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1.
Pharmacol Res ; 157: 104866, 2020 07.
Article in English | MEDLINE | ID: covidwho-1318930

ABSTRACT

COVID-19 is a medical emergency, with 20 % of patients presenting with severe clinical manifestations. From the pathogenetic point of view, COVID-19 mimics two other well-known diseases characterized by cytokine storm and hyper-activation of the immune response, with consequent organ damage: acute graft-versus-host disease (aGVHD) and macrophage activation syndrome (MAS). Hematologists are confident with these situations requiring a prompt therapeutic approach for switching off the uncontrolled cytokine release; here, we discuss pros and cons of drugs that are already employed in hematology in the light of their possible application in COVID-19. The most promising drugs might be: Ruxolitinib, a JAK1/2 inhibitor, with a rapid and powerful anti-cytokine effect, tyrosine kinase inhibitors (TKIs), with their good anti-inflammatory properties, and perhaps the anti-Cd26 antibody Begelomab. We also present immunological data from gene expression experiments where TKIs resulted effective anti-inflammatory and pro-immune drugs. A possible combined treatment algorithm for COVID-19 is here proposed.


Subject(s)
Coronavirus Infections/drug therapy , Hematology/methods , Pneumonia, Viral/drug therapy , Betacoronavirus/drug effects , COVID-19 , Graft vs Host Disease/drug therapy , Humans , Macrophage Activation Syndrome/drug therapy , Pandemics , SARS-CoV-2
2.
Cureus ; 13(6): e15604, 2021 Jun 11.
Article in English | MEDLINE | ID: covidwho-1271055

ABSTRACT

Coronavirus disease 2019 (COVID-19) is associated with various cardiovascular manifestations, including myocarditis, myocardial infarction, and arrhythmias. A prothrombotic state is the primary underlying pathogenic mechanism. While cardiac arrhythmias manifest more commonly amongst critically ill COVID-19 populations, ventricular arrhythmias have been reported only in few cases. This report describes a case of a 95-year-old African American man with COVID-19, who developed sustained monomorphic ventricular tachycardia, which progressed to an electrical storm. The case highlights the importance of high clinical suspicion, early recognition of electrical abnormalities in patients with active COVID-19 infection, and its ability to precipitate fatal ventricular arrhythmia. Also, we provide a literature review on the electrical storm in COVID-19 patients, highlighting the pathophysiologic mechanisms and the management of this deadly arrhythmia.

3.
FASEB J ; 35(6): e21666, 2021 06.
Article in English | MEDLINE | ID: covidwho-1242109

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 is responsible for coronavirus disease 2019 (COVID-19). While COVID-19 is often benign, a subset of patients develops severe multilobar pneumonia that can progress to an acute respiratory distress syndrome. There is no cure for severe COVID-19 and few treatments significantly improved clinical outcome. Dexamethasone and possibly aspirin, which directly/indirectly target the biosynthesis/effects of numerous lipid mediators are among those options. Our objective was to define if severe COVID-19 patients were characterized by increased bioactive lipids modulating lung inflammation. A targeted lipidomic analysis of bronchoalveolar lavages (BALs) by tandem mass spectrometry was done on 25 healthy controls and 33 COVID-19 patients requiring mechanical ventilation. BALs from severe COVID-19 patients were characterized by increased fatty acids and inflammatory lipid mediators. There was a predominance of thromboxane and prostaglandins. Leukotrienes were also increased, notably LTB4 , LTE4 , and eoxin E4 . Monohydroxylated 15-lipoxygenase metabolites derived from linoleate, arachidonate, eicosapentaenoate, and docosahexaenoate were also increased. Finally yet importantly, specialized pro-resolving mediators, notably lipoxin A4 and the D-series resolvins, were also increased, underscoring that the lipid mediator storm occurring in severe COVID-19 involves pro- and anti-inflammatory lipids. Our data unmask the lipid mediator storm occurring in the lungs of patients afflicted with severe COVID-19. We discuss which clinically available drugs could be helpful at modulating the lipidome we observed in the hope of minimizing the deleterious effects of pro-inflammatory lipids and enhancing the effects of anti-inflammatory and/or pro-resolving lipid mediators.


Subject(s)
COVID-19 , Leukotriene B4/metabolism , Leukotriene E4/analogs & derivatives , Leukotriene E4/metabolism , Lipoxins/metabolism , Lung , SARS-CoV-2/metabolism , Adult , COVID-19/metabolism , COVID-19/pathology , COVID-19/therapy , Female , Humans , Lung/metabolism , Lung/pathology , Lung/virology , Male , Middle Aged
4.
Clin Infect Dis ; 72(7): 1247-1250, 2021 04 08.
Article in English | MEDLINE | ID: covidwho-1174886

ABSTRACT

Hyperinflammation is associated with increased mortality in coronavirus disease 2019 (COVID-19). In this retrospective, uncontrolled patient cohort with moderate -severe COVID-19, treatment with baricitinib plus hydroxychloroquine was associated with recovery in 11 of 15 patients. Baricitinib for the treatment of COVID-19 should be further investigated in randomized, controlled clinical trials.


Subject(s)
COVID-19 , Antiviral Agents/therapeutic use , Azetidines , COVID-19/drug therapy , Humans , Purines , Pyrazoles , Retrospective Studies , SARS-CoV-2 , Sulfonamides , Treatment Outcome
5.
J Intern Med ; 289(1): 97-115, 2021 01.
Article in English | MEDLINE | ID: covidwho-1153555

ABSTRACT

BACKGROUND: SARS-CoV-2 coronavirus infection ranges from asymptomatic through to fatal COVID-19 characterized by a 'cytokine storm' and lung failure. Vitamin D deficiency has been postulated as a determinant of severity. OBJECTIVES: To review the evidence relevant to vitamin D and COVID-19. METHODS: Narrative review. RESULTS: Regression modelling shows that more northerly countries in the Northern Hemisphere are currently (May 2020) showing relatively high COVID-19 mortality, with an estimated 4.4% increase in mortality for each 1 degree latitude north of 28 degrees North (P = 0.031) after adjustment for age of population. This supports a role for ultraviolet B acting via vitamin D synthesis. Factors associated with worse COVID-19 prognosis include old age, ethnicity, male sex, obesity, diabetes and hypertension and these also associate with deficiency of vitamin D or its response. Vitamin D deficiency is also linked to severity of childhood respiratory illness. Experimentally, vitamin D increases the ratio of angiotensin-converting enzyme 2 (ACE2) to ACE, thus increasing angiotensin II hydrolysis and reducing subsequent inflammatory cytokine response to pathogens and lung injury. CONCLUSIONS: Substantial evidence supports a link between vitamin D deficiency and COVID-19 severity but it is all indirect. Community-based placebo-controlled trials of vitamin D supplementation may be difficult. Further evidence could come from study of COVID-19 outcomes in large cohorts with information on prescribing data for vitamin D supplementation or assay of serum unbound 25(OH) vitamin D levels. Meanwhile, vitamin D supplementation should be strongly advised for people likely to be deficient.


Subject(s)
Angiotensin-Converting Enzyme 2/metabolism , COVID-19/ethnology , Ethnicity , SARS-CoV-2 , Thrombosis/etiology , Vitamin D Deficiency/ethnology , COVID-19/metabolism , Comorbidity , Global Health , Humans , Risk Factors , Thrombosis/ethnology , Thrombosis/metabolism , Vitamin D Deficiency/metabolism
7.
Dermatol Ther (Heidelb) ; 11(2): 339-345, 2021 Apr.
Article in English | MEDLINE | ID: covidwho-1083623

ABSTRACT

INTRODUCTION: The inflammation storm involved in coronavirus disease 2019 (COVID-19) infection and worsening and the psychological stress derived from current quarantine conditions can affect the course of many skin and scalp conditions. This study examined the possible effects of COVID-19 on alopecia areata (AA) relapse in patients suffering from these scalp conditions during the pandemic. METHODS: The study was carried out in the form of an observational cross-sectional type using a questionnaire sent by mail to a cohort of patients affected by AA during the pandemic from March 2020 to October 2020. RESULTS: During the pandemic, AA relapse was reported in 42.5% of the participants who also declared COVID-19 infection, confirmed by nasopharyngeal swab or hematological analysis. The relapse was reported about 2 months later COVID-19 infection (median of 2.14 months) and 74.0% of these participants continue to experience AA symptoms when the survey was proposed. Only 12.5% of participants reported AA relapse in the absence of COVID-19 infection. CONCLUSIONS: The present study reported a significant relapse in patients suffering from AA and infected by COVID-19. This phenomenon could be attributed to the inflammation storm typical of COVID-19 infection and the psychological stress derived from quarantine conditions.

8.
Front Psychiatry ; 12: 638866, 2021.
Article in English | MEDLINE | ID: covidwho-1080439
9.
Chest ; 159(1): e7-e11, 2021 01.
Article in English | MEDLINE | ID: covidwho-1064922

ABSTRACT

Coronavirus disease 2019 (COVID-19) has resulted in significant morbidity and mortality because of a lack of effective therapies. Therapeutic strategies under investigation target the overactive cytokine response with anti-cytokine or immunomodulators therapies. We present a unique case of severe cytokine storm resistant to multiple anti-cytokine therapies, but eventually responsive to etoposide. Thus, etoposide may have a role as salvage therapy in treatment of cytokine storm in COVID-19. To our knowledge, this is the first reported case of use of etoposide in COVID-19.


Subject(s)
COVID-19/complications , Cytokine Release Syndrome/drug therapy , Cytokine Release Syndrome/etiology , Etoposide/therapeutic use , Aged , Female , Humans , Salvage Therapy/methods , Severity of Illness Index
10.
Adv Ther ; 38(1): 782-791, 2021 01.
Article in English | MEDLINE | ID: covidwho-1064616

ABSTRACT

INTRODUCTION: The COVID-19 global pandemic caused by the novel coronavirus, SARS-CoV-2, and the consequent morbidity and mortality attributable to progressive hypoxemia and subsequent respiratory failure threaten to overrun hospital critical care units globally. New agents that address the hyperinflammatory "cytokine storm" and hypercoagulable pathology seen in these patients may be a promising approach to treat patients, minimize hospital stays, and ensure hospital wards and critical care units are able to operate effectively. Dociparstat sodium (DSTAT) is a glycosaminoglycan derivative of heparin with robust anti-inflammatory properties, with the potential to address underlying causes of coagulation disorders with substantially reduced risk of bleeding compared to commercially available heparin. METHODS: This study is a randomized, double-blind, placebo-controlled, phase 2/3 trial to determine the safety and efficacy of DSTAT added to standard of care in hospitalized adults with COVID-19 who require supplemental oxygen. Phase 2 will enroll 12 participants in each of two dose-escalating cohorts to confirm the safety of DSTAT in this population. Following review of the data, an additional 50 participants will be enrolled. Contingent upon positive results, phase 3 will enroll approximately 450 participants randomized to DSTAT or placebo. The primary endpoint is the proportion of participants who survive and do not require mechanical ventilation through day 28. DISCUSSION: Advances in standard of care, recent emergency use authorizations, and positive data with dexamethasone have likely contributed to an increasing proportion of patients who are surviving without the need for mechanical ventilation. Therefore, examining the time to improvement in the NIAID score will be essential to provide a measure of drug effect on recovery. Analysis of additional endpoints, including supportive biomarkers (e.g., IL-6, HMGB1, soluble-RAGE, D-dimer), will be performed to further define the effect of DSTAT in patients with COVID-19 infection. TRIAL REGISTRATION: ClinicalTrials.gov identifier; NCT04389840, Registered 13 May 2020.


Subject(s)
Acute Lung Injury/drug therapy , Anti-Inflammatory Agents/therapeutic use , COVID-19/complications , COVID-19/drug therapy , Heparin/therapeutic use , Respiratory Insufficiency/drug therapy , Acute Lung Injury/etiology , Adult , Aged , Aged, 80 and over , Double-Blind Method , Female , Humans , Male , Middle Aged , Respiratory Insufficiency/etiology , SARS-CoV-2/drug effects , Treatment Outcome
11.
Lancet Infect Dis ; 21(1): 25-26, 2021 01.
Article in English | MEDLINE | ID: covidwho-1059342
12.
Can J Respir Ther ; 56: 25-31, 2020.
Article in English | MEDLINE | ID: covidwho-1060415

ABSTRACT

The global pandemic COVID-19 is a contagious disease and its mortality rates ranging from 1% to 5% are likely due to acute respiratory distress syndrome (ARDS), and cytokine storm. A significant proportion of patients who require intubation succumb to the disease, despite the availability of ventilators and the best treatment practices. Researchers worldwide are in search of anti-inflammatory medicines in the hope of finding a cure for COVID-19. Low-level laser therapy (LLLT) has strong, anti-inflammatory effects confirmed by meta-analyses, and it may be therapeutic to ARDS. LLLT has been used for pain management, wound healing, and other health conditions by physicians, physiotherapists, and nurses worldwide for decades. In addition, it has been used in veterinary medicine for respiratory tract disease such as pneumonia. Laser light with low-power intensity is applied to the surface of the skin to produce local and systemic effects. Based on the clinical experience, peer-reviewed studies, and solid laboratory data in experimental animal models, LLLT attenuates cytokine storm at multiple levels and reduces the major inflammatory metabolites. LLLT is a safe, effective, low-cost modality without any side-effects that may be combined with conventional treatment of ARDS. We summarize the effects of LLLT on pulmonary inflammation and we provide a protocol for augmenting medical treatment in COVID-19 patients. LLLT combined with conventional medical therapy has the potential to prevent the progression of COVID-19, minimize the length of time needed on a ventilator, enhance the healing process, and shorten recovery time.

13.
J Clin Med ; 9(9)2020 Sep 14.
Article in English | MEDLINE | ID: covidwho-1021973

ABSTRACT

The repurposing of colchicine for the treatment of COVID-19 was suggested based in its immunomodulatory, anti-inflammatory, and anti-viral properties. We performed a single-center propensity score matched cohort study, including all consecutive COVID-19 patients admitted to a community hospital between 1 March 2020 and 30 May 2020. Patients were stratified according to the receipt of colchicine. The primary endpoint was defined as in-hospital death within 28-days follow-up. Secondary endpoints included favorable change in the Ordinal Scale for Clinical Improvement on days 14 and 28 versus baseline, proportion of patients not requiring supplemental oxygen on days 14 and 28, and proportion of patients discharged by day 28. In total data for 303 PCR positive COVID-19 patients were extracted and 66 patients were included in the 1:1 matched cohort study. At the end of the 28 day follow-up, patients receiving colchicine were approximately five times more likely to be discharged (odds ratio, 5.0; 95% confidence interval, 1.25-20.1; p = 0.023) and when comparing mortality, there were 3 deaths (9.1%) in patients receiving colchicine versus 11 deaths (33.3%) in the groups receiving standard of care (odds ratio, 0.20; 95% confidence interval, 0.05-0.80; p = 0.023). These observations warrant further investigation in large controlled clinical trials.

15.
Front Immunol ; 11: 1782, 2020.
Article in English | MEDLINE | ID: covidwho-945655

ABSTRACT

As the SARS-CoV-2 virus wreaks havoc on the populations, health care infrastructures and economies of nations around the world, finding ways to protect health care workers and bolster immune responses in the general population while we await an effective vaccine will be the difference between life and death for many people. Recent studies show that innate immune populations may possess a form of memory, termed Trained Immunity (TRIM), where innate immune cells undergo metabolic, mitochondrial, and epigenetic reprogramming following exposure to an initial stimulus that results in a memory phenotype of enhanced immune responses when exposed to a secondary, heterologous, stimulus. Throughout the literature, it has been shown that the induction of TRIM using such inducers as the BCG vaccine and ß-glucan can provide protection through altered immune responses against a range of viral infections. Here we hypothesize a potential role for ß-glucan in decreasing worldwide morbidity and mortality due to COVID-19, and posit several ideas as to how TRIM may actually shape the observed epidemiological phenomena related to COVID-19. We also evaluate the potential effects of ß-glucan in relation to the immune dysregulation and cytokine storm observed in COVID-19. Ultimately, we hypothesize that the use of oral ß-glucan in a prophylactic setting could be an effective way to boost immune responses and abrogate symptoms in COVID-19, though clinical trials are necessary to confirm the efficacy of this treatment and to further examine differential effects of ß-glucan's from various sources.


Subject(s)
Antiviral Agents/therapeutic use , Betacoronavirus , Coronavirus Infections/diet therapy , Coronavirus Infections/immunology , Dietary Fiber/therapeutic use , Immunologic Memory/drug effects , Pneumonia, Viral/diet therapy , Pneumonia, Viral/immunology , beta-Glucans/therapeutic use , Administration, Oral , Adult , Age Factors , Animals , Antiviral Agents/administration & dosage , Antiviral Agents/immunology , Antiviral Agents/pharmacology , BCG Vaccine/immunology , COVID-19 , Child , Coronavirus Infections/blood , Coronavirus Infections/virology , Cytokines/blood , Dietary Fiber/administration & dosage , Epigenesis, Genetic/immunology , Humans , Immunity, Innate/drug effects , Pandemics , Pneumonia, Viral/blood , Pneumonia, Viral/virology , Pre-Exposure Prophylaxis , SARS-CoV-2 , beta-Glucans/administration & dosage , beta-Glucans/immunology , beta-Glucans/pharmacology
16.
J Clin Med ; 9(9)2020 Sep 21.
Article in English | MEDLINE | ID: covidwho-892454

ABSTRACT

Coronavirus disease 2019 (COVID-19) patients can develop interstitial pneumonia, which, in turn, can evolve into acute respiratory distress syndrome (ARDS). This is accompanied by an inflammatory cytokine storm. severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) has proteins capable of promoting the cytokine storm, especially in patients with comorbidities, including obesity. Since currently no resolutive therapy for ARDS has been found and given the scientific literature regarding the use of adenosine, its application has been hypothesized. Through its receptors, adenosine is able to inhibit the acute inflammatory process, increase the protection capacity of the epithelial barrier, and reduce the damage due to an overactivation of the immune system, such as that occurring in cytokine storms. These features are known in ischemia/reperfusion models and could also be exploited in acute lung injury with hypoxia. Considering these hypotheses, a COVID-19 patient with unresponsive respiratory failure was treated with adenosine for compassionate use. The results showed a rapid improvement of clinical conditions, with negativity of SARS-CoV2 detection.

17.
BMC Pulm Med ; 20(1): 269, 2020 Oct 16.
Article in English | MEDLINE | ID: covidwho-873971

ABSTRACT

BACKGROUND: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes coronavirus disease 2019 (COVID-19) has spread to almost 100 countries, infected over 31 M patients and resulted in 961 K deaths worldwide as of 21st September 2020. The major clinical feature of severe COVID-19 requiring ventilation is acute respiratory distress syndrome (ARDS) with multi-functional failure as a result of a cytokine storm with increased serum levels of cytokines. The pathogenesis of the respiratory failure in COVID-19 is yet unknown, but diffuse alveolar damage with interstitial thickening leading to compromised gas exchange is a plausible mechanism. Hypoxia is seen in the COVID-19 patients, however, patients present with a distinct phenotype. Intracellular levels of nitric oxide (NO) play an important role in the vasodilation of small vessels. To elucidate the intracellular levels of NO inside of RBCs in COVID-19 patients compared with that of healthy control subjects. METHODS: We recruited 14 COVID-19 infected cases who had pulmonary involvement of their disease, 4 non-COVID-19 healthy controls (without pulmonary involvement and were not hypoxic) and 2 hypoxic non-COVID-19 patients subjects who presented at the Masih Daneshvari Hospital of Tehran, Iran between March-May 2020. Whole blood samples were harvested from patients and intracellular NO levels in 1 × 106 red blood cells (RBC) was measured by DAF staining using flow cytometry (FACS Calibour, BD, CA, USA). RESULTS: The Mean florescent of intensity for NO was significantly enhanced in COVID-19 patients compared with healthy control subjects (P ≤ 0.05). As a further control for whether hypoxia induced this higher intracellular NO, we evaluated the levels of NO inside RBC of hypoxic patients. No significant differences in NO levels were seen between the hypoxic and non-hypoxic control group. CONCLUSIONS: This pilot study demonstrates increased levels of intracellular NO in RBCs from COVID-19 patients. Future multi-centre studies should examine whether this is seen in a larger number of COVID-19 patients and whether NO therapy may be of use in these severe COVID-19 patients.


Subject(s)
Carbon Dioxide/metabolism , Coronavirus Infections/metabolism , Erythrocytes/metabolism , Hypoxia/metabolism , Nitric Oxide/metabolism , Oxygen/metabolism , Pneumonia, Viral/metabolism , Adult , Aged , Aged, 80 and over , Asymptomatic Diseases , Betacoronavirus , Blood Gas Analysis , COVID-19 , Case-Control Studies , Coronavirus Infections/blood , Coronavirus Infections/complications , Female , Flow Cytometry , Humans , Hypoxia/blood , Hypoxia/etiology , Male , Middle Aged , Pandemics , Partial Pressure , Pilot Projects , Pneumonia, Viral/blood , Pneumonia, Viral/complications , Pulmonary Disease, Chronic Obstructive/blood , Pulmonary Disease, Chronic Obstructive/complications , Pulmonary Disease, Chronic Obstructive/metabolism , SARS-CoV-2 , Vasodilation , Young Adult
18.
Int Immunopharmacol ; 89(Pt B): 107082, 2020 Dec.
Article in English | MEDLINE | ID: covidwho-872153

ABSTRACT

Severe acute respiratory syndrome Coronavirus-2 (SARS-CoV-2) is responsible for recent ongoing public health emergency in the world. Sharing structural and behavioral similarities with its ancestors [SARS and Middle East Respiratory Syndrome (MERS)], SARS-CoV-2 has lower fatality but faster transmission. We have gone through a long path to recognize SARS and MERS, therefore our knowledge regarding SARS-CoV-2 is not raw. Various responses of the immune system account for the wide spectrum of clinical manifestations in Coronavirus disease-2019 (COVID-19). Given the innate immune response as the front line of defense, it is immediately activated after the virus entry. Consequently, adaptive immune response is activated to eradicate the virus. However, this does not occur in every case and immune response is the main culprit causing the pathological manifestations of COVID-19. Lethal forms of the disease are correlated with inefficient and/or insufficient immune responses associated with cytokine storm. Current therapeutic approach for COVID-19 is in favor of suppressing extreme inflammatory responses, while maintaining the immune system alert and responsive against the virus. This could be contributing along with administration of antiviral drugs in such patients. Furthermore, supplementation with different compounds, such as vitamin D, has been tested to modulate the immune system responses. A thorough understanding of chronological events in COVID-19 contributing to the development of a highly efficient treatment has not figured out yet. This review focuses on the virus-immune system interaction as well as currently available and potential therapeutic approaches targeting immune system in the treatment of COVID-19 patients.


Subject(s)
COVID-19/immunology , Immunotherapy , SARS-CoV-2 , Adaptive Immunity , Angiotensin-Converting Enzyme 2/physiology , COVID-19/drug therapy , COVID-19/etiology , Humans , Immune System/drug effects , Immunity, Innate , Virus Internalization , Vitamin D/pharmacology
19.
Lancet Respir Med ; 8(12): 1233-1244, 2020 12.
Article in English | MEDLINE | ID: covidwho-867256

ABSTRACT

The description of a so-called cytokine storm in patients with COVID-19 has prompted consideration of anti-cytokine therapies, particularly interleukin-6 antagonists. However, direct systematic comparisons of COVID-19 with other critical illnesses associated with elevated cytokine concentrations have not been reported. In this Rapid Review, we report the results of a systematic review and meta-analysis of COVID-19 studies published or posted as preprints between Nov 1, 2019, and April 14, 2020, in which interleukin-6 concentrations in patients with severe or critical disease were recorded. 25 COVID-19 studies (n=1245 patients) were ultimately included. Comparator groups included four trials each in sepsis (n=5320), cytokine release syndrome (n=72), and acute respiratory distress syndrome unrelated to COVID-19 (n=2767). In patients with severe or critical COVID-19, the pooled mean serum interleukin-6 concentration was 36·7 pg/mL (95% CI 21·6-62·3 pg/mL; I2=57·7%). Mean interleukin-6 concentrations were nearly 100 times higher in patients with cytokine release syndrome (3110·5 pg/mL, 632·3-15 302·9 pg/mL; p<0·0001), 27 times higher in patients with sepsis (983·6 pg/mL, 550·1-1758·4 pg/mL; p<0·0001), and 12 times higher in patients with acute respiratory distress syndrome unrelated to COVID-19 (460 pg/mL, 216·3-978·7 pg/mL; p<0·0001). Our findings question the role of a cytokine storm in COVID-19-induced organ dysfunction. Many questions remain about the immune features of COVID-19 and the potential role of anti-cytokine and immune-modulating treatments in patients with the disease.


Subject(s)
COVID-19/blood , Cytokine Release Syndrome/blood , Interleukin-6/blood , Biomarkers/blood , COVID-19/immunology , Cytokine Release Syndrome/immunology , Humans , Interleukin-6/immunology , Respiratory Distress Syndrome/blood , Respiratory Distress Syndrome/immunology , Sepsis/blood , Sepsis/immunology , Severity of Illness Index
20.
Biomed Pharmacother ; 132: 110886, 2020 Dec.
Article in English | MEDLINE | ID: covidwho-866443

ABSTRACT

Host excessive inflammatory immune response to SARS-CoV-2 infection is thought to underpin the pathogenesis of COVID-19 associated severe pneumonitis and acute lung injury (ALI) or acute respiratory distress syndrome (ARDS). Once an immunological complication like cytokine storm occurs, anti-viral based monotherapy alone is not enough. Additional anti-inflammatory treatment is recommended. It must be noted that anti-inflammatory drugs such as JAK inhibitors, IL-6 inhibitors, TNF-α inhibitors, colchicine, etc., have been either suggested or are under trials for managing cytokine storm in COVID-19 infections. Natural astaxanthin (ASX) has a clinically proven safety profile and has antioxidant, anti-inflammatory, and immunomodulatory properties. There is evidence from preclinical studies that supports its preventive actions against ALI/ARDS. Moreover, ASX has a potent PPARs activity. Therefore, it is plausible to speculate that ASX could be considered as a potential adjunctive supplement. Here, we summarize the mounting evidence where ASX is shown to exert protective effect by regulating the expression of pro-inflammatory factors IL-1ß, IL-6, IL-8 and TNF-α. We present reports where ASX is shown to prevent against oxidative damage and attenuate exacerbation of the inflammatory responses by regulating signaling pathways like NF-ĸB, NLRP3 and JAK/STAT. These evidences provide a rationale for considering natural astaxanthin as a therapeutic agent against inflammatory cytokine storm and associated risks in COVID-19 infection and this suggestion requires further validation with clinical studies.


Subject(s)
COVID-19/drug therapy , Cytokines/antagonists & inhibitors , Fibrinolytic Agents/therapeutic use , SARS-CoV-2/drug effects , Animals , Antiviral Agents/pharmacology , Antiviral Agents/therapeutic use , COVID-19/blood , COVID-19/immunology , Cytokines/blood , Cytokines/immunology , Fibrinolytic Agents/pharmacology , Humans , Risk Factors , SARS-CoV-2/immunology , Xanthophylls/pharmacology , Xanthophylls/therapeutic use
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