白三烯的抑制及其在1型糖尿病发病机制中的潜在作用:孟鲁司特作为治疗剂的意义:一个病例报告。

Frontiers in clinical diabetes and healthcare Pub Date : 2024-12-19 eCollection Date: 2024-01-01 DOI:10.3389/fcdhc.2024.1494470
Pavel Fatulla, Ingela Ström, Christine Lingblom, Marcus Lind
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引用次数: 0

摘要

导论:1型糖尿病涉及免疫介导的胰岛素生成β细胞的破坏,嗜酸性粒细胞可能发挥重要作用。最近的研究表明,白三烯抑制可能影响这一过程。本病例报告提出了一种新的观察,孟鲁司特是一种白三烯受体拮抗剂,可以降低成人潜伏性自身免疫性糖尿病(LADA)患者的胰岛素需求。一名患有LADA的55岁男性患者在使用孟鲁司特治疗呼吸道症状后,胰岛素剂量显著降低。该患者最初于2018年被诊断为LADA,一直在接受胰岛素治疗。孟鲁司特治疗因呼吸道症状开始,导致胰岛素需用量降低60.5%,停药后胰岛素需用量增加。随后的孟鲁司特疗程导致胰岛素降低87.9%。尽管继续使用孟鲁司特降低胰岛素的效果减弱,但患者报告餐后高血糖减少。血液检查显示,尽管胰岛素剂量减少,但血糖水平稳定。结论:本病例提示孟鲁司特可能通过其对嗜酸性粒细胞的抗炎作用降低1型糖尿病患者的胰岛素需求。这些发现强调需要进一步研究孟鲁司特在1型糖尿病治疗中的作用及其保持β细胞功能或减少胰岛素依赖的潜力。
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Inhibition of leukotrienes and their potential role in type 1 diabetes pathogenesis: implications for montelukast as a therapeutic agent: a case report.

Introduction: Type 1 diabetes involves immune-mediated destruction of insulin-producing beta cells, with eosinophils potentially playing a significant role. Recent studies suggest that leukotriene inhibition might influence this process. This case report presents a novel observation of montelukast, a leukotriene receptor antagonist, reducing insulin requirements in a patient with Latent Autoimmune Diabetes in Adults (LADA). A 55-year-old male with LADA experienced substantial reductions in insulin dosage when treated with montelukast for respiratory symptoms. Initially diagnosed with LADA in 2018, the patient had been on insulin therapy. Montelukast therapy, initiated due to respiratory symptoms, led to a 60.5% reduction in insulin requirements which increased upon discontinuation. A subsequent montelukast course resulted in an 87.9% insulin reduction. Although the insulin-lowering effect diminished with continued montelukast use, the patient reported reduced postprandial hyperglycemia. Blood tests indicated stable glucose levels despite reduced insulin doses.

Conclusions: This case suggests that montelukast may reduce insulin needs in type 1 diabetes patients, potentially through its anti-inflammatory effects on eosinophils. These findings highlight the need for further research into montelukast's role in type 1 diabetes management and its potential to preserve beta-cell function or reduce insulin dependence.

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