First confirmed case of multisystem inflammatory syndrome in adult in Egypt.

Key Clinical Message: Our case report demonstrates extremely uncommon data associated with MIS-A, such as cholestatic jaundice, anemia, and quickly progressing pneumonia. IVIG and pulse steroid medications are the best treatments for improving clinical outcomes. Abstract: We report a case of multiple organ dysfunctions due to MIS-A in an adult with a history of suspected COVID-19. Our case demonstrates extremely uncommon data associated with MIS-A, such as cholestatic jaundice, anemia, and quickly progressing pneumonia. IVIG and pulse steroid medications are the best treatments for improving clinical outcomes.

SARS‐CoV‐2 induced HDL dysfunction may affect the host's response to and recovery from COVID‐19

Introduction Covid‐19 is linked with the development of cardio‐metabolic disorders, including dyslipidemia, dysregulation of high‐density lipoprotein (HDL), and low‐density lipoprotein (LDL). Furthermore, SARS‐Co‐2 infection is associated with noteworthy changes in lipid profile, which is suggested as a possible biomarker to support the diagnosis and management of Covid‐19. Methods This paper adopts the literature review method to obtain information about how Covid‐19 affects high‐risk group patients and may cause severe and critical effects due to the development of acute lung injury and acute respiratory distress syndrome. A narrative and comprehensive review is presented. Results Reducing HDL in Covid‐19 is connected to the disease severity and poor clinical outcomes, suggesting that high HDL serum levels could benefit Covid‐19. SARS‐CoV‐2 binds HDL, and this complex is attached to the co‐localized receptors, facilitating viral entry. Therefore, SARS‐CoV‐2 infection may induce the development of dysfunctional HDL through different mechanisms, including induction of inflammatory and oxidative stress with activation of inflammatory signaling pathways. In turn, the induction of dysfunctional HDL induces the activation of inflammatory signaling pathways and oxidative stress, increasing Covid‐19 severity. Conclusions Covid‐19 is linked with the development of cardio‐metabolic disorders, including dyslipidemia in general and dysregulation of high‐density lipoprotein and low‐density lipoprotein. Therefore, the present study aimed to overview the causal relationship between dysfunctional high‐density lipoprotein and Covid‐19. While Covid‐19 is linked with the development of cardio‐metabolic disorders, including dyslipidemia and dysregulation of high‐density lipoprotein and low‐density lipoprotein, this study aimed to overview the causal relationship between dysfunctional high‐density lipoprotein and Covid‐19.

Mixed storm in SARS‐CoV‐2 infection: A narrative review and new term in the Covid‐19 era

Coronavirus disease 2019 (Covid‐19) is caused by a novel severe acute respiratory syndrome coronavirus virus type 2 (SARS‐CoV‐2) leading to the global pandemic worldwide. Systemic complications in Covid‐19 are mainly related to the direct SARS‐CoV‐2 cytopathic effects, associated hyperinflammation, hypercytokinemia, and the development of cytokine storm (CS). As well, Covid‐19 complications are developed due to the propagation of oxidative and thrombotic events which may progress to a severe state called oxidative storm and thrombotic storm (TS), respectively. In addition, inflammatory and lipid storms are also developed in Covid‐19 due to the activation of inflammatory cells and the release of bioactive lipids correspondingly. Therefore, the present narrative review aimed to elucidate the interrelated relationship between different storm types in Covid‐19 and the development of the mixed storm (MS). In conclusion, SARS‐CoV‐2 infection induces various storm types including CS, inflammatory storm, lipid storm, TS and oxidative storm. These storms are not developing alone since there is a close relationship between them. Therefore, the MS seems to be more appropriate to be related to severe Covid‐19 than CS, since it develops in Covid‐19 due to the intricate interface between reactive oxygen species, proinflammatory cytokines, complement activation, coagulation disorders, and activated inflammatory signaling pathway. SARS‐CoV‐2 infection induces various storm types including cytokine storm (CS), inflammatory storm, lipid storm, thrombotic storm (TS), and oxidative storm. These storms are not developing alone since there is a close relationship between them. Therefore, the mixed storm seems to be more appropriate to be related to severe Covid‐19 than CS, since it develops in Covid‐19 due to the intricate interface between reactive oxygen species, proinflammatory cytokines, complement activation, coagulation disorders, and activated inflammatory signaling pathway

The potential role of scavenger receptor B type I (SR‐BI) in SARS‐CoV‐2 infection

Scavenger receptor type B I (SR‐BI), the major receptor for high‐density lipoprotein (HDL) mediates the delivery of cholesterol ester and cholesterol from HDL to the cell membrane. SR‐BI is implicated as a receptor for entry of severe acute respiratory syndrome coronavirus type 2 (SARS‐CoV‐2). SR‐BI is colocalized with the angiotensin‐converting enzyme 2 (ACE2) increasing the binding and affinity of SARS‐CoV‐2 to ACE2 with subsequent viral internalization. SR‐BI regulates lymphocyte proliferation and the release of pro‐inflammatory cytokines from activated macrophages and lymphocytes. SR‐BI is reduced during COVID‐19 due to consumption by SARS‐CoV‐2 infection. COVID‐19‐associated inflammatory changes and high angiotensin II (AngII) might be possible causes of repression of SR‐BI in SARS‐CoV‐2 infection. In conclusion, the downregulation of SR‐BI in COVID‐19 could be due to direct invasion by SARS‐CoV‐2 or through upregulation of pro‐inflammatory cytokines, inflammatory signaling pathways, and high circulating AngII. Reduction of SR‐BI in COVID‐19 look like ACE2 may provoke COVID‐19 severity through exaggeration of the immune response. Further studies are invoked to clarify the potential role of SR‐BI in the pathogenesis of COVID‐19 that could be protective rather than detrimental. We illustrate that Scavenger receptor type B I (SR‐BI), the major receptor for high‐density lipoprotein (HDL) mediates delivery of cholesterol ester and cholesterol from HDL to the cell membrane. SR‐BI is implicated as a receptor for entry of severe acute respiratory syndrome coronavirus type 2 (SARS‐CoV‐2). Downregulation of SR‐BI in COVID‐19 could be due to direct invasion by SARS‐CoV‐2 or through upregulation of pro‐inflammatory cytokines, inflammatory signaling pathways and high circulating AngII.

Immunological interactions in helminths-SARS CoV-2 coinfection: Could old enemy be a friend today?

Helminths are metazoan parasites affecting about one third of the worldwide population. Chronic helminth infections (CHIs) confer immunological tolerance to harmless and self-antigens mediated by regulatory T cells (Treg) that are up-regulated. In coronavirus disease 2019 (COVID-19), abnormal adaptive immune response and unrestrained innate immune response could result in local and systemic immune-mediated tissue damage. COVID-19 and CHIs establish complicated immune interactions due to SARS-CoV-2-induced immunological stimulation and CHIs-induced immunological tolerance. However, COVID-19 severity in patients with CHIs is mild, as immuno-suppressive anti-inflammatory cytokines counterbalance the risk of cytokine storm. Here, an overview of the interplay between helminths and COVID-19 severity is given. CHIs through helminth-derived molecules may suppress SARS-CoV-2 entry and associated hyperinflammation through attenuation of the TLR4/NF-kB signalling pathway. In addition, CHIs may reduce the COVID-19 severity by reducing the SARS-CoV-2 entry points at ACE2/DPP4/CD147 axis in the initial phase and immunomodulation in the late phase of the disease by suppressing TLR4/NF-kB signalling pathway.

Mixed storm in SARS-CoV-2 infection: A narrative review and new term in the Covid-19 era.

Coronavirus disease 2019 (Covid-19) is caused by a novel severe acute respiratory syndrome coronavirus virus type 2 (SARS-CoV-2) leading to the global pandemic worldwide. Systemic complications in Covid-19 are mainly related to the direct SARS-CoV-2 cytopathic effects, associated hyperinflammation, hypercytokinemia, and the development of cytokine storm (CS). As well, Covid-19 complications are developed due to the propagation of oxidative and thrombotic events which may progress to a severe state called oxidative storm and thrombotic storm (TS), respectively. In addition, inflammatory and lipid storms are also developed in Covid-19 due to the activation of inflammatory cells and the release of bioactive lipids correspondingly. Therefore, the present narrative review aimed to elucidate the interrelated relationship between different storm types in Covid-19 and the development of the mixed storm (MS). In conclusion, SARS-CoV-2 infection induces various storm types including CS, inflammatory storm, lipid storm, TS and oxidative storm. These storms are not developing alone since there is a close relationship between them. Therefore, the MS seems to be more appropriate to be related to severe Covid-19 than CS, since it develops in Covid-19 due to the intricate interface between reactive oxygen species, proinflammatory cytokines, complement activation, coagulation disorders, and activated inflammatory signaling pathway.

The potential role of scavenger receptor B type I (SR-BI) in SARS-CoV-2 infection.

Scavenger receptor type B I (SR-BI), the major receptor for high-density lipoprotein (HDL) mediates the delivery of cholesterol ester and cholesterol from HDL to the cell membrane. SR-BI is implicated as a receptor for entry of severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2). SR-BI is colocalized with the angiotensin-converting enzyme 2 (ACE2) increasing the binding and affinity of SARS-CoV-2 to ACE2 with subsequent viral internalization. SR-BI regulates lymphocyte proliferation and the release of pro-inflammatory cytokines from activated macrophages and lymphocytes. SR-BI is reduced during COVID-19 due to consumption by SARS-CoV-2 infection. COVID-19-associated inflammatory changes and high angiotensin II (AngII) might be possible causes of repression of SR-BI in SARS-CoV-2 infection. In conclusion, the downregulation of SR-BI in COVID-19 could be due to direct invasion by SARS-CoV-2 or through upregulation of pro-inflammatory cytokines, inflammatory signaling pathways, and high circulating AngII. Reduction of SR-BI in COVID-19 look like ACE2 may provoke COVID-19 severity through exaggeration of the immune response. Further studies are invoked to clarify the potential role of SR-BI in the pathogenesis of COVID-19 that could be protective rather than detrimental.

The potential role of SARS‐CoV‐2 infection in acute coronary syndrome and type 2 myocardial infarction (T2MI): Intertwining spread

Coronavirus disease 2019 (COVID‐19) is a novel pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2). It has been shown that SARS‐CoV‐2 infection‐induced inflammatory and oxidative stress and associated endothelial dysfunction may lead to the development of acute coronary syndrome (ACS). Therefore, this review aimed to ascertain the link between severe SARS‐CoV‐2 infection and ACS. ACS is a spectrum of acute myocardial ischemia due to a sudden decrease in coronary blood flow, ranging from unstable angina to myocardial infarction (MI). Primary or type 1 MI (T1MI) is mainly caused by coronary plaque rupture and/or erosion with subsequent occlusive thrombosis. Secondary or type 2 MI (T2MI) is due to cardiac and systemic disorders without acute coronary atherothrombotic disruption. Acute SARS‐CoV‐2 infection is linked with the development of nonobstructive coronary disorders such as coronary vasospasm, dilated cardiomyopathy, myocardial fibrosis, and myocarditis. Furthermore, SARS‐CoV‐2 infection is associated with systemic inflammation that might affect coronary atherosclerotic plaque stability through augmentation of cardiac preload and afterload. Nevertheless, major coronary vessels with atherosclerotic plaques develop minor inflammation during COVID‐19 since coronary arteries are not initially and primarily targeted by SARS‐CoV‐2 due to low expression of angiotensin‐converting enzyme 2 in coronary vessels. In conclusion, SARS‐CoV‐2 infection through hypercytokinemia, direct cardiomyocyte injury, and dysregulation of the renin‐angiotensin system may aggravate underlying ACS or cause new‐onset T2MI. As well, arrhythmias induced by anti‐COVID‐19 medications could worsen underlying ACS. SARS‐CoV‐2 infection through hypercytokinemia, direct cardiomyocyte injury, and dysregulation of the renin‐angiotensin system may aggravate acute coronary syndrome (ACS) or cause new‐onset type 2 myocardial infarction. As well, arrhythmias induced by anti‐COVID‐19 medications could worsen ACS.

The potential role of SARS-CoV-2 infection in acute coronary syndrome and type 2 myocardial infarction (T2MI): Intertwining spread.

Coronavirus disease 2019 (COVID-19) is a novel pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It has been shown that SARS-CoV-2 infection-induced inflammatory and oxidative stress and associated endothelial dysfunction may lead to the development of acute coronary syndrome (ACS). Therefore, this review aimed to ascertain the link between severe SARS-CoV-2 infection and ACS. ACS is a spectrum of acute myocardial ischemia due to a sudden decrease in coronary blood flow, ranging from unstable angina to myocardial infarction (MI). Primary or type 1 MI (T1MI) is mainly caused by coronary plaque rupture and/or erosion with subsequent occlusive thrombosis. Secondary or type 2 MI (T2MI) is due to cardiac and systemic disorders without acute coronary atherothrombotic disruption. Acute SARS-CoV-2 infection is linked with the development of nonobstructive coronary disorders such as coronary vasospasm, dilated cardiomyopathy, myocardial fibrosis, and myocarditis. Furthermore, SARS-CoV-2 infection is associated with systemic inflammation that might affect coronary atherosclerotic plaque stability through augmentation of cardiac preload and afterload. Nevertheless, major coronary vessels with atherosclerotic plaques develop minor inflammation during COVID-19 since coronary arteries are not initially and primarily targeted by SARS-CoV-2 due to low expression of angiotensin-converting enzyme 2 in coronary vessels. In conclusion, SARS-CoV-2 infection through hypercytokinemia, direct cardiomyocyte injury, and dysregulation of the renin-angiotensin system may aggravate underlying ACS or cause new-onset T2MI. As well, arrhythmias induced by anti-COVID-19 medications could worsen underlying ACS.

Is it about time to develop social surgery?

The need for social surgery is nowadays more dire than ever, due to the exponential increase of the driving factors of surgical diseases in modern societies. During the last decades, high rates of urbanization have been linked to increased incidence of colon, liver, pancreas cancer and appendicitis.9 Sedentary lifestyle and obesity have translated into higher orthopedic surgical volumes.10 Climate change has jeopardized surgical supply chains, influenced surgery and pregnancy complications and increased the risk for massive trauma in the context of natural disaster.11 Finally, the COVID-19 pandemic has put a strain on surgical care and training, prolonged surgical waiting lists, hindered operable non - communicable diseases' (NCDs) screening and early diagnosis.12 Even though innovation in surgery has made big leaps in personalizing surgical planning, advancing minimally invasive approaches and improving surgical outcomes, the risk of losing the race to the mounting drivers of surgical morbidity is significant. This sets a reminder of the hippocratic doctrine of prevention over treatment, in the sense that preventing surgical disease and their complications can safeguard the access of those with non - preventable disease to better surgical care.

Commiphora myrrh: a phytochemical and pharmacological update.

Medicinal plants have a long track record of use in history, and one of them is Commiphora myrrh which is commonly found in the southern part of Arabia, the northeastern part of Africa, in Somalia, and Kenya. Relevant literatures were accessed via Google Scholar, PubMed, Scopus, and Web of Science to give updated information on the phytochemical constituents and pharmacological action of Commiphora myrrh. It has been used traditionally for treating wounds, mouth ulcers, aches, fractures, stomach disorders, microbial infections, and inflammatory diseases. It is used as an antiseptic, astringent, anthelmintic, carminative, emmenagogue, and as an expectorant. Phytochemical studies have shown that it contains terpenoids (monoterpenoids, sesquiterpenoids, and volatile/essential oil), diterpenoids, triterpenoids, and steroids. Its essential oil has applications in cosmetics, aromatherapy, and perfumery. Research has shown that it exerts various biological activities such as anti-inflammatory, antioxidant, anti-microbial, neuroprotective, anti-diabetic, anti-cancer, analgesic, anti-parasitic, and recently, it was found to work against respiratory infections like COVID-19. With the advancement in drug development, hopefully, its rich phytochemical components can be explored for drug development as an insecticide due to its great anti-parasitic activity. Also, its interactions with drugs can be fully elucidated.This review highlights an updated information on the history, distribution, traditional uses, phytochemical components, pharmacology, and various biological activities of Commiphora myrrh. Graphical summary of the phytochemical and pharmacological update of Commiphora myrrh.

Heparanase is the possible link between monkeypox and Covid-19: robust candidature in the mystic and present perspective.

Heparanase (HPSE) is an endoglycosidase cleaves heparan sulfate (HS) and this contributes to the degradation and remodeling of the extracellular matrix. HS cleaved by HPSE induces activation of autophagy and formation of autophagosommes which facilitate binding of HPSE to the HS and subsequent release of growth factors. The interaction between HPSE and HS triggers releases of chemokines and cytokines which affect inflammatory response and cell signaling pathways with development of hyperinflammation, cytokine storm (CS) and coagulopathy. HPSE expression is induced by both SARS-CoV-2 and monkeypox virus (MPXV) leading to induction release of pro-inflammatory cytokines, endothelial dysfunction and thrombotic events. Co-infection of MPX with SARS-CoV-2 may occur as we facing many outbreaks of MPX cases during Covid-19 pandemic. Therefore, targeting of HPSE by specific inhibitors may reduce the risk of complications in both SARS-CoV-2 and MPXV infections. Taken together, HPSE could be a potential link between MPX with SARS-CoV-2 in Covid-19 era.

The potential link between Covid-19 and multiple myeloma: A new saga.

BACKGROUND: Covid-19 is considered a primary respiratory disease-causing viral pneumonia and, in severe cases, leads to acute lung injury and acute respiratory distress syndrome (ARDS). In addition, though, extra-pulmonary manifestations of Covid-19 have been shown. Furthermore, severe acute respiratory distress syndrome coronavirus type 2 (SARS-CoV-2) infection may coexist with several malignancies, including multiple myeloma (MM). METHODS: This critical literature review aimed to find the potential association between SARS-CoV-2 infection and MM in Covid-19 patients with underlying MM. Narrative literature and databases search revealed that ARDS is developed in both MM and Covid-19 due to hypercalcemia and proteasome dysfunction. RESULTS: Notably, the expression of angiogenic factors and glutamine deficiency could link Covid-19 severity and MM in the pathogenesis of cardiovascular complications. MM and Covid-19 share thrombosis as a typical complication; unlike thrombosis in Covid-19, which reflects disease severity, thrombosis does not reflect disease severity in MM. In both conditions, thromboprophylaxis is essential to prevent pulmonary thrombosis and other thromboembolic disorders. Moreover, Covid-19 may exacerbate the development of acute kidney injury and neurological complications in MM patients. CONCLUSION: These findings highlighted that MM patients might be a risk group for Covid-19 severity due to underlying immunosuppression and most of those patients need specific management in the Covid-19 era.

Telehealth has comparable outcomes to in-person diabetic foot care during the COVID-19 pandemic.

BACKGROUND: The coronavirus disease 2019 (COVID-19) pandemic has posed obstacles to the delivery of diabetic foot care. In response to this remote healthcare services have been deployed offering monitoring, follow-up, and referral services to patients with diabetic foot ulcers and related conditions. Although, remote diabetic foot care has been studied before the COVID-19 pandemic as an alternative to in-person care, the peculiar situation of the pandemic, which dictates that remote care would be the sole available option for healthcare practitioners and patients, necessitates an evaluation of the relevant knowledge obtained since the beginning of the severe acute respiratory syndrome coronavirus 2 outbreak. AIM: To perform a thorough search in PubMed/Medline and Cochrane to identify original records on the topic. METHODS: To identify relevant peer-reviewed publications and gray literature, the authors searched PubMed-MEDLINE and Cochrane Library-Cochrane Central Register of Controlled Trials starting September 27 till October 31, 2021. The reference lists of the selected sources and relevant systematic reviews were also hand-searched to identify potentially relevant resources. Otherwise, the authors searched Reference Citation Analysis (https://www.referencecitationanalysis.com/). RESULTS: A number of randomized prospective studies, case series, and case reports have shown that the effectiveness of remote care is comparable to in-person care in terms of hospitalizations, amputations, and mortality. The level of satisfaction of patients' receiving this type of care was high. The cost of remote healthcare was not significantly lower than in - person care though. CONCLUSION: It is noteworthy that remote care during the COVID-19 pandemic appeared to be more effective and well - received than remote care in the past. Nevertheless, larger studies spanning over longer time intervals are necessary in order to validate these results and provide additional insights.

Burnout und Abhängigkeit bei ärztlichem Personal zeitlos und während der COVID-19-Pandemie am Beispiel der Chirurgie und Anästhesie Burnout and dependence among medical personnel timeless and during the COVID-19 pandemic, using surgery and anesthesia as examples

Hintergrund Die COVID-19(„coronavirus disease 2019“)-Pandemie wirkt sich auf die psychische Gesundheit und das berufliche Verhalten von Chirurgen und Chirurginnen und Anästhesisten und Anästhesistinnen aus und scheint einen Einfluss auf die Substanzabhängigkeit zu haben. Fragestellung Welche Gründe gibt es für das Auftreten einer Substanzabhängigkeit und einem Burnout bei Chirurgen und Chirurginnen und Anästhesisten und Anästhesistinnen zeitlos und während der COVID-19-Pandemie und welche Verbesserungsmaßnahmen könnten im klinischen Alltag helfen? Material und Methoden Es wurde eine Literaturrecherche in Form einer systematischen Übersicht („systematic review“) zu Studien und Übersichtsarbeiten durchgeführt, die für das Thema relevant sind. Ergebnisse Im Laufe der Jahre hat sich gezeigt, dass Chirurgen bzw. Chirurginnen und Anästhesisten bzw. Anästhesistinnen aufgrund ihres direkten Zugangs zu Medikamenten in der Klinik und der arbeitsbezogenen Stressbelastung zur Drogenabhängigkeit neigen. Insbesondere Chirurgen und Chirurginnen und Anästhesisten und Anästhesistinnen schienen eine erhöhte Neigung zur Suchterkrankungen und ein erhöhtes Burnout-Risiko in der Pandemie vorzuweisen. Schlussfolgerungen Präventive Maßnahmen zugunsten besserer Arbeitsbedingungen in der Chirurgie und Anästhesie und eine bessere Drogenkontrolle (nicht nur wegen der Ausgabe, sondern auch wegen der richtigen Drogentests) sowie mehr Therapie- und Wiedereingliederungsprogramme unter psychiatrischer Begleitung und in Zusammenarbeit mit einem multidisziplinären Team sind sinnvoll.

[Burnout and dependence among medical personnel timeless and during the COVID-19 pandemic, using surgery and anesthesia as examples]. / Burnout und Abhängigkeit bei ärztlichem Personal zeitlos und während der COVID-19-Pandemie am Beispiel der Chirurgie und Anästhesie.

BACKGROUND: The COVID-19 pandemic affects the mental health and professional behavior of surgeons and anesthesiologists and seems to have an impact on substance dependence. QUESTION: What are the reasons for the occurrence of substance dependence and burnout in surgeons and anesthesiologists timelessly and during the COVID-19 pandemic and what improvement measures could help in the clinical practice? MATERIAL AND METHODS: A literature search was conducted in the form of a systematic review of studies and review articles relevant to the topic. RESULTS: Over the years it has been shown that surgeons and anesthesiologists are prone to drug dependence due to their direct access to medications in the clinical field and work-related stress. In particular, surgeons and anesthesiologists appeared to have an increased propensity for addictive diseases and an increased risk of burnout in the pandemic. CONCLUSION: Preventive measures in favor of better working conditions in surgery and anesthesia and better drug control (not only for dispensing but also for correct drug testing), as well as more treatment and reintegration programs under psychiatric supervision and in collaboration with a multidisciplinary team are meaningful.