Key points: -Patients with severe coronavirus disease 2019 may have neck endothelial inflammation, pseudo-aneurysm and an increased risk of bleeding, especially during neck surgical procedures.-The management of vascular lesions may be performed through interventional radiological procedures that may be useful to reduce the risk of virus aerosolization and healthcare provider contamination.-Neck pseudo-aneurysm may be managed through percutaneous glue injection under ultrasonography guidance while active hemorrhage may be managed by endovascular embolization with coil.

IImmunodeficiency and hyperinflammation characterize COVID-19 associated states; thus, repurposing of multiple cytokine and/or anti-cytokine drugs currently being used in other therapeutic areas has been suggested as a potential therapeutic strategy in COVID-19 patients. Clinical trials involving these drugs target the most frequent and life-threatening peripheral consequences of the disease, mainly focusing on lung, heart, and coagulation functions; however, a growing number of reports describe a wide range of COVID-associated neurological manifestations (altogether defined as neuro-COVID) including anosmia, seizures, confusion, stroke, encephalopathy, and paralysis. Notably, the underlying pathophysiological mechanisms for neuro-COVID may also include dysregulation of cytokines/chemokines, deficiencies in the innate immune response, and autoimmunity. This suggests that therapeutic attempts with drugs targeting cytokine-mediated inflammation in peripheral organs could also positively affect neuro-COVID manifestations. As a matter of fact, some of these drugs have also been scrutinized for their potential efficacy in treating neuroinflammatory diseases such as optic neuromyelitis, epilepsy, stroke, and traumatic brain injury, among others. On the other hand, anti-cytokine drugs, by impairing relevant physiological activities exerted by these mediators in the CNS, may also be endowed with significant neurological risk. Therefore, the primary aim of the present manuscript is to review the available preclinical and clinical data regarding the neurological effects of the drugs targeting cytokine-mediated inflammation, in order to raise awareness about their potentially beneficial or detrimental neurological consequences when used to treat COVID-19 patients.

Many hospitals will continue to see a surge in COVID-19 cases and halt of elective cases, while others pass the surge and begin to restart elective surgeries. Regardless of the phase each hospital encounters, the safety of both patients and staff must be taken into account.1,2 This case report describes a patient who underwent urgent coronary artery bypass grafting (CABG) at the beginning of the COVID-19 surge. The initial postoperative course was uneventful and the patient was discharged on postoperative day 4. The patient presented nearly two weeks later with a subsequent severe COVID-19 infection complicated by STEMI and stroke. This case not only demonstrates the risks and potential complications of caring for cardiac surgery patients during the COVID-19 pandemic, it is the only known reported case of a patient developing severe COVID-19 infection after a CABG resulting in STEMI and stroke due to hypercoagulable state associated with COVID-19.

We present prolonged viral shedding in an immunocompromised HIV patient with a literature review of risk factors for prolonged viral shedding and its implications for isolation strategies. We explore the role of PCR-CT-value (cycle threshold) as an instrument for guiding isolation policies and the impact of HIV on Covid-19.

Background: The aim of this study includes to discuss the clinical, laboratory, and chest computed tomography (CT) in pediatric patients with 2019 novel coronavirus (COVID‐19) infection. Material and Methods: The clinical, laboratory, and chest CT features of 17 pediatric inpatients with COVID‐19 infection confirmed by pharyngeal swab COVID‐19 polymerase chain reaction(PCR). All clinical and laboratory data have been recorded and analyzed during march-june 2020 . Chest CT have been performed to all Covid 19 PCR confirmed patients and radiologicall view have been noted. Results: Seventeen pediatric patients with a history of close contact with COVID‐19 diagnosed family members included to the study. Fever (10/17, 58%) and cough (13/17, 76%) were the most common symptoms. For laboratory findings, c reactive protein elevation (15/17, 88%) seem to be the most finding. A total of 4 patients presented with unilateral pulmonary lesions (4/17, 23%), 9 with bilateral pulmonary lesions (9/17, 52%) and 13 cases showed bilateral diffuse covid pattern on chest CT (13/17, 76%). Non-spesific consolidation with was observed in 8 patients (8/17, 47%), ground‐glass opacities were observed in 11 patients (11/17, 64%), nodules were observed in 7 patients (7/17, 41%), and tiny nodules were observed in 2 patients (2/17, 11%). Conclusion: In pediatric patients with positive COVID‐19 nucleic acid test from pharyngeal swab samples; the early detection of lesions by CT can be efficient; in management and early treatment for pediatric patients. However; early chest CT screening and COVİD-19 PCR testing together can be more efficent in diagnose. Keywords: Covid-19, viral pneumenia, chest computed tomography (CT), childeren.

The novel coronavirus named SARS-CoV-2 caused human epidemic all over the world at breathtaking speed. It is of great concern for the research community to understand the evolutionary origin and molecular characteristics of this virus. With more and more isolates are sequenced, it is possible to estimate the genomic variation and evolution of SARS-CoV-2. In this study, 17,229 complete genomes of SARS-CoV-2 were analyzed to characterize the genomic diversity. Using Doc2vec algorithm, we got the the genome embeddings of SARS-CoV-2 isolates as well as its related virus species. The results showed that the distance estimated from genome embedding is different from sequence alignment. Additionally, a frequently happened mutations (C to T/U) in -25 upstream of the ORF1ab start codon were identified. On protein level, it seemed that the mutations appeared with unequal distribution among the proteins. ORF1ab, S, ORF3a, ORF8 and N proteins were easier to tolerate mutations while the other proteins showed high conservation among the isolates.

36-year-old man with past medical history of liver cirrhosis presented to the ED during COVID-19 pandemic peak with a history of shortness of breath on minimal exertion, mild cough and fever. Findings on physical examination included hypoxic, tachypnoea, ascites, pedal edema and digital clubbing. No abnormal sounds were heard on lung and heart auscultation. Due to the high suspicion of COVID-19, tests were performed. Thoracic CT scan demonstrated neither ground glass opacities nor consolidation. SARS-CoV-2 testing was negative. ABG showed a PaO2 of 51 mm Hg with an A-a gradient of 68 mm Hg. A targeted history revealed platypnoea-orthodeoxia syndrome. Contrast echocardiography with saline was consistent with a diagnosis of hepatopulmonary syndrome. Patient was discharged with long-term oxygen. Currently, the patient is on the waiting list for a liver transplant.

In December 2019, the COVID-19 outbreak began in Wuhan, China, and soon announced as a pandemic in March 2020 and Iran was no exception. Since COVID-19 is a newly emerging disease, no definite treatment exists and therapy is based upon supportive care. Many treatment regimens have been proposed and some of which have shown promising results that may be considered as the treatment of COVID-19 in the near future if confirmed by further studies. As there is no gold standard for the treatment of COVID-19 and many physicians in different countries prescribe a combination of drugs, we prescribed a combination of drugs. based on the above evidence to patients referring to our clinic. We monitored and analyzed patients with mild to moderate symptoms with the inclusion criteria of either confirmed COVID-19 cases by RT-PCR or had close contact with confirmed cases having symptoms of headache, sore throat, cough, diarrhea, unjustifiable symptoms in favor of vasculitis, and any cutaneous manifestations which last for more than 5 days. A total of thirty-three patients were included and then visited daily with their vital parameters being recorded directly. All thirty-three patients recovered from the disease with no complication after receiving the treatment and in follow up visits. Although a definite treatment for SARS-CoV-2 still remains a matter of debate, this treatment regimen showed effective treatment in patients with mild to moderate symptoms. Undoubtedly, further researches and papers are needed to be done to prove the effectiveness of this treatment regimen.

Background: Following the remarkable spread of coronavirus disease 2019 (COVID-19), worldwide, it quickly became apparent that many public health systems worldwide were not prepared to manage such a pandemic. We aimed to assess the perceptions of primary care physicians (PCPs) in Jordan toward their role during COVID-19. Methods: A cross-sectional study using a self-administered questionnaire was performed. The study participants included PCPs from the Ministry of Health, academic institutions, and the private sector in Jordan. Results: A total of 221 PCPs participated in the study. Most participants reported not having received any training on infection control (59.7%) or COVID-19 (81%). More than half PCPs (53.4%) felt positive about the way patients received and/or complied with their instructions. More than half PCPs (55.7%) educated their patients on protective measures against COVID-19 infection and considered this as part of their role and responsibility. Over 80% of the participants would apply social distancing, hand sanitation, facial masks, and patient education, but only half (51.1%) reported planning to order COVID-19 test kits. Conclusions: PCPs had a positive attitude toward controlling COVID-19 infection and showed a willingness to educate patients on how to protect themselves. However, PCPs should be provided special training on COVID-19.

SARS-CoV-2 is neutralized by proteins that block receptor-binding sites on spikes that project from the viral envelope. In particular, substantial research investment has advanced monoclonal antibody therapies to the clinic where there are signs of partial efficacy in reducing viral burden and hospitalization. An alternative is to use the host entry receptor, ACE2, as a soluble decoy that broadly blocks SARS-associated coronaviruses with limited potential for viral escape. Here, we summarize efforts to engineer higher affinity variants of soluble ACE2 that rival the potency of affinity-matured antibodies. Strategies have also been used to increase the valency of ACE2 decoys for avid spike interactions and to improve pharmacokinetics via IgG fusions. Finally, the intrinsic catalytic activity of ACE2 for the turnover of the vasoconstrictor angiotensin II may directly address COVID-19 symptoms and protect against lung and cardiovascular injury, conferring dual mechanisms of action unachievable by monoclonal antibodies. Soluble ACE2 derivatives therefore have the potential to be next generation therapeutics for addressing the immediate needs of the current pandemic and possible future outbreaks.

Marciano Lee1, Elise Anderson1, Ali Farooq1, Mohammed Yasin1, Yazan Alkawaleet1, Frank Annie2Charleston Area Medical Center, Department of Cardiology, 3200 MacCorkle Ave. SE,Charleston, WV 25304CAMC Health Education and Research Institute, 3200 MacCorkle Ave. SE,Charleston, WV 25304Corresponding:Frank Annie MA; MPA; PhDResearch Scientist (Department of Cardiology)CAMC Health Education and Research Institute3200 MacCorkle Ave. SE,Charleston, WV 25304Cell 304 -395 – 3830Phone 304-388-9921Fax: 304-388-9921Email: Frank.H.Annie@camc.orgKeywords:COVID-19, GEMFIBROZIL, IMMUNE MODULATING TREATMENTAbstract:The current Covid-19 viral infection has been declared a pandemic causing significant global morbidity and mortality predominantly from the manifestation of severe acute respiratory syndrome (SARS). It has been designated as SARS-CoV 2. Epidemiological studies show predilection in patients with associated chronic medical conditions including those with cardiovascular disease. Exaggerated host immune response known as cytokine storm syndrome (CSS) leading to acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) is the proposed mechanism for the development of SARS in Covid-19 infection. Gemfibrozil has proven benefits in patients with cardiovascular disease. More importantly, it has established anti-inflammatory, anti-oxidative, and anti-migratory properties. Gemfibrozil has shown survival benefits as immune modulation of ALI/ARDS from viral pathogens. This article reviews the potential of gemfibrozil as adjuntive immue modulating therapy for SARS associated with Covid-19 infected patients who have associated cardiovascular disease.Introduction:The severe acute respiratory syndrome (SARS) seen in Covid-19 infection share similarities with previous coronavirus epidemics, particularly SARS-CoV 1 and the Middle East Respiratory Syndrome (MERS-CoV). (1) It has been designated SARS-CoV 2. Acute lung injury (ALI) with subsequent development of acute respiratory distress syndrome (ARDS) from robust host hyper-immune response is the proposed pathophysiological mechanism. This so called ”cytokine storm” may be independent of viral load and replication. (2) Thus, the rationale for adding immune modulating strategies on top of antiviral/antimicrobial therapies is warranted to prevent this complication and hopefully improve survival. The development of ALI/ARDS amplifies mortality in Covid-19 infection, more so in patients with associated chronic medical conditions including cardiovascular disease. (3)Gemfibrozil, a drug discovered over 40 years ago, have beneficial effects and safety profile in both primary and secondary prevention of cardiovascular disease. (4) In addition to its lipid lowering ability, it has important immune modulating properties that inhibit pro-inflammatory factors involved in cytokine storms.(5) It is a peroxisome proliferators-activated receptor (PPAR) agonist known to reduce the release of inflammatory cytokines including interleukin-6 (IL-6), tumor necrosing factors (TNF) and interferon-gamma (IFN-g).IL-6 elevation have been reported as an important marker of severity with Covid-19 infection. (3) Together with other markers for inflammation such as CRP, the degree of IL-6 elevation correlates with increased morbidity and mortality.Gemfibrozil has shown survival benefits by attenuating ALI/ARDS development from viral etiologies. (6) Since gemfibrozil is currently indicated for patients with cardiovascular disease, its adjunctive use does not have to be repurposed for SARS associated with Covid-19 infection. Therefore, Gemfibrozil’s potential as an immune modulating strategy to prevent ALI/ARDS cannot be ignored.Immune Modulating Targets for Gemfibrozil in Covid-19 SARS pathogenesis:Gemfibrozil has been shown to attenuate pro-inflammatory effects of disease states through its immune-modulating, anti-inflammatory and anti-migratory properties. (5). It belongs to the fibrate family of drugs used to lower plasma lipds and cholesterol. They are one of several known synthetic lignads acting as agonists to the PPARs. (7) Their action in turn decrease serum levels of TNF, IFN-g and IL-6. (8,9)As an an anti-inflammatory, gemfibrozil reduces superoxide production and expression of nuclear factor kB (NF-kB). (10) Moreover, it inhibits astrocyte production of TNF, IL-1b, IL-6 and nitric oxide (NO) production. (11) Gemfibrozil also promotes the production of anti-inflammatory cytokine IL-4. (12) It reduces the production of C-reactive protein (CRP), TNF-a and IL-6 in peripheral blood mononuclear cells. It inhibits the production of cyclooxygenase-2 (COX-2) and prostaglandins. (13)As an immune-modulating agent, gemfibrozil attenuates pro-inflammatory transcription factor activation. This includes IFN-g regulatory factor 1 (IRF-1)bidning to gamma activation site (GAS), nuclear factor-kB (NF-kB), activator protein 1 (AP-1), and CCAT/enhancer binding protein beta (C/EBPb). (5) It also promotes switching of T helper (Th) cells from the pro-inflammatory Th1 to anti-inflammatory Th2. Production of Th2-specific cytokines is amplified including IL-4, IL-5 and IL-10. (14)As an anti-oxidant, gemfibrozil not only prevents low density lipoprotein (LDL) peroxidation but also acts on other signals of inflammation. Reactive oxygen species (ROS) have emerged as important signaling molecules during inflammatory conditions. Excessive ROS generation results in damage to most cellular components of the living organism. Gemfibrozil is known to inhibit ROS-mediated inflammation. (15) It has free radical scavenging ability as well. Its para-hydroxyl metabolite has been shown to reduce the burden of ROS. (16)As an anti-migratory agent, gemfibrozil affects the expression of cell-surface adhesion molecules icluding intracellular adhesion molecule 1 (ICAM-1), VCAM-1 and selectins inhibiting trans endothelial migration of mononuclear cells and macrophages. (17) It also down-regulates the expression of chemokines including monocyte chemotactic protein 1 (MCP-1), macrophage inflammatory protein 1 (MIP-1), monokines induced by IFN-g (MIG) and IL-8. The expression of IL-8 induces inflammation, monocyte/macrophage recruitment, angiogenesis and vascular smooth muscle migration. Thus, gemfibrozil can function as an anti-migratory factor by down-regulating the expression of different soluble chemokines and inhibit the expression of different cell surface proteins and selectins.Discussion:Over the years, viral pathogens including Influenzas and Coronaviruses cause ALI/ARDS from excessive release of pro-inflammatory cytokines and chemokines described in cytokine storm syndromes. They induce much higher transcription and up regulation of TNF genes including TNF related aptoptosis-inducing lignad and TNF-mRNA in human monocyte-derived macrophages. (18) This macrophage activation syndrome (MAS) seen with the current SARS-CoV 2 may be a dysregulated host response to Covid-19 viral induced immunosuppression and lymphopenia leading to unintended ALI/ARDS consequences at the site of infection. (19) The development of ALI/ARDS and the need for ventilator support portends to increased mortality rates. Markers of inflammation including CRP and IL-6 have been used as surrogates for MAS, and their degree of elevation have correlated well with disease severity. (3)Experiments with SARS-CoV indicate that MAS induced cytokine storms result more from amplification of gene related inflammatory signals regardless of viral load. In one model, immune modulation of receptor sites or alteration of recruitment signals resulted in dramatic improvement in host survival with viral load remaining constant. (20) This suggests that immune modulating therapy may have as important a role in addition to antiviral therapy in altering the course of Covid-19 infection. Reports of clinical improvement have been reported with the adjuvant use of IL-6 antagonists including tocilizumab. However, cost and repurposing use of these medications may be limiting factors.Gemfibrozil has been in clinical use for patients with cardiovascular disease and has achieved generic status. In addition, it has vital immune modulating properties against cytokine storms that mitigate the development of ALI/ARDS from both viral and nonviral pathogens. (21). It not only reduces the levels of IL-6, TNF and IFN-g. But it has also been shown to attneuate gene recruiting signals of inflammation utlizing human equivalent dosing. In one animal study, the adjuvant use of gemfibrozil resulted in enhanced host survival that developed ALI/ARDS from viral pathogens. (6) Enhanced survival is seen even after exposure to the virus. This implies that gemfibrozil has the potential to be a treatment rather than a preventive therapy in human disease.Therefore, the potential of gemfibrozil as adjunct immune modulating therapy in conjunction with antiviral treatment for SARS associated with Covid-19 infection in patients with associated cardiovascular disease is emphasized.References:1. Petrosillo N, Vicenconte G, et al. Covid-19, SARS and MERS: are they closely related? JCMI. 20202. Smits S, Lang A, et al. Exacerbated inane host response to SARS-CoV in aged non-human primates. PLos Patholog. 20103. Zhou F, Du R, et al. Clinical course and risk factors for mortality of adult inpatients with Covid-19 in Wuhan, China: a retrospective cohort study. Lancet. 2020. 3954. Rubins HB, Robins SJ, et al. Gemfibrozil for the secondary prevention of coronary aretery disease inmen with low levels of high-density lipoprotein cholesterol. Veterans Affairs high-density lipoprotein cholesterol intervention trial group. N Engl J Med. 1999. 341: 410-4185. Roy A, Pahan K, et al. Gemfibrozil, stretching the arms beyond lipid lowering. Immunopharmacol Immunotoxicol. 2009. 31: 339-3516. Budd A, Alleva L, et al. Increased survival after gemfibrozil treatment of severe mouse influenza. Antimicrobial Agents and Chemotherapy. 2007. 2965-29687. Berger J, Moler DE. The mechanisms of action of PPARs. Annu Rev Med. 53: 409-4358. Madej A, Okopien B, et al. Effects of fenofibrate on plasma cytokine concentrations in patients with atherosclerosis and hyperlipoproteinemia IIb. Int J Clin Pharmacol. 36: 345-3499. Staels B, Koenig W, et al. Activation of human oartic smooth muscle cells is inhibited by PPARa. Nature. 303: 790-79310. Calkin AC, Cooper KA, et al. Gemfibrozil decreases atherosclerosis in experimental diabetes in association with a reduction in oxidative stress and inflammation. Diabetologia. 49: 766-77411. Xu J, Chavis JA, et al. Gemfibrozil reduces release of tumor necrosis factor-alpha in peripheral blood mononuclear cells from healthy subjects and patients with coronary heart disease. Clin Chem Acta. 332: 61-6712. Lovette-Racke AE, Hussain RZ, et al. Peroxisome proliferator-activated receptor-alpha agonists as therapy for autoimmune diesease. J Immunol. 172: 5790-579813. neve BP, Frutchart JC, et al. Role of PPAR in atherosclerosis. Biochem Pharmacol. 2000. 60: 1245-125014. Heyworth PG, Bohl BP, et al. Rac translocates independently of the neutrophil NADPH oxidase components p47phox and p67phox. Evidence for its ineteraction with flavocytochrome b558. J Biol Chem. 1994. 269: 30749-3075215. Aviram M, Rosenblat M, et al. Atorvastatin and gemfibrozil metabolites, but not the parent drugs, are potent antioxidants against lipoprotein oxidation. Ahterosclerosis. 1998. 138: 271-28016. Dasgupta S, Roy A, et al. Gemfibrozil ameliorates relapsing-remitting experimental autoimmune encephalomyelitis of peroxisome proliferator-acivated receptor-alpha. Molecular Pharmacol. 2007. 72: 934-94617. Zhou JF, Law HK, et al. Functional tumor necrosis factor-related apoptosis-inducing ligand production by avian flu influenza virus-infected macrophages. J Infect Dis. 193: 945-95318. Xu J, Shi I, et al. Pathological findings of Covid-19 associated with acute respiratory distress syndrome. Lancet. 2020. Epub ahead of print19. McGonagle D, Sharif K, et al. The role of cytokines including interleukin-6 in Covid-19 induced pneumonia and macrophage activation syndrome-like disease. J AutRev. 2020. 10253720. Channappanavar AR, Fehr R, et al. Dysregulated type 1 interferon and inflammatory monocytes-macrophage responses cause lethal pneumonia in SARS-CoV infected mice. Cell Host Microbe. 2016.19: 181-19321. Kim YS, Kim JK, et al. The peroxisome proliferator-activated receptor-alpha agonist gemfibrozil promotes defense against mycobacterium abcessus infections. Cells. 2020. 9: 648

Background: Coronavirus Disease 2019 (Covid-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), along with its cardiovascular, gastrointestinal, hematologic, mucocutaneous, respiratory, neurological, renal and testicular manifestations and further complications constitutes one of the deadliest pandemics in modern history. A common pathogenetic mechanism of these complications seems to be the Covid-19-induced excessive immune response of uncontrolled release of interleukins, chemokines, interferons, tumor necrosis factors and colony-stimulating factors, the so called cytokine storm syndrome. Severe anaphylactic reactions with profound hypotension or hypoxemia can be also associated with release of pro-inflammatory cytokines. Aim: Careful investigation for similarities in clinical manifestations and correlated multi-organ complications of Covid-19 with other viral infections including dengue and human immunodeficiency viruses together with the action of inflammatory cells inducing the Kounis syndrome could provide a better understanding on pathophysiolgy and trigger mechanisms, elucidating potential preventing and therapeutic strategies. Methods: A search was performed in Medline (via PubMed), for current literature on the pathophysiology, causality, clinical appearance, variance, prevention, and treatment of Covid-19, anaphylaxis with profuse hypotension and the Kounis anaphylaxis associated acute coronary syndrome. Results: Insights from research in allergy/anaphylaxis-associated cardiac syndromes and Covid-19, suggest that the same key immune cells are invollved in cardiovascular complications of Covid-19 and the anaphylaxis-associated Kounis syndrome. The myocardial injury in patients with Covid-19 has been attributed to coronary spasm, plaque rupture and microthrombi, hypoxic injury or cytokine storm and shares the same patho-physiology with the 3 clinical variants of Kounis syndrome. Conclusion: The patho-physiology, etiology, clinical manifestations and therapeutic approaches of the severe Covid-19 and their associations might be proved beneficial for future treatments. Early immunological interventions targeting inflammatory markers that are predictive of worse disease outcome would be more beneficial than those blocking late-appearing cytokine related storm. Individualized, tailored to each patient treatment approach is required in Covid-19 cases

Objective: To investigate the causes of early COVID-19 complicated with platelets(PLT) abnormality, and to analyze the possible mechanisms. Methods: The case datum of early COVID-19 complicated with PLT increase or decrease was collected. (125-350) ×109/L defined as the normal level of PLT(Group C), <125×109/L was defined as the PLT decrease group (Group A), >350×109/L defined as the PLT increase group (Group B) . The data were analyzed after collected. Results: Our statistical results showed that the incidence of COVID-19 combined PLT decreased was about 11.94% and the incidence of combined PLT increased was about 9.33% at admission. Compared with Group B and C, Group A showed a significant decrease in white blood cell, neutrophil and CD4 (P<0.05). The lymphocyte in Group A and C decreased significantly, but not find in Group B (P<0.05). Compared with Group A and C, IL-4 was increased in Group B, but lymphocyte decline was not significant (P>0.05). Conclusion: PLT abnormalities occur in all patients with different types of COVID-19. It may be related to the severity of inflammation and infection, immune regulation and megakaryocyte function, etc.

Evaluation of population-based COVID-19 control measures informs strategies to quell the current pandemic and reduce the impact of those yet to come. Effective COVID-19 control measures may simultaneously reduce the incidence of other acute respiratory infections (ARIs) due to shared transmission modalities. To assess the impact of stay-at-home orders and other physical distancing measures on the prevalence of ARI-related symptoms, we compared symptoms reported by prospective college cohorts enrolled during two consecutive academic years. ARI-related symptoms declined following campus closure and implementation of stay-at-home orders, demonstrating the impact of population-based physical distancing measures on control of a broad range of respiratory infections.

Aim: The common cardiac toxicities of hydroxychloroquine (HCQ) and azithromycin(AZ) are not well defined in COVID -19 patients . The purpose of this study was to evaluate ventricular repolarization in COVID-19 patients treated with HCQ and AZ using iCEB, Tp-e interval, Tp-e/QT ratio, and Tp-e/QTc ratio. Methods: This retrospective study enrolled 164 patients diagnosed with COVID-19 pneumonia in the Emergency Department (ED) and then transferred to the medical floor or ICU in April 2020 Result: A total of 164 patients were mean aged 47 ± 18 years (range, 18-97 years) and 83 (50.6%) were women in study population. Group HTQ had 38 patients , Group HTQ + AZ had 126 patients. On the 5th day of hospitalization heart rates (HR) were significantly lower than ED (p<0,001). On the 5th day of hospitalization QTc , QT max (V5-V6), QTmin, Tp-e (V5-V6) and iCEB values were significantly higher than ED (p=0,01and all the rest p<0,001 respectively). On the 5th day of hospitalization iCEB values of HTZ+AZ group were statistically significant higher than iCEB values of HTQ group (p=0,03). iCEBc had strong correlation between Tp-e/QT (V5). iCEBc had strong negative correlation between Tp-e (V5). Conclusion: The iCEB values were significant increased after HTQ and AZ treatment in COVID-19 patients. We think that iCEB is a more sensitive marker than QT prolongation in predicting the risk of multi-drug arrhythmia.

Angiotensin Converting Enzyme 2 (ACE2) is the receptor the new coronavirus SARS-CoV-2 binds to for cell entry. ACE2 is also an important player in the Renin Angiotensin System (RAS). ACE2 and RAS appears to be central in coronavirus disease (Covid-19) pathophysiology. Covid-19 might be regarded as a virus-induced “RAS disorder”. Drugs acting upon RAS components may offer potential therapeutic value in Covid-19. The authors advocate diminazene aceturate (DIZE), a putative ACE2 activator, as a feasible treatment option unduly disregarded a priori, likely due to lack of licensing for human use. However, DIZE has been extensively employed in African trypanosomiasis patients with little toxicity reported. With the current pandemic causing health issues on a large scale worldwide, the properties of DIZE remain to be investigated in Covid-19. A drug that is available, inexpensive and with a long track record of safe usage should be considered, particularly while effective alternatives remain scarce.

Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can cause thyroid hormonal disorders. In addition, tracheal compression by thyroid nodules can aggravate hypoxia in critically-ill patients. No studies have investigated the effect of thyroid nodules on the prognosis of patients with COVID-19. In this study, we investigated the effect of thyroid hormonal disorders and thyroid nodules on the prognosis of patients with COVID-19. Material and Methods: This prospective study was conducted at the Şırnak State Hospital (Pandemic hospital in Turkey) between 15 March and 15 August 2020. We evaluated thyroid hormonal disorder and thyroid nodules in 125 patients who were admitted to the non-intensive care unit (non-ICU) due to mild COVID-19 pneumonia (group 1) and 125 critically-ill patients who were admitted to the ICU (group 2). Results: Thyroid stimulating hormone levels (TSH) were not significantly different between groups 1 and 2 ; however, group 2 patients had significantly lower levels of free thyroxine (FT4) and free triiodothyronine (FT3) as compared to group 1 (p = 0.005, p < 0.0001, respectively). FT3 level showed a negative correlation with length of hospital stay and C-reactive protein level (rho: −0.216, p: 0.001; rho: - 0.383, p < 0.0001). Overt thyroid disorder was observed in 13 patients [2 patients in group 1 (both with overt thyrotoxicosis) and 11 patients in group 2 (3 overt hypothyroidism, 8 overt thyrotoxicosis) (p = 0.01)]. Thyroid nodules sized ≥1 cm were found in 9 patients (7 %) in group 1 and 32 patients (26%) in group 2 (p < 0.0001). Conclusion: Overt thyroid hormonal disorders were more common in critically-ill COVID-19 patients. FT3 level at hospital admission is a potential prognostic marker of COVID-19 patients. Thyroid nodules may be associated with severe COVID-19 disease.

WHO guidance has incorrect recommendation in Oral health care involving AGPs. Air flow plays a key role in mitigating COVID-19 infection since airborne particles travel by air currents.

Background: The interplay between COVID-19 pandemic and asthma in children is still unclear. We evaluated the impact of COVID-19 on childhood asthma outcomes. Methods: The PeARL multinational cohort included 1,054 children with asthma and 505 non-asthmatic children aged between 4-18 years from 25 pediatric departments, from 15 countries globally. We compared the frequency of acute respiratory and febrile presentations during the first wave of the COVID-19 pandemic between groups and with data available from the previous year. In children with asthma, we also compared current and historical disease control. Results: During the pandemic, children with asthma experienced fewer upper respiratory tract infections, episodes of pyrexia, emergency visits, hospital admissions, asthma attacks and hospitalizations due to asthma, in comparison to the preceding year. Sixty-six percent of asthmatic children had improved asthma control while in 33% the improvement exceeded the minimal clinically important difference. Pre-bronchodilatation FEV1 and peak expiratory flow rate were improved during the pandemic. When compared to non-asthmatic controls, children with asthma were not at increased risk of LRTIs, episodes of pyrexia, emergency visits or hospitalizations during the pandemic. However, an increased risk of URTIs emerged. Conclusion: Childhood asthma outcomes, including control, were improved during the first wave of the COVID-19 pandemic, probably because of reduced exposure to asthma triggers and increased treatment adherence. The decreased frequency of acute episodes does not support the notion that childhood asthma may be a risk factor for COVID-19. Furthermore, the potential for improving childhood asthma outcomes through environmental control becomes apparent.

The emergence of coronavirus diseases (COVID-19) has presented a global health threat. The number of COVID-19 cases continues to increase in Africa; this poses a challenge to the African healthcare system, particularly the intensive care unit (ICU). More so, individuals with severe COVID-19 would often have a prolonged intensive care stay, requiring mechanical ventilation and sedation and this may increase their risk of developing physical, cognitive and psychosocial impairments. These post-ICU sequelae of morbidities have been termed Post Intensive Care Syndrome. The African healthcare system needs to be prepared to manage the adverse effects of Post Intensive Care Syndrome (PICS) largely characterized by a decline in functional capacity and health-related quality of life. It is thus expedient that multi-targeted measures such as early rehabilitation, adequate screening, patient/caregiver education and post-discharge rehabilitation be adopted to combat imminent poor health outcomes in COVID-19 survivors. In this editorial, we provided a brief review of PICS and highlighted strategies for preventing and managing PICS in the critically ill within the African context Key words: Pandemic, COVID-19 Survivors, African healthcare, Intensive Care Unit, Rehabilitation

This case series identified a sub cohort of healthcare workers with COVID-19 who experienced a prolonged symptomatic course and remained unable to return to work for many weeks. It notes their demographic and clinical characteristics and suggest ways to support them returning to work in a graded and supported manner.

Aim: To show if lower urinary tract symptoms (LUTS) could be symptoms of COVID-19 with validated questionnaires. Methods: The 96 COVID-19 patients who were hospitalized at a tertiary center were collected retrospectively. After the exclusion criteria, 46 patients were consisted as the study population. The male and female patients then fill formed the International Prostate Symptom Score and Urinary Symptom Profile respectively. All patients responded to these questions for the three period. Results: 27 female (58.6 %) and 19 male (41.4 %) COVID-19 patients answered the questions In the male patients, while there were no statistically significant differences in the total IPSS, the voiding IPSS score, and quality of life between the three periods (p=0.148; p=0.933, p=0.079, respectively), the storage IPSS scores had a significant difference between the three periods (p=0.05). In the female patients, low stream scores, were similar between the three periods (p=0.368). The scores of stress incontinence and an overactive bladder had a significant difference between the three periods (p=0.05 and p=0.05). Conclusion: LUTS, especially storage symptoms, might be one of the initial symptoms of COVID-19 and the clinicians should evaluate LUTS with other known symptoms of the virus when a patient is suspected of having COVID-19.

ABSTRACT Aim: To investigate the effect of COVID-19 on sexual dysfunction in women. Materials and Methods: The women diagnosed with COVID-19 and hospitalized at a tertiary hospital were included. They completed the Introductory Data Form, the Female Sexual Function Index-(FSFI), and the Short Form-36 Quality of Life Scale (SF-36). Results: 15 women between the ages of 19-49 who completed the treatment protocol, discharged at least 14 days before, and who had not been diagnosed as sexual dysfunction sexually active earlier were included to the study. It was detected that weekly sexual intercourse before and after COVID-19 significantly differed (p=0.047). The frequency of relationships decreased statistically after COVID-19. The mean value of the FSFI satisfaction score differs from COVID-19 before and after diagnosis (p=0.012). The mean satisfaction score before COVID-19 was 3.47, and after COVID-19 was 2.93. The score of the subgroups of FSFI did not differ from COVID-19 before and after diagnosis (p>0.050). The median value of SF-36 pain differs from COVID-19 before and after diagnosis (p=0.008). Conclusion: it was concluded that the frequency of sexual intercourse, sexual satisfaction in women decreased after COVID-19 disease, and the quality of life scores did not change in a statistically significant way.

Background – Studies investigating the relation between baseline liver abnormality and COVID-19 patients’ outcomes during hospitalization are scarce. The aim of the study is to address and characterize this clinically important association. Methods – Retrospective single-center study of adults hospitalized with COVID-19 infection for whom the baseline liver function tests up to one year prior to the admission were available. The study cohort included hospitalized patients from COVID-19 wards and specialized COVID-19 intensive care unit. Subjects were divided into a normal and abnormal baseline LFT groups that were then compared with respect to demographic characteristics, co-morbidities and patients’ outcomes during hospitalization. Results – 133 of 444 subjects met the inclusion criteria and were included in the study. Of them, 50/133 (37.6%) had abnormal baseline LFTs. The mean age of the cohort subjects was 65.7 ± 22.1 years and the mean BMI was 28.7 ± 13.0. Subjects with abnormal LFTs were more likely to die (22% versus 4.8%, p = 0.004) or require mechanical ventilation (16% versus 4.8%, p = 0.03) during hospitalization when compared to their normal LFT counterparts. Multivariate analysis revealed that abnormal baseline LFT (OR 6, 95% CI 2.0 – 18.4) was the strongest predictor of death or requiring mechanical ventilation followed by diabetes mellitus (OR 4.5, 95% CI 1.3 – 14.8) and congestive heart failure (OR 3.9, 95% CI 1.2 – 12.5). Conclusion - patients known to have a baseline LFTs abnormality appear to be at an increased risk for death or mechanical ventilation during hospitalization with COVID-19.