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1.
Front Med (Lausanne) ; 9: 835421, 2022.
Article in English | MEDLINE | ID: covidwho-2099159

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection causes a disease (COVID-19) with multisystem involvement. The world is now entering a phase of post-COVID-19 manifestations in this pandemic. Secondary hemophagocytic lymphohistiocytosis (sHLH) is a life-threatening hyperinflammatory event triggered by viral infections, including SARS-CoV-2. Both Multisystem Inflammatory Syndrome-Adults (MIS-A) and Cytokine Storm Syndrome (CSS) are considered close differentials of sHLH and add to the spectrum of Post-acute COVID-19 syndrome (PACS). In this report, we presented the case of a middle-aged Asian man who was initially discharged upon recovery from severe COVID-19 infection after 17 days of hospitalization to a private institute and later came to our hospital 13 days post-discharge. Here, he was diagnosed with sHLH, occurring as an extension of CSS, with delayed presentation falling within the spectrum of PACS. The diagnosis of sHLH was made holistically with the HLH-2004 criteria. Our patient initially responded to intravenous immunoglobulin (IVIG) and dexamethasone, later complicated by disseminated Candida auris infection and had a fatal outcome. Though many cases of HLH during active COVID-19 and a few cases post COVID-19 recovery have been reported, based on H-score, which has limitations as a diagnostic tool. We report the first case report of post-COVID-19 sHLH using the HLH-2004 criteria, complicated by disseminated Candidemia, emphasizing that the care of patients with COVID-19 does not conclude at the time of hospital discharge. We highlight the importance of surveillance in the post-COVID phase for early detection of sHLH which may predispose to fatal opportunistic infections (OIs).

2.
Blood Purif ; : 1-8, 2022 Nov 02.
Article in English | MEDLINE | ID: covidwho-2098076

ABSTRACT

INTRODUCTION: High-flux hemodialysis membranes may modulate the cytokine storm of SARS-CoV-2, but their impact on chronic hemodialysis (CHD) patients is unknown. The aim of the study was the evaluation of asymmetric cellulose triacetate (ATA) and polymethylmethacrylate (PMMA) dialyzers on inflammatory markers and clinical outcomes in CHD patients with SARS-CoV-2. METHODS: A prospective, observational study on CHD patients with SARS-CoV-2 was carried out. Patients were enrolled from March 2020 to May 2021. Pre- and postdialysis C-reactive protein (CRP), procalcitonin (PCT), and interleukin-6 (IL-6) were determined at each session. Patients who underwent on-line hemodiafiltration (OLHDF) with a PMMA dialyzer were compared with those treated with OLHDF with a ATA dialyzer. The primary endpoint was the differences in the reduction ratio per session (RR) of CRP, PCT, IL-6, and IL-6 RR >25%. RESULTS: We consecutively enrolled 74 CHD patients with COVID-19, 48 were treated with ATA membrane, and 26 with PMMA. Median IL-6 RR was higher in the ATA group compared to PMMA (17.08%, IQR -9.0 to 40.0 vs. 2.95%, IQR -34.63 to 27.32). Median CRP RR was 7.77% (IQR 2.47-13.77) in the ATA group versus 4.8% (IQR -2.65 to 11.38) in the PMMA group (p = 0.0017). Median PCT-RR% was 77.38% (IQR 70.92-82.97) in ATA group versus 54.59% (IQR 42.62-63.16) in the PMMA group (p < 0.0001). A multiple logistic regression analysis with IL-6 RR >25% as the outcome including the membrane employed, pre-dialysis IL-6, CRP, PCT, and ferritin showed that ATA led to a higher probability to reach the outcome (OR 1.891, 95% CI 1.273-2.840, p = 0.0018) while higher CRP favors the risk of lower IL-6 RR values (OR 0.910, 95% CI 0.868-0.949, p ≤ 0.0001). CONCLUSIONS: In SARS-CoV-2 CHD patients treated with OLHDF, ATA showed a better anti-inflammatory profile, regarding IL-6 RR, compared to PMMA.

3.
Int Immunopharmacol ; 113(Pt B): 109428, 2022 Nov 07.
Article in English | MEDLINE | ID: covidwho-2095518

ABSTRACT

Coronavirus disease 2019 (COVID-19) outbreak has become a global public health emergency and has led to devastating results. Mounting evidence proposes that the disease causes severe pulmonary involvement and influences different organs, leading to a critical situation named multi-organ failure. It is yet to be fully clarified how the disease becomes so deadly in some patients. However, it is proven that a condition called "cytokine storm" is involved in the deterioration of COVID-19. Although beneficial, sustained production of cytokines and overabundance of inflammatory mediators causing cytokine storm can lead to collateral vital organ damages. Furthermore, cytokine storm can cause post-COVID-19 syndrome (PCS), an important cause of morbidity after the acute phase of COVID-19. Herein, we aim to explain the possible pathophysiology mechanisms involved in COVID-19-related cytokine storm and its association with multi-organ failure and PCS. We also discuss the latest advances in finding the potential therapeutic targets to control cytokine storm wishing to answer unmet clinical demands for treatment of COVID-19.

4.
Ter Arkh ; 94(5): 668-674, 2022 Jun 17.
Article in Russian | MEDLINE | ID: covidwho-2091500

ABSTRACT

AIM: To study the effect of levilimab or baricitinib in combination with standard therapy (ST) on the incidence of severe viral pneumonia associated with a new coronavirus infection COVID-19. MATERIALS AND METHODS: A multicenter, open-label observational study of the efficacy and safety of levilimab in combination with ST (group 1, n=100), baricitinib in combination with ST (group 2, n=139), or in comparison with ST (group 3, n=200) in outpatients with verified CT-1 pneumonia. RESULTS: According to the results of laboratory tests, patients treated with levilimab in combination with ST had the best dynamics of changes in CRP from reliably the highest level (mg/L) to the lowest in comparison with other groups. In the group of patients with ST, in contrast to the other groups, no dynamics of CRP was observed by day 5 of therapy. In group of hospitalized patients initially receiving levilimab in addition to ST, the rate of transfer to the intensive care unit (2 patients, 9.52%) and length of stay (4 days) was significantly lower compared to the values in patients in both the baricitinib group in combination with ST (7 patients, 15.56%; 5 days [interquartile range 36.5]) and in patients receiving ST alone (7 patients, 15.56%; 5 days [interquartile range 36.5]). Also in hospitalized patients we observed no statistically significant intergroup differences in the incidence of infectious complications and thromboembolic events, which confirms the safety of including levilimab or baricitinib in COVID-19 pathogenetic therapy regimens. Observational results support the hypothesis that the initial inclusion of levilimab or baricitinib in addition to ST is accompanied by a reduced risk of viral pneumonia progression. CONCLUSION: The addition of levilimab or baricitinib to the therapy regimen for coronavirus infection during the outpatient phase has demonstrated a preemptive anti-inflammatory effect and reduced the probability of lung tissue damage progression.


Subject(s)
COVID-19 , Pneumonia, Viral , Humans , COVID-19/drug therapy , Outpatients , SARS-CoV-2 , Pneumonia, Viral/complications , Pneumonia, Viral/drug therapy , Anti-Inflammatory Agents/therapeutic use , Treatment Outcome
5.
Curr Drug Targets ; 2022 Oct 25.
Article in English | MEDLINE | ID: covidwho-2089597

ABSTRACT

Infection with SARS-CoV-2 leads to COVID-19 which can manifest in various ways from asymptomatic or mild disease to acute respiratory distress syndrome. The occurrence of dysregulated inflammatory responses in the form of a cytokine storm has been reported in patients with severe COVID-19. Infection can also lead to dysfunctional hemostasis reflected in d-dimer and fibrin degradation product levels. Components of the coagulation and inflammatory systems can interact with each other to result in a procoagulation or proinflammatory state. The interplay between coagulation and inflammation has been elucidated for various diseases. In this article, we will discuss the occurrence of cytokine storms and dysfunctional hemostasis induced in COVID-19.

6.
Curr Pharm Des ; 2022 Oct 27.
Article in English | MEDLINE | ID: covidwho-2089590

ABSTRACT

BACKGROUND-AIM: In this narrative review, firstly we describe the characteristics of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the pathogenesis of its infection in humans. Later, the importance of mast cells in SARS-CoV-2 infection and their role in Coronavirus Disease 2019 (COVID-19) will be discussed. SARS-CoV-2 is a transmissible agent frequently detected in some mammalian species and nowadays also in humans. METHODS: Literature data published in PubMed that covered mast cells' role in cytokine release syndrome and related manifestations of COVID-19 disease was reviewed by the authors independently and collectively. Recommendations for the management of cytokine release syndrome and related manifestations were made by the authors. RESULTS: Mast cells are concentrated in environments where they encounter viruses, bacteria, and toxins, especially in the skin, nasal mucosa, lungs, airways, gastrointestinal tract, and meninges, to prevent their entry into the human body. Once SARS-CoV-2 enters the host, it stimulates one of them, mast cells, together with pre-existing innate immune cells that form a defensive barrier in the submucosa of the respiratory tract and nasal cavities against pathogenic microorganisms. The roles of mast cells in SARS-CoV-2 -induced hyper inflammation and cytokine storms have recently been one of the hot topics mostly discussed in the literature. CONCLUSION: Physicians should keep in mind the mast cells' role in cytokine release syndrome and related manifestations of COVID-19 disease. Mast cell-targeting therapies (eg, H1 and H2 receptor antagonists) can reduce the severity and course of the disease when used after complications associated with COVID-19 are suspected or seen.

7.
J Pharm Anal ; 2022 Oct 22.
Article in English | MEDLINE | ID: covidwho-2082761

ABSTRACT

SARS-CoV-2-induced cytokine storms constitute the primary cause of COVID-19 progression, severity, criticality, and death. Glucocorticoid and anti-cytokine therapies have been frequently administered to treat COVID-19 but have had limited clinical efficacy in severe and critical cases. Nevertheless, the weaknesses of these treatment modalities have prompted the development of anti-inflammatory therapy against this infection. We found that the broad-spectrum anti-inflammatory agent inosine downregulated proinflammatory IL-6, upregulated anti-inflammatory IL-10, and ameliorated acute inflammatory lung injury caused by multiple infectious agents. Inosine significantly improved survival in mice infected with SARS-CoV-2. It indirectly impeded TANK-binding kinase 1 (TBK1) phosphorylation by binding stimulator of interferon genes (STING) and glycogen synthase kinase-3ß (GSK3ß), inhibited the activation and nuclear translocation of the downstream transcription factors IRF3 and NF-κB, and downregulated IL-6 in the sera and lung tissues of mice infected with lipopolysaccharide (LPS), H1N1, or SARS-CoV-2. Thus, inosine administration is feasible for clinical anti-inflammatory therapy against severe and critical COVID-19. Moreover, targeting TBK1 is a promising strategy for inhibiting cytokine storms and mitigating acute inflammatory lung injury induced by SARS-CoV-2 and other infectious agents.

8.
Int J Mol Sci ; 23(21)2022 Oct 22.
Article in English | MEDLINE | ID: covidwho-2081827

ABSTRACT

Systemic juvenile idiopathic arthritis (sJIA) and its complication, macrophage activation syndrome (sJIA-MAS), are rare but sometimes very serious or even critical diseases of childhood that can occasionally be characterized by nonspecific clinical signs and symptoms at onset-such as non-remitting high fever, headache, rash, or arthralgia-and are biologically accompanied by an increase in acute-phase reactants. For a correct positive diagnosis, it is necessary to rule out bacterial or viral infections, neoplasia, and other immune-mediated inflammatory diseases. Delays in diagnosis will result in late initiation of targeted therapy. A set of biomarkers is useful to distinguish sJIA or sJIA-MAS from similar clinical entities, especially when arthritis is absent. Biomarkers should be accessible to many patients, with convenient production and acquisition prices for pediatric medical laboratories, as well as being easy to determine, having high sensitivity and specificity, and correlating with pathophysiological disease pathways. The aim of this review was to identify the newest and most powerful biomarkers and their synergistic interaction for easy and accurate recognition of sJIA and sJIA-MAS, so as to immediately guide clinicians in correct diagnosis and in predicting disease outcomes, the response to treatment, and the risk of relapses. Biomarkers constitute an exciting field of research, especially due to the heterogeneous nature of cytokine storm syndromes (CSSs) in the COVID era. They must be selected with utmost care-a fact supported by the increasingly improved genetic and pathophysiological comprehension of sJIA, but also of CSS-so that new classification systems may soon be developed to define homogeneous groups of patients, although each with a distinct disease.


Subject(s)
Arthritis, Juvenile , COVID-19 , Macrophage Activation Syndrome , Humans , Child , Macrophage Activation Syndrome/diagnosis , Macrophage Activation Syndrome/drug therapy , Macrophage Activation Syndrome/etiology , Arthritis, Juvenile/diagnosis , Arthritis, Juvenile/drug therapy , COVID-19/diagnosis , Biomarkers
9.
Front Microbiol ; 13: 1007081, 2022.
Article in English | MEDLINE | ID: covidwho-2080195

ABSTRACT

Recognition of viral infection by pattern recognition receptors is paramount for a successful immune response to viral infection. However, an unbalanced proinflammatory response can be detrimental to the host. Recently, multiple studies have identified that the SARS-CoV-2 spike protein activates Toll-like receptor 4 (TLR4), resulting in the induction of proinflammatory cytokine expression. Activation of TLR4 by viral glycoproteins has also been observed in the context of other viral infection models, including respiratory syncytial virus (RSV), dengue virus (DENV) and Ebola virus (EBOV). However, the mechanisms involved in virus-TLR4 interactions have remained unclear. Here, we review viral glycoproteins that act as pathogen-associated molecular patterns to induce an immune response via TLR4. We explore the current understanding of the mechanisms underlying how viral glycoproteins are recognized by TLR4 and discuss the contribution of TLR4 activation to viral pathogenesis. We identify contentious findings and research gaps that highlight the importance of understanding viral glycoprotein-mediated TLR4 activation for potential therapeutic approaches.

10.
Int Arch Allergy Immunol ; : 1-11, 2022 Oct 14.
Article in English | MEDLINE | ID: covidwho-2079118

ABSTRACT

INTRODUCTION: Cytokine storm and critical COVID-19 pneumonia are caused in at least 10% of patients by inborn errors of or auto-Abs to type I IFNs. The pathogenesis of life-threatening COVID-19 pneumonia in other patients remains unknown. METHODS: This study was conducted at Masih Daneshvari Hospital, Tehran, Iran. In the period of study, 75 confirmed cases of COVID-19 with presentations ranging from mild upper respiratory tract infection to lower respiratory tract infection, including moderate, severe, and critical disease, were recruited. Expression of STING mRNA was measured in peripheral blood mononuclear cells (PBMCs) and compared between patients with different severity and outcome. RESULTS: There was a significant negative correlation between age and STING expression level (p value = 0.010). Patients with "severe to critical" illness had a 20-fold lower STING expression level compared to the "mild to moderate" group (p value = 0.001). Also, the results showed lower expressions of STING in the patients admitted to the ICU (p value = 0.015). Patients who finally died had lower expression of STING at the time of sampling (p value = 0.041). CONCLUSION: STING mRNA expression in PBMCs was significantly lower in older COVID-19 cases, the patients with more severe illness, who needed intensive care, and who eventually died.

11.
Cannabis Cannabinoid Res ; 7(5): 582-590, 2022 10.
Article in English | MEDLINE | ID: covidwho-2077548

ABSTRACT

The coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory distress syndrome coronavirus 2 (SARS-Cov-2), was identified for the first time in late 2019 in China, resulting in a global pandemic of massive impact. Despite a fast development and implementation of vaccination strategies, and the scouting of several pharmacological treatments, alternative effective treatments are still needed. In this regard, cannabinoids represent a promising approach because they have been proven to exhibit several immunomodulatory, anti-inflammatory, and antiviral properties in COVID-19 disease models and related pathological conditions. This mini-review aims at providing a practical brief overview of the potential applications of cannabinoids so far identified for the treatment and prevention of COVID-19, finally considering key aspects related to their technological and clinical implementation.


Subject(s)
COVID-19 , Cannabinoids , Humans , COVID-19/drug therapy , SARS-CoV-2 , Cannabinoids/pharmacology , Antiviral Agents/pharmacology , Anti-Inflammatory Agents
12.
Immunopharmacol Immunotoxicol ; : 1-3, 2022 Oct 19.
Article in English | MEDLINE | ID: covidwho-2077370

ABSTRACT

NETosis is a type of neutrophil extinction that outcome in the liberation of extracellular chromatin and protein accumulation, which contains antiviral proteins, produced by an external pathogen. Neutrophils can show bipolar action in special circumstances. This event, along with other circumstances, involves COVID-19. Neutrophil extracellular traps (NETs) are involved in the pathogenesis of COVID-19 by creating a pro-inflammatory and pre-coagulation state that leads to numerous organ losses. This form of host defense, which is promoted by neutrophils, is closely related to the known cytokine storm in severe COVID-19 patients. Hence, these two elements reveal possibly the treatment of the target for SARS-CoV-2 infections intense.

13.
Indian J Clin Biochem ; : 1-7, 2021 Nov 10.
Article in English | MEDLINE | ID: covidwho-2075674

ABSTRACT

SARS-CoV-2 is the third coronavirus to have caused severe disease in humans in the last two decades, with approximately 5% of all patients and 20% of hospitalized patients experiencing severe symptoms, necessitating intensive care. The occurrence of Cytokine Storm has been implicated in the immune-pathogenesis of severe COVID-19. This is associated with cardiac injury, precipitated by cytokine mediated imbalance of coagulation and fibrinolysis, in the lung alveoli. In the absence of proven therapeutic agents, combinations of anti-viral drugs, immune-modulators and other adjunctive therapies have been tried in different clinical settings. A total of 128 confirmed cases of severe COVID-19 admitted to BLK-MAX Super Speciality Hospital between 16th of June to 31st of July, 2020 were included in this study. The correlation of age, gender, first value (on admission) of serum IL-6 and D-dimer, and impact of Tocilizumab and Remdesivir therapy on clinical outcome (28-day mortality), was evaluated in confirmed cases of severe COVID-19. The mortality rate was highest in the age group above 70 years. The incidence of death was significantly higher in males above 50 years, when age and gender were considered together. IL-6 and D-dimer levels >70 pg/mL and > 0.5µg FEU/mL respectively, were associated with poor outcome. 85.3% of patients treated with Remdesivir showed clinical improvement. When Tocilizumab and Remdisivir were administered together, 44.0% of patients survived while 56% expired. 79.7% of patients survived while 20.3% expired when neither Tocilizumab nor Remdesivir was administered.

14.
International Journal of Pediatrics-Mashhad ; 10(9):16745-16757, 2022.
Article in English | Web of Science | ID: covidwho-2071491

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) provokes the host immune responses and induces severe respiratory syndrome by overreaction of immune cells. IL-1 beta is a proinflammatory cytokine highly associated with the related inflammation and cytokine storm, and several IL-1 beta antagonists are being used to treat cytokine release syndrome (CRS). Accordingly, some studies and clinical trials are investigating the effects of IL-1 beta antagonists for controlling Coronavirus disease 2019 (COVID-19) associated CRS. Here, we will review any interaction and association between IL-1 beta and SARS-CoV-2 infection.

15.
Microorganisms ; 10(10)2022 Oct 10.
Article in English | MEDLINE | ID: covidwho-2071644

ABSTRACT

The coronavirus disease 2019 (COVID-19) pandemic began in January 2020 in Wuhan, China, with a new coronavirus designated SARS-CoV-2. The principal cause of death from COVID-19 disease quickly emerged as acute respiratory distress syndrome (ARDS). A key ARDS pathogenic mechanism is the "Cytokine Storm", which is a dramatic increase in inflammatory cytokines in the blood. In the last two years of the pandemic, a new pathology has emerged in some COVID-19 survivors, in which a variety of long-term symptoms occur, a condition called post-acute sequelae of COVID-19 (PASC) or "Long COVID". Therefore, there is an urgent need to better understand the mechanisms of the virus. The spike protein on the surface of the virus is composed of joined S1-S2 subunits. Upon S1 binding to the ACE2 receptor on human cells, the S1 subunit is cleaved and the S2 subunit mediates the entry of the virus. The S1 protein is then released into the blood, which might be one of the pivotal triggers for the initiation and/or perpetuation of the cytokine storm. In this study, we tested the hypothesis that the S1 spike protein is sufficient to activate inflammatory signaling and cytokine production, independent of the virus. Our data support a possible role for the S1 spike protein in the activation of inflammatory signaling and cytokine production in human lung and intestinal epithelial cells in culture. These data support a potential role for the SARS-CoV-2 S1 spike protein in COVID-19 pathogenesis and PASC.

16.
J Pers Med ; 12(10)2022 Oct 17.
Article in English | MEDLINE | ID: covidwho-2071576

ABSTRACT

BACKGROUND: Immune dysregulation has been linked to morbidity and mortality in COVID-19 patients. Understanding the immunology of COVID-19 is critical for developing effective therapies, diagnostics, and prophylactic strategies to control the disease. AIM: The aim of this study was to correlate cytokine and chemokine serum levels with COVID-19 disease severity and mortality. SUBJECTS AND METHODS: A total of 60 hospitalized patients from the Tabuk region of Saudi Arabia with confirmed COVID-19 were included in the study. At hospital admission, the IL-1 ß, IL-2, IL-8, IL-10, LT-B4, and CCL-2 serum levels were measured. The cytokine levels in COVID-19 patients were compared to the levels in 30 healthy matched control subjects. RESULTS: The IL-1 ß, IL-2, LTB-4, CCL-2, and IL-8 levels (but not IL-10) were significantly higher in all COVID-19 patients (47 survivors and 13 non-survivors) compared with the levels in the healthy control group. In the non-survivor COVID-19 patients, patients' age, D-dimer, and creatinine kinase were significantly higher, and IL-1 ß, IL-2, and IL-8 were significantly lower compared with the levels in the survivors. CONCLUSION: Mortality rates in COVID-19 patients are associated with increased age and a failure to mount an effective immune response rather than developing a cytokine storm. These results warrant the personalized treatment of COVID-19 patients based on cytokine profiling.

17.
Cytokine Growth Factor Rev ; 2022 Oct 13.
Article in English | MEDLINE | ID: covidwho-2068864

ABSTRACT

The development of therapies for SARS-CoV-2 infection, based on virus biology and pathology, and of large- and small-scale randomized controlled trials, have brought forward several antiviral and immunomodulatory drugs targeting the disease severity. Casirivimab/Imdevimab monoclonal antibodies and convalescent plasma to prevent virus entry, Remdesivir, Molnupiravir, and Paxlovid nucleotide analogs to prevent viral replication, a variety of repurposed JAK-STAT signaling pathway inhibitors, corticosteroids, and recombinant agonists/antagonists of cytokine and interferons have been found to provide clinical benefits in terms of mortality and hospitalization. However, current treatment options face multiple clinical needs, and therefore, in this review, we provide an update on the challenges of the existing therapeutics and highlight drug development strategies for COVID-19 therapy, based on ongoing clinical trials, meta-analyses, and clinical case reports.

18.
Carbohydr Polym ; 297: 120032, 2022 Dec 01.
Article in English | MEDLINE | ID: covidwho-2068751

ABSTRACT

The cytokine storm is highly associated with inflammatory-type disease severity and patients' survival. Plant polysaccharides, the main natural phytomedicine source, have a great potential to be an effective drug to treat cytokine storm. Herein we found that a polymeric acemannan (ABPA1) isolated from Aloe Vera Barbadensis extract C (AVBEC) exerted prominent inhibitory effects on inflammation-induced cytokine storm. The results displayed that ABPA1 effectively suppressed LPS-induced proinflammatory cytokines release in vitro. Moreover, ABPA1 treatment alleviated the cytokine storm and tissue damage in LPS- and IAV-induced mouse pneumonia models, and altered the phenotypic balance of macrophages in lung tissues. Functionally, ABPA1 enhanced macrophage M2 polarization and phagocytosis in RAW264.7 cells and inhibited LPS-induced M1 polarization. Mechanistically, ABPA1 enhanced mitochondrial metabolism and OXPHOS through activated PI3K/Akt/GSK-3ß signalling pathway. Overall, our findings suggest that ABPA1 may modulate macrophage activation and mitochondrial metabolism by targeting PI3K/Akt/GSK-3ß signalling pathway, thereby alleviating cytokine storm and inflammation.


Subject(s)
Aloe , Aloe/metabolism , Animals , Cytokine Release Syndrome , Cytokines/metabolism , Glycogen Synthase Kinase 3 beta/metabolism , Lipopolysaccharides/pharmacology , Macrophages , Mannans , Mice , Phosphatidylinositol 3-Kinases/metabolism , Plant Extracts/pharmacology , Polysaccharides/pharmacology , Proto-Oncogene Proteins c-akt/metabolism
19.
Indian Journal of Critical Care Medicine ; 26(10):1069-1071, 2022.
Article in English | EMBASE | ID: covidwho-2066999
20.
New Armenian Medical Journal ; 16(2):33-37, 2022.
Article in English | EMBASE | ID: covidwho-2067788

ABSTRACT

COVID-19 caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is re-sponsible for the recent global pandemic, with increasing number of cases reported globally. Our understanding of this novel respiratory virus deepens, it is increasingly clear that its effects extend beyond that of the respiratory system and can be extended to the almost all organ systems. SARS-CoV-2 causes lung inflammation which progresses to cytokine storm in the most severe cases. The lungs of patients with COVID-19 show extensive alveolar and interstitial inflammation. COVID-19 causes a spectrum of complications, with frequent involvement of the hemostatic system and there is a high incidence of venous thromboembolism in hospitalized COVID-19 patients, particularly those with severe illness. There is evidence of current body knowledge that COVID-19 induced by microvascular angiopathy can lead to a wide range of tissue pathology and clinical complications, such as Kawasaki disease, Buerger's syndrome and other systemic inflammatory disorders. Thromboangiitis obliterans (TAO) or Buerger's disease is a segmental occlusive inflammatory condition of arteries and veins, characterized by thrombosis and recana-lization of the affected vessels. Limb infection at diagnosis was associated with a 4-fold higher risk of amputation. Smoking cessation was strongly associated with a lower rate of vascular events and amputation. TAO appears more likely to be a systemic disorder rather than a localized vasculopathy. Therefore, treatment protocols based on systemic treatment of TAO patients may be more helpful than localized treatment, such as bypass surgery and endovascular procedures. We present a case of a 53-years-old male with positive SARS-CoV-2 PCR test. Furter exami-nation showed that patient had pneumonia, moreover, based on the duplex scan results the diagnosis of thromboangiitis obliterans (TAO) or Buerger's disease was confirmed. This disease itself is associated with a high risk of thrombosis and alongside with COVID-19 can cause unpredict-able outcome. Patient underwent the day-round observation, received the appropriate treatment and was successfully discharged from the hospital on the day 11. Copyright © 2022, Yerevan State Medical University. All rights reserved.

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