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一例病例报告及系统文献综述:胰岛素诱导的Ⅲ型超敏反应

A case report and systematic literature review: insulin-induced type III hypersensitivity reaction.

作者信息

Meredith Rebecca R, Patel Pooja, Huang Polly, Onyenekwu Chinelo Pamela, Rai Herleen, Tversky Jody, Alvarez-Arango Santiago

机构信息

Division of Hospital Medicine, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States.

Division of Allergy and Clinical Immunology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States.

出版信息

Front Allergy. 2024 Feb 21;5:1357901. doi: 10.3389/falgy.2024.1357901. eCollection 2024.

DOI:10.3389/falgy.2024.1357901
PMID:38469413
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10926194/
Abstract

Insulin-induced type III hypersensitivity reactions (HSRs) are exceedingly rare and pose complex diagnostic and management challenges. We describe a case of a 43-year-old woman with type 1 diabetes mellitus (DM), severe insulin resistance, and subcutaneous nodules at injection sites, accompanied by elevated anti-insulin IgG autoantibodies. Treatment involved therapeutic plasma exchange (TPE) and intravenous immunoglobulin (IVIg) as bridge therapy, followed by long-term immunosuppression, which reduced autoantibody levels and improved insulin tolerance. Given the limited treatment guidelines, we conducted a comprehensive literature review, identifying 16 similar cases. Most patients were females with a median age of 36.5 years; 63% had type 1 DM, and 44% had concurrent insulin resistance (56% with elevated autoantibodies). Treatment approaches varied, with glucocorticoids used in 67% of cases. Patients with type 1 DM were less responsive to steroids than those with type 2 DM, and had a more severe course. Of those patients with severe disease necessitating immunosuppression, 66% had poor responses or experienced relapses. The underlying mechanism of insulin-induced type III HSRs remains poorly understood. Immunosuppressive therapy reduces anti-insulin IgG autoantibodies, leading to short-term clinical improvement and improved insulin resistance, emphasizing their crucial role in the condition. However, the long-term efficacy of immunosuppression remains uncertain and necessitates continuous evaluation and further research.

摘要

胰岛素诱导的III型超敏反应(HSR)极为罕见,给诊断和管理带来了复杂的挑战。我们描述了一例43岁1型糖尿病(DM)女性患者,该患者存在严重胰岛素抵抗,注射部位有皮下结节,伴有抗胰岛素IgG自身抗体升高。治疗包括采用治疗性血浆置换(TPE)和静脉注射免疫球蛋白(IVIg)作为过渡治疗,随后进行长期免疫抑制,这降低了自身抗体水平并改善了胰岛素耐受性。鉴于治疗指南有限,我们进行了全面的文献综述,确定了16例类似病例。大多数患者为女性,中位年龄为36.5岁;63%患有1型DM,44%同时存在胰岛素抵抗(56%自身抗体升高)。治疗方法各不相同,67%的病例使用了糖皮质激素。1型DM患者对类固醇的反应不如2型DM患者,病程也更严重。在那些需要免疫抑制的重症患者中,66%反应不佳或复发。胰岛素诱导的III型HSR的潜在机制仍知之甚少。免疫抑制治疗可降低抗胰岛素IgG自身抗体,带来短期临床改善并改善胰岛素抵抗,强调了其在该病中的关键作用。然而,免疫抑制的长期疗效仍不确定,需要持续评估和进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/460a/10926194/d9a8a47a1f3a/falgy-05-1357901-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/460a/10926194/b87bda6ed509/falgy-05-1357901-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/460a/10926194/d9a8a47a1f3a/falgy-05-1357901-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/460a/10926194/b87bda6ed509/falgy-05-1357901-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/460a/10926194/d9a8a47a1f3a/falgy-05-1357901-g002.jpg

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本文引用的文献

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Case Report: Insulin hypersensitivity in youth with type 1 diabetes.病例报告:1 型糖尿病青少年的胰岛素超敏。
Front Endocrinol (Lausanne). 2023 Oct 20;14:1226231. doi: 10.3389/fendo.2023.1226231. eCollection 2023.
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Injection Site Reaction to Various Insulins as Type III Allergy With Urticarial Vasculitis in a Patient With Type I Diabetes Mellitus.1 型糖尿病患者发生 III 型过敏反应致各种胰岛素注射部位反应,伴荨麻疹性血管炎。
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Insulin Reactions: What Do You Do When Your Treatment's the Trigger?
胰岛素反应:当你的治疗成为诱因时该怎么办?
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Serious diabetic ketoacidosis induced by insulin allergy and anti-insulin antibody in an individual with type 2 diabetes mellitus.2 型糖尿病患者因胰岛素过敏和抗胰岛素抗体导致严重糖尿病酮症酸中毒。
J Diabetes Investig. 2022 Oct;13(10):1788-1792. doi: 10.1111/jdi.13838. Epub 2022 May 31.
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Insulin Allergy to Detemir Followed by Rapid Onset of Diabetic Ketoacidosis: A Case Report and Literature Review.德谷胰岛素过敏致糖尿病酮症酸中毒快速发作 1 例报告并文献复习
Front Endocrinol (Lausanne). 2022 Mar 8;13:844040. doi: 10.3389/fendo.2022.844040. eCollection 2022.
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Clin Case Rep. 2020 Aug 30;8(12):2759-2762. doi: 10.1002/ccr3.3200. eCollection 2020 Dec.
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