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两名接受西他列汀和维生素D3治疗的1型糖尿病患者实现了四年临床缓解。

Four-year clinical remission of type 1 diabetes mellitus in two patients treated with sitagliptin and vitamin D3.

作者信息

Pinheiro Marcelo Maia, Pinheiro Felipe Moura Maia, Torres Margareth Afonso

机构信息

Pharmaceutical Assistance Center of the State of Mato Grosso , Cuiaba , Brazil.

Faculdade de Medicina da Universidade de Cuiabá-UNIC , Cuiaba , Brazil.

出版信息

Endocrinol Diabetes Metab Case Rep. 2016;2016. doi: 10.1530/EDM-16-0099. Epub 2016 Dec 21.

DOI:10.1530/EDM-16-0099
PMID:28035286
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5184778/
Abstract

UNLABELLED

Type 1 diabetes mellitus (T1DM) is a chronic disease characterized by autoimmune destruction of pancreatic beta cells and inadequate insulin production. Remission criteria in T1DM take into account serum levels of C-peptide and glycosylated hemoglobin, as well as the dose of insulin administered to the patient. However, remission of T1DM lasting longer than 1 year is rare. We describe here the cases of two young women who presented with positive glutamic acid decarboxylase (GAD) antibody and classic clinical manifestations of T1DM. Both patients had a prior history of Hashimoto's thyroiditis. They were initially treated with a basal-bolus regimen of insulin (glargine and lispro/glulisine). Once their blood glucose levels were controlled, they were started on oral sitagliptin 100 mg and vitamin D3 5000 IU daily. After this therapy, both patients achieved clinical diabetes remission for 4 years, along with a decrease in anti-GAD antibody levels. These benefits were probably associated with immunological effects of these medications. Inhibition of dipeptidyl peptidase 4 (DPP-4) in animal models deregulates Th1 immune response, increases secretion of Th2 cytokines, activates CD4CD25FoxP3 regulatory T-cells and prevents IL-17 production. Vitamin D3 also activates CD4CD25FoxP3 regulatory T-cells, and these medications combined can improve the immune response in patients with new-onset T1DM and probably promote sustained clinical remission.

LEARNING POINTS

The use of sitagliptin and vitamin D3 in patients with new-onset type 1 diabetes mellitus (T1DM) may help decrease the daily insulin requirement by delaying beta cell loss and improving endogenous insulin production.The use of sitagliptin and vitamin D3 in new-onset T1DM could help regulate the imbalance between Th17 and Treg cells.Age 14 years or above, absence of ketoacidosis and positive C-peptide levels in patients with T1DM are good criteria to predict prolonged T1DM remission.The determination of anti-GAD antibodies and C-peptide levels could be helpful in the follow-up of patients in use of sitagliptin and vitamin D3, which could be associated with prolonged T1DM clinical remission.

摘要

未标注

1型糖尿病(T1DM)是一种慢性疾病,其特征是胰腺β细胞发生自身免疫性破坏且胰岛素分泌不足。T1DM的缓解标准考虑血清C肽水平、糖化血红蛋白水平以及给予患者的胰岛素剂量。然而,T1DM持续缓解超过1年的情况很少见。我们在此描述两名年轻女性的病例,她们谷氨酸脱羧酶(GAD)抗体呈阳性且有T1DM的典型临床表现。两名患者既往均有桥本甲状腺炎病史。她们最初接受胰岛素(甘精胰岛素和赖脯胰岛素/谷赖胰岛素)的基础 - 餐时方案治疗。一旦血糖水平得到控制,她们开始每日口服西格列汀100毫克和维生素D3 5000国际单位。经过这种治疗,两名患者均实现了4年的临床糖尿病缓解,同时抗GAD抗体水平降低。这些益处可能与这些药物的免疫作用有关。在动物模型中,抑制二肽基肽酶4(DPP - 4)可调节Th1免疫反应,增加Th2细胞因子的分泌,激活CD4CD25FoxP3调节性T细胞并阻止IL - 17的产生。维生素D3也可激活CD4CD25FoxP3调节性T细胞,并且这些药物联合使用可改善新发T1DM患者的免疫反应,并可能促进持续的临床缓解。

学习要点

在新发1型糖尿病(T1DM)患者中使用西格列汀和维生素D3可能通过延缓β细胞丢失和改善内源性胰岛素分泌来帮助减少每日胰岛素需求量。在新发T1DM中使用西格列汀和维生素D3有助于调节Th17和Treg细胞之间的失衡。T1DM患者年龄14岁及以上、无酮症酸中毒且C肽水平阳性是预测T1DM长期缓解的良好标准。测定抗GAD抗体和C肽水平有助于对使用西格列汀和维生素D3的患者进行随访,这可能与T1DM的长期临床缓解有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f423/5184778/264d3185b16b/edmcr-2016-160099-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f423/5184778/3c0817326613/edmcr-2016-160099-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f423/5184778/2be555216e5b/edmcr-2016-160099-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f423/5184778/dd2d04f2bfb5/edmcr-2016-160099-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f423/5184778/264d3185b16b/edmcr-2016-160099-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f423/5184778/3c0817326613/edmcr-2016-160099-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f423/5184778/2be555216e5b/edmcr-2016-160099-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f423/5184778/dd2d04f2bfb5/edmcr-2016-160099-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f423/5184778/264d3185b16b/edmcr-2016-160099-g004.jpg

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