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1.
Diagnosis and Treatment of Spinal Cord Injury ; : 131-146, 2022.
Article in English | Scopus | ID: covidwho-2060200

ABSTRACT

Spinal cord injuries cause not only a loss of mobility and sensibility, but also numerous chronic disorders such as: immunosuppression, higher rates of hypertension, neurogenic bladder, blood circulation impairments, and at T8 or above levels of injury, respiratory muscle weakness that can lead to breathing failure. All these conditions make chronic patients susceptible to infections due to a lowered immune system. The aim of this chapter is to analyze the clinical presentation of Covid-19 in patients with spinal cord injury. The authors pretend to make pause to understand if this emergent disease, which is deadly hitting our general population, behaves in the same way in these special patients, to understand if the spinal cord injury condition is acting as a risk factor for morbidity or not, and why. For this purpose, we want to explore the role that the immune system plays in causing infection in patients with spinal cord injury. Some spinal cord-injured patients develop a dysregulation of the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis, which negatively affects all immune processes. Therefore, the combination of this situation with other locally impaired conditions provide the suitable environment for developing an infection, as it occurs in urinary tract infections, the most frequent infection in these patients, because of the presence of a neurogenic bladder and the use of catheters to facilitate its voiding;or in pulmonary infections, the severest ones, because of the respiratory muscle weakness, dysphagia disorders, pulmonary edema, and the use of ventilators to assist with breathing. The physiopathology of these infections helps us to understand its appropriate diagnosis, treatment, and methods of prevention. Most of the published studies show a tendency of milder initial symptoms and a less severe evolution of the Covid-19 disease in spinal cord-injured patients, but currently further validation is needed to support or reject it. The altered immune response could play a critical role in the clinical presentation of these patients. Close observation of neurofunctional outcomes, especially with the help of the International Standards for Neurological Classification of the Spinal Cord Injury (ISNCSCI) Worksheet, is needed to conclude if this infection produces sensory and motor deficits in these patients. Telemedicine has demonstrated to be a useful and effective tool to provide access to medical healthcare to these chronically affected patients, especially under pandemic restriction. © 2022 Elsevier Inc. All rights reserved.

2.
Clin Immunol ; 245: 109133, 2022 Sep 29.
Article in English | MEDLINE | ID: covidwho-2049019

ABSTRACT

About one out of eight people to convalesce from COVID-19 suffer from the so called Long COVID, a syndrome of non-specific symptoms with unclear pathogenesis. In a recent study published in Cell Long COVID participants reporting respiratory symptoms had low cortisol levels. In an as yet unpublished analysis from Yale University low plasma cortisol levels discriminated Long COVID from asymptomatic convalescent or healthy non-infected controls. Although various immune perturbations were present in Long COVID, low levels of cortisol were prominent and strikingly, depression and anxiety were increased. It has become clear that Long COVID features may be similar to those described in myalgic encephalomyelitis/chronic fatigue syndrome, post-SARS sickness syndrome, and various chronic stress syndromes which have been linked to hypocortisolemia. Notably, lack of response of the hypothalamic-pituitary-adrenal axis to hypocortisolemia shows a suppressed axis in Long COVID. We suggest that the inability of hypothalamic-pituitary-adrenal axis to recover after the acute illness, perhaps due to protracted stress in predisposed individuals, may represent the pathogenetic basis of the Long COVID-associated clinical and immunological manifestations.

3.
The Yale Journal of Biology and Medicine ; 95(1):165-170, 2022.
Article in English | ProQuest Central | ID: covidwho-2045794

ABSTRACT

The relationship between chronic stress and chronic disease (including mental illness) is well established: HPA-axis hyperactivity leads to hormonal dysregulation of primary mediators (eg, glucocorticoids, cytokines, etc.), allostatic overload, and neurological degradation, followed by clinical manifestations of disease. Amid the largest public health crisis of the century lay a myriad of challenges pushing people beyond their limit. From experiencing loss of connection or dealing with loss of life to financial shocks of COVID-19 lockdowns or infection by the SARS-CoV-2 virus, stress is at an all-time high, threatening both brain and mental health at scale. Fortunately, there is a way forward: the neuroscience of resilience teaches us that it is possible to resist, recover, and redirect the brain from trauma to re-establish balance in the body and improve well-being. At the same time, health follows a social gradient: adverse and protective psychosocial factors are shaped by wider social and economic determinants of health. This paper argues the neurobiology of stress is not separate from health disparities linked to adverse factors (ie, stress) created by complex social and economic contexts. Therefore, the field of neuroscience is challenged to inform multi-context and multi-level approaches and engage with decision-makers to enact policies and interventions aimed at promoting the resilient element in a wider population health context. Undoubtedly, achieving such a goal for current and future generations to benefit and lead healthier lives requires a heroic effort from all key stakeholders. The cost of willful neglect to resolve these issues is too expensive.

4.
Psychoneuroendocrinology ; 145: 105894, 2022 11.
Article in English | MEDLINE | ID: covidwho-1996501

ABSTRACT

The COVID-19 pandemic can be characterized as a chronic stressor affecting the hypothalamic-pituitary-adrenal (HPA) axis, indexed by glucocorticoids (e.g., cortisol). We investigated whether salivary cortisol level is increased during a lockdown and whether a lockdown condition affects the association between loneliness, specific COVID-19 related stressors and salivary cortisol level. We conducted a smartphone-based ecological momentary assessment (EMA) study with 280 participants in Germany who experienced at least mild loneliness and distress amid COVID-19 from August 2020 to March 2021. We measured their momentary loneliness and COVID-related stressors including worries, information seeking behaviors and feelings of restriction during "no-lockdown" or "lockdown" stages amid COVID-19. Their salivary cortisol was measured 4 times on the last day of a 7-day EMA study. We found a significant increase in salivary cortisol levels during lockdown compared to no-lockdown. Lockdown stage was found to moderate the relationship between momentary loneliness and salivary cortisol level, i.e., loneliness was positively related to cortisol level specifically during lockdown. Mechanisms explaining the effect of forced social isolation on the association between loneliness and salivary cortisol need to be investigated in future studies.


Subject(s)
COVID-19 , Hydrocortisone , Communicable Disease Control , Humans , Hypothalamo-Hypophyseal System , Loneliness , Pandemics , Pituitary-Adrenal System , Saliva , Stress, Psychological
5.
Int J Mol Sci ; 23(13)2022 Jun 30.
Article in English | MEDLINE | ID: covidwho-1917523

ABSTRACT

Coronavirus disease 2019 (COVID-19) is a highly heterogeneous disease regarding severity, vulnerability to infection due to comorbidities, and treatment approaches. The hypothalamic-pituitary-adrenal (HPA) axis has been identified as one of the most critical endocrine targets of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that might significantly impact outcomes after infection. Herein we review the rationale for glucocorticoid use in the setting of COVID-19 and emphasize the need to have a low index of suspicion for glucocorticoid-induced adrenal insufficiency, adjusting for the glucocorticoid formulation used, dose, treatment duration, and underlying health problems. We also address several additional mechanisms that may cause HPA axis dysfunction, including critical illness-related corticosteroid insufficiency, the direct cytopathic impacts of SARS-CoV-2 infection on the adrenals, pituitary, and hypothalamus, immune-mediated inflammations, small vessel vasculitis, microthrombotic events, the resistance of cortisol receptors, and impaired post-receptor signaling, as well as the dissociation of ACTH and cortisol regulation. We also discuss the increased risk of infection and more severe illness in COVID-19 patients with pre-existing disorders of the HPA axis, from insufficiency to excess. These insights into the complex regulation of the HPA axis reveal how well the body performs in its adaptive survival mechanism during a severe infection, such as SARS-CoV-2, and how many parameters might disbalance the outcomes of this adaptation.


Subject(s)
COVID-19 , Pituitary-Adrenal System , Glucocorticoids/therapeutic use , Humans , Hydrocortisone , Hypothalamo-Hypophyseal System , SARS-CoV-2
6.
Evidence-Based Practice of Anesthesiology (Fourth Edition) ; : 217-225, 2023.
Article in English | ScienceDirect | ID: covidwho-1881583

ABSTRACT

Perioperative glucocorticoid replacement has been used in a variety of clinical conditions. Glucocorticoids have several benefits, such as antiinflammatory and immunosuppressant effects. Routine perioperative use, however, has been limited by side effects, lack of efficacy, and conflicting trial results. Nevertheless, glucocorticoid replacement is indicated in certain situations, including refractory septic shock, early moderate-to-severe acute respiratory distress syndrome, severe COVID-19, and relative adrenal insufficiency in patients undergoing surgical procedures. Further investigations are required to determine optimal glucocorticoid dosing and timing, identify patient subsets who benefit from replacement therapy, and reconcile conflicting results from clinical studies.

7.
Int J Environ Res Public Health ; 19(8)2022 04 13.
Article in English | MEDLINE | ID: covidwho-1785712

ABSTRACT

The COVID-19 pandemic has a major impact on society, particularly affecting its vulnerable members, including pregnant women and their unborn children. Pregnant mothers reported fear of infection, fear of vertical transmission, fear of poor birth and child outcomes, social isolation, uncertainty about their partner's presence during medical appointments and delivery, increased domestic abuse, and other collateral damage, including vaccine hesitancy. Accordingly, pregnant women's known vulnerability for mental health problems has become a concern during the COVID-19 pandemic, also because of the known effects of prenatal stress for the unborn child. The current narrative review provides a historical overview of transgenerational effects of exposure to disasters during pregnancy, and the role of maternal prenatal stress. We place these effects into the perspective of the COVID-19 pandemic. Hereby, we aim to draw attention to the psychological impact of the COVID-19 pandemic on women of reproductive age (15-49 year) and its potential associated short-term and long-term consequences for the health of children who are conceived, carried, and born during this pandemic. Timely detection and intervention during the first 1000 days is essential to reduce the burden of transgenerational effects of the COVID-19 pandemic.


Subject(s)
COVID-19 , COVID-19/epidemiology , Female , Humans , Pandemics , Parturition/psychology , Pregnancy , Pregnant Women/psychology , Stress, Psychological/epidemiology , Stress, Psychological/etiology
8.
Cureus ; 14(3): e23021, 2022 Mar.
Article in English | MEDLINE | ID: covidwho-1742938

ABSTRACT

Coronavirus disease 2019 (COVID-19) can affect multiple organs and systems, including the endocrine system. Its symptoms can last for months, resulting in post-COVID-19 conditions, among others. A small number of patients have central adrenal insufficiency (CAI) months after recovery from COVID-19; nevertheless, its pathogenesis has not been fully elucidated. The insulin tolerance test (ITT) is a gold standard test assessing the hypothalamic-pituitary-adrenal axis, and the corticotropin-releasing hormone (CRH) test is useful for differentiating CAI into secondary (pituitary) and tertiary (hypothalamic) adrenal insufficiency. We present a case of new-onset CAI in a young female patient who had no medical history other than COVID-19. Adrenocorticotropin hormone and cortisol responded poorly to both insulin-induced hypoglycemia and CRH administration. These findings suggest that the pituitary gland may be the primary site of hypothalamic-pituitary-adrenal dysfunction, although magnetic resonance imaging of the pituitary gland was unremarkable. To our knowledge, this is possibly the first and only case report of new-onset secondary adrenal insufficiency after recovery from COVID-19 in which the ITT and the CRH test were performed and highly suggestive for the pathogenesis of not only post-COVID-19 CAI but also post-COVID-19 conditions.

9.
Endocr Regul ; 55(3): 174-181, 2021 Sep 13.
Article in English | MEDLINE | ID: covidwho-1408880

ABSTRACT

The pathophysiology of COVID comprises an exaggerated pro-inflammatory response. Hypothalamic-pituitary-adrenal (HPA) axis has a crucial role in various inflammatory conditions and modulated immunological response. Limited evidence is available regarding the incidence and the effect of HPA dysfunction in COVID-19. Although the cortisol levels have only been estimated in a few studies, the dehydroepiandrosterone sulfate (DHEAS) release from the adrenal gland has not been explored yet. In this mini review, the authors discuss the role of dehydroepiandrosterone (DHEA) and DHEAS in the acute stress response and immunological modulation. Various effects of DHEAS have been demonstrated in different diseases. The specific inhibitory effect of DHEA on interleukin 6 (IL-6) could be of paramount importance in COVID-19. Further, DHEA supplementation has already been proposed in inflammatory conditions, like rheumatoid arthritis. DHEAS levels in COVID-19 may help to understand the HPA axis dysfunction as well as the possibility of repurposing DHEA as a drug for mitigating the pro-inflammatory COVID-19.


Subject(s)
COVID-19 , Dehydroepiandrosterone Sulfate/metabolism , Dehydroepiandrosterone/therapeutic use , Hypothalamo-Hypophyseal System , Immunologic Factors/therapeutic use , COVID-19/diagnosis , COVID-19/drug therapy , COVID-19/immunology , COVID-19/metabolism , Humans , Hypothalamo-Hypophyseal System/immunology , Hypothalamo-Hypophyseal System/metabolism
10.
Neurobiol Stress ; 14: 100296, 2021 May.
Article in English | MEDLINE | ID: covidwho-1051996

ABSTRACT

The COVID-19 pandemic continues to strongly affect people with health disadvantages, creating a heavy burden on medical systems and societies worldwide. Research is growing rapidly and recently revealed that stress-related factors such as socio-economic status, may also play a pivotal role. However, stress research investigating the underlying psychoneuroimmune interactions is missing. Here we address the question whether stress-associated neuroendocrine-immune mechanisms can possibly contribute to an increase in SARS-CoV-2 infections and influence the course of COVID-19 disease. Additionally, we discuss that not all forms of stress (e.g. acute versus chronic) are detrimental and that some types of stress could attenuate infection-risk and -progression. The overall aim of this review is to motivate future research efforts to clarify whether psychosocial interventions have the potential to optimize neuroendocrine-immune responses against respiratory viral infections during and beyond the COVID-19 pandemic. The current state of research on different types of stress is summarized in a comprehensive narrative review to promote a psychoneuroimmune understanding of how stress and its mediators cortisol, (nor)adrenaline, neuropeptides and neurotrophins can shape the immune defense against viral diseases. Based on this understanding, we describe how people with high psychosocial stress can be identified, which behaviors and psychosocial interventions may contribute to optimal stress management, and how psychoneuroimmune knowledge can be used to improve adequate care for COVID-19 and other patients with viral infections.

11.
Endocr Pract ; 27(2): 83-89, 2021 Feb.
Article in English | MEDLINE | ID: covidwho-1002515

ABSTRACT

OBJECTIVE: To study the adrenocortical response to an acute coronavirus disease-2019 (COVID-19) infection. METHODS: Morning plasma cortisol, adrenocorticotropic hormone (ACTH), and dehydroepiandrosterone sulfate levels were measured in 28 consecutive patients with COVID-19 (16 men, 12 women, median age 45.5 years, range 25-69 years) on day 1 to 2 of hospital admission. These tests were repeated twice in 20 patients and thrice in 15 patients on different days. The hormone levels were correlated with severity of the disease. RESULTS: The median morning cortisol level was 196 (31-587) nmol/L. It was <100 nmol/L in 8 patients (28.6%), <200 nmol/L in 14 patients (50%), and <300 nmol/L in 18 patients (64.3%). The corresponding ACTH values had a median of 18.5 ng/L (range 4-38 ng/L), and the ACTH level was <10 ng/L in 7 patients (26.9%), <20 ng/L in 17 patients (60.7%), and <30 ng/L in 23 patients (82.1%). The repeated testing on different days showed a similar pattern. Overall, if a cutoff level of <300 nmol/L is considered abnormal in the setting of acute disease, 9 patients (32%) had cortisol levels below this limit, regardless of whether the test was done only once (3 patients) or 3 times (6 patients). When the disease was more severe, the patients had lower cortisol and ACTH levels, suggesting a direct link between the COVID-19 infection and impaired glucocorticoid response. CONCLUSION: Unexpectedly, the adrenocortical response in patients with COVID-19 infection was impaired, and a significant percentage of the patients had plasma cortisol and ACTH levels consistent with central adrenal insufficiency.


Subject(s)
COVID-19 , Hypothalamo-Hypophyseal System , Adrenocorticotropic Hormone , Adult , Aged , Female , Humans , Hydrocortisone , Male , Middle Aged , Pituitary-Adrenal System , SARS-CoV-2
12.
Front Physiol ; 11: 890, 2020.
Article in English | MEDLINE | ID: covidwho-719750

ABSTRACT

Background: Covid-19 is an infectious disease caused by an invasion of the alveolar epithelial cells by coronavirus 19. The most severe outcome of the disease is the Acute Respiratory Distress Syndrome (ARDS) combined with hypoxemia and cardiovascular damage. ARDS and co-morbidities are associated with inflammatory cytokine storms, sympathetic hyperactivity, and respiratory dysfunction. Hypothesis: In the present paper, we present and justify a novel potential treatment for Covid19-originated ARDS and associated co-morbidities, based on the non-invasive stimulation of the auricular branch of the vagus nerve. Methods: Auricular vagus nerve stimulation activates the parasympathetic system including anti-inflammatory pathways (the cholinergic anti-inflammatory pathway and the hypothalamic pituitary adrenal axis) while regulating the abnormal sympatho-vagal balance and improving respiratory control. Results: Along the paper (1) we expose the role of the parasympathetic system and the vagus nerve in the control of inflammatory processes (2) we formulate our physiological and methodological hypotheses (3) we provide a large body of clinical and preclinical data that support the favorable effects of auricular vagus nerve stimulation in inflammation, sympatho-vagal balance as well as in respiratory and cardiac ailments, and (4) we list the (few) possible collateral effects of the treatment. Finally, we discuss auricular vagus nerve stimulation protective potential, especially in the elderly and co-morbid population with already reduced parasympathetic response. Conclusions: Auricular vagus nerve stimulation is a safe clinical procedure and it could be either an effective treatment for ARDS originated by Covid-19 and similar viruses or a supplementary treatment to actual ARDS therapeutic approaches.

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