Delayed Onset of Central Hypocortisolism in a Patient Recovering From COVID-19

新冠肺炎康复患者中枢性低皮质醇症延迟发作

阅读:1

Abstract

OBJECTIVE: The objective of this report is to highlight the possible but little-known association between coronavirus disease 2019 (COVID-19) and delayed onset of central hypocortisolism, which may be of significant clinical importance. METHODS: We describe a patient who developed new-onset central hypocortisolism in the convalescent phase of mild COVID-19, which has not been previously reported. RESULTS: A 47-year-old man with recent COVID-19 upper respiratory tract infection developed new-onset persistent dyspepsia and eosinophilia for which multiple investigations were normal. He was eventually diagnosed with central hypocortisolism, as evidenced by 8 AM cortisol level of 19 nmol/L (normal, 133-537 nmol/L) and adrenocorticotropic hormone of 7.1 ng/mL (normal, 10.0-60.0 ng/mL). He was started on hydrocortisone, which led to resolution of both dyspepsia and eosinophilia. At the same time, an interesting thyroid function trend was observed-an initial increase in both free thyroxine and thyroid stimulating hormone was followed by temporary central hypothyroidism before subsequent spontaneous recovery. On follow-up 3 weeks later, the patient remained hypocortisolemic. CONCLUSION: COVID-19 may be associated with the delayed onset of central hypocortisolism in its convalescent phase. Although various mechanisms are possible, hypothalamic-pituitary activation during systemic illness, followed by a rebound decrease in activity after recovery, is consistent with the clinical course and thyroid function trend in this patient. It is essential that physicians consider endocrinopathies in the differential diagnosis of such cases, given the risk of life-threatening adrenal crises and their possible contribution to persistent symptoms following recovery from COVID-19.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。