冠状病毒感染背景下2型糖尿病患者低肾素血症性低醛固酮增多症表现为自主神经病变1例临床病例

N. Pertseva, T. Chursinova, A.A. Gryshniakova
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引用次数: 0

摘要

冠状病毒病(COVID-19)通常与内分泌并发症相关。本文描述了1例2型糖尿病合并COVID-19患者的临床病例,首次需要基础胰岛素治疗,其次出现明显的动脉低血压。患者胰腺β细胞损伤的机制尚存争议。在分析糖尿病病程特点后,我们发现患者急性起病,年龄44岁,伴有明显的高血糖和酮症,需要胰岛素治疗。在很长一段时间内,不需要胰岛素治疗,病人服用二甲双胍,体重超标,没有β细胞抗原抗体。也不可能排除SARS-CoV-2对胰腺β细胞分泌功能的影响。因此,临床病例是有趣的,因为它们的分析不仅有助于了解这种感染的发生和进展机制,而且有助于其并发症的诊断和治疗。我们报道了一例罕见的2型糖尿病患者在COVID-19感染后出现低肾素血症性低醛固酮增多症的临床病例。低肾素血症性低醛固酮增多症病程的一个特点是患者无电解质紊乱,伴有严重的动脉低血压,肾素和醛固酮抑制。我们认为,在COVID-19的背景下,低肾素血症性低醛固酮增多症与慢性糖尿病并发症的进展有关,主要是自主神经病变。为了改善已确定的疾病,使用矿物皮质激素进行替代治疗。在选择氟化可的松剂量时监测血压、体液潴留症状和电解质水平。患者已观察14个月,至今仍需要氟化可的松替代治疗。自主神经障碍是影响患者生活质量的独立危险因素,是导致心血管疾病死亡的重要因素,执业医师应重视自主神经障碍的诊断。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hyporeninemic hypoaldosteronism as a manifestation of autonomic neuropathy in a patient with type 2 diabetes mellitus against the background of coronavirus disease. A clinical case
Coronavirus disease (COVID-19) is often associated with endocrine complications. The article describes a clinical case of the patient with type 2 diabetes mellitus and COVID-19 after which, for the first time, there was a need for basal-bolus insulin therapy, and secondly, a significant arterial hypotension occurred. The mechanism of damage to β-cells of the pancreas in the patient is debatable. After analyzing the features of diabetes course, we found an acute onset of the disease at the age of 44 years with pronounced hyperglycemia and ketosis, which required insulin therapy. Then for a long time there was no need in insulin therapy, and the patient took metformin, having overweight, no antibodies to β-cell antigens. It is also impossible to exclude the effect of SARS-CoV-2 on the secretory function of β-cells of the pancreas. Accordingly, clinical cases are interesting, as their analysis helps to understand not only the mecha­nism of development and progression of this infection, but also the diagnosis and treatment of its complications. We have described a rare clinical case of the hyporeninemic hypoaldosteronism in the patient with type 2 diabetes mellitus after COVID-19 infection. A feature of the hyporeninemic hypoaldosteronism course was the absence of electrolyte disorders in the patient, with severe arterial hypotension, suppression of renin and aldosterone. We believe that the hyporeninemic hypoaldosteronism has been associated with the progression of chronic diabetes complications, mainly autonomic neuropathy against the background of COVID-19. To improve the identified disorders, replacement therapy with mineralocorticoids was prescribed. The blood pressure, symptoms of fluid retention and electrolyte levels were monitored when selecting the dose of fludrocortisone. The patient has been under observation for 14 months, the need for fludrocortisone replacement therapy persists to this day. Practicing doctors need to pay attention to the diagnosis of autonomic disorders, which reduce the patients’ quality of life and are an independent risk factor for cardiovascular mortality.
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