La ghiandola pituitaria
While respiratory symptoms dominate the initial presentation, mounting evidence suggests that the virus can also affect various organ systems, including the endocrine glands.
This article discusses the findings of a study investigating adrenal insufficiency (AI) in patients with COVID-19 pneumonia, highlighting its prevalence, potential underlying mechanisms, and clinical implications.
Prevalence of AI in COVID-19 Pneumonia
The study under scrutiny revealed that AI is a common complication in patients with COVID-19 pneumonia. Among the cohort of patients examined, 10 out of 11 patients (90.9%) manifested central hypocortisolism, indicating a significant association between the infection and adrenal dysfunction.
Furthermore, it was observed that a considerable proportion of patients (55%) experienced clinical symptoms of long COVID, such as fatigue, insomnia, and dyspnea.
Role of ACE2 Receptor in AI Mechanism
The underlying mechanism of AI in COVID-19 patients is likely linked to the ACE2 receptor, which serves as the primary functional receptor for SARS-CoV and SARS-CoV-2 infections. The presence of ACE2 mRNA in various human tissues, including endocrine glands like the adrenal and pituitary glands, suggests that these glands could be targeted by the virus.
ACE2 receptors facilitate viral entry in conjunction with S glycoprotein priming by the host cell transmembrane serine protease 2.
Pituitary Disruption and Primary AI in COVID-19
Numerous studies have reported cases of pituitary disruption after SARS-CoV-2 infection, including various pituitary-related conditions like central AI, central diabetes insipidus, hypothalamic hypogonadism, lymphocytic hypophysitis, and pituitary apoplexy. Additionally, primary AI has been documented in COVID-19 patients.
The findings from these studies, including the current one, indicate that both pituitary and adrenal functions may be affected by SARS-CoV-2 infection.
Impact of BMI and Obesity on AI Risk
The study results further suggest that high BMI is significantly associated with an increased risk of AI in COVID-19 patients. This association may be attributed to the high ACE2 expression in adipose tissue, leading to an elevated viral burden and subsequent damage to the endocrine glands.
Additionally, metabolic dysfunction and dysregulation of the renin–angiotensin pathway may contribute to the increased proinflammatory phenotype associated with obesity, which in turn worsens the severity of COVID-19.
Comparison with Previous Studies
Contrasting findings between this study and others can be attributed to differences in the corticotropin stimulation test (CST) methodologies and the timing of adrenal function evaluation. The low-dose CST utilized in this study likely improved the detection of mild or early onset AI compared to the standard CST used in other investigations. Furthermore, the differences in severity and duration of COVID-19 in study participants may explain the variations in AI prevalence.
Strengths and Limitations of the Study
The study’s strengths include the use of a high cut-off value for serum cortisol and a low-dose CST, both of which likely reduced false-positive results. Additionally, imaging studies were performed to investigate other potential causes of AI in most of the patients with AI. However, the small sample size and the single-center setting are limitations that may limit the generalizability of the results. Furthermore, the focus on severe COVID-19 pneumonia might not fully represent patients with milder forms of the disease.
Clinical Implications and Conclusion
The study emphasizes the importance of monitoring endocrine complications in patients with a history of SARS-CoV-2 infection. For patients presenting with clinical symptoms like shock, nausea, vomiting, and fatigue, AI should be excluded as a potential diagnosis. Additionally, individuals with long COVID syndrome may benefit from an analysis of hypothalamic–pituitary axis function.
Further research is needed to fully understand the mechanisms of AI following SARS-CoV-2 infection, and larger studies are required to confirm these findings and gain a better understanding of the prevalence and mechanisms of AI in patients with COVID-19 pneumonia.