scholarly journals Multi-Organ Involvement in COVID-19: Beyond Pulmonary Manifestations

2021 ◽  
Vol 10 (3) ◽  
pp. 446
Author(s):  
Vikram Thakur ◽  
Radha Kanta Ratho ◽  
Pradeep Kumar ◽  
Shashi Kant Bhatia ◽  
Ishani Bora ◽  
...  

Coronavirus Disease 19 (COVID-19), due to severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has become an on-going global health emergency affecting over 94 million cases with more than 2 million deaths globally. Primarily identified as atypical pneumonia, it has developed into severe acute respiratory distress syndrome (ARDS), a multi-organ dysfunction with associated fatality. Ever since its emergence, COVID-19 with its plethora of clinical presentations has signalled its dynamic nature and versatility of the disease process. Being a disease with droplet transmission has now assumed the proportion of a suspected airborne nature which, once proved, poses a Herculean task to control. Because of the wide distribution of the human angiotensin-converting enzyme-2 (hACE2) receptors, known for its transmission, we envisage its multiorgan spread and extensive disease distribution. Thus, an extensive review of the extrapulmonary organotropism of SARS-CoV-2 with organ-specific pathophysiology and associated manifestations like dermatological complications, myocardial dysfunction, gastrointestinal symptoms, neurologic illnesses, hepatic and renal injury is needed urgently. The plausible mechanism of site-specific viral invasion is also discussed to give a comprehensive understanding of disease complexity, to help us to focus on research priorities and therapeutic strategies to counter the disease progression. A note on the latest advancements in vaccine research will enlighten the scientific world and equip it for better preparedness.

2020 ◽  
Vol 10 (01) ◽  
pp. e137-e140
Author(s):  
Mosaad Abdel-Aziz ◽  
Nada M. Abdel-Aziz ◽  
Dina M. Abdel-Aziz ◽  
Noha Azab

AbstractThe clinical manifestations of novel coronavirus disease 2019 (COVID-19) vary from mild flu-like symptoms to severe fatal pneumonia. However, children with COVID-19 may be asymptomatic or may have mild clinical symptoms. The aim of this study was to investigate clinical features of pediatric COVID-19 and to search for the factors that may mitigate the disease course. We reviewed the literature to realize the clinical features, laboratory, and radiographic data that may be diagnostic for COVID-19 among children. Also, we studied the factors that may affect the clinical course of the disease. Fever, dry cough, and fatigue are the main symptoms of pediatric COVID-19, sometimes flu-like symptoms and/or gastrointestinal symptoms may be present. Although some infected children may be asymptomatic, a recent unusual hyperinflammatory reaction with overlapping features of Kawasaki's disease and toxic shock syndrome in pediatric COVID-19 has been occasionally reported. Severe acute respiratory syndrome-coronvirus-2 (SARS-CoV-2) nucleic acid testing is the corner-stone method for the diagnosis of COVID-19. Lymphocyte count and other inflammatory markers are not essentially diagnostic; however, chest computed tomography is highly specific. Factors that may mitigate the severity of pediatric COVID-19 are home confinement with limited children activity, trained immunity caused by compulsory vaccination, the response of the angiotensin-converting enzyme 2 receptors in children is not the same as in adults, and that children are less likely to have comorbidities. As infected children may be asymptomatic or may have only mild respiratory and/or gastrointestinal symptoms that might be missed, all children for families who have a member diagnosed with COVID-19 should be investigated.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Shaun Khanna ◽  
Aditya Bhat ◽  
Henry H Chen ◽  
Kennith Gu ◽  
Gary Gan ◽  
...  

Introduction: Myocarditis is an inflammatory disease process with growing clinical relevance in the current COVID-19 pandemic. Acute-phase myocarditis is known to result in subclinical changes in left ventricular (LV) function despite normal LV ejection fraction (LVEF), as assessed by myocardial deformation indices. The presence of right ventricular (RV) and left atrial (LA) subclinical dysfunction however has not been well described in current literature. Hypothesis: Myocarditis patients have subclinical impairment of LV, RV and LA function as assessed by global longitudinal strain (GLS) on speckle tracking echocardiography. Methods: Consecutive patients with clinical diagnosis of myocarditis admitted to our institution during 2013-2018 were assessed (n=76). Patients who did not meet appropriate diagnostic criteria (n=14), had impaired LVEF or prior cardiac disease (n=8) or poor transthoracic echocardiogram images (n=14) were excluded from analysis. Clinical and echocardiographic parameters were compared to age- , gender- and risk factor- matched controls. GLS was performed by two independent observers using vendor independent software (TomTec Arena, Germany v4.6). Results: The final cohort consisted 40 patients with myocarditis (age 44.3±16.7, 60% male) and 40 matched controls (44.5±16.6, 60% male). No significant differences in baseline clinical characteristics were observed between groups. No differences in LVEF, indexed LV mass, RV fractional area change, indexed LA volume or TR pressure gradient (p>0.05 for all) were demonstrated between the two groups. Patients with myocarditis had a lower mean LV strain (GLS%: -16.4±2.9 vs -19.7±2.7, p=0.0001), a lower mean RV Free Wall Strain (FWS) (GLS%: -22.1±4.1 vs -26.2±6.9, p=0.03) and a lower mean LA reservoir strain (GLS%: 27.5±4.6 vs. 33.7±6.3, p<0.0001) when compared to controls. Conclusions: Our results demonstrate the presence of significant subclinical global myocardial dysfunction despite normal traditional echocardiographic indices, in patients with acute-phase myocarditis. Routine assessment of GLS may identify such patients for early targeted cardiac therapy.


2020 ◽  
Vol 25 (10) ◽  
pp. 1108-1122 ◽  
Author(s):  
Dawid Maciorowski ◽  
Samir Z. El Idrissi ◽  
Yash Gupta ◽  
Brian J. Medernach ◽  
Michael B. Burns ◽  
...  

In December of 2019, an outbreak of a novel coronavirus flared in Wuhan, the capital city of the Hubei Province, China. The pathogen has been identified as a novel enveloped RNA beta-coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The virus SARS-CoV-2 is associated with a disease characterized by severe atypical pneumonia known as coronavirus 2019 (COVID-19). Typical symptoms of this disease include cough, fever, malaise, shortness of breath, gastrointestinal symptoms, anosmia, and, in severe cases, pneumonia.1 The high-risk group of COVID-19 patients includes people over the age of 60 years as well as people with existing cardiovascular disease and/or diabetes mellitus. Epidemiological investigations have suggested that the outbreak was associated with a live animal market in Wuhan. Within the first few months of the outbreak, cases were growing exponentially all over the world. The unabated spread of this deadly and highly infectious virus is a health emergency for all nations in the world and has led to the World Health Organization (WHO) declaring a pandemic on March 11, 2020. In this report, we consolidate and review the available clinically and preclinically relevant results emanating from in vitro animal models and clinical studies of drugs approved for emergency use as a treatment for COVID-19, including remdesivir, hydroxychloroquine, and lopinavir-ritonavir combinations. These compounds have been frequently touted as top candidates to treat COVID-19, but recent clinical reports suggest mixed outcomes on their efficacies within the current clinical protocol frameworks.


Author(s):  
Annalise E Zemlin ◽  
Owen J Wiese

Since the first cases of atypical pneumonia linked to the Huanan Seafood Wholesale Market in Wuhan, China, were described in late December 2019, the global landscape has changed radically. In March 2020, the World Health Organization declared COVID-19 a global pandemic, and at the time of writing this review, just over three million individuals have been infected with more than 200,000 deaths globally. Numerous countries are in ‘lockdown’, social distancing is the new norm, even the most advanced healthcare systems are under pressure, and a global economic recession seems inevitable. A novel coronavirus (SARS-CoV-2) was identified as the aetiological agent. From experience with previous coronavirus epidemics, namely the severe acute respiratory syndrome (SARS) and Middle East Respiratory Syndrome (MERS) in 2004 and 2012 respectively, it was postulated that the angiotensin-converting enzyme-2 (ACE2) receptor is a possible port of cell entry. ACE2 is part of the renin-angiotensin system and is also associated with lung and cardiovascular disorders and inflammation. Recent studies have confirmed that ACE2 is the port of entry for SARS-CoV-2. Male sex, advanced age and a number of associated comorbidities have been identified as risk factors for infection with COVID-19. Many high-risk COVID-19 patients with comorbidities are on ACE inhibitors and angiotensin receptor blockers, and this has sparked debate about whether to continue these treatment regimes. Attention has also shifted to ACE2 being a target for future therapies or vaccines against COVID-19. In this review, we discuss COVID-19 and its complex relationship with ACE2.


Problems relating to the gastrointestinal system are frequently seen in emergency and urgent care settings. Gastrointestinal signs and symptoms may relate directing to a problem in the gastrointestinal tract or may be a feature of another disease process. For example, vomiting and abdominal pain are often seen in diabetic ketoacidosis. This chapter provides detailed guidance on how to assess a patient with abdominal pain and other gastrointestinal symptoms. Appropriate investigations are identified, with their suggested indications. The remainder of this chapter covers the nursing assessment, investigations, and initial management of a comprehensive list of gastrointestinal problems, including injuries to abdominal organs.


2020 ◽  
Vol 6 (2) ◽  
Author(s):  
Eugenio Boccalone ◽  
Veronica Maria Lanni ◽  
Valerio Massimo Magro

In 2019, a new coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), aroused the attention of the entire world. It causes an acute respiratory disease, by involving the same receptor, i.e. the angiotensin-converting enzyme 2, as that for severe acute respiratory syndrome coronavirus (SARS-CoV), mainly spreads through the respiratory tract. The clinical symptoms in patients with of SARS-CoV-2 include fever, cough, dyspnea, fatigue and in a small percentage of patients also gastrointestinal symptoms have been reported...


2021 ◽  
Vol 8 (9) ◽  
pp. 2848
Author(s):  
Krishna Ramavath ◽  
Siddharth S. Rao ◽  
Nyna Sindhu ◽  
Tushar Parmeshwar ◽  
Pranay Palle

COVID-19 disease is caused by severe acute respiratory syndrome corona virus-2 (SARS-CoV-2) which can cause respiratory symptoms more. It can cause gastrointestinal symptoms also due to this RNA virus protein binding to the angiotensin converting enzyme 2 (ACE2) receptors which are abundantly present in stomach, small intestine, large intestine and liver. The gastrointestinal manifestations of COVID-19 disease can present as acute surgical abdomen which can create diagnostic dilemma. We presented a case of COVID-19 disease, admitted in our hospital. Later he had symptoms of acute surgical abdomen symptoms like sudden onset abdominal pain, nausea, vomiting and loose stool without blood. He was properly evaluated and conservatively managed. The gastrointestinal manifestations of COVID-19 disease can present as acute surgical abdomen. So, these patients properly evaluated and then only surgical plan will be made according pathology.


2021 ◽  
Vol 12 ◽  
Author(s):  
Elizabeth M. Sajdel-Sulkowska

SARS-CoV-2, primarily considered a respiratory virus, is increasingly recognized as having gastrointestinal aspects based on its presence in the gastrointestinal (GI) tract and feces. SARS-CoV-2 uses as a receptor angiotensin-converting enzyme 2 (ACE-2), a critical member of the renin-angiotensin-aldosterone system (RAAS) involved in the regulation of blood pressure and fluid system. In addition to the systemic endocrine functions, RAAS components are also involved in intracrine and organ-specific local functions. The angiotensin-converting enzyme 2 (ACE-2) is a key component of RAAS and a receptor for SARS-CoV-2. It is expressed in many tissues with gastrointestinal (GI) tract ACE-2 levels far exceeding those in the respiratory tract. SARS-CoV-2 binding to its receptor results in a deficiency of ACE-2 activity in endocrine, intracrine, and local lung and GI tract ACE-2. The local ACE-2 has different organ-specific functions, including hypertension-independent activities; dysregulations of these functions may contribute to multiorgan COVID-19 pathology, its severity, long-term effects, and mortality. We review supporting evidence from this standpoint. Notably, COVID-19 comorbidities involving hypertension, obesity, heart disease, kidney disease, and diabetes are associated with gastrointestinal problems and display ACE-2 deficits. While RAAS inhibitors target both endocrine and intracrine ACE-2 activity, the deficit of the local ACE-2 activity in the lungs and more so in the gut have not been targeted. Consequently, the therapeutic approach to COVID-19 should be carefully reconsidered. Ongoing clinical trials testing oral probiotic bound ACE-2 delivery are promising.


2021 ◽  
Vol 52 (2) ◽  
pp. 160-164
Author(s):  
Zoran Matković ◽  
Nataša Đekić-Matković

The COVID-19 pandemic has recently spread worldwide presenting primarily in form of pneumonia. Gastrointestinal manifestations such as nausea, vomiting, diarrhoea and abdominal pain are less common than respiratory symptoms. However, critically ill patients may develop digestive complications including acute pseudo-obstruction of colon-Ogilvie syndrome. Gastrointestinal symptoms can manifest before the onset of typical respiratory symptoms. Common mucosal immune response underly both-pulmonary and gastrointestinal manifestations (high expression of angiotensin-converting enzyme 2 receptors). This article described a 75-year old female patient who arise Ogilvie syndrome during viral bilateral pneumonia induced by COVID-19. Patient also had an absolute tachyarrhythmia and hearth failure. Diameter of caecum, ascending and transverse colon was 12 to 14 cm. The walls of this segment of large bowel were deserosed, with threatening perforation. Right colectomy was performed. Nine days after the surgery, despite all therapeutic measures taken, there was a fatal outcome due to pulmonary thromboembolisation.


2021 ◽  
Author(s):  
Christoph Hofmann ◽  
Erik A Blackwood ◽  
Tobias Jakobi ◽  
Clara Sandmann ◽  
Julia Groß ◽  
...  

Cardiac myocyte death during heart failure is particularly detrimental, given that cardiac muscle exhibits limited regenerative potential. Protein aggregation was previously observed in end-stage heart failure, suggesting protein-misfolding in cardiac myocytes as a contributor to the disease process. However, the relationship between protein-misfolding, cardiac myocyte death, and myocardial dysfunction is yet to be clearly established. Here, we showed that protein synthesis and the unfolded protein response (UPR) declined as a function of mammalian postnatal development, especially in tissues with low mitotic activity, such as the heart. A deeper examination in animals models showed that compared to neonatal cardiac myocytes, adult cardiac myocytes expressed lower levels of the adaptive UPR transcription factor, ATF6, as well as lower levels of numerous ATF6-regulated genes, which was associated with susceptibility to ER stress-induced cell death. Further reduction of the ATF6-dependent gene program in ATF6 knock-out mice led to the accumulation of misfolded proteins in the myocardium and impaired myocardial function in response to cardiac stress, indicating that ATF6 plays a critical adaptive role in the setting of cardiac disease. Thus, strategies to increase ATF6 aimed at balancing proteostasis in cardiac myocytes might be a fruitful avenue for the development of novel therapies for heart disease and other age-associated diseases.


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