AdapterOcean/med_alpaca_standardized_cluster_96_std

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Answer this question truthfully	instruction	0	49,670	96	148,600
The appearance of abdominal pain has no fixed pattern of appearance in the COVID-19 clinical course. Abdominal pain may be the acute presenting symptom or one of numerous symptoms in a COVID-19 patient with intensity ranging from mild to severe. A complication reported is gut perforation due to ischemia. Patients may present with gut perforation as the first sign of COVID-19 infection. Upper GI bleed (due to esophageal mucosal damage as observed on endoscopy) has been reported among 4% of patients with other GI symptoms such as abdominal pain related to novel coronavirus infection. It is not known whether bleeding is a complication of other entities or a separate phenomenon in COVID-19 infection but has been mentioned together with abdominal pain. The esophagus, stomach, duodenum and stool have been tested positive for viral RNA. Prognosis: In a meta-analysis by Mao R. et al. the odds of severe disease among patients with abdominal pain as one of the gastrointestinal symptoms were 7.10.	output	1	49,670	96	148,601
What is abdominal pain associated with COVID-19?	input	2	49,670	96	148,602
Answer this question truthfully	instruction	0	51,383	96	153,739
COVID-19 can involve many organs leading to organ failure, one of which is kidneys that manifest with mild proteinuria to advanced acute kidney injury (AKI). Early reports from China revealed that COVID-19 rarely involves the kidneys, as Acute Renal Failure was not seen among COVID-19 hospitalized patients and mild BUN or creatinine rise 10.8% and mild proteinuria 7.2% occurred. However, recent study found 75.4% of hospitalized patients with COVID-19 pneumonia developed hematuria, proteinuria, and AKI. But, these findings are not significantly different from other critical diseases. AKI is frequently seen among patients with COVID-19 hospitalized in ICU, with prevalence of 0.6-29% in China "Acute Kidney Injury in COVID-19 Patients \| COVID-19". and 22.2% in the USA. While, the real incidence of AKI in critcally ill patients with COVID-19 is estimated between 27-85%. "Acute Kidney Injury in COVID-19 Patients \| COVID-19". Angiotensin-converting enzyme 2 (ACE2), which is a primary receptor for SARS-CoV-2 entry into cells, mostly presents in renal tubular epithelial cells as well as lungs and heart. Despite kidney injury following COVID-19 infection is less frequent than severe lung injury, ACE2: ACE ratio is higher in the kidneys compared to the respiratory system. (1:1 in the kidneys VS 1:20 in the respiratory system) After SARS-CoV-2 enters through the nasal cavity, it may travel to the kidneys and enters the bloodstream leading to severe inflammatory response activation and cytokine storm. It is thought that AKI following COVID-19 is the result of: Sepsis Hypovolemia and Hypotension Hypoxemia Blood clots formation, leading to impaired blood flow in the renal arterioles. AKI is more likely to develop in the late stages of COVID-19 in critically ill patients. Severe COVID-19 pneumonia and severe acute respiratory distress syndrome are associated with developing AKI. Approximately half of the new AKI cases following COVID-19 is mild with good short-term prognosis. If no improvement occurs during follow-up, it is contributed to higher mortality. Patients in the early stages of kidney failure may be asymptomatic. If left untreated, patients may progress to develop Azotemia and Uremia, which occur due to the buildup of waste materials in the blood. Symptoms of kidney injury include: Nausea and Vomiting Weakness Fatigue Confusion Weight loss Loss of appetite Oliguria or Anuria Fluid retention, leading edema and swelling of face and extremities Electrolyte imbalance; High level of Potassium which leads to cardiac arrhythmia Laboratory Findings Elevated BUN level Plasma BUN-creatinine ratio> 20 in prerenal AKI Plasma BUN-creatinine ratio< 15 in renal AKI or Acute Tubular Necrosis Based on KDIGO definition for the diagnosis of AKI : Elevated serum Creatinine by ≥0.3 mg/dl (≥26.5 μmol/l) within 48 hours; or Elevated serum Creatinine to ≥1.5 times baseline within the previous 7 days; or Urine volume < 0.5 ml/kg/h for >6 hours Fractional excretion of sodium (FENa) (FENa)< 1% in prerenal AKI (FENa)> 2% in renal AKI or Acute Tubular Necrosis Urinary sediment Hyaline casts in prerenal AKI Granular or Muddy brown casts in renal AKI or Acute Tubular Necrosis Electrocardiogram There are no specific ECG findings associated with AKI. However, electrolyte disturbances such as hyperkalemia might lead to various ECG abnormalities. Management of AKI following COVID-19 includes treatment of infection, identifying electrolyte disorders, and intravenous fluid administration. Early diagnosis and treatment of AKI in patients with COVID-19 can avoid the progression of AKI into ESRD and reduce mortality. Treatment of AKI following COVID-19 includes: Correction of hypovolemia and hypotension by the administration of adequate intravenous fluid Correction of electrolyte disturbances Renal Replacement Therapy If AKI is unresponsive to conservative therapy In volume overload conditions Modality of choice in unstable hemodynamic status and ESRD Anticoagulants in hypercoagulable conditions Sequential extracorporeal therapy	output	1	51,383	96	153,740
What are the renal complications of COVID-19?	input	2	51,383	96	153,741
Answer this question truthfully	instruction	0	52,713	96	157,729
Coronavrus Disease 2019 (COVID-19) is caused by a virus named severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). To browse the causes of diabetes, click here.	output	1	52,713	96	157,730
What is the effect of COVID-19 on individuals with diabetes?	input	2	52,713	96	157,731
Answer this question truthfully	instruction	0	55,369	96	165,697
COVID-19 is caused by a virus called severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) that belongs to the order nidovirale, family coronaviridae. Abnormal production of adipokines and cytokines such as tumor necrosis factor-alpha and interferons in diabetic patients have been associated with impairment in immune system and increased susceptibility to infections. COVID-19 has been related to cytokine storm and beta cell damage. The latter effects added to the own nature of COVID-19 lead to the following conditions: Hyperglycemia at the time of admission New onset diabetes Aggravated metabolic control in a diabetic patient The following factors have been demonstrated as responsible mechanisms which increase the risk of infections in diabetes: Reduction of Interleukin production Neutrophil dysfunction Decreased phagocytic activity and chemotaxis Decreased T cell activity Immobilized granulocytes Poor circulation, especially with concurrent peripheral vascular disease (PVD)	output	1	55,369	96	165,698
In what ways does COVID-19 impact people who have diabetes?	input	2	55,369	96	165,699
Please summerize the given abstract to a title	instruction	0	77,269	96	231,397
"Silent Hypoxemia" Leads to Vicious Cycle of Infection, Coagulopathy and Cytokine Storm in COVID-19: Can Prophylactic Oxygen Therapy Prevent It?	output	1	77,269	96	231,398
Humankind is facing its worst pandemic of the twenty-first century, due to infection of a novel coronavirus named as SARS-CoV2, started from Wuhan in China. Till now, 15 million people are infected, causing more than 600,000 deaths. The disease, commonly known as, COVID-19, was initially thought to be associated with ARDS only, but later on revealed to have many unexplained and atypical clinical features like coagulopathy and cytokinemia, leading to multi-organ involvements. The patients also suffer from 'Silent Hypoxemia', where there is no immediate respiratory signs and symptoms even though alarmingly low SpO2 level. We hypothesize that this covert hypoxemia may lead to molecular changes exacerbating coagulopathy and cytokine storm in COVID19 patients, which again, in turn, causes a vicious cycle of more hypoxemia/hypoxia and progression of the infection to more severe stages through HIF-1α dependent pathway. Although molecular mechanisms are yet to be substantiated by scientific evidence, hypoxemia remains an independent worsening factor in serious COVID 19 patients. Keeping all in mind, we propose that even in the early and asymptomatic cases, prophylactic oxygen therapy to be initiated to break the vicious cycle and to reduce the mortality in COVID 19 to save precious human lives.	input	2	77,269	96	231,399
Please summerize the given abstract to a title	instruction	0	77,298	96	231,484
Lipid-lowering therapy in high cardiovascular risk patients during COVID-19 pandemic: keep focused on the target.	output	1	77,298	96	231,485
To the Editor COVID-19 (COrona VIrus Disease) patients with cardiovascular (CV) disease, multiple CV risk factors or comorbidities (i.e., arterial hypertension and diabetes) were shown to be more prone to a worse prognosis. SARS-CoV-2 is a still unknown enemy and the role of concomitant cardiovascular therapies has been controversial in the early stages, particularly with regard to Angiotensin-Converting Enzyme inhibitors...	input	2	77,298	96	231,486
Please summerize the given abstract to a title	instruction	0	77,336	96	231,598
Symptomatic Carotid Artery Thrombosis in a Patient Recently Recovered From a COVID-19 Infection	output	1	77,336	96	231,599
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2), was initially discovered in December 2019 in China and rapidly spread all over the world to become a pandemic. The most common symptoms of a disease are fever, cough, generalized body ache, weakness, dyspnoea, nausea, vomiting, and diarrhea. Among vascular complications of COVID-19, the venous thrombotic complications, like pulmonary embolism and lower limb deep veins thrombosis, are not uncommon. But data about arterial thrombotic complications of COVID-19, especially carotid thrombosis, are still limited. We are describing a case of stroke due to thrombosis of the right carotid arteries, in a patient who had recovered from asymptomatic COVID-19. A 66-year-old male with arterial hypertension presented to the emergency department with a history of repeated collapse, dysarthria, weakness in the left extremities, and a drop in the left angle of his mouth (National Institutes of Health Stroke Scale [NIHSS]-4). The patient was swabbed for COVID-19 which was negative. A computed tomography angiography (CTA) was obtained which showed thrombosis in the branching point of the brachiocephalic trunk (BCT) continuing into the right subclavian artery (SA) and also into the right common carotid artery (CCA), with a subtotal occlusion of the right CCA, extending into the internal carotid artery (ICA) as well. From the apical lung tissue caught during the CT scan, bilateral, irregular widespread ground-glass opacifications, as well as consolidations and small reticular changes were seen in the lungs, which is typical for COVID-19 infection. A quantitative antibody test for COVID-19 infection was performed with the results showing a strong positivity for IgG antibodies, indicating previous COVID-19 infection. The patient was indicated for a standard carotid thrombectomy, which was performed without complications. It seems that one of the important factors that led to the formation of the thrombus in the carotid arteries was COVID-19 infection-induced inflammation in the atherosclerotic carotid vessels and generalized hypercoagulability as well as hyperviscosity. COVID-19 infection is an independent and important risk factor for the formation of an arterial thrombus during the acute illness and in the early post-COVID-19 period also, regardless of the severity of its course. Prophylactic anticoagulation is needed not only at the time of acute illness but also at the early post-COVID-19 time.	input	2	77,336	96	231,600
Please summerize the given abstract to a title	instruction	0	77,389	96	231,757
COVID-19 and liver transplantation	output	1	77,389	96	231,758
The effect of coronavirus disease 2019 (COVID-19) on liver transplantation programmes and recipients is still not completely understood but overall involves the risk of donor-derived transmission, the reliability of diagnostic tests, health-care resource utilization and the effect of immunosuppression. This Comment reviews the effect of COVID-19 on liver transplantation and summarizes recommendations for donor and recipient management.	input	2	77,389	96	231,759
Please summerize the given abstract to a title	instruction	0	77,398	96	231,784
Lower urinary tract symptoms (LUTS) related to COVID-19: Review article	output	1	77,398	96	231,785
The pandemic of the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) or Coronavirus Disease 2019 (COVID-19) is still ongoing. The outbreak of this new emerging contagious disease has impacted a wide range of sectors including health and economics. Much information about COVID-19 has been discovered by many laboratories, and action taken in various ways as quickly as possible to inhibit the outbreak. It was found that COVID-19 is a ribonucleic acid virus (RNA virus) that can cause infection among humans. Moreover, it can mutate and spread contagiously mainly through the respiratory system. The most common symptoms are cough and fever. Many patients could develop to either pneumonitis or respiratory failure. The SARS-CoV-2 virus can infect various organs, the main infections being in lungs and rectum. In these cases, many laboratories can isolate the virus from oropharyngeal and nasopharyngeal swab and then apply the reverse transcription polymerase chain reaction (RT-PCR) test to identify the COVID-19 virus. Many of the viral infections can cause cystitis by immunologic response. There is a study that showed the SARS-CoV-2 virus could be isolated from the urine sample. The patients had significant changes in urinary storage for frequency, urgency, and urinary incontinence during infected period, which improved after the disease resolved. Moreover, there is a study that reported that the COVID-19 patients who had the International Prostate Symptom Score (IPSS) scores of 20 to 35 had significantly longer hospital stays, more frequent intensive care requirements, and higher mortality rates. Therefore, physician and medical personnel should be aware of the irritative voiding symptoms that might be the presenting symptoms of COVID-19. Furthermore, as many studies have shown that the virus can be excreted in urine, thus, the virus could be contagious via urinary contamination.	input	2	77,398	96	231,786
Please summerize the given abstract to a title	instruction	0	77,431	96	231,883
Characterization of respiratory microbial dysbiosis in hospitalized COVID-19 patients	output	1	77,431	96	231,884
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused a global pandemic of Coronavirus disease 2019 (COVID-19). However, the microbial composition of the respiratory tract and other infected tissues as well as their possible pathogenic contributions to varying degrees of disease severity in COVID-19 patients remain unclear. Between 27 January and 26 February 2020, serial clinical specimens (sputum, nasal and throat swab, anal swab and feces) were collected from a cohort of hospitalized COVID-19 patients, including 8 mildly and 15 severely ill patients in Guangdong province, China. Total RNA was extracted and ultra-deep metatranscriptomic sequencing was performed in combination with laboratory diagnostic assays. We identified distinct signatures of microbial dysbiosis among severely ill COVID-19 patients on broad spectrum antimicrobial therapy. Co-detection of other human respiratory viruses (including human alphaherpesvirus 1, rhinovirus B, and human orthopneumovirus) was demonstrated in 30.8% (4/13) of the severely ill patients, but not in any of the mildly affected patients. Notably, the predominant respiratory microbial taxa of severely ill patients were Burkholderia cepacia complex (BCC), Staphylococcus epidermidis, or Mycoplasma spp. (including M. hominis and M. orale). The presence of the former two bacterial taxa was also confirmed by clinical cultures of respiratory specimens (expectorated sputum or nasal secretions) in 23.1% (3/13) of the severe cases. Finally, a time-dependent, secondary infection of B. cenocepacia with expressions of multiple virulence genes was demonstrated in one severely ill patient, which might accelerate his disease deterioration and death occurring one month after ICU admission. Our findings point to SARS-CoV-2-related microbial dysbiosis and various antibiotic-resistant respiratory microbes/pathogens in hospitalized COVID-19 patients in relation to disease severity. Detection and tracking strategies are needed to prevent the spread of antimicrobial resistance, improve the treatment regimen and clinical outcomes of hospitalized, severely ill COVID-19 patients.	input	2	77,431	96	231,885
Please summerize the given abstract to a title	instruction	0	77,467	96	231,991
Coagulopathy and thromboembolic events in patients with SARS-CoV-2 infection: pathogenesis and management strategies	output	1	77,467	96	231,992
In October 2019, a viral infectious disease appeared in the city of Wuhan in China. A new betacoronavirus, SARS-CoV-2, has been recognized as the responsible pathogen in this infection. Although coronavirus disease is principally expressed as a pulmonary infection, critical SARS-CoV-2 infection is frequently complicated with coagulopathy, and thromboembolic events are recognizable in several patients. Dehydration, acute inflammatory condition, protracted immobilization during disease, existence of multiple cardiovascular risk factors such as diabetes, obesity or hypertension, previous coronary artery disease, ischemic stroke, peripheral artery disease are frequent comorbidities in SARS-CoV-2 hospitalized subjects, which possibly augment thrombo-embolic risk. However, other causal factors can still be identified such as unrestricted angiotensin II action, the use of immunoglobulins, an increased production of adhesion molecules able to induce vascular inflammation and endothelial activation, complement stimulation, excessive production of neutrophil extracellular traps (NETs), and increased platelet count. Low-molecular-weight heparin should be chosen as early treatment because of its anti-inflammatory action and its ability to antagonize histones and so defend the endothelium. However, several therapeutic possibilities have also been proposed such as fibrinolytic treatment, drugs that target NETs, and complement inhibition. Nevertheless, although the violence of the pandemic may suggest the use of heroic treatments to reduce the frightening mortality that accompanies SARS-CoV-2 infection, we believe that experimental treatments should only be used within approved and controlled protocols, the only ones that can provide useful and specify information on the validity of the treatments.	input	2	77,467	96	231,993
Please summerize the given abstract to a title	instruction	0	77,520	96	232,150
Optic neuritis following SARS-CoV-2 infection	output	1	77,520	96	232,151
The most common neurologic symptoms in COVID-19 are headache, anosmia, and dysgeusia. Optic neuritis is an unusual manifestation of SARS-CoV-2 infection. We report a case of a patient who initially consulted for vision loss in the absence of respiratory symptoms. She was diagnosed with optic neuritis following SARS-CoV-2 infection. Delay in diagnosis of neuro-ophthalmic manifestations of COVID-19 may lead to irreversible optic atrophy. A mechanism in which viral antigens would induce an immune response against self-proteins, or direct SARS Cov-2 infection of the central nervous system, may be involved in optic nerve injury.	input	2	77,520	96	232,152
Please summerize the given abstract to a title	instruction	0	77,541	96	232,213
Demyelinating Disease of the Central Nervous System Concurrent With COVID-19	output	1	77,541	96	232,214
Neurological diseases related to coronavirus disease-2019 (COVID-19) are increasingly reported. We report here three cases that presented with subtle neurologic findings manifesting within a range of 15 days to four months after their COVID-19 diagnoses. Magnetic resonance imaging showed acute multifocal periventricular and subcortical demyelinating lesions. Some of the lesions showed contrast enhancement and diffusion restriction. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) PCR was found in the cerebrospinal fluid of just one patient. All patients received intravenous methylprednisolone therapy. In this report, we aim to discuss the aspects of possible COVID-19-related demyelination that support a diagnosis of multiple sclerosis (MS) or acute disseminated encephalomyelitis (ADEM).	input	2	77,541	96	232,215
Please summerize the given abstract to a title	instruction	0	77,557	96	232,261
Posterior Reversible Encephalopathy Syndrome: A Rare Complication in COVID-19	output	1	77,557	96	232,262
The coronavirus disease 2019 (COVID-19) has a broad spectrum of manifestations. Neurological complications are not uncommon in patients with COVID-19. We report the case of a middle-aged man who presented with a cough and fever. He had a decreased oxygen saturation and required supplementary oxygen therapy. During his stay, he developed an unexplained seizure. Computed tomography of the brain revealed vasogenic edema located posteriorly. Subsequently, magnetic resonance imaging demonstrated subcortical white-matter hyperdensities, in keeping with the diagnosis of posterior reversible encephalopathy syndrome, an exceedingly rare manifestation in COVID-19. This condition should be kept in mind when encountering unexplained neurological manifestations that developed in patients with COVID-19.	input	2	77,557	96	232,263
Please summerize the given abstract to a title	instruction	0	77,572	96	232,306
New-Onset Transient Global Amnesia: A Clinical Challenge in an Air Medical Transportation Pilot With a History of Coronavirus Disease 2019	output	1	77,572	96	232,307
A 43-year-old male Bell 214C helicopter pilot presented to the emergency ward with flu-like syndrome. His nasopharyngeal severe acute respiratory syndrome coronavirus 2 real-time polymerase chain reaction test was positive, and a chest computed tomographic scan confirmed coronavirus disease 2019 pneumonia. He was admitted, received treatment, was discharged, and returned to flying. During the mission debrief, copilots who had flown with him reported that he experienced episodes of in-flight dizziness and blacked out. They occurred briefly during the cruise and hovering flight, perhaps for a few seconds of disorientation and unconsciousness. Rapid identification of the copilot and control of the helicopter prevented any incident or accident. Afterward, he explained the sudden onset and unexpected brief periods of loss of consciousness after a headache. The flight safety office referred him to the aviation medical center for further investigations. The cardiovascular, neurologic, laboratory, and toxicologic assessments were inconclusive with the approach to sudden-onset transient loss of consciousness. The only abnormal finding was hippocampus lesions on brain magnetic resonance imaging (MRI). Because of the possible diagnosis of transient global amnesia, the aviation medical examiner suspended him from flight duties until complete recovery and the absence of any probable complications.	input	2	77,572	96	232,308
Please summerize the given abstract to a title	instruction	0	77,722	96	232,756
Rationale for targeting Complement in COVID‐19	output	1	77,722	96	232,757
A novel coronavirus, SARS‐CoV‐2, has recently emerged in China and spread internationally, posing a health emergency to the global community. COVID‐19 caused by SARS‐CoV‐2 is associated with an acute respiratory illness that varies from mild to the life‐threatening acute respiratory distress syndrome (ARDS). The complement system is part of the innate immune arsenal against pathogens, which many viruses can evade or employ to mediate cell entry. The immunopathology and acute lung injury orchestrated through the influx of pro‐inflammatory macrophages and neutrophils can be directly activated by complement components to prime an overzealous cytokine storm. The manifestations of severe COVID‐19 such as the ARDS, sepsis and multiorgan failure have an established relationship with activation of the complement cascade. We have collected evidence from all the current studies we are aware of on SARS‐CoV‐2 immunopathogenesis and the preceding literature on SARS‐CoV‐1 and MERS‐CoV infection linking severe COVID‐19 disease directly with dysfunction of the complement pathways. This information lends support for a therapeutic anti‐inflammatory strategy against complement, where a number of clinically ready potential therapeutic agents are available.	input	2	77,722	96	232,758
Please summerize the given abstract to a title	instruction	0	77,727	96	232,771
Impact of COVID-19 on biochemical parameters: a narrative review	output	1	77,727	96	232,772
Coronaviruses have been a major threat to public health globally since last decades Coronaviruses are enveloped and positive-stranded RNA genome After SARS and MERS, SARS-CoV-2 is the third known coronavirus causing fatal respiratory diseases in humans In the initial stage of SARS-CoV-2 infection, clinical features are quite nonspecific and not all suspected patients can be tested to exclude or confirm the diagnosis The clinical course of the disease may cause changes in laboratory parameters Early identification of causative agent SARS-CoV-2 and monitoring the blood biochemical parameters helps in assessment of disease severity and proper monitoring of the disease In this review, the research studies on biochemical markers in COVID-19 till 31st August 2020 are retrieved and selected articles are reviewed These data are extremely important in assessing the evolution of the disease, prognosis and directing therapeutic interventions In the view of that the present study aimed to discuss the impact of biochemical markers in COVID-19	input	2	77,727	96	232,773
Please summerize the given abstract to a title	instruction	0	77,734	96	232,792
Skin manifestations of COVID-19 in children: Part 1	output	1	77,734	96	232,793
The current COVID-19 pandemic is caused by the SARS-CoV-2 coronavirus. The initial recognized symptoms were respiratory, sometimes culminating in severe respiratory distress requiring ventilation, and causing death in a percentage of those infected. As time has passed, other symptoms have been recognized. The initial reports of cutaneous manifestations were from Italian dermatologists, probably because Italy was the first European country to be heavily affected by the pandemic. The overall clinical presentation, course and outcome of SARS-CoV-2 infection in children differ from those in adults as do the cutaneous manifestations of childhood. In this review, we summarize the current knowledge on the cutaneous manifestations of COVID-19 in children after thorough and critical review of articles published in the literature and from the personal experience of a large panel of paediatric dermatologists in Europe. In Part 1, we discuss one of the first and most widespread cutaneous manifestation of COVID-19, chilblain-like lesions. In Part 2, we review other manifestations, including erythema multiforme, urticaria and Kawasaki disease-like inflammatory multisystemic syndrome, while in Part 3, we discuss the histological findings of COVID-19 manifestations, and the testing and management of infected children, for both COVID-19 and any other pre-existing conditions.	input	2	77,734	96	232,794
Please summerize the given abstract to a title	instruction	0	77,889	96	233,257
Mechanisms and consequences of COVID-19 associated liver injury: What can we affirm?	output	1	77,889	96	233,258
Since the first reports of coronavirus disease 2019 (COVID-19) cases in December 2019 in China, numerous papers have been published describing a high frequency of liver injury associated with severe acute respiratory syndrome coronavirus 2 infection, many of them proposing a link between these findings and patient outcomes. Increases in serum aminotransferase levels (ranging from 16% to 62%) and bilirubin levels (ranging from 5% to 21%) have been reported and seem to be more often observed in patients with severe forms of COVID-19. Although absolute changes in these parameters are frequently seen, other variables, such as the ratio above the upper limit of normal, the onset of liver injury as a complication in severe cases and histopathological findings, reinforce that liver changes are of dubious clinical relevance in the course of this disease. Other factors must also be considered in these analyses, such as the repercussions of hemodynamic changes, the presence of thrombotic events, and, mainly, the possible drug-induced liver injury with the current, yet off-label, treatment. This paper aimed to analyze the currently available data on liver injury in patients with COVID-19.	input	2	77,889	96	233,259
Please summerize the given abstract to a title	instruction	0	77,944	96	233,422
COVID-19: unravelling the clinical progression of nature's virtually perfect biological weapon	output	1	77,944	96	233,423
Coronavirus disease 2019 (COVID-19) pandemic has shocked the world and caused morbidity and mortality on an unprecedented level in the era of modern medicine Evidence generated to-date on the virulence and pathogenicity of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) suggests that COVID-19 may be considered a perfect storm, caused by a nature's virtually perfect biological weapon This conclusion is supported by an updated analysis of pathogenesis and clinical progression of this infectious disease It is now readily apparent that COVID-19 is not a clear-cut disorder, but is instead a gradually evolving pathology, characterized by a series of stages sustained by different molecular and biological mechanisms The disease can hence be divided in at least five different phases (incubation, respiratory, pro-inflammatory, pro-thrombotic, and death or remission) Whilst the virus triggers direct cytopathic injury during the initial stage of illness, in the following evolving phases, it is the host itself that undergoes an almost suicidal reaction, sustained, amplified and maintained by the immune, complement and hemostatic systems Another peculiar property making SARS-CoV-2 a devious and vicious pathogen is the biophysical structure of its receptor biding domain, which needs to be primed by human proteases, thus being less efficiently targetable by the host immune system The unique pathophysiology of COVID-19 requires the customization of therapy by individual patient characteristics and according to the phase-specific, evolving derangement of the multiple biological pathways	input	2	77,944	96	233,424
Please summerize the given abstract to a title	instruction	0	77,945	96	233,425
Prior and novel coronaviruses, Coronavirus Disease 2019 (COVID-19), and human reproduction: what is known?	output	1	77,945	96	233,426
OBJECTIVE: To summarize current understanding of the effects of novel and prior coronaviruses on human reproduction, specifically male and female gametes, and in pregnancy. DESIGN: Review of English publications in PubMed and Embase to April 6, 2020. METHOD(S): Articles were screened for reports including coronavirus, reproduction, pathophysiology, and pregnancy. INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): Reproductive outcomes, effects on gametes, pregnancy outcomes, and neonatal complications. RESULT(S): Seventy-nine reports formed the basis of the review. Coronavirus binding to cells involves the S1 domain of the spike protein to receptors present in reproductive tissues, including angiotensin-converting enzyme-2 (ACE2), CD26, Ezrin, and cyclophilins. Severe Acute Respiratory Syndrome Coronavirus 1 (SARS-CoV-1) may cause severe orchitis leading to germ cell destruction in males. Reports indicate decreased sperm concentration and motility for 72-90 days following Coronavirus Disease 2019 (COVID-19) infection. Gonadotropin-dependent expression of ACE2 was found in human ovaries, but it is unclear whether SARS-Coronavirus 2 (CoV-2) adversely affects female gametogenesis. Evidence suggests that COVID-19 infection has a lower maternal case fatality rate than SARS or Middle East respiratory syndrome (MERS), but anecdotal reports suggest that infected, asymptomatic women may develop respiratory symptoms postpartum. Coronavirus Disease 2019 infections in pregnancy are associated with preterm delivery. Postpartum neonatal transmission from mother to child has been reported. CONCLUSION(S): Coronavirus Disease 2019 infection may affect adversely some pregnant women and their offspring. Additional studies are needed to assess effects of SARS-CoV-2 infection on male and female fertility.	input	2	77,945	96	233,427
Please summerize the given abstract to a title	instruction	0	77,976	96	233,518
Unexpected BP Sensitivity to Angiotensin II in a Patient With Coronavirus Disease 2019, ARDS, and Septic Shock	output	1	77,976	96	233,519
We report the case of an 88-year-old man with coronavirus disease 2019 (COVID-19) who presented with ARDS and septic shock. The patient had exquisite BP sensitivity to low-dose angiotensin II (Ang-2), allowing for rapid liberation from high-dose vasopressors. We hypothesize that sensitivity to Ang-2 might be related to biological effect of severe acute respiratory syndrome coronavirus 2 infection. The case is suggestive of a potential role for synthetic Ang-2 for patients with COVID-19 and septic shock. Further studies are needed to confirm our observed clinical efficacy.	input	2	77,976	96	233,520
Please summerize the given abstract to a title	instruction	0	78,033	96	233,689
COVID-19 Associated Pulmonary Aspergillosis (CAPA)—From Immunology to Treatment	output	1	78,033	96	233,690
Like severe influenza, coronavirus disease-19 (COVID-19) resulting in acute respiratory distress syndrome (ARDS) has emerged as an important disease that predisposes patients to secondary pulmonary aspergillosis, with 35 cases of COVID-19 associated pulmonary aspergillosis (CAPA) published until June 2020. The release of danger-associated molecular patterns during severe COVID-19 results in both pulmonary epithelial damage and inflammatory disease, which are predisposing risk factors for pulmonary aspergillosis. Moreover, collateral effects of host recognition pathways required for the activation of antiviral immunity may, paradoxically, contribute to a highly permissive inflammatory environment that favors fungal pathogenesis. Diagnosis of CAPA remains challenging, mainly because bronchoalveolar lavage fluid galactomannan testing and culture, which represent the most sensitive diagnostic tests for aspergillosis in the ICU, are hindered by the fact that bronchoscopies are rarely performed in COVID-19 patients due to the risk of disease transmission. Similarly, autopsies are rarely performed, which may result in an underestimation of the prevalence of CAPA. Finally, the treatment of CAPA is complicated by drug–drug interactions associated with broad spectrum azoles, renal tropism and damage caused by SARS-CoV-2, which may challenge the use of liposomal amphotericin B, as well as the emergence of azole-resistance. This clinical reality creates an urgency for new antifungal drugs currently in advanced clinical development with more promising pharmacokinetic and pharmacodynamic profiles.	input	2	78,033	96	233,691
Please summerize the given abstract to a title	instruction	0	78,089	96	233,857
COVID-19 and liver damage	output	1	78,089	96	233,858
An outbreak of unknown pneumonia, caused by the novel severe acute respiratory syndrome coronavirus (SARS-CoV-2), was reported in China at the end of December 2019. On February 11, 2020, the World Health Organization officially named SARS-CoV-2 infection COVID-19 (Coronavirus Disease 2019). The most common clinical manifestation of COVID-19 is pneumonia. However, with the spread of the COVID-19 pandemic and analysis of clinical data, symptoms that are not characteristic of "atypical" pneumonia have been identified in patients. Neurological symptoms, skin and eye damage, etc., are described. The extrapulmonary presence of SARS-CoV-2 was also detected in cholangiocytes. Virus-induced effects, systemic inflammation ("cytokine storm"), hypoxia, hypovolemia, hypotension in shock, druginduced hepatotoxicity, etc., are considered possible factors of liver damage. In 14-53 % of COVID-19 patients, changes in biochemical parameters, which usually do not require drug therapy, can be recorded. Acute hepatitis is very rare. However, special attention should be given to COVID-19 patients at risk: after liver transplantation; receiving immunosuppressants and antiviral drugs; and in cases of decompensated cirrhosis, acute-on-chronic liver failure, and hepatocellular carcinoma. Constant data sharing and open access to research data, new technologies, and up-to-date guidelines are required.	input	2	78,089	96	233,859
Please summerize the given abstract to a title	instruction	0	78,154	96	234,052
Covid-19 and oral diseases: Crosstalk, synergy or association?	output	1	78,154	96	234,053
The coronavirus disease 2019 (Covid-19) is a viral infection caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that clinically affects multiple organs of the human body. Cells in the oral cavity express viral entry receptor angiotensin-converting enzyme 2 that allows viral replication and may cause tissue inflammation and destruction. Recent studies have reported that Covid-19 patients present oral manifestations with multiple clinical aspects. In this review, we aim to summarise main signs and symptoms of Covid-19 in the oral cavity, its possible association with oral diseases, and the plausible underlying mechanisms of hyperinflammation reflecting crosstalk between Covid-19 and oral diseases. Ulcers, blisters, necrotising gingivitis, opportunistic coinfections, salivary gland alterations, white and erythematous plaques and gustatory dysfunction were the most reported clinical oral manifestations in patients with Covid-19. In general, the lesions appear concomitant with the loss of smell and taste. Multiple reports show evidences of necrotic/ulcerative gingiva, oral blisters and hypergrowth of opportunistic oral pathogens. SARS-CoV-2 exhibits tropism for endothelial cells and Covid-19-mediated endotheliitis can not only promote inflammation in oral tissues but can also facilitate virus spread. In addition, elevated levels of proinflammatory mediators in patients with Covid-19 and oral infectious disease can impair tissue homeostasis and cause delayed disease resolution. This suggests potential crosstalk of immune-mediated pathways underlying pathogenesis. Interestingly, few reports suggest recurrent herpetic lesions and higher bacterial growth in Covid-19 subjects, indicating SARS-CoV-2 and oral virus/bacteria interaction. Larger cohort studies comparing SARS-CoV-2 negative and positive subjects will reveal oral manifestation of the virus on oral health and its role in exacerbating oral infection.	input	2	78,154	96	234,054
Please summerize the given abstract to a title	instruction	0	78,217	96	234,241
Guillain-Barré syndrome associated with COVID-19 disease	output	1	78,217	96	234,242
Clinical manifestations of COVID-19 are known to be variable with growing evidence of nervous system involvement. In this case report, we describe the symptoms of a patient infected with SARS-CoV-2 whose clinical course was complicated with Guillain-Barré syndrome (GBS). We present a case of a 58-year-old woman who was initially diagnosed with COVID-19 pneumonia due to symptoms of fever and cough. Two weeks later, after the resolution of upper respiratory tract symptoms, she developed symmetric ascending quadriparesis and paresthesias. The diagnosis of GBS was made through cerebrospinal fluid analysis and she was successfully treated with intravenous immunoglobulin administration.	input	2	78,217	96	234,243
Please summerize the given abstract to a title	instruction	0	78,373	96	234,709
A Systematic Review of Cases of Acute Respiratory Distress Syndrome in the Coronavirus Disease 2019 Pandemic	output	1	78,373	96	234,710
The outbreak of coronavirus disease 2019 (COVID-19) was declared a global pandemic after it spread to 213 countries and has the highest total number of cases worldwide. About 80% of COVID-19 infections are mild or asymptomatic and never require hospitalization but about 5% of patients become critically ill and develop acute respiratory distress syndrome (ARDS). The widely used management for ARDS in COVID-19 has been in line with the standard approach, but the need to adjust the treatment protocols has been questioned based on the reports of higher mortality risk among those requiring mechanical ventilation. Treatment options for this widespread disease are limited and there are no definitive therapies or vaccines until now. Although some antimalarial and antiviral drugs may prove effective against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), their safety and efficacy are still under clinical trials. We conducted a systematic review of case reports on ARDS in SARS-CoV-2 infection to summarize the clinical presentation, laboratory and chest imaging findings, management protocols, and outcome of ARDS in COVID-19-positive patients. We need more data and established studies for the effective management of the novel SARS-CoV-2 and to reduce mortality in high-risk patients.	input	2	78,373	96	234,711
Please summerize the given abstract to a title	instruction	0	78,435	96	234,895
Surgically treated reactive arthritis of the ankle after COVID-19 infection: A case report	output	1	78,435	96	234,896
A 37-year-old man developed right ankle pain and swelling six days after being diagnosed with coronavirus disease (COVID-19). Despite conservative treatment, his ankle symptoms persisted. Magnetic resonance imaging and computed tomography showed synovial hypertrophy and bone erosion in the ankle. Following arthroscopic synovectomy, performed 69 days after the COVID-19 diagnosis, the pain improved significantly. The clinical course was consistent with that of reactive arthritis following severe acute respiratory syndrome coronavirus 2 infection. The pathological findings resembled rheumatoid nodules. The bone erosion may have originated from the inflammatory pathway, which resembles the mechanism of rheumatoid arthritis.	input	2	78,435	96	234,897
Please summerize the given abstract to a title	instruction	0	78,447	96	234,931
Microglial Implications in SARS-CoV-2 Infection and COVID-19: Lessons From Viral RNA Neurotropism and Possible Relevance to Parkinson’s Disease	output	1	78,447	96	234,932
Since December 2019, humankind has been experiencing a ravaging severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) outbreak, the second coronavirus pandemic in a decade after the Middle East respiratory syndrome coronavirus (MERS-CoV) disease in 2012. Infection with SARS-CoV-2 results in Coronavirus disease 2019 (COVID-19), which is responsible for over 3.1 million deaths worldwide. With the emergence of a second and a third wave of infection across the globe, and the rising record of multiple reinfections and relapses, SARS-CoV-2 infection shows no sign of abating. In addition, it is now evident that SARS-CoV-2 infection presents with neurological symptoms that include early hyposmia, ischemic stroke, meningitis, delirium and falls, even after viral clearance. This may suggest chronic or permanent changes to the neurons, glial cells, and/or brain vasculature in response to SARS-CoV-2 infection or COVID-19. Within the central nervous system (CNS), microglia act as the central housekeepers against altered homeostatic states, including during viral neurotropic infections. In this review, we highlight microglial responses to viral neuroinfections, especially those with a similar genetic composition and route of entry as SARS-CoV-2. As the primary sensor of viral infection in the CNS, we describe the pathogenic and neuroinvasive mechanisms of RNA viruses and SARS-CoV-2 vis-à-vis the microglial means of viral recognition. Responses of microglia which may culminate in viral clearance or immunopathology are also covered. Lastly, we further discuss the implication of SARS-CoV-2 CNS invasion on microglial plasticity and associated long-term neurodegeneration. As such, this review provides insight into some of the mechanisms by which microglia could contribute to the pathophysiology of post-COVID-19 neurological sequelae and disorders, including Parkinson’s disease, which could be pervasive in the coming years given the growing numbers of infected and re-infected individuals globally.	input	2	78,447	96	234,933
Please summerize the given abstract to a title	instruction	0	78,476	96	235,018
The Emerging Threat of (Micro)Thrombosis in COVID-19 and Its Therapeutic Implications	output	1	78,476	96	235,019
The recent emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the ensuing global pandemic has presented a health emergency of unprecedented magnitude. Recent clinical data has highlighted that coronavirus disease 2019 (COVID-19) is associated with a significant risk of thrombotic complications ranging from microvascular thrombosis, venous thromboembolic disease, and stroke. Importantly, thrombotic complications are markers of severe COVID-19 and are associated with multiorgan failure and increased mortality. The evidence to date supports the concept that the thrombotic manifestations of severe COVID-19 are due to the ability of SARS-CoV-2 to invade endothelial cells via ACE-2 (angiotensin-converting enzyme 2), which is expressed on the endothelial cell surface. However, in patients with COVID-19 the subsequent endothelial inflammation, complement activation, thrombin generation, platelet, and leukocyte recruitment, and the initiation of innate and adaptive immune responses culminate in immunothrombosis, ultimately causing (micro)thrombotic complications, such as deep vein thrombosis, pulmonary embolism, and stroke. Accordingly, the activation of coagulation (eg, as measured with plasma D-dimer) and thrombocytopenia have emerged as prognostic markers in COVID-19. Given thrombotic complications are central determinants of the high mortality rate in COVID-19, strategies to prevent thrombosis are of critical importance. Several antithrombotic drugs have been proposed as potential therapies to prevent COVID-19-associated thrombosis, including heparin, FXII inhibitors, fibrinolytic drugs, nafamostat, and dipyridamole, many of which also possess pleiotropic anti-inflammatory or antiviral effects. The growing awareness and mechanistic understanding of the prothrombotic state of COVID-19 patients are driving efforts to more stringent diagnostic screening for thrombotic complications and to the early institution of antithrombotic drugs, for both the prevention and therapy of thrombotic complications. The shifting paradigm of diagnostic and treatment strategies holds significant promise to reduce the burden of thrombotic complications and ultimately improve the prognosis for patients with COVID-19.	input	2	78,476	96	235,020
Please summerize the given abstract to a title	instruction	0	78,619	96	235,447
Coronavirus disease 2019 respiratory disease in children: clinical presentation and pathophysiology	output	1	78,619	96	235,448
PURPOSE OF REVIEW: Pediatric coronavirus disease 2019 (COVID-19) respiratory disease is a distinct entity from adult illness, most notable in its milder phenotype. This review summarizes the current knowledge of the clinical patterns, cellular pathophysiology, and epidemiology of COVID-19 respiratory disease in children with specific attention toward factors that account for the maturation-related differences in disease severity. RECENT FINDINGS: Over the past 14 months, knowledge of the clinical presentation and pathophysiology of COVID-19 pneumonia has rapidly expanded. The decreased disease severity of COVID-19 pneumonia in children was an early observation. Differences in the efficiency of viral cell entry and timing of immune recognition and response between children and adults remain at the center of ongoing research. SUMMARY: The clinical spectrum of COVID-19 respiratory disease in children is well defined. The age-related differences protecting children from severe disease and death remain incompletely understood.	input	2	78,619	96	235,449
Please summerize the given abstract to a title	instruction	0	78,702	96	235,696
COVID-19 and Long-Term Outcomes: Lessons from Other Critical Care Illnesses and Potential Mechanisms	output	1	78,702	96	235,697
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel coronavirus that is currently causing a pandemic and has been termed Coronavirus disease 2019 (COVID-19). The elderly or those with preexisting conditions like diabetes, hypertension, coronary heart disease, chronic obstructive pulmonary disease, cerebrovascular disease, or kidney dysfunction are more likely to develop severe cases when infected. COVID-19 patients admitted to the intensive care unit (ICU) have higher mortality than non-ICU patients. Critical illness has consistently posed a challenge not only in terms of mortality, but also in regard to long-term outcomes of survivors. Patients who survive acute critical illness including, but not limited to, pulmonary and systemic insults associated with ARDS, pneumonia, systemic inflammation, and mechanical ventilation, will likely suffer from Post-ICU Syndrome (PICS), a phenomenon of cognitive, psychiatric, and/or physical disability following treatment in the ICU. Post-ICU morbidity and mortality continues to be a cause for concern when considering large-scale studies showing 12-month mortality risks of 11.8% to 21%. Previous studies have demonstrated that multiple mechanisms, including cytokine release, mitochondrial dysfunction and even amyloids may lead to end-organ dysfunction in patients. We hypothesize that COVID-19 infection will lead to PICS via potentially similar mechanisms as other chronic critical illness and cause long-term morbidity and mortality in patients. We consider a variety of mechanisms and questions that not only consider the short-term impact of the COVID-19 pandemic, but its long-term effects that may not yet be imagined. This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives License 4.0 (http://creativecommons.org/licenses/by-nc-nd/4.0/).	input	2	78,702	96	235,698
Please summerize the given abstract to a title	instruction	0	78,753	96	235,849
Coronaviruses and Central Nervous System Manifestations	output	1	78,753	96	235,850
SARS-CoV-2 is a highly pathogenic coronavirus that has caused an ongoing worldwide pandemic. Emerging in Wuhan, China in December 2019, the virus has spread rapidly around the world. Corona virus disease 2019 (COVID-19), which is caused by SARS-CoV-2, has resulted in significant morbidity and mortality. The most prominent symptoms of SARS-CoV-2 infection are respiratory. However, accumulating evidence highlights involvement of the central nervous system (CNS). This includes headache, anosmia, meningoencephalitis, acute ischemic stroke, and several presumably post/para-infectious syndromes and altered mental status not explained by respiratory etiologies. Interestingly, previous studies in animal models emphasized the neurotropism of coronaviruses; thus, these CNS manifestations of COVID-19 are not surprising. This minireview scans the literature regarding the involvement of the CNS in coronavirus infections in general, and in regard to the recent SARS-CoV-2, specifically.	input	2	78,753	96	235,851
Please summerize the given abstract to a title	instruction	0	78,785	96	235,945

Answer this question truthfully

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The appearance of abdominal pain has no fixed pattern of appearance in the COVID-19 clinical course. Abdominal pain may be the acute presenting symptom or one of numerous symptoms in a COVID-19 patient with intensity ranging from mild to severe. A complication reported is gut perforation due to ischemia. Patients may present with gut perforation as the first sign of COVID-19 infection. Upper GI bleed (due to esophageal mucosal damage as observed on endoscopy) has been reported among 4% of patients with other GI symptoms such as abdominal pain related to novel coronavirus infection. It is not known whether bleeding is a complication of other entities or a separate phenomenon in COVID-19 infection but has been mentioned together with abdominal pain. The esophagus, stomach, duodenum and stool have been tested positive for viral RNA. Prognosis: In a meta-analysis by Mao R. et al. the odds of severe disease among patients with abdominal pain as one of the gastrointestinal symptoms were 7.10.

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What is abdominal pain associated with COVID-19?

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COVID-19 can involve many organs leading to organ failure, one of which is kidneys that manifest with mild proteinuria to advanced acute kidney injury (AKI). Early reports from China revealed that COVID-19 rarely involves the kidneys, as Acute Renal Failure was not seen among COVID-19 hospitalized patients and mild BUN or creatinine rise 10.8% and mild proteinuria 7.2% occurred. However, recent study found 75.4% of hospitalized patients with COVID-19 pneumonia developed hematuria, proteinuria, and AKI. But, these findings are not significantly different from other critical diseases. AKI is frequently seen among patients with COVID-19 hospitalized in ICU, with prevalence of 0.6-29% in China "Acute Kidney Injury in COVID-19 Patients | COVID-19". and 22.2% in the USA. While, the real incidence of AKI in critcally ill patients with COVID-19 is estimated between 27-85%. "Acute Kidney Injury in COVID-19 Patients | COVID-19". Angiotensin-converting enzyme 2 (ACE2), which is a primary receptor for SARS-CoV-2 entry into cells, mostly presents in renal tubular epithelial cells as well as lungs and heart. Despite kidney injury following COVID-19 infection is less frequent than severe lung injury, ACE2: ACE ratio is higher in the kidneys compared to the respiratory system. (1:1 in the kidneys VS 1:20 in the respiratory system) After SARS-CoV-2 enters through the nasal cavity, it may travel to the kidneys and enters the bloodstream leading to severe inflammatory response activation and cytokine storm. It is thought that AKI following COVID-19 is the result of: Sepsis Hypovolemia and Hypotension Hypoxemia Blood clots formation, leading to impaired blood flow in the renal arterioles. AKI is more likely to develop in the late stages of COVID-19 in critically ill patients. Severe COVID-19 pneumonia and severe acute respiratory distress syndrome are associated with developing AKI. Approximately half of the new AKI cases following COVID-19 is mild with good short-term prognosis. If no improvement occurs during follow-up, it is contributed to higher mortality. Patients in the early stages of kidney failure may be asymptomatic. If left untreated, patients may progress to develop Azotemia and Uremia, which occur due to the buildup of waste materials in the blood. Symptoms of kidney injury include: Nausea and Vomiting Weakness Fatigue Confusion Weight loss Loss of appetite Oliguria or Anuria Fluid retention, leading edema and swelling of face and extremities Electrolyte imbalance; High level of Potassium which leads to cardiac arrhythmia Laboratory Findings Elevated BUN level Plasma BUN-creatinine ratio> 20 in prerenal AKI Plasma BUN-creatinine ratio< 15 in renal AKI or Acute Tubular Necrosis Based on KDIGO definition for the diagnosis of AKI : Elevated serum Creatinine by ≥0.3 mg/dl (≥26.5 μmol/l) within 48 hours; or Elevated serum Creatinine to ≥1.5 times baseline within the previous 7 days; or Urine volume < 0.5 ml/kg/h for >6 hours Fractional excretion of sodium (FENa) (FENa)< 1% in prerenal AKI (FENa)> 2% in renal AKI or Acute Tubular Necrosis Urinary sediment Hyaline casts in prerenal AKI Granular or Muddy brown casts in renal AKI or Acute Tubular Necrosis Electrocardiogram There are no specific ECG findings associated with AKI. However, electrolyte disturbances such as hyperkalemia might lead to various ECG abnormalities. Management of AKI following COVID-19 includes treatment of infection, identifying electrolyte disorders, and intravenous fluid administration. Early diagnosis and treatment of AKI in patients with COVID-19 can avoid the progression of AKI into ESRD and reduce mortality. Treatment of AKI following COVID-19 includes: Correction of hypovolemia and hypotension by the administration of adequate intravenous fluid Correction of electrolyte disturbances Renal Replacement Therapy If AKI is unresponsive to conservative therapy In volume overload conditions Modality of choice in unstable hemodynamic status and ESRD Anticoagulants in hypercoagulable conditions Sequential extracorporeal therapy

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What are the renal complications of COVID-19?

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Coronavrus Disease 2019 (COVID-19) is caused by a virus named severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). To browse the causes of diabetes, click here.

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What is the effect of COVID-19 on individuals with diabetes?

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COVID-19 is caused by a virus called severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) that belongs to the order nidovirale, family coronaviridae. Abnormal production of adipokines and cytokines such as tumor necrosis factor-alpha and interferons in diabetic patients have been associated with impairment in immune system and increased susceptibility to infections. COVID-19 has been related to cytokine storm and beta cell damage. The latter effects added to the own nature of COVID-19 lead to the following conditions: Hyperglycemia at the time of admission New onset diabetes Aggravated metabolic control in a diabetic patient The following factors have been demonstrated as responsible mechanisms which increase the risk of infections in diabetes: Reduction of Interleukin production Neutrophil dysfunction Decreased phagocytic activity and chemotaxis Decreased T cell activity Immobilized granulocytes Poor circulation, especially with concurrent peripheral vascular disease (PVD)

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In what ways does COVID-19 impact people who have diabetes?

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165,699

Please summerize the given abstract to a title

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77,269

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231,397

"Silent Hypoxemia" Leads to Vicious Cycle of Infection, Coagulopathy and Cytokine Storm in COVID-19: Can Prophylactic Oxygen Therapy Prevent It?

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Humankind is facing its worst pandemic of the twenty-first century, due to infection of a novel coronavirus named as SARS-CoV2, started from Wuhan in China. Till now, 15 million people are infected, causing more than 600,000 deaths. The disease, commonly known as, COVID-19, was initially thought to be associated with ARDS only, but later on revealed to have many unexplained and atypical clinical features like coagulopathy and cytokinemia, leading to multi-organ involvements. The patients also suffer from 'Silent Hypoxemia', where there is no immediate respiratory signs and symptoms even though alarmingly low SpO2 level. We hypothesize that this covert hypoxemia may lead to molecular changes exacerbating coagulopathy and cytokine storm in COVID19 patients, which again, in turn, causes a vicious cycle of more hypoxemia/hypoxia and progression of the infection to more severe stages through HIF-1α dependent pathway. Although molecular mechanisms are yet to be substantiated by scientific evidence, hypoxemia remains an independent worsening factor in serious COVID 19 patients. Keeping all in mind, we propose that even in the early and asymptomatic cases, prophylactic oxygen therapy to be initiated to break the vicious cycle and to reduce the mortality in COVID 19 to save precious human lives.

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231,399

Please summerize the given abstract to a title

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231,484

Lipid-lowering therapy in high cardiovascular risk patients during COVID-19 pandemic: keep focused on the target.

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231,485

To the Editor COVID-19 (COrona VIrus Disease) patients with cardiovascular (CV) disease, multiple CV risk factors or comorbidities (i.e., arterial hypertension and diabetes) were shown to be more prone to a worse prognosis. SARS-CoV-2 is a still unknown enemy and the role of concomitant cardiovascular therapies has been controversial in the early stages, particularly with regard to Angiotensin-Converting Enzyme inhibitors...

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231,486

Please summerize the given abstract to a title

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77,336

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231,598

Symptomatic Carotid Artery Thrombosis in a Patient Recently Recovered From a COVID-19 Infection

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231,599

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2), was initially discovered in December 2019 in China and rapidly spread all over the world to become a pandemic. The most common symptoms of a disease are fever, cough, generalized body ache, weakness, dyspnoea, nausea, vomiting, and diarrhea. Among vascular complications of COVID-19, the venous thrombotic complications, like pulmonary embolism and lower limb deep veins thrombosis, are not uncommon. But data about arterial thrombotic complications of COVID-19, especially carotid thrombosis, are still limited. We are describing a case of stroke due to thrombosis of the right carotid arteries, in a patient who had recovered from asymptomatic COVID-19. A 66-year-old male with arterial hypertension presented to the emergency department with a history of repeated collapse, dysarthria, weakness in the left extremities, and a drop in the left angle of his mouth (National Institutes of Health Stroke Scale [NIHSS]-4). The patient was swabbed for COVID-19 which was negative. A computed tomography angiography (CTA) was obtained which showed thrombosis in the branching point of the brachiocephalic trunk (BCT) continuing into the right subclavian artery (SA) and also into the right common carotid artery (CCA), with a subtotal occlusion of the right CCA, extending into the internal carotid artery (ICA) as well. From the apical lung tissue caught during the CT scan, bilateral, irregular widespread ground-glass opacifications, as well as consolidations and small reticular changes were seen in the lungs, which is typical for COVID-19 infection. A quantitative antibody test for COVID-19 infection was performed with the results showing a strong positivity for IgG antibodies, indicating previous COVID-19 infection. The patient was indicated for a standard carotid thrombectomy, which was performed without complications. It seems that one of the important factors that led to the formation of the thrombus in the carotid arteries was COVID-19 infection-induced inflammation in the atherosclerotic carotid vessels and generalized hypercoagulability as well as hyperviscosity. COVID-19 infection is an independent and important risk factor for the formation of an arterial thrombus during the acute illness and in the early post-COVID-19 period also, regardless of the severity of its course. Prophylactic anticoagulation is needed not only at the time of acute illness but also at the early post-COVID-19 time.

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Please summerize the given abstract to a title

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77,389

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231,757

COVID-19 and liver transplantation

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The effect of coronavirus disease 2019 (COVID-19) on liver transplantation programmes and recipients is still not completely understood but overall involves the risk of donor-derived transmission, the reliability of diagnostic tests, health-care resource utilization and the effect of immunosuppression. This Comment reviews the effect of COVID-19 on liver transplantation and summarizes recommendations for donor and recipient management.

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77,398

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231,784

Lower urinary tract symptoms (LUTS) related to COVID-19: Review article

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The pandemic of the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) or Coronavirus Disease 2019 (COVID-19) is still ongoing. The outbreak of this new emerging contagious disease has impacted a wide range of sectors including health and economics. Much information about COVID-19 has been discovered by many laboratories, and action taken in various ways as quickly as possible to inhibit the outbreak. It was found that COVID-19 is a ribonucleic acid virus (RNA virus) that can cause infection among humans. Moreover, it can mutate and spread contagiously mainly through the respiratory system. The most common symptoms are cough and fever. Many patients could develop to either pneumonitis or respiratory failure. The SARS-CoV-2 virus can infect various organs, the main infections being in lungs and rectum. In these cases, many laboratories can isolate the virus from oropharyngeal and nasopharyngeal swab and then apply the reverse transcription polymerase chain reaction (RT-PCR) test to identify the COVID-19 virus. Many of the viral infections can cause cystitis by immunologic response. There is a study that showed the SARS-CoV-2 virus could be isolated from the urine sample. The patients had significant changes in urinary storage for frequency, urgency, and urinary incontinence during infected period, which improved after the disease resolved. Moreover, there is a study that reported that the COVID-19 patients who had the International Prostate Symptom Score (IPSS) scores of 20 to 35 had significantly longer hospital stays, more frequent intensive care requirements, and higher mortality rates. Therefore, physician and medical personnel should be aware of the irritative voiding symptoms that might be the presenting symptoms of COVID-19. Furthermore, as many studies have shown that the virus can be excreted in urine, thus, the virus could be contagious via urinary contamination.

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77,431

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231,883

Characterization of respiratory microbial dysbiosis in hospitalized COVID-19 patients

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused a global pandemic of Coronavirus disease 2019 (COVID-19). However, the microbial composition of the respiratory tract and other infected tissues as well as their possible pathogenic contributions to varying degrees of disease severity in COVID-19 patients remain unclear. Between 27 January and 26 February 2020, serial clinical specimens (sputum, nasal and throat swab, anal swab and feces) were collected from a cohort of hospitalized COVID-19 patients, including 8 mildly and 15 severely ill patients in Guangdong province, China. Total RNA was extracted and ultra-deep metatranscriptomic sequencing was performed in combination with laboratory diagnostic assays. We identified distinct signatures of microbial dysbiosis among severely ill COVID-19 patients on broad spectrum antimicrobial therapy. Co-detection of other human respiratory viruses (including human alphaherpesvirus 1, rhinovirus B, and human orthopneumovirus) was demonstrated in 30.8% (4/13) of the severely ill patients, but not in any of the mildly affected patients. Notably, the predominant respiratory microbial taxa of severely ill patients were Burkholderia cepacia complex (BCC), Staphylococcus epidermidis, or Mycoplasma spp. (including M. hominis and M. orale). The presence of the former two bacterial taxa was also confirmed by clinical cultures of respiratory specimens (expectorated sputum or nasal secretions) in 23.1% (3/13) of the severe cases. Finally, a time-dependent, secondary infection of B. cenocepacia with expressions of multiple virulence genes was demonstrated in one severely ill patient, which might accelerate his disease deterioration and death occurring one month after ICU admission. Our findings point to SARS-CoV-2-related microbial dysbiosis and various antibiotic-resistant respiratory microbes/pathogens in hospitalized COVID-19 patients in relation to disease severity. Detection and tracking strategies are needed to prevent the spread of antimicrobial resistance, improve the treatment regimen and clinical outcomes of hospitalized, severely ill COVID-19 patients.

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231,991

Coagulopathy and thromboembolic events in patients with SARS-CoV-2 infection: pathogenesis and management strategies

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In October 2019, a viral infectious disease appeared in the city of Wuhan in China. A new betacoronavirus, SARS-CoV-2, has been recognized as the responsible pathogen in this infection. Although coronavirus disease is principally expressed as a pulmonary infection, critical SARS-CoV-2 infection is frequently complicated with coagulopathy, and thromboembolic events are recognizable in several patients. Dehydration, acute inflammatory condition, protracted immobilization during disease, existence of multiple cardiovascular risk factors such as diabetes, obesity or hypertension, previous coronary artery disease, ischemic stroke, peripheral artery disease are frequent comorbidities in SARS-CoV-2 hospitalized subjects, which possibly augment thrombo-embolic risk. However, other causal factors can still be identified such as unrestricted angiotensin II action, the use of immunoglobulins, an increased production of adhesion molecules able to induce vascular inflammation and endothelial activation, complement stimulation, excessive production of neutrophil extracellular traps (NETs), and increased platelet count. Low-molecular-weight heparin should be chosen as early treatment because of its anti-inflammatory action and its ability to antagonize histones and so defend the endothelium. However, several therapeutic possibilities have also been proposed such as fibrinolytic treatment, drugs that target NETs, and complement inhibition. Nevertheless, although the violence of the pandemic may suggest the use of heroic treatments to reduce the frightening mortality that accompanies SARS-CoV-2 infection, we believe that experimental treatments should only be used within approved and controlled protocols, the only ones that can provide useful and specify information on the validity of the treatments.

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232,150

Optic neuritis following SARS-CoV-2 infection

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The most common neurologic symptoms in COVID-19 are headache, anosmia, and dysgeusia. Optic neuritis is an unusual manifestation of SARS-CoV-2 infection. We report a case of a patient who initially consulted for vision loss in the absence of respiratory symptoms. She was diagnosed with optic neuritis following SARS-CoV-2 infection. Delay in diagnosis of neuro-ophthalmic manifestations of COVID-19 may lead to irreversible optic atrophy. A mechanism in which viral antigens would induce an immune response against self-proteins, or direct SARS Cov-2 infection of the central nervous system, may be involved in optic nerve injury.

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232,213

Demyelinating Disease of the Central Nervous System Concurrent With COVID-19

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232,214

Neurological diseases related to coronavirus disease-2019 (COVID-19) are increasingly reported. We report here three cases that presented with subtle neurologic findings manifesting within a range of 15 days to four months after their COVID-19 diagnoses. Magnetic resonance imaging showed acute multifocal periventricular and subcortical demyelinating lesions. Some of the lesions showed contrast enhancement and diffusion restriction. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) PCR was found in the cerebrospinal fluid of just one patient. All patients received intravenous methylprednisolone therapy. In this report, we aim to discuss the aspects of possible COVID-19-related demyelination that support a diagnosis of multiple sclerosis (MS) or acute disseminated encephalomyelitis (ADEM).

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2

77,541

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232,215

Please summerize the given abstract to a title

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0

77,557

96

232,261

Posterior Reversible Encephalopathy Syndrome: A Rare Complication in COVID-19

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232,262

The coronavirus disease 2019 (COVID-19) has a broad spectrum of manifestations. Neurological complications are not uncommon in patients with COVID-19. We report the case of a middle-aged man who presented with a cough and fever. He had a decreased oxygen saturation and required supplementary oxygen therapy. During his stay, he developed an unexplained seizure. Computed tomography of the brain revealed vasogenic edema located posteriorly. Subsequently, magnetic resonance imaging demonstrated subcortical white-matter hyperdensities, in keeping with the diagnosis of posterior reversible encephalopathy syndrome, an exceedingly rare manifestation in COVID-19. This condition should be kept in mind when encountering unexplained neurological manifestations that developed in patients with COVID-19.

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2

77,557

96

232,263

Please summerize the given abstract to a title

instruction

0

77,572

96

232,306

New-Onset Transient Global Amnesia: A Clinical Challenge in an Air Medical Transportation Pilot With a History of Coronavirus Disease 2019

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1

77,572

96

232,307

A 43-year-old male Bell 214C helicopter pilot presented to the emergency ward with flu-like syndrome. His nasopharyngeal severe acute respiratory syndrome coronavirus 2 real-time polymerase chain reaction test was positive, and a chest computed tomographic scan confirmed coronavirus disease 2019 pneumonia. He was admitted, received treatment, was discharged, and returned to flying. During the mission debrief, copilots who had flown with him reported that he experienced episodes of in-flight dizziness and blacked out. They occurred briefly during the cruise and hovering flight, perhaps for a few seconds of disorientation and unconsciousness. Rapid identification of the copilot and control of the helicopter prevented any incident or accident. Afterward, he explained the sudden onset and unexpected brief periods of loss of consciousness after a headache. The flight safety office referred him to the aviation medical center for further investigations. The cardiovascular, neurologic, laboratory, and toxicologic assessments were inconclusive with the approach to sudden-onset transient loss of consciousness. The only abnormal finding was hippocampus lesions on brain magnetic resonance imaging (MRI). Because of the possible diagnosis of transient global amnesia, the aviation medical examiner suspended him from flight duties until complete recovery and the absence of any probable complications.

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77,572

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232,308

Please summerize the given abstract to a title

instruction

0

77,722

96

232,756

Rationale for targeting Complement in COVID‐19

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1

77,722

96

232,757

A novel coronavirus, SARS‐CoV‐2, has recently emerged in China and spread internationally, posing a health emergency to the global community. COVID‐19 caused by SARS‐CoV‐2 is associated with an acute respiratory illness that varies from mild to the life‐threatening acute respiratory distress syndrome (ARDS). The complement system is part of the innate immune arsenal against pathogens, which many viruses can evade or employ to mediate cell entry. The immunopathology and acute lung injury orchestrated through the influx of pro‐inflammatory macrophages and neutrophils can be directly activated by complement components to prime an overzealous cytokine storm. The manifestations of severe COVID‐19 such as the ARDS, sepsis and multiorgan failure have an established relationship with activation of the complement cascade. We have collected evidence from all the current studies we are aware of on SARS‐CoV‐2 immunopathogenesis and the preceding literature on SARS‐CoV‐1 and MERS‐CoV infection linking severe COVID‐19 disease directly with dysfunction of the complement pathways. This information lends support for a therapeutic anti‐inflammatory strategy against complement, where a number of clinically ready potential therapeutic agents are available.

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2

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96

232,758

Please summerize the given abstract to a title

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0

77,727

96

232,771

Impact of COVID-19 on biochemical parameters: a narrative review

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1

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232,772

Coronaviruses have been a major threat to public health globally since last decades Coronaviruses are enveloped and positive-stranded RNA genome After SARS and MERS, SARS-CoV-2 is the third known coronavirus causing fatal respiratory diseases in humans In the initial stage of SARS-CoV-2 infection, clinical features are quite nonspecific and not all suspected patients can be tested to exclude or confirm the diagnosis The clinical course of the disease may cause changes in laboratory parameters Early identification of causative agent SARS-CoV-2 and monitoring the blood biochemical parameters helps in assessment of disease severity and proper monitoring of the disease In this review, the research studies on biochemical markers in COVID-19 till 31st August 2020 are retrieved and selected articles are reviewed These data are extremely important in assessing the evolution of the disease, prognosis and directing therapeutic interventions In the view of that the present study aimed to discuss the impact of biochemical markers in COVID-19

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232,773

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232,792

Skin manifestations of COVID-19 in children: Part 1

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1

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232,793

The current COVID-19 pandemic is caused by the SARS-CoV-2 coronavirus. The initial recognized symptoms were respiratory, sometimes culminating in severe respiratory distress requiring ventilation, and causing death in a percentage of those infected. As time has passed, other symptoms have been recognized. The initial reports of cutaneous manifestations were from Italian dermatologists, probably because Italy was the first European country to be heavily affected by the pandemic. The overall clinical presentation, course and outcome of SARS-CoV-2 infection in children differ from those in adults as do the cutaneous manifestations of childhood. In this review, we summarize the current knowledge on the cutaneous manifestations of COVID-19 in children after thorough and critical review of articles published in the literature and from the personal experience of a large panel of paediatric dermatologists in Europe. In Part 1, we discuss one of the first and most widespread cutaneous manifestation of COVID-19, chilblain-like lesions. In Part 2, we review other manifestations, including erythema multiforme, urticaria and Kawasaki disease-like inflammatory multisystemic syndrome, while in Part 3, we discuss the histological findings of COVID-19 manifestations, and the testing and management of infected children, for both COVID-19 and any other pre-existing conditions.

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2

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232,794

Please summerize the given abstract to a title

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0

77,889

96

233,257

Mechanisms and consequences of COVID-19 associated liver injury: What can we affirm?

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1

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Since the first reports of coronavirus disease 2019 (COVID-19) cases in December 2019 in China, numerous papers have been published describing a high frequency of liver injury associated with severe acute respiratory syndrome coronavirus 2 infection, many of them proposing a link between these findings and patient outcomes. Increases in serum aminotransferase levels (ranging from 16% to 62%) and bilirubin levels (ranging from 5% to 21%) have been reported and seem to be more often observed in patients with severe forms of COVID-19. Although absolute changes in these parameters are frequently seen, other variables, such as the ratio above the upper limit of normal, the onset of liver injury as a complication in severe cases and histopathological findings, reinforce that liver changes are of dubious clinical relevance in the course of this disease. Other factors must also be considered in these analyses, such as the repercussions of hemodynamic changes, the presence of thrombotic events, and, mainly, the possible drug-induced liver injury with the current, yet off-label, treatment. This paper aimed to analyze the currently available data on liver injury in patients with COVID-19.

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233,259

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0

77,944

96

233,422

COVID-19: unravelling the clinical progression of nature's virtually perfect biological weapon

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233,423

Coronavirus disease 2019 (COVID-19) pandemic has shocked the world and caused morbidity and mortality on an unprecedented level in the era of modern medicine Evidence generated to-date on the virulence and pathogenicity of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) suggests that COVID-19 may be considered a perfect storm, caused by a nature's virtually perfect biological weapon This conclusion is supported by an updated analysis of pathogenesis and clinical progression of this infectious disease It is now readily apparent that COVID-19 is not a clear-cut disorder, but is instead a gradually evolving pathology, characterized by a series of stages sustained by different molecular and biological mechanisms The disease can hence be divided in at least five different phases (incubation, respiratory, pro-inflammatory, pro-thrombotic, and death or remission) Whilst the virus triggers direct cytopathic injury during the initial stage of illness, in the following evolving phases, it is the host itself that undergoes an almost suicidal reaction, sustained, amplified and maintained by the immune, complement and hemostatic systems Another peculiar property making SARS-CoV-2 a devious and vicious pathogen is the biophysical structure of its receptor biding domain, which needs to be primed by human proteases, thus being less efficiently targetable by the host immune system The unique pathophysiology of COVID-19 requires the customization of therapy by individual patient characteristics and according to the phase-specific, evolving derangement of the multiple biological pathways

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2

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Please summerize the given abstract to a title

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233,425

Prior and novel coronaviruses, Coronavirus Disease 2019 (COVID-19), and human reproduction: what is known?

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OBJECTIVE: To summarize current understanding of the effects of novel and prior coronaviruses on human reproduction, specifically male and female gametes, and in pregnancy. DESIGN: Review of English publications in PubMed and Embase to April 6, 2020. METHOD(S): Articles were screened for reports including coronavirus, reproduction, pathophysiology, and pregnancy. INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): Reproductive outcomes, effects on gametes, pregnancy outcomes, and neonatal complications. RESULT(S): Seventy-nine reports formed the basis of the review. Coronavirus binding to cells involves the S1 domain of the spike protein to receptors present in reproductive tissues, including angiotensin-converting enzyme-2 (ACE2), CD26, Ezrin, and cyclophilins. Severe Acute Respiratory Syndrome Coronavirus 1 (SARS-CoV-1) may cause severe orchitis leading to germ cell destruction in males. Reports indicate decreased sperm concentration and motility for 72-90 days following Coronavirus Disease 2019 (COVID-19) infection. Gonadotropin-dependent expression of ACE2 was found in human ovaries, but it is unclear whether SARS-Coronavirus 2 (CoV-2) adversely affects female gametogenesis. Evidence suggests that COVID-19 infection has a lower maternal case fatality rate than SARS or Middle East respiratory syndrome (MERS), but anecdotal reports suggest that infected, asymptomatic women may develop respiratory symptoms postpartum. Coronavirus Disease 2019 infections in pregnancy are associated with preterm delivery. Postpartum neonatal transmission from mother to child has been reported. CONCLUSION(S): Coronavirus Disease 2019 infection may affect adversely some pregnant women and their offspring. Additional studies are needed to assess effects of SARS-CoV-2 infection on male and female fertility.

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2

77,945

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233,427

Please summerize the given abstract to a title

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0

77,976

96

233,518

Unexpected BP Sensitivity to Angiotensin II in a Patient With Coronavirus Disease 2019, ARDS, and Septic Shock

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1

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We report the case of an 88-year-old man with coronavirus disease 2019 (COVID-19) who presented with ARDS and septic shock. The patient had exquisite BP sensitivity to low-dose angiotensin II (Ang-2), allowing for rapid liberation from high-dose vasopressors. We hypothesize that sensitivity to Ang-2 might be related to biological effect of severe acute respiratory syndrome coronavirus 2 infection. The case is suggestive of a potential role for synthetic Ang-2 for patients with COVID-19 and septic shock. Further studies are needed to confirm our observed clinical efficacy.

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2

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233,520

Please summerize the given abstract to a title

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0

78,033

96

233,689

COVID-19 Associated Pulmonary Aspergillosis (CAPA)—From Immunology to Treatment

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233,690

Like severe influenza, coronavirus disease-19 (COVID-19) resulting in acute respiratory distress syndrome (ARDS) has emerged as an important disease that predisposes patients to secondary pulmonary aspergillosis, with 35 cases of COVID-19 associated pulmonary aspergillosis (CAPA) published until June 2020. The release of danger-associated molecular patterns during severe COVID-19 results in both pulmonary epithelial damage and inflammatory disease, which are predisposing risk factors for pulmonary aspergillosis. Moreover, collateral effects of host recognition pathways required for the activation of antiviral immunity may, paradoxically, contribute to a highly permissive inflammatory environment that favors fungal pathogenesis. Diagnosis of CAPA remains challenging, mainly because bronchoalveolar lavage fluid galactomannan testing and culture, which represent the most sensitive diagnostic tests for aspergillosis in the ICU, are hindered by the fact that bronchoscopies are rarely performed in COVID-19 patients due to the risk of disease transmission. Similarly, autopsies are rarely performed, which may result in an underestimation of the prevalence of CAPA. Finally, the treatment of CAPA is complicated by drug–drug interactions associated with broad spectrum azoles, renal tropism and damage caused by SARS-CoV-2, which may challenge the use of liposomal amphotericin B, as well as the emergence of azole-resistance. This clinical reality creates an urgency for new antifungal drugs currently in advanced clinical development with more promising pharmacokinetic and pharmacodynamic profiles.

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78,033

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233,691

Please summerize the given abstract to a title

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0

78,089

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233,857

COVID-19 and liver damage

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233,858

An outbreak of unknown pneumonia, caused by the novel severe acute respiratory syndrome coronavirus (SARS-CoV-2), was reported in China at the end of December 2019. On February 11, 2020, the World Health Organization officially named SARS-CoV-2 infection COVID-19 (Coronavirus Disease 2019). The most common clinical manifestation of COVID-19 is pneumonia. However, with the spread of the COVID-19 pandemic and analysis of clinical data, symptoms that are not characteristic of "atypical" pneumonia have been identified in patients. Neurological symptoms, skin and eye damage, etc., are described. The extrapulmonary presence of SARS-CoV-2 was also detected in cholangiocytes. Virus-induced effects, systemic inflammation ("cytokine storm"), hypoxia, hypovolemia, hypotension in shock, druginduced hepatotoxicity, etc., are considered possible factors of liver damage. In 14-53 % of COVID-19 patients, changes in biochemical parameters, which usually do not require drug therapy, can be recorded. Acute hepatitis is very rare. However, special attention should be given to COVID-19 patients at risk: after liver transplantation; receiving immunosuppressants and antiviral drugs; and in cases of decompensated cirrhosis, acute-on-chronic liver failure, and hepatocellular carcinoma. Constant data sharing and open access to research data, new technologies, and up-to-date guidelines are required.

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233,859

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78,154

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234,052

Covid-19 and oral diseases: Crosstalk, synergy or association?

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1

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234,053

The coronavirus disease 2019 (Covid-19) is a viral infection caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that clinically affects multiple organs of the human body. Cells in the oral cavity express viral entry receptor angiotensin-converting enzyme 2 that allows viral replication and may cause tissue inflammation and destruction. Recent studies have reported that Covid-19 patients present oral manifestations with multiple clinical aspects. In this review, we aim to summarise main signs and symptoms of Covid-19 in the oral cavity, its possible association with oral diseases, and the plausible underlying mechanisms of hyperinflammation reflecting crosstalk between Covid-19 and oral diseases. Ulcers, blisters, necrotising gingivitis, opportunistic coinfections, salivary gland alterations, white and erythematous plaques and gustatory dysfunction were the most reported clinical oral manifestations in patients with Covid-19. In general, the lesions appear concomitant with the loss of smell and taste. Multiple reports show evidences of necrotic/ulcerative gingiva, oral blisters and hypergrowth of opportunistic oral pathogens. SARS-CoV-2 exhibits tropism for endothelial cells and Covid-19-mediated endotheliitis can not only promote inflammation in oral tissues but can also facilitate virus spread. In addition, elevated levels of proinflammatory mediators in patients with Covid-19 and oral infectious disease can impair tissue homeostasis and cause delayed disease resolution. This suggests potential crosstalk of immune-mediated pathways underlying pathogenesis. Interestingly, few reports suggest recurrent herpetic lesions and higher bacterial growth in Covid-19 subjects, indicating SARS-CoV-2 and oral virus/bacteria interaction. Larger cohort studies comparing SARS-CoV-2 negative and positive subjects will reveal oral manifestation of the virus on oral health and its role in exacerbating oral infection.

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234,054

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0

78,217

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234,241

Guillain-Barré syndrome associated with COVID-19 disease

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Clinical manifestations of COVID-19 are known to be variable with growing evidence of nervous system involvement. In this case report, we describe the symptoms of a patient infected with SARS-CoV-2 whose clinical course was complicated with Guillain-Barré syndrome (GBS). We present a case of a 58-year-old woman who was initially diagnosed with COVID-19 pneumonia due to symptoms of fever and cough. Two weeks later, after the resolution of upper respiratory tract symptoms, she developed symmetric ascending quadriparesis and paresthesias. The diagnosis of GBS was made through cerebrospinal fluid analysis and she was successfully treated with intravenous immunoglobulin administration.

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234,243

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78,373

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234,709

A Systematic Review of Cases of Acute Respiratory Distress Syndrome in the Coronavirus Disease 2019 Pandemic

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234,710

The outbreak of coronavirus disease 2019 (COVID-19) was declared a global pandemic after it spread to 213 countries and has the highest total number of cases worldwide. About 80% of COVID-19 infections are mild or asymptomatic and never require hospitalization but about 5% of patients become critically ill and develop acute respiratory distress syndrome (ARDS). The widely used management for ARDS in COVID-19 has been in line with the standard approach, but the need to adjust the treatment protocols has been questioned based on the reports of higher mortality risk among those requiring mechanical ventilation. Treatment options for this widespread disease are limited and there are no definitive therapies or vaccines until now. Although some antimalarial and antiviral drugs may prove effective against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), their safety and efficacy are still under clinical trials. We conducted a systematic review of case reports on ARDS in SARS-CoV-2 infection to summarize the clinical presentation, laboratory and chest imaging findings, management protocols, and outcome of ARDS in COVID-19-positive patients. We need more data and established studies for the effective management of the novel SARS-CoV-2 and to reduce mortality in high-risk patients.

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234,711

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0

78,435

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234,895

Surgically treated reactive arthritis of the ankle after COVID-19 infection: A case report

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A 37-year-old man developed right ankle pain and swelling six days after being diagnosed with coronavirus disease (COVID-19). Despite conservative treatment, his ankle symptoms persisted. Magnetic resonance imaging and computed tomography showed synovial hypertrophy and bone erosion in the ankle. Following arthroscopic synovectomy, performed 69 days after the COVID-19 diagnosis, the pain improved significantly. The clinical course was consistent with that of reactive arthritis following severe acute respiratory syndrome coronavirus 2 infection. The pathological findings resembled rheumatoid nodules. The bone erosion may have originated from the inflammatory pathway, which resembles the mechanism of rheumatoid arthritis.

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2

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234,897

Please summerize the given abstract to a title

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0

78,447

96

234,931

Microglial Implications in SARS-CoV-2 Infection and COVID-19: Lessons From Viral RNA Neurotropism and Possible Relevance to Parkinson’s Disease

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234,932

Since December 2019, humankind has been experiencing a ravaging severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) outbreak, the second coronavirus pandemic in a decade after the Middle East respiratory syndrome coronavirus (MERS-CoV) disease in 2012. Infection with SARS-CoV-2 results in Coronavirus disease 2019 (COVID-19), which is responsible for over 3.1 million deaths worldwide. With the emergence of a second and a third wave of infection across the globe, and the rising record of multiple reinfections and relapses, SARS-CoV-2 infection shows no sign of abating. In addition, it is now evident that SARS-CoV-2 infection presents with neurological symptoms that include early hyposmia, ischemic stroke, meningitis, delirium and falls, even after viral clearance. This may suggest chronic or permanent changes to the neurons, glial cells, and/or brain vasculature in response to SARS-CoV-2 infection or COVID-19. Within the central nervous system (CNS), microglia act as the central housekeepers against altered homeostatic states, including during viral neurotropic infections. In this review, we highlight microglial responses to viral neuroinfections, especially those with a similar genetic composition and route of entry as SARS-CoV-2. As the primary sensor of viral infection in the CNS, we describe the pathogenic and neuroinvasive mechanisms of RNA viruses and SARS-CoV-2 vis-à-vis the microglial means of viral recognition. Responses of microglia which may culminate in viral clearance or immunopathology are also covered. Lastly, we further discuss the implication of SARS-CoV-2 CNS invasion on microglial plasticity and associated long-term neurodegeneration. As such, this review provides insight into some of the mechanisms by which microglia could contribute to the pathophysiology of post-COVID-19 neurological sequelae and disorders, including Parkinson’s disease, which could be pervasive in the coming years given the growing numbers of infected and re-infected individuals globally.

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2

78,447

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234,933

Please summerize the given abstract to a title

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0

78,476

96

235,018

The Emerging Threat of (Micro)Thrombosis in COVID-19 and Its Therapeutic Implications

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The recent emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the ensuing global pandemic has presented a health emergency of unprecedented magnitude. Recent clinical data has highlighted that coronavirus disease 2019 (COVID-19) is associated with a significant risk of thrombotic complications ranging from microvascular thrombosis, venous thromboembolic disease, and stroke. Importantly, thrombotic complications are markers of severe COVID-19 and are associated with multiorgan failure and increased mortality. The evidence to date supports the concept that the thrombotic manifestations of severe COVID-19 are due to the ability of SARS-CoV-2 to invade endothelial cells via ACE-2 (angiotensin-converting enzyme 2), which is expressed on the endothelial cell surface. However, in patients with COVID-19 the subsequent endothelial inflammation, complement activation, thrombin generation, platelet, and leukocyte recruitment, and the initiation of innate and adaptive immune responses culminate in immunothrombosis, ultimately causing (micro)thrombotic complications, such as deep vein thrombosis, pulmonary embolism, and stroke. Accordingly, the activation of coagulation (eg, as measured with plasma D-dimer) and thrombocytopenia have emerged as prognostic markers in COVID-19. Given thrombotic complications are central determinants of the high mortality rate in COVID-19, strategies to prevent thrombosis are of critical importance. Several antithrombotic drugs have been proposed as potential therapies to prevent COVID-19-associated thrombosis, including heparin, FXII inhibitors, fibrinolytic drugs, nafamostat, and dipyridamole, many of which also possess pleiotropic anti-inflammatory or antiviral effects. The growing awareness and mechanistic understanding of the prothrombotic state of COVID-19 patients are driving efforts to more stringent diagnostic screening for thrombotic complications and to the early institution of antithrombotic drugs, for both the prevention and therapy of thrombotic complications. The shifting paradigm of diagnostic and treatment strategies holds significant promise to reduce the burden of thrombotic complications and ultimately improve the prognosis for patients with COVID-19.

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2

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235,020

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78,619

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235,447

Coronavirus disease 2019 respiratory disease in children: clinical presentation and pathophysiology

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PURPOSE OF REVIEW: Pediatric coronavirus disease 2019 (COVID-19) respiratory disease is a distinct entity from adult illness, most notable in its milder phenotype. This review summarizes the current knowledge of the clinical patterns, cellular pathophysiology, and epidemiology of COVID-19 respiratory disease in children with specific attention toward factors that account for the maturation-related differences in disease severity. RECENT FINDINGS: Over the past 14 months, knowledge of the clinical presentation and pathophysiology of COVID-19 pneumonia has rapidly expanded. The decreased disease severity of COVID-19 pneumonia in children was an early observation. Differences in the efficiency of viral cell entry and timing of immune recognition and response between children and adults remain at the center of ongoing research. SUMMARY: The clinical spectrum of COVID-19 respiratory disease in children is well defined. The age-related differences protecting children from severe disease and death remain incompletely understood.

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2

78,619

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235,449

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78,702

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235,696

COVID-19 and Long-Term Outcomes: Lessons from Other Critical Care Illnesses and Potential Mechanisms

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1

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235,697

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel coronavirus that is currently causing a pandemic and has been termed Coronavirus disease 2019 (COVID-19). The elderly or those with preexisting conditions like diabetes, hypertension, coronary heart disease, chronic obstructive pulmonary disease, cerebrovascular disease, or kidney dysfunction are more likely to develop severe cases when infected. COVID-19 patients admitted to the intensive care unit (ICU) have higher mortality than non-ICU patients. Critical illness has consistently posed a challenge not only in terms of mortality, but also in regard to long-term outcomes of survivors. Patients who survive acute critical illness including, but not limited to, pulmonary and systemic insults associated with ARDS, pneumonia, systemic inflammation, and mechanical ventilation, will likely suffer from Post-ICU Syndrome (PICS), a phenomenon of cognitive, psychiatric, and/or physical disability following treatment in the ICU. Post-ICU morbidity and mortality continues to be a cause for concern when considering large-scale studies showing 12-month mortality risks of 11.8% to 21%. Previous studies have demonstrated that multiple mechanisms, including cytokine release, mitochondrial dysfunction and even amyloids may lead to end-organ dysfunction in patients. We hypothesize that COVID-19 infection will lead to PICS via potentially similar mechanisms as other chronic critical illness and cause long-term morbidity and mortality in patients. We consider a variety of mechanisms and questions that not only consider the short-term impact of the COVID-19 pandemic, but its long-term effects that may not yet be imagined. This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives License 4.0 (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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235,698

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78,753

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235,849

Coronaviruses and Central Nervous System Manifestations

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235,850

SARS-CoV-2 is a highly pathogenic coronavirus that has caused an ongoing worldwide pandemic. Emerging in Wuhan, China in December 2019, the virus has spread rapidly around the world. Corona virus disease 2019 (COVID-19), which is caused by SARS-CoV-2, has resulted in significant morbidity and mortality. The most prominent symptoms of SARS-CoV-2 infection are respiratory. However, accumulating evidence highlights involvement of the central nervous system (CNS). This includes headache, anosmia, meningoencephalitis, acute ischemic stroke, and several presumably post/para-infectious syndromes and altered mental status not explained by respiratory etiologies. Interestingly, previous studies in animal models emphasized the neurotropism of coronaviruses; thus, these CNS manifestations of COVID-19 are not surprising. This minireview scans the literature regarding the involvement of the CNS in coronavirus infections in general, and in regard to the recent SARS-CoV-2, specifically.

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78,753

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235,851

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78,785

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235,945

Datasets:

AdapterOcean
/

med_alpaca_standardized_cluster_96_std

Dataset Card for "med_alpaca_standardized_cluster_96_std"