The Impact of COVID-19 Viral Infection on the Hypothalamic-Pituitary-Adrenal Axis

COVID-19 and Endocrine Disorders – Emerging Links in this Puzzle

“…The levels are found to be lower in patients with more severe disease, and critically ill COVID-19 patients have lower cortisol levels than those with critical illness without COVID-19. [ 11 ] In this respect, the present study by Kumar et al . differs – severe cases appeared to have higher basal and stimulated serum cortisol than mild cases; although, critical illness-related corticosteroid insufficiency (CIRCI) was reported by Kumar et al .…”

Problems of Pathogenesis and Pathogenetic Therapy of COVID-19 from the Perspective of the General Theory of Pathological Systems (General Pathological Processes)

“…At the same time, cortisol levels and the hospital anxiety and sadness scale (HADS) were considerably greater in COVID-19 patients who died than in survivors [ 224 ]. Other authors, on the other hand, found COVID-19 symptoms of adrenal insufficiency in the most severe COVID-19 patients despite low cortisol and ACTH levels [ 225 ]. Another study found that essential SARS-CoV-2 receptors, such as ACE2 and TMPRSS2, are co-localized in adrenal cells, and that cortisol levels are lower in COVID-19-positive critically ill patients than in COVID-19-negative critically ill patients [ 226 ].…”

Endocrine risk factors for COVID-19: Endogenous and exogenous glucocorticoid excess

“…However, because of the expression of angiotensin-converting enzyme 2 (ACE2) in many endocrine glands [82,83], endocrine organs are likely to be involved in COVID-19 [6,84]. Alzahrani and colleagues reported on an impaired adrenocortical response in 28 patients with COVID-19 with plasma cortisol and ACTH concentrations indicating central adrenal insufficiency [85]. The authors found an inverse correlation between disease severity and [70] 20-47 % Corona et al [9] • Optimization of medical treatment is recommended to improve the eventual clinical course of COVID-19 Hypercoagulability [63] 54 % Levi et al [62] • Strict monitoring of coagulation parameters • Treatment with low-molecular-weight heparin is recommended, especially for hospitalized, moderately to severely ill patients Immune impairments [45] 21-51% Wu et al [116] • Due to a poor immune response, febrile response in the early phase might be limited • Because of the increased risk of secondary infections, prolonged antiviral treatment and empirical prophylaxis with broad-spectrum antibiotics should be considered in hospitalized cases of COVID-19 and florid CS Obesity [117] 32-41 % Rottoli et al [118] • Patients with CS and visceral obesity should be carefully monitored in case of COVID-19, due to an increased morbidity and mortality Atherosclerosis/ cardiovascular diseases [68] 27-31 % Zou et al [8] • Optimization of medical treatment is recommended to improve the eventual clinical course of COVID-19 Myopathy [75] 60-82 % De Giorgio et al [119] • Dyspnea might be enhanced due to left ventricular cardiomyopathy and/or thoracic muscle weakness in patients with CS Dyslipidemia [120] 38-71 % Zuin et al [121] • Optimization of medical treatment is recommended to improve the eventual clinical course of COVID-19 Mental illness [122] 50-81 % Barcella et al [123] • As mental illness is associated with an unfavorable outcome in patients with COVID-19, neuropsychiatric disorders in patients with CS should be considered and adequately treated Obstructive sleep apnea [115] 50 % Strausz et al [124] • Consistent therapy is recommended to improve the risk profile and prevent secondary consequences such as hypertension, reduced physical performance and further systemic effects above-mentioned report of Tan and colleagues on higher cortisol concentrations in patients with COVID-19…”

“…As the HPA axis function of the majority recovered within a year, the authors suggested a reversible hypophysitis or direct hypothalamic injury induced by the virus [89]. Whether the beneficial effects of dexamethasone in the treatment of COVID-19 is due to general supportive benefits of GCs in critical ill patients, mitigation of the cytokine release syndrome and ARDS [12,90], the treatment of undiagnosed adrenal insufficiency [83,85], or the suppression of endogenous cortisol secretion with reduced effects on mineralocorticoid receptors [53], has to be clarified in the future.…”