Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich Heine University Düsseldorf, Auf'm Hennekamp 65, 40225, Düsseldorf, Germany.
Medical Faculty, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
Semin Immunopathol. 2019 Jul;41(4):477-489. doi: 10.1007/s00281-019-00730-x. Epub 2019 Feb 18.
Depression is a frequent comorbidity of type 1 diabetes (T1D) and type 2 diabetes (T2D). Depression and diabetes are linked by a bidirectional relationship, but the underlying mechanisms are still incompletely understood. Experimental, observational and intervention studies showed that inflammatory processes contribute to the development of depression in animal models and humans. Given the high risk of morbidity and mortality in patients with the double burden of diabetes and depression, this review provides an overview of epidemiological studies that addressed the relationship between biomarkers of inflammation and depressive symptoms or depression in diabetes patients. In patients with T1D, there is some evidence that higher levels of high-sensitivity C-reactive protein (hsCRP), IL-6, IL-1 receptor antagonist (IL-1RA) and sICAM-1 may be related to depressive symptoms or (for hsCRP) lower treatment response. For T2D, hsCRP, IL-1RA, CCL2 and adiponectin or its isoforms were associated with depressive symptoms in at least two studies, whereas positive associations of IL-1β, IL-6 and IL-18 with depressive symptoms or depression were reported from single cohorts. However, the number of studies is too low for any meaningful meta-analysis. Prospective life course studies including both patients with T1D and T2D, a comprehensive assessment of systemic inflammation and repeated assessment of depressive symptoms should represent a future research priority to clarify to what extent subclinical inflammation affects the risk of depression in patients with diabetes. A better understanding of the role of inflammatory processes may help to identify subtypes of depression with partly different pathogenesis, which could have consequences with respect to therapeutic options including immunomodulation.
抑郁症是 1 型糖尿病（T1D）和 2 型糖尿病（T2D）的常见合并症。抑郁症和糖尿病之间存在双向关系，但潜在机制仍不完全清楚。实验、观察和干预研究表明，炎症过程在动物模型和人类中导致了抑郁症的发展。鉴于糖尿病和抑郁症双重负担患者的发病率和死亡率较高，本综述提供了对解决炎症生物标志物与糖尿病患者抑郁症状或抑郁症之间关系的流行病学研究的概述。在 T1D 患者中，有一些证据表明，较高水平的高敏 C 反应蛋白（hsCRP）、IL-6、IL-1 受体拮抗剂（IL-1RA）和 sICAM-1 可能与抑郁症状或（对于 hsCRP）治疗反应降低有关。对于 T2D，至少有两项研究表明 hsCRP、IL-1RA、CCL2 和脂联素或其同工型与抑郁症状相关，而来自单个队列的报告则表明 IL-1β、IL-6 和 IL-18 与抑郁症状或抑郁症呈正相关。然而，研究数量太少，无法进行任何有意义的荟萃分析。包括 T1D 和 T2D 患者的前瞻性生命历程研究、对全身炎症的全面评估以及对抑郁症状的反复评估应成为未来的研究重点，以明确亚临床炎症在多大程度上影响糖尿病患者的抑郁风险。更好地了解炎症过程的作用可能有助于确定部分不同发病机制的抑郁亚型，这可能会对包括免疫调节在内的治疗选择产生影响。
