Gerganova Antonina, Assyov Yavor, Kamenov Zdravko
Department of Internal Medicine, Medical University - Sofia, Sofia, Bulgaria.
Clinic of Endocrinology, University Hospital Alexandrovska, Sofia, Bulgaria.
Front Clin Diabetes Healthc. 2022 Apr 7;3:826006. doi: 10.3389/fcdhc.2022.826006. eCollection 2022.
The novel severe acute respiratory distress syndrome-coronavirus 2 (SARS-CoV-2) has caused one of the most substantial pandemics that has affected humanity in the last century. At the time of the preparation of this review, it has caused the death of around 5 million people around the globe. There is ample evidence linking higher mortality risk rates from Coronavirus disease-19 (COVID-19) with male gender, advancing age and comorbidities, such as obesity, arterial hypertension, cardiovascular disease, chronic obstructive pulmonary disease, diabetes mellitus, and cancer. Hyperglycemia has been found to be accompanying COVID-19 not only in individuals with overt diabetes. Many authors claim that blood glucose levels should also be monitored in non-diabetic patients; moreover, it has been confirmed that hyperglycemia worsens the prognosis even without pre-existing diabetes. The pathophysiological mechanisms behind this phenomenon are complex, remain controversial, and are poorly understood. Hyperglycemia in the setting of COVID-19 could be a consequence of deterioration in pre-existing diabetes, new-onset diabetes, stress-induced or iatrogenic due to substantial usage of corticosteroids within the context of a severe COVID-19 infection. It is also plausible that it might be a result of adipose tissue dysfunction and insulin resistance. Last but not least, SARS-CoV-2 is also claimed to trigger sporadically direct β-cell destruction and β-cell autoimmunity. Pending further validations with longitudinal data are needed to legitimize COVID-19 as a potential risk factor for the development of diabetes. Hereby, we present an emphasized critical review of the available clinical data in an attempt to unravel the complex mechanisms behind hyperglycemia in COVID-19 infection. The secondary endpoint was to evaluate the bidirectional relationship between COVID-19 and diabetes mellitus. As the worldwide pandemic is still expanding, demand for answering these questions is arising. It will be of immense help for the management of COVID-19 patients, as well as for the implementation of post-discharge policies for patients with a high risk of developing diabetes.
新型严重急性呼吸综合征冠状病毒2(SARS-CoV-2)引发了上世纪以来影响人类的最严重大流行之一。在撰写本综述时,它已导致全球约500万人死亡。有充分证据表明,冠状病毒病19(COVID-19)导致的较高死亡风险率与男性、年龄增长以及肥胖、动脉高血压、心血管疾病、慢性阻塞性肺疾病、糖尿病和癌症等合并症有关。高血糖不仅在显性糖尿病患者中伴随COVID-19出现。许多作者主张,非糖尿病患者也应监测血糖水平;此外,已证实即使没有糖尿病病史,高血糖也会使预后恶化。这一现象背后的病理生理机制复杂,仍存在争议,且了解甚少。COVID-19背景下的高血糖可能是由于原有糖尿病病情恶化、新发糖尿病、应激诱导或在严重COVID-19感染情况下大量使用皮质类固醇导致的医源性因素。也有可能是脂肪组织功能障碍和胰岛素抵抗的结果。最后但同样重要的是,有人声称SARS-CoV-2也会偶尔引发直接的β细胞破坏和β细胞自身免疫。需要进一步的纵向数据验证,以使COVID-19成为糖尿病发生的潜在风险因素合法化。在此,我们对现有临床数据进行重点批判性综述,试图阐明COVID-19感染中高血糖背后的复杂机制。次要终点是评估COVID-19与糖尿病之间的双向关系。由于全球大流行仍在扩大,回答这些问题的需求日益增加。这将对COVID-19患者的管理以及对有糖尿病高风险患者实施出院后政策有极大帮助。