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1.
Oncol Nurs Forum ; 49(3): 207-211, 2022 May 01.
Article in English | MEDLINE | ID: covidwho-1846882

ABSTRACT

OBJECTIVES: Little is known about the biologic mechanisms of chronic chemotherapy-induced peripheral neuropathy (CIPN) pain. The purpose of this secondary analysis was to explore salivary cortisol patterns among cancer survivors with chronic CIPN pain to provide preliminary data regarding the role of hypothalamic-pituitary-adrenal axis dysregulation in the pathophysiology of this condition. SAMPLE & SETTING: 13 cancer survivors with chronic CIPN pain recruited from the breast, gastrointestinal, and gynecologic cancer centers at Dana-Farber Cancer Institute in Boston, Massachusetts. METHODS & VARIABLES: Salivary cortisol was collected on awakening, 30 minutes after awakening, and before going to bed on two consecutive days. Cortisol awakening response and diurnal cortisol slope were calculated by averaging results across two days. RESULTS: Cortisol was available from 13 participants. The median cortisol awakening response was -0.03 mcg/dl, and the average diurnal cortisol slope was -0.24 mcg/dl. IMPLICATIONS FOR NURSING: Mechanism-based treatments are needed for cancer survivors with chronic CIPN pain. Nurse scientists may use study results to explore stress-related mechanisms of chronic CIPN pain.


Subject(s)
Antineoplastic Agents , Peripheral Nervous System Diseases , Adenosine Monophosphate , Biomarkers , Circadian Rhythm , Female , Humans , Hydrocortisone , Hypothalamo-Hypophyseal System , Pain , Peripheral Nervous System Diseases/chemically induced , Pituitary-Adrenal System , Saliva
2.
Signal Transduct Target Ther ; 7(1): 137, 2022 04 25.
Article in English | MEDLINE | ID: covidwho-1805598

ABSTRACT

Whether and how innate antiviral response is regulated by humoral metabolism remains enigmatic. We show that viral infection induces progesterone via the hypothalamic-pituitary-adrenal axis in mice. Progesterone induces downstream antiviral genes and promotes innate antiviral response in cells and mice, whereas knockout of the progesterone receptor PGR has opposite effects. Mechanistically, stimulation of PGR by progesterone activates the tyrosine kinase SRC, which phosphorylates the transcriptional factor IRF3 at Y107, leading to its activation and induction of antiviral genes. SARS-CoV-2-infected patients have increased progesterone levels, and which are co-related with decreased severity of COVID-19. Our findings reveal how progesterone modulates host innate antiviral response, and point to progesterone as a potential immunomodulatory reagent for infectious and inflammatory diseases.


Subject(s)
COVID-19 , SARS-CoV-2 , Animals , Antiviral Agents , COVID-19/genetics , Humans , Hypothalamo-Hypophyseal System , Immunity, Innate/genetics , Mice , Pituitary-Adrenal System , Progesterone/pharmacology
3.
Brain Behav Immun ; 103: 19-27, 2022 07.
Article in English | MEDLINE | ID: covidwho-1773120

ABSTRACT

The global spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has led to the lasting pandemic of coronavirus disease 2019 (COVID-19) and the post-acute phase sequelae of heterogeneous negative impacts in multiple systems known as the "long COVID." The mechanisms of neuropsychiatric complications of long COVID are multifactorial, including long-term tissue damages from direct CNS viral involvement, unresolved systemic inflammation and oxidative stress, maladaptation of the renin-angiotensin-aldosterone system and coagulation system, dysregulated immunity, the dysfunction of neurotransmitters and hypothalamus-pituitaryadrenal (HPA) axis, and the psychosocial stress imposed by societal changes in response to this pandemic. The strength of safety, well-acceptance, and accumulating scientific evidence has now afforded nutritional medicine a place in the mainstream of neuropsychiatric intervention and prophylaxis. Long chain omega-3 polyunsaturated fatty acids (omega-3 or n-3 PUFAs) might have favorable effects on immunity, inflammation, oxidative stress and psychoneuroimmunity at different stages of SARS-CoV-2 infection. Omega-3 PUFAs, particularly EPA, have shown effects in treating mood and neurocognitive disorders by reducing pro-inflammatory cytokines, altering the HPA axis, and modulating neurotransmission via lipid rafts. In addition, omega-3 PUFAs and their metabolites, including specialized pro-resolvin mediators, accelerate the process of cleansing chronic inflammation and restoring tissue homeostasis, and therefore offer a promising strategy for Long COVID. In this article, we explore in a systematic review the putative molecular mechanisms by which omega-3 PUFAs and their metabolites counteract the negative effects of long COVID on the brain, behavior, and immunity.


Subject(s)
COVID-19 , Fatty Acids, Omega-3 , COVID-19/complications , Fatty Acids , Fatty Acids, Omega-3/therapeutic use , Humans , Hypothalamo-Hypophyseal System , Inflammation/drug therapy , Pituitary-Adrenal System , SARS-CoV-2
4.
Am J Physiol Regul Integr Comp Physiol ; 322(3): R161-R169, 2022 03 01.
Article in English | MEDLINE | ID: covidwho-1770007

ABSTRACT

Arginine vasopressin (AVP) is produced in the paraventricular (PVN) and supraoptic nuclei (SON). Peripheral AVP, which is secreted from the posterior pituitary, is produced in the magnocellular division of the PVN (mPVN) and SON. In addition, AVP is produced in the parvocellular division of the PVN (pPVN), where corticotrophin-releasing factor (CRF) is synthesized. These peptides synergistically modulate the hypothalamic-pituitary-adrenal (HPA) axis. Previous studies have revealed that the HPA axis was activated by hypovolemia. However, the detailed dynamics of AVP in the pPVN under hypovolemic state has not been elucidated. Here, we evaluated the effects of hypovolemia and hyperosmolality on the hypothalamus, using AVP-enhanced green fluorescent protein (eGFP) transgenic rats. Polyethylene glycol (PEG) or 3% hypertonic saline (HTN) was intraperitoneally administered to develop hypovolemia or hyperosmolality. AVP-eGFP intensity was robustly upregulated at 3 and 6 h after intraperitoneal administration of PEG or HTN in the mPVN. While in the pPVN, eGFP intensity was significantly increased at 6 h after intraperitoneal administration of PEG with significant induction of Fos-immunoreactive (-ir) neurons. Consistently, eGFP mRNA, AVP hnRNA, and CRF mRNA in the pPVN and plasma AVP and corticosterone were significantly increased at 6 h after intraperitoneal administration of PEG. The results suggest that AVP and CRF syntheses in the pPVN were activated by hypovolemia, resulting in the activation of the HPA axis.


Subject(s)
Arginine Vasopressin/genetics , Green Fluorescent Proteins/genetics , Hypothalamo-Hypophyseal System/metabolism , Hypovolemia/metabolism , Paraventricular Hypothalamic Nucleus/metabolism , Animals , Corticosterone/blood , Corticotropin-Releasing Hormone/genetics , Corticotropin-Releasing Hormone/metabolism , Disease Models, Animal , Genes, Reporter , Green Fluorescent Proteins/biosynthesis , Hypothalamo-Hypophyseal System/physiopathology , Hypovolemia/genetics , Hypovolemia/physiopathology , Injections, Intraperitoneal , Male , Paraventricular Hypothalamic Nucleus/physiopathology , Polyethylene Glycols/administration & dosage , Proto-Oncogene Proteins c-fos/metabolism , Rats, Transgenic , Rats, Wistar , Saline Solution, Hypertonic/administration & dosage , Supraoptic Nucleus/metabolism , Supraoptic Nucleus/physiopathology , Time Factors , Up-Regulation
5.
Lancet Diabetes Endocrinol ; 10(3): 221-230, 2022 03.
Article in English | MEDLINE | ID: covidwho-1665596

ABSTRACT

Current evidence suggests that severity and mortality of COVID-19 is higher in men than in women, whereas women might be at increased risk of COVID-19 reinfection and development of long COVID. Differences between sexes have been observed in other infectious diseases and in the response to vaccines. Sex-specific expression patterns of proteins mediating virus binding and entry, and divergent reactions of the immune and endocrine system, in particular the hypothalamic-pituitary-adrenal axis, in response to acute stress might explain the higher severity of COVID-19 in men. In this Personal View, we discuss how sex hormones, comorbidities, and the sex chromosome complement influence these mechanisms in the context of COVID-19. Due to its role in the severity and progression of SARS-CoV-2 infections, we argue that sexual dimorphism has potential implications for disease treatment, public health measures, and follow-up of patients predisposed to the development of long COVID. We suggest that sex differences could be considered in future pandemic surveillance and treatment of patients with COVID-19 to help to achieve better disease stratification and improved outcomes.


Subject(s)
COVID-19 , Health Status Disparities , Sex Characteristics , COVID-19/complications , COVID-19/epidemiology , COVID-19/physiopathology , Female , Humans , Hypothalamo-Hypophyseal System , Male , Pituitary-Adrenal System , Public Health
6.
Trials ; 23(1): 4, 2022 Jan 03.
Article in English | MEDLINE | ID: covidwho-1606541

ABSTRACT

BACKGROUND: Cardiogenic shock (CS) is a life-threatening condition characterized by circulatory insufficiency caused by an acute dysfunction of the heart pump. The pathophysiological approach to CS has recently been enriched by the tissue consequences of low flow, including inflammation, endothelial dysfunction, and alteration of the hypothalamic-pituitary-adrenal axis. The aim of the present trial is to evaluate the impact of early low-dose corticosteroid therapy on shock reversal in adults with CS. METHOD/DESIGN: This is a multicentered randomized, double-blind, placebo-controlled trial with two parallel arms in adult patients with CS recruited from medical, cardiac, and polyvalent intensive care units (ICU) in France. Patients will be randomly allocated into the treatment or control group (1:1 ratio), and we will recruit 380 patients (190 per group). For the treatment group, hydrocortisone (50 mg intravenous bolus every 6 h) and fludrocortisone (50 µg once a day enterally) will be administered for 7 days or until discharge from the ICU. The primary endpoint is catecholamine-free days at day 7. Secondary endpoints include morbidity and all-cause mortality at 28 and 90 days post-randomization. Pre-defined subgroups analyses are planned, including: postcardiotomy, myocardial infarction, etomidate use, vasopressor use, and adrenal profiles according the short corticotropin stimulation test. Each patient will be followed for 90 days. All analyses will be conducted on an intention-to-treat basis. DISCUSSION: This trial will provide valuable evidence about the effectiveness of low dose of corticosteroid therapy for CS. If effective, this therapy might improve outcome and become a therapeutic adjunct for patients with CS. TRIAL REGISTRATION: ClinicalTrials.gov , NCT03773822 . Registered on 12 December 2018.


Subject(s)
COVID-19 , Shock, Cardiogenic , Adult , Humans , Hypothalamo-Hypophyseal System , Multicenter Studies as Topic , Pituitary-Adrenal System , Randomized Controlled Trials as Topic , SARS-CoV-2 , Shock, Cardiogenic/diagnosis , Shock, Cardiogenic/drug therapy , Treatment Outcome
7.
Med Sci (Paris) ; 37(11): 1047-1054, 2021 Nov.
Article in French | MEDLINE | ID: covidwho-1585739

ABSTRACT

Hypothalamus stimulation by inflammatory and / or stress signals can trigger activation of the HPA (hypothalamic-pituitary-adrenal) axis, which includes the hypothalamus, pituitary and adrenal gland. Acute activation of the HPA axis is fundamental for the fight or flight response. It allows a maximal energy mobilization available for an effort, whilst erasing fatigue. On the contrary, the chronic activation of this axis decreases muscle efficiency and leads to chronic fatigue. In this second part of our review will be discussed several strategic points that need to be considered for attempting to understand and treat together inflammation and chronic fatigue.


TITLE: Mécanismes sous-jacents à la fatigue chronique, un symptôme trop souvent négligé - II. De l'immunité dérégulée à la neuroinflammation et ses conséquences. ABSTRACT: L'activation de l'hypothalamus par des signaux inflammatoires et/ou de stress peut déclencher celle de l'axe HPA (hypothalamic-pituitary-adrenal axis), qui intègre l'hypothalamus, l'hypophyse et la glande surrénale. L'activation aiguë de l'axe HPA est fondamentale pour la réponse fight or flight (« combats ou fuis ¼). Elle permet de mobiliser un maximum d'énergie pour un effort, tout en effaçant la fatigue. En revanche, son activation chronique diminue l'efficacité musculaire et entraîne une fatigue chronique. On discutera dans cette partie de plusieurs points stratégiques à considérer pour tenter de comprendre et de traiter ensemble inflammation et fatigue chroniques.


Subject(s)
Fatigue Syndrome, Chronic , Hypothalamo-Hypophyseal System , Fatigue Syndrome, Chronic/etiology , Humans , Pituitary Gland , Pituitary-Adrenal System
8.
Food Funct ; 12(22): 11241-11249, 2021 Nov 15.
Article in English | MEDLINE | ID: covidwho-1545659

ABSTRACT

The discovery of psychobiotics has improved the therapeutic choices available for clinical mental disorders and shows promise for regulating mental health in people by combining the properties of food and medicine. A Pediococcus acidilactici strain CCFM6432 was previously isolated and its mood-regulating effect was investigated in this study. Viable bacteria were given to chronically stressed mice for five weeks, and then the behavioral, neurobiological, and gut microbial changes were determined. CCFM6432 significantly reduced stress-induced anxiety-like behaviors, mitigated hypothalamic-pituitary-adrenal (HPA) axis hyperactivity, and reversed the abnormal expression of hippocampal phosphorylated CREB and the c-Fos protein. In particular, CCFM6432 improved the gut microbial composition by inhibiting the over-proliferated pathogenic bacteria (e.g., Escherichia-shigella) and promoting beneficial bacteria growth (e.g., Bifidobacterium). Lactic acid, rather than bacteriocin, was further confirmed as the key compound that determined the antimicrobial activity of CCFM6432. Collectively, these results first proved the psychobiotic potential of the Pediococcus acidilactici strain. Ingestion of CCFM6432, or fermented food containing it, may facilitate mental health management in daily life, especially during the COVID-19 pandemic.


Subject(s)
Anxiety/microbiology , Gastrointestinal Microbiome/drug effects , Hypothalamo-Hypophyseal System/drug effects , Lactic Acid/pharmacology , Pediococcus acidilactici , Probiotics/pharmacology , Animals , CREB-Binding Protein/metabolism , Hippocampus/metabolism , Mice , Mice, Inbred C57BL , Proto-Oncogene Proteins c-fos/metabolism
9.
Intensive Care Med ; 46(12): 2284-2296, 2020 12.
Article in English | MEDLINE | ID: covidwho-1451948

ABSTRACT

Current literature addressing the pharmacological principles guiding glucocorticoid (GC) administration in ARDS is scant. This paucity of information may have led to the heterogeneity of treatment protocols and misinterpretation of available findings. GCs are agonist compounds that bind to the GC receptor (GR) producing a pharmacological response. Clinical efficacy depends on the magnitude and duration of exposure to GR. We updated the meta-analysis of randomized trials investigating GC treatment in ARDS, focusing on treatment protocols and response. We synthesized the current literature on the role of the GR in GC therapy including genomic and non-genomic effects, and integrated current clinical pharmacology knowledge of various GCs, including hydrocortisone, methylprednisolone and dexamethasone. This review addresses the role dosage, timing of initiation, mode of administration, duration, and tapering play in achieving optimal response to GC therapy in ARDS. Based on RCTs' findings, GC plasma concentration-time profiles, and pharmacodynamic studies, optimal results are most likely achievable with early intervention, an initial bolus dose to achieve close to maximal GRα saturation, followed by a continuous infusion to maintain high levels of response throughout the treatment period. In addition, patients receiving similar GC doses may experience substantial between-patient variability in plasma concentrations affecting clinical response. GC should be dose-adjusted and administered for a duration targeting clinical and laboratory improvement, followed by dose-tapering to achieve gradual recovery of the suppressed hypothalamic-pituitary-adrenal (HPA) axis. These findings have practical clinical relevance. Future RCTs should consider these pharmacological principles in the study design and interpretation of findings.


Subject(s)
Glucocorticoids , Respiratory Distress Syndrome , Humans , Hypothalamo-Hypophyseal System , Methylprednisolone , Pituitary-Adrenal System , Respiratory Distress Syndrome/drug therapy
10.
Food Funct ; 12(22): 11241-11249, 2021 Nov 15.
Article in English | MEDLINE | ID: covidwho-1493239

ABSTRACT

The discovery of psychobiotics has improved the therapeutic choices available for clinical mental disorders and shows promise for regulating mental health in people by combining the properties of food and medicine. A Pediococcus acidilactici strain CCFM6432 was previously isolated and its mood-regulating effect was investigated in this study. Viable bacteria were given to chronically stressed mice for five weeks, and then the behavioral, neurobiological, and gut microbial changes were determined. CCFM6432 significantly reduced stress-induced anxiety-like behaviors, mitigated hypothalamic-pituitary-adrenal (HPA) axis hyperactivity, and reversed the abnormal expression of hippocampal phosphorylated CREB and the c-Fos protein. In particular, CCFM6432 improved the gut microbial composition by inhibiting the over-proliferated pathogenic bacteria (e.g., Escherichia-shigella) and promoting beneficial bacteria growth (e.g., Bifidobacterium). Lactic acid, rather than bacteriocin, was further confirmed as the key compound that determined the antimicrobial activity of CCFM6432. Collectively, these results first proved the psychobiotic potential of the Pediococcus acidilactici strain. Ingestion of CCFM6432, or fermented food containing it, may facilitate mental health management in daily life, especially during the COVID-19 pandemic.


Subject(s)
Anxiety/microbiology , Gastrointestinal Microbiome/drug effects , Hypothalamo-Hypophyseal System/drug effects , Lactic Acid/pharmacology , Pediococcus acidilactici , Probiotics/pharmacology , Animals , CREB-Binding Protein/metabolism , Hippocampus/metabolism , Mice , Mice, Inbred C57BL , Proto-Oncogene Proteins c-fos/metabolism
11.
Contemp Clin Trials ; 111: 106616, 2021 12.
Article in English | MEDLINE | ID: covidwho-1487636

ABSTRACT

Opioid Use Disorders (OUDs) and drug overdose deaths are increasing at alarmingly high rates in the United States. Stress and dysregulation in biologic stress response systems such as the hypothalamic-pituitary-adrenal axis and noradrenergic system appear to play an important role in the pathophysiology of substance use disorders and relapse to drug use, particularly for women. Alpha-2 adrenergic agonist medications effectively decrease noradrenergic activity and have demonstrated benefit in preventing relapse to substance use and decreasing stress-reactivity and craving in cocaine- and nicotine-dependent women, compared to men. Alpha-2 adrenergic agonists may help decrease stress reactivity in individuals with OUDs and prevent relapse to drug use, but gender differences have yet to be systematically explored. We describe the rationale, study design and methodology of a randomized, double-blind, placebo-controlled clinical trial examining gender differences in stress, craving and drug use among adult men and women with OUD taking methadone or buprenorphine and randomly assigned to an alpha-2 adrenergic agonist, lofexidine, compared to placebo. In addition, we describe methods for measuring daily stress, craving and drug use in participant's natural environment as well as participant's physiological (i.e., heart rate, cortisol) and psychological (i.e., stress, craving) response to laboratory social and drug cue stressors. Lastly, we detail methods adopted to sustain research activity while following guidelines for the COVID-19 pandemic. ClinicalTrials.gov Registration Number: NCT03718065.


Subject(s)
Analgesics, Opioid , COVID-19 , Clonidine/analogs & derivatives , Craving , Humans , Hypothalamo-Hypophyseal System , Pandemics , Pituitary-Adrenal System , Recurrence , SARS-CoV-2
12.
Int J Mol Sci ; 22(21)2021 Oct 25.
Article in English | MEDLINE | ID: covidwho-1480799

ABSTRACT

The hypothalamus-pituitary-adrenal (HPA) axis was described as the principal component of the stress response 85 years ago, along with the acute-phase reaction, and the defense response at the tissue level. The orchestration of these processes is essential since systemic inflammation is a double-edged sword; whereas inflammation that is timely and of appropriate magnitude is beneficial, exuberant systemic inflammation incites tissue damage with potentially devastating consequences. Apart from its beneficial cardiovascular and metabolic effects, cortisol exerts a significant immunoregulatory role, a major attribute being that it restrains the excessive inflammatory reaction, thereby preventing unwanted tissue damage. In this review, we will discuss the role of the HPA axis in the normal stress response and in critical illness, especially in critically ill patients with coronavirus disease 2019 (COVID-19). Finally, a chapter will be dedicated to the findings from clinical studies in critical illness and COVID-19 on the expression of the mediator of glucocorticoid actions, the glucocorticoid receptor (GCR).


Subject(s)
COVID-19/metabolism , Hypothalamo-Hypophyseal System/metabolism , Hypothalamo-Hypophyseal System/virology , Pituitary-Adrenal System/metabolism , Pituitary-Adrenal System/virology , Receptors, Glucocorticoid/metabolism , Critical Illness , Glucocorticoids/metabolism , Humans , Stress, Physiological
13.
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
14.
Int J Mol Sci ; 22(15)2021 Jul 26.
Article in English | MEDLINE | ID: covidwho-1344938

ABSTRACT

Adaptation of organisms to stressors is coordinated by the hypothalamic-pituitary-adrenal axis (HPA), which involves glucocorticoids (GCs) and glucocorticoid receptors (GRs). Although the effects of GCs are well characterized, their impact on brain adaptation to hypoxia/ischemia is still understudied. The brain is not only the most susceptible to hypoxic injury, but also vulnerable to GC-induced damage, which makes studying the mechanisms of brain hypoxic tolerance and resistance to stress-related elevation of GCs of great importance. Cross-talk between the molecular mechanisms activated in neuronal cells by hypoxia and GCs provides a platform for developing the most effective and safe means for prevention and treatment of hypoxia-induced brain damage, including hypoxic pre- and post-conditioning. Taking into account that hypoxia- and GC-induced reprogramming significantly affects the development of organisms during embryogenesis, studies of the effects of prenatal and neonatal hypoxia on health in later life are of particular interest. This mini review discusses the accumulated data on the dynamics of the HPA activation in injurious and non-injurious hypoxia, the role of the brain GRs in these processes, interaction of GCs and hypoxia-inducible factor HIF-1, as well as cross-talk between GC and hypoxic signaling. It also identifies underdeveloped areas and suggests directions for further prospective studies.


Subject(s)
Disease Resistance , Glucocorticoids/metabolism , Hypothalamo-Hypophyseal System/metabolism , Hypoxia, Brain/metabolism , Ischemic Preconditioning , Pituitary-Adrenal System/metabolism , Signal Transduction , Animals , Humans , Hypothalamo-Hypophyseal System/pathology , Hypoxia, Brain/prevention & control , Pituitary-Adrenal System/pathology
15.
J Clin Neurosci ; 91: 283-287, 2021 Sep.
Article in English | MEDLINE | ID: covidwho-1333598

ABSTRACT

The new coronavirus (COVID-19) has emerged now in the world as a pandemic. The SARS-CoV-2 infection causes variant common symptoms, such as dry cough, tiredness, dyspnea, fever, myalgia, chills, headache, chest pain, and conjunctivitis. Different organs may be affected by COVID-19, such as the respiratory system, gastrointestinal tract, kidneys, and CNS. However, the information about the COVID-19 infection in the CNS is insufficient. We do know that the virus can enter the central nervous system (CNS) via different routes, causing symptoms such as dizziness, headache, seizures, loss of consciousness, and depression. Depression is the most common disorder among all neurological symptoms following COVID-19 infection, although the mechanism of COVID-19-induced depression is not yet clear. The aim of the present study is to investigate the probable mechanisms of COVID-19-induced depression. The reasons for depression in infected patients may be due to social and pathological factors including social quarantine, economic problems, stress, changes in the HPA axis, inflammation due to the entry of proinflammatory cytokines into the CNS, production of inflammatory cytokines by microglia, mitochondrial disorders, damage to the hippocampus, and malnutrition. By evaluating different factors involved in COVID-19-induced depression, we have concluded that depression can be minimized by controlling stress, preventing the cytokine storm with appropriate anti-inflammatory drugs, and proper nutrition.


Subject(s)
COVID-19 , Depression/epidemiology , Depression/etiology , Humans , Hypothalamo-Hypophyseal System , Pituitary-Adrenal System , SARS-CoV-2
16.
Rev Endocr Metab Disord ; 23(2): 233-250, 2022 04.
Article in English | MEDLINE | ID: covidwho-1303352

ABSTRACT

Patients with endogenous or exogenous glucocorticoid (GC) excess exhibit a range of side effects, including an increased risk of infections. Via both mechanism, immune impairments and cardiometabolic concomitant diseases, patients with GC excess could be at increased risk for COVID-19. The impact on incidence and outcome of a SARS-CoV-2 infection in this population are not yet completely clear. This review aims to compile the data available to date and to discuss the existing literature on this topic. Further we highlight potential effects of SARS-CoV-2 on the hypothalamic-pituitary-adrenal axis as well as the influence of endogenous or exogenous GC excess on SARS-CoV-2 mRNA vaccination. There is growing evidence suggesting an increased risk of infection and severe outcome in patients with high-dose GC therapy after contracting SARS-CoV-2. The few data and case reports on patients with endogenous GC excess and SARS-CoV-2 infection point in a similar direction: chronic GC excess seems to be associated with an unfavorable course of COVID-19. Whether this is mainly a primary immune-mediated effect, or also triggered by the many GC-associated comorbidities in this population, is not yet fully understood. Patients with endogenous or exogenous GC excess should be considered as a vulnerable group during the SARS-CoV-2 pandemic. Regardless of the cause, vaccination and consistent surveillance and control of associated comorbidities are recommended.


Subject(s)
COVID-19 , Glucocorticoids , Glucocorticoids/adverse effects , Humans , Hypothalamo-Hypophyseal System , Pituitary-Adrenal System , Risk Factors , SARS-CoV-2
17.
Säo Paulo med. j ; 139(4): 398-404, Jul.-Aug. 2021. tab, graf
Article in English | WHO COVID, LILACS (Americas) | ID: covidwho-1288720

ABSTRACT

ABSTRACT BACKGROUND: Critical diseases usually cause hypercortisolemia via activation of the hypothalamic-pituitary-adrenal axis. OBJECTIVES: To investigate the relationship between serum total cortisol level and mortality among coronavirus disease 2019 (COVID-19) patients in the intensive care unit (ICU), at the time of their admission. DESIGN AND SETTING: Prospective study developed in a pandemic hospital in the city of Şırnak, Turkey. METHODS: We compared the serum total cortisol levels of 285 patients (141 COVID-19-negative patients and 144 COVID-19-positive patients) followed up in the ICU. RESULTS: The median cortisol level of COVID-19-positive patients was higher than that of COVID-19 negative patients (21.84 μg/dl versus 16.47 μg/dl; P < 0.001). In multivariate logistic regression analysis, mortality was associated with higher cortisol level (odds ratio: 1.20; 95% confidence interval: 1.08-1.35; P = 0.001). The cortisol cutoff point was 31 μg/dl (855 nmol/l) for predicting mortality among COVID-19-positive patients (area under the curve 0.932; sensitivity 59%; and specificity 95%). Among the COVID-19 positive patients with cortisol level ≤ 31 μg/dl (79%; 114 patients), the median survival was higher than among those with cortisol level > 31 μg/dl (21%; 30 patients) (32 days versus 19 days; log-rank test P < 0.001). CONCLUSION: Very high cortisol levels are associated with severe illness and increased risk of death, among COVID-19 patients in the ICU.


Subject(s)
Humans , Hydrocortisone , COVID-19 , Pituitary-Adrenal System , Prospective Studies , SARS-CoV-2 , Hypothalamo-Hypophyseal System , Intensive Care Units
18.
Psychoneuroendocrinology ; 132: 105345, 2021 10.
Article in English | MEDLINE | ID: covidwho-1284482

ABSTRACT

Loneliness is associated with multiple forms of psychopathology in youth. However, we do not yet know how loneliness gets "under the skin" in ways that may impact the long-term health and development of early adolescents. In particular, loneliness may influence youths' patterns of diurnal cortisol, an index of hypothalamic-pituitary-adrenal (HPA) axis functioning and a central predictor of health across the lifespan. The current severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2, or COVID-19) pandemic represents a salient period in which to study the consequences of loneliness, as recent work has provided evidence that the physical-distancing measures put in place to contain the virus have resulted in greater loneliness, particularly among youth. Thus, the current study aimed to examine the prospective association between loneliness during the COVID-19 pandemic and diurnal cortisol in early adolescents. We found that greater loneliness was associated with higher levels of cortisol at waking and a blunted cortisol awakening response (CAR). These results held even when controlling for covariates that can influence diurnal trajectories of cortisol. Critically, this pattern of HPA-axis functioning increases risk for adverse mental and physical health outcomes across adolescence and into adulthood. This study is the first to examine the prospective association between loneliness and diurnal cortisol in early adolescence, and the first to identify mechanisms that contribute to biological markers of distress during the COVID-19 pandemic. Findings underscore the importance of developing and distributing strategies to mitigate feelings of loneliness among youth.


Subject(s)
COVID-19 , Circadian Rhythm , Hydrocortisone/metabolism , Hypothalamo-Hypophyseal System/metabolism , Loneliness/psychology , Pituitary-Adrenal System/metabolism , Adolescent , Female , Humans , Hydrocortisone/analysis , Male , Pituitary-Adrenal Function Tests , SARS-CoV-2 , Saliva/chemistry
19.
Int J Mol Sci ; 22(13)2021 Jun 23.
Article in English | MEDLINE | ID: covidwho-1282517

ABSTRACT

The coronavirus disease 2019 (COVID-19) caused by infection of the severe respiratory syndrome coronavirus-2 (SARS-CoV-2) significantly impacted human society. Recently, the synthetic pure glucocorticoid dexamethasone was identified as an effective compound for treatment of severe COVID-19. However, glucocorticoids are generally harmful for infectious diseases, such as bacterial sepsis and severe influenza pneumonia, which can develop respiratory failure and systemic inflammation similar to COVID-19. This apparent inconsistency suggests the presence of pathologic mechanism(s) unique to COVID-19 that renders this steroid effective. We review plausible mechanisms and advance the hypothesis that SARS-CoV-2 infection is accompanied by infected cell-specific glucocorticoid insensitivity as reported for some other viruses. This alteration in local glucocorticoid actions interferes with undesired glucocorticoid to facilitate viral replication but does not affect desired anti-inflammatory properties in non-infected organs/tissues. We postulate that the virus coincidentally causes glucocorticoid insensitivity in the process of modulating host cell activities for promoting its replication in infected cells. We explore this tenet focusing on SARS-CoV-2-encoding proteins and potential molecular mechanisms supporting this hypothetical glucocorticoid insensitivity unique to COVID-19 but not characteristic of other life-threatening viral diseases, probably due to a difference in specific virally-encoded molecules and host cell activities modulated by them.


Subject(s)
Antiviral Agents/pharmacology , COVID-19/drug therapy , Dexamethasone/pharmacology , Hypothalamo-Hypophyseal System/physiology , Inflammation/drug therapy , Host Microbial Interactions , Humans , Immunity, Innate , SARS-CoV-2/drug effects , SARS-CoV-2/physiology , Severity of Illness Index , Virus Replication/drug effects
20.
Medicina (Kaunas) ; 57(6)2021 May 27.
Article in English | MEDLINE | ID: covidwho-1256605

ABSTRACT

The current COVID-19 pandemic has necessitated the need to find healthcare solutions that boost or support immunity. There is some evidence that high-velocity, low-amplitude (HVLA) controlled vertebral thrusts have the potential to modulate immune mediators. However, the mechanisms of the link between HVLA controlled vertebral thrusts and neuroimmune function and the associated potential clinical implications are less clear. This review aims to elucidate the underlying mechanisms that can explain the HVLA controlled vertebral thrust--neuroimmune link and discuss what this link implies for clinical practice and future research needs. A search for relevant articles published up until April 2021 was undertaken. Twenty-three published papers were found that explored the impact of HVLA controlled vertebral thrusts on neuroimmune markers, of which eighteen found a significant effect. These basic science studies show that HVLA controlled vertebral thrust influence the levels of immune mediators in the body, including neuropeptides, inflammatory markers, and endocrine markers. This narravtive review discusses the most likely mechanisms for how HVLA controlled vertebral thrusts could impact these immune markers. The mechanisms are most likely due to the known changes in proprioceptive processing that occur within the central nervous system (CNS), in particular within the prefrontal cortex, following HVLA spinal thrusts. The prefrontal cortex is involved in the regulation of the autonomic nervous system, the hypothalamic-pituitary-adrenal axis and the immune system. Bi-directional neuro-immune interactions are affected by emotional or pain-related stress. Stress-induced sympathetic nervous system activity also alters vertebral motor control. Therefore, there are biologically plausible direct and indirect mechanisms that link HVLA controlled vertebral thrusts to the immune system, suggesting HVLA controlled vertebral thrusts have the potential to modulate immune function. However, it is not yet known whether HVLA controlled vertebral thrusts have a clinically relevant impact on immunity. Further research is needed to explore the clinical impact of HVLA controlled vertebral thrusts on immune function.


Subject(s)
COVID-19 , Manipulation, Spinal , Humans , Hypothalamo-Hypophyseal System , Pandemics , Pituitary-Adrenal System , SARS-CoV-2
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