Direct Viral Damage Research Articles

Suspected intracranial hypertension in COVID-19 patients with severe respiratory failure.

COVID-19 patients may exhibit neurological symptoms due to direct viral damage, systemic inflammatory syndrome, or treatment side effects. Mechanical ventilation in patients with severe respiratory failure often requires sedation and neuromuscular blockade, hindering thorough clinical examinations. This study aimed to investigate neurological involvement through clinical and noninvasive techniques and to detect signs of intracranial hypertension in these patients. We conducted a prospective observational study on mechanically ventilated COVID-19 adult patients admitted to our ICU, following standard of care protocols for ventilation and permissive hypercapnia. Data were collected at three time points: admission day (T1), day seven (T7), and day fourteen (T14). At each time point, patients underwent multimodal noninvasive neurological monitoring, including clinical examination, pupillary reactivity, transcranial color doppler of the middle cerebral artery (MCA), and optic nerve sheath diameter (ONSD) assessed via ultrasound (US). Head computer tomography (CT) was performed at T1 and T14. A limited subset of patients had a follow-up examination six months after ICU discharge. Seventy-nine patients were recruited; most were under deep sedation and neuromuscular blockade at T1. Pupillary size, symmetry, and reactivity were normal, as was the MCA mean velocity. However, ONSD, assessed by both US and CT, appeared enlarged, suggesting raised intracranial pressure (ICP). In a subgroup of 12 patients, increased minute ventilation was associated with a significant decrease in US-ONSD, corresponding to a drop in paCO2. At follow-up, twelve patients showed no long-term neurological sequelae, and US-ONSD was decreased in all of them. In this cohort, enlarged ONSD was detected during non-invasive neurological monitoring, suggesting a raised ICP, with hypercapnia playing a prominent role. Further studies are needed to explore ONSD behavior in other samples of mechanically ventilated, hypercapnic patients.

Case Report: Asymptomatic SARS-COV2 infection triggering recurrent Takotsubo syndrome

Takotsubo syndrome (TTS) is a rare disease mimicking acute coronary syndrome, often triggered by physical or emotional stress, and characterized by transient left ventricular dysfunction. Recurrences are described in about 5% of cases and may have different clinical and imaging patterns. In the present report, SARS-COV-2 infection, even in the absence of symptoms and overt emotional stress, seems correlated with recurrence of TTS, due to the absence of other recognized triggers. The hypothesis is that in predisposed patients, events like catecholamine-induced myocyte injury, direct viral damage, cytokine storm, immune-mediated damage, and procoagulant state, all possibly induced by the infection, may elicit endothelial dysfunction as substrate for TTS onset.

Evaluation of the Clinical Effectiveness of the Drug Laennec in Complex Rehabilitation of Patients with Post-COVID Syndrome: a Randomized Trial

INTRODUCTION. The development of post-COVID syndrome is accompanied by an increase in markers of systemic inflammation, a violation of the detoxification function of the liver, caused by both direct viral damage to hepatocytes and an increased iatrogenic load on the hepatobiliary system due to polypharmacy. AIM. Studying the use of the drug Laennec in the rehabilitation period as a hepatoprotector and immunomodulator in patients with post-COVID syndrome. MATERIALS AND METHODS. The study included 40 patients with post-COVID syndrome aged 30 to 60 years, with steatosis and steatohepatitis (increased levels of liver transaminases). The clinical effectiveness of Laennec was assessed based on the dynamics of pro-inflammatory biomarkers, liver metabolism indicators, as well as functional tests and psychological questionnaires. RESULTS. The inclusion of Laennec in the rehabilitation program for patients with post-COVID syndrome leads to a more pronounced improvement in lipid metabolism parameters, correction of liver metabolism parameters, a decrease in the level of pro-inflammatory biomarkers, and an improvement in the quality of life of patients than in the control group. DISCUSSION. Significantly significant positive dynamics in the severity of complaints of general weakness and sleep disturbance, as well as indicators of memory impairment and impaired concentration in the main group could indicate the achievement of anabolic, neurotrophic and bioenergetic effects of the Laennec drug. A significantly significant decrease in the level of liver transaminases in the main group indicates the hepatoprotective effect of the drug Laennec, due to the amino acids, vitamins and microelements included in the drug, which support the reactions of phases 1 and 2 of liver detoxification. Normalization of elevated pro-inflammatory markers (ferritin, IL-6, CRP) in patients of the main group may indicate the presence of anti-inflammatory and immunoregulatory effects of the Laennec drug. CONCLUSIONS. A course prescription of the drug Laennec for the purpose of correcting pro-inflammatory markers and hepatoprotection can be recommended for use in complex non-drug rehabilitation to increase its clinical effectiveness, as well as improve subjective indicators of the quality of life of patients with post-COVID syndrome.

Recent pathogenetic aspects of hearing loss in COVID: A literature review

The World Health Organisation predicts that by 2050, up to 10% of the world's population will need rehabilitation to address disability-related hearing loss. The purpose of this study was to identify the main mechanisms of hearing loss associated with Severe Acute Respiratory Syndrome Coronavirus 2 infection. The study included modern English-language scientific publications, mainly those with a high citation index, through the professional platforms MEDLINE/PubMed and Index Medicus. A total of 48 sources were selected. Research papers devoted to the development of conductive or sensorineural hearing loss, which occurred directly as a result of a viral disease, or is associated with the processes that accompany it (treatment, concomitant pathology, vaccination, etc.), were analysed. It was found that the development of viral-induced hearing loss in COVID has a multifactorial nature. The heterogeneity of audiological changes is primarily conditioned by direct viral damage to auditory analyser cells that express membrane receptors of the angiotensin converting enzyme of the second type. In addition, there is a reactivation of latent viral infection, extravasation of exudate into the middle ear cavity, blood clotting disorders, immune-mediated cell damage, local and generalised inflammatory reactions that affect both sound conduction and sound perception in one ear or both. Some cases of audiological disorders may also be of iatrogenic origin, since post-vaccination complications and ototoxic effects of medications used in the treatment of COVID-19 are not excluded, which should be considered by clinicians at all levels of healthcare to effectively manage a specific clinical scenario

Exploring the Therapeutic Potential of Glycyrrhizic Acid in Liver Implication in Dengue Infection: A Case Report

Dengue is one of the most common infectious diseases affecting humans. The virus is transmitted between humans by the Aedes mosquito. It occurs hyperendemically in tropical and subtropical climates worldwide. Dengue infection can affect numerous organs, with the liver being the most frequently affected organ. The clinical spectrum of liver disorders ranges from mild elevation of transaminase enzymes to severe conditions such as acute liver failure. Several mechanisms have been proposed to describe hepatic dysfunction observed in dengue fever and dengue hemorrhagic fever, such as immunological injury, hypoxic injury, and direct viral damage due to reduced hepatic perfusion during shock. Glycyrrhizic acid, extracted in the form of glycyrrhizin from the root of the licorice plant Glycyrrhiza glabra, is referred to as Stronger Neo-Minophagen-C (SNMC®). It has shown effectiveness in reducing serum aminotransferase and bilirubin levels, attenuating hepatocyte apoptosis, and producing endogenous interferon. The following is a case report of a 23-year-old woman with dengue fever and elevated liver enzyme level. The patient’s vital signs were stable. A physical examination revealed no abnormalities. A complete blood count test showed thrombocytopenia without an elevation of the hematocrit. AST level was 901 U/L after admission. Causes of other hepatitis infections, such as hepatitis A, B, and C, were excluded. The dengue IgM and IgG antibody levels were reactive. After several days of hospitalization, the patient experienced clinical improvement after supportive therapy and the administration of glicyrrhizic acid or SNMC®.

A Case of Dengue Meningitis Manifested as a Part of Expanded Dengue Syndrome

Dengue is a prevalent arthropod-borne viral disease in tropical and subtropical areas of the globe. Dengue clinical manifestations include asymptomatic infections; undifferentiated fever; dengue fever, which is characterized by fever, headache, retro orbital pain, myalgia, and arthralgia; and a severe form of the disease denominated dengue hemorrhagic fever/dengue shock syndrome, characterized by hemoconcentration, thrombocytopenia, and bleeding tendency. However, atypical manifestations, such as liver, central nervous system, and cardiac involvement, have been increasingly reported called expanded dengue syndrome. We report a 35 years old lady with atypical and rare presentation of dengue disease marked by meningitis. Condition improved after conservative treatment. Neurological complications in dengue are now increasingly observed with the most common case is aseptic meningitis. Dengue meningitis is self-limiting in almost all cases. Hepatic failure rarely dominates the clinical picture in adults. The main mechanism of dengue meningitis is still unknown though both direct viral infection and immune mediated damage have been suggested to be the cause. To avoid otherwise preventable morbidity and mortality, physicians should have a high index of suspicion for neurological complications in patients with dengue illness and should manage this accordingly

Pathogenesis of pulmonary fibrosis

A literature review reflects data on the mechanisms of pulmonary fibrosis after a novel coronavirus infection associated with the SARS-COV2 virus. Factors contributing to post-COVID lung remodeling are considered. According to the literature, in the mechanism of pulmonary fibrosis, during the course of the disease and during the recovery period, both direct viral damage and death of alveolocytes and endothelium, the development of a systemic inflammatory reaction due to inadequate secretion of cytokines, especially type 2, which are activators of the proliferation of fibroblasts and myofibroblasts, are important. The influence of angiogenesis disorders and vascular dysfunction on pneumofibrosis was noted. Attention is also paid to the relationship between the development of pulmonary fibrosis and abnormal activation of the renin-angiotensin-aldosterone system. In combination with the action of many factors, especially germinal ones, an imbalance between profibrogenic and antifibrogenic action develops and fibrosis occurs.

Phenomenological structure of anxiety disorders in persons who have transferred COVID-19

The SARS-CoV-2 virus is neurotropic because its adhesion protein has a high affinity for Angiotensin-Converting Enzyme 2 receptors, which are expressed, among other things, on the endothelium of cerebral capillaries. There are several theories of the pathogenesis of brain damage in COVID-19: direct viral damage, hypoxia/ischemia and systemic inflamma-tion, autoimmune damage. The study was conducted to study the clinical and psychopatho-logical features of anxiety disorders in patients who suffered from COVID-19. During 2020–2022, 94 patients (49 men and 55 women) with an average age of (33.0±5.0) years who suf-fered from COVID-19 and were diagnosed with anxiety disorders were examined. According to the results of the study was found: a characteristic low mood background; feeling anxious; unmotivated anxiety; internal tension with inability to relax; anxious fears; intrusive anxious thoughts that intensify in the evening and at night, which prevents falling asleep; attacks of fear, which are accompanied by suffocation, a feeling of unreality, fear of death; exaggerated wariness; inability to control anxiety; feeling of loss of control over one's life; irritability; decreased ability to concentrate; motor tension; autonomic hyperactivity; sleep disorders. The data obtained in the course of the study formed the basis for the development of a com-prehensive personalized program for the correction of anxiety disorders in patients with COVID-19 with differentiated use of psychopharmacotherapy, psychotherapy and psy-choeducation. It was concluded that patients are characterized by pronounced manifestations of anxiety disorders: prolonged anxiety-depressive reaction, panic disorder, generalized anx-iety disorder; anxiety disorder of an organic nature. Keywords: SARS-CoV-2 virus, neurotropic virus, anxiety, depressive states.

Acute cerebral edema: a lethal neurological complication in a patient with COVID-19 infection. Case report and literature review

Introduction. COVID-19 can damage the nervous system by direct viral damage to the neural cells or by immunopathology. More serious medical conditions such as cerebral edema, neuronal degeneration, encephalitis, acute disseminated encephalomyelitis, Guillain-Barre syndrome, Bickerstaff’s brainstem encephalitis, Miller-Fisher syndrome, polyneuritis, toxic encephalopathy, and stroke can occur.Case report. We report a case of a 40-year-old patient with previous history of hypertension and no other chronic disease who was admitted to the hospital with respiratory distress due to SARS-CoV-2-induced bilateral pneumonia. A few days later, he developed worsening respiratory function with an acute seizure episode. Head CT scan revealed subarachnoid hemorrhage with diffuse cerebral edema as a lethal neurological complication, possibly secondary to COVID-19.Discussion. COVID-19 induces CNS damage through various mechanisms including ACE-2 receptor damage, cytokine storm syndrome, secondary hypoxia, blood-brain barrier disruption, and neuroinflammation. Neurological symptoms correlate with the severity of COVID-19 disease and may range from asymptomatic infection to severe and lethal forms. Acute cerebral edema, as illustrated by our case, may result from a combination of diffuse en dothelial dysfunction, cytokine release syndrome, and hypoxic damage from pulmonary dysfunction.

The nature of kidney damage causing the development of acute renal failure in patients with COVID-19 (according to morphological studies)

The literature review presents data on the study of the nature of kidney damage in patients with COVID-19 with acute renal insufficiency according to histo-morphological lifetime and postmortem studies of the kidneys during the peak of the epidemic of infection in 2020-2022. In the analysis, the role of direct viral damage to tissues and organ cells is questioned. The frequency of diagnosis of glomerular, tubular, interstitial and vascular lesions is specified, the significance of the presence of variants of the apolipoprotein-1 (APOL1) gene in patients with severe respiratory complications of acute viral infection is assessed.

Secondary Sclerosing Cholangitis After SARS-CoV2: ICU Ketamine Use or Virus-Specific Biliary Tropism and Injury in the Context of Biliary Ischemia in Critically Ill Patients?

From the beginning of the Severe Acute Respiratory Syndrome CoronaVirus-2 (SARS-CoV2) pandemic, different cases of a cholangiopathy with features of secondary sclerosing cholangitis in critically ill patients (SSC-CIP) have been reported. Patients developing it are generally recovering from severe Coronavirus disease 19 (COVID-19) and required intensive care unit (ICU) admission and mechanical ventilation. Many of them have been administered with ketamine during their ICU stay. The pathogenesis of this novel disease is still debated, and, since prognosis is poor, efforts are needed in order to better understand it. In this review, we focused our attention on COVID-19 SSC clinical, imaging, and histology findings in order to clarify the different pathogenetic options, particularly in regard of the ischemic-direct viral damage and ketamine-related theories, beginning with a recapitulation of SSC-CIP and ketamine-induced cholangiopathy in abusers. The research has been conducted using PubMed and Google Scholar databases. Key-words were "Secondary Sclerosing Cholangiopathy", "SSC-CIP", "Secondary Sclerosing Cholangiopathy in critically ill patients", "Ketamine and cholangiopathy", "Ketamine abusers and liver disease", "Ketamine-related cholangiopathy", "SARS-CoV2 infection and liver disease", "post Covid-19 secondary sclerosing cholangitis", "Covid-19 cholangiopathy". Many authors, based on the clinical, histological, imaging, and prognostic features of the disease, have pointed out the similarities between post COVID-19 SSC and SSC-CIP; however, peculiar features in the former were not previously observed. Therefore, a direct viral cytopathic action and SARS-CoV2-related coagulopathy are considered the most likely causes. On the other hand, ketamine, with the available data, cannot be surely linked as the main determinant cause of cholangiopathy. Moreover, ketamine-induced cholangitis (KIC) presentation is different from post COVID-19 SSC. Its role as a cofactor precipitating the disease cannot be ruled out. Post COVID-19 SSC is a rare clinical entity following severe COVID-19 disease. The most accepted theory is that a sum of different insults determines the disease: biliary ischemia, direct viral damage, toxic bile, possibly worsened by ketamine and hyperinflammation due to the cytokine storm. Given the severe prognosis of the disease, with persistent cholangiopathy, organ failure, and orthotopic liver transplantation (OLT), further study on this novel clinical entity is needed.

A scientific perspective of how and why Omicron is less severe than SARS-CoV-2

Abstract Omicron is currently the dominant variant of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the coronavirus responsible for the coronavirus disease 2019 (COVID-19) pandemic. Omicron is associated with mild symptoms, although it can cause harmful effects in high-risk patient populations. Omicron and COVID-19 affect multiple organ systems, including the respiratory system, gastrointestinal tract, cardiovascular system, central nervous system, ophthalmic system, genitourinary tract, and musculoskeletal system. COVID-19 infects additional organ systems, including the hematological system, hepatobiliary system, renal system, and dermatologic system. The viral-induced complications were compared to discuss the effects of Omicron versus the authentic SARS-CoV-2 virus, revealing less detrimental outcomes for Omicron. Moreover, COVID-19 is more likely to infect older adults, males, and obesity with mild to severe symptoms. Omicron causes mild symptoms in younger populations and overweight females. Data were acquired using PubMed, Centers for Disease Prevention and Control, and the World Health Organization. COVID-19 and Omicron mechanisms causing organ system-related complications are likely because of the natural immune response to the active infection, the uncontrollable release of cytokines causing cytokine release syndrome, and direct viral damage through angiotensin-converting enzyme 2/transmembrane serine protease 2 receptor binding and entrance to the host cell for infection.

SARS-CoV-2, vaccination or autoimmunity as causes of cardiac inflammation. Which form prevails?

The causes of cardiac inflammation during the COVID-19 pandemic are manifold and complex, and may have changed with different virus variants and vaccinations. The underlying viral etiology is self-evident, but its role in the pathogenic process is diverse. The view of many pathologists that myocyte necrosis and cellular infiltrates are indispensable for myocarditis does not suffice and contradicts the clinical criteria of myocarditis, i.e., acombination of serological evidence of necrosis based on troponins or MRI features of necrosis, edema, and inflammation based on prolonged T1 and T2times and late gadolinium enhancement. The definition of myocarditis is still debated by pathologists and clinicians. We have learned that myocarditis and pericarditis can be induced by the virus via different pathways of action such as direct viral damage to the myocardium through the ACE2 receptor. Indirect damage occurs via immunological effector organs such as the innate immune system by macrophages and cytokines, and then later the acquired immune system via Tcells, overactive proinflammatory cytokines, and cardiac autoantibodies. Cardiovascular diseases lead to more severe courses of SARS-CoV‑2 disease. Thus, heart failure patients have adouble risk for complicated courses and lethal outcome. So do patients with diabetes, hypertension, and renal insufficiency. Independent of the definition, myocarditis patients benefitted from intensive hospital care, ventilation, if needed, and cortisone treatment. Postvaccination myocarditis and pericarditis affect primarily young male patients after the second RNA vaccine. Both are rare events but severe enough to deserve our full attention, because treatment according to current guidelines is available and necessary.

Analysis Descriptive of Anosmia and Dysgeusia in SARS CoV-2 Patients: Overview of Epidemiology, Pathogenesis, Prognosis, and Treatment Options

Introduction: SARS CoV-2 (COVID-19) is a respiratory infectious disease whose cause has been identified as the seventh type of the coronavirus family that attacks humans. Common symptoms among patients with COVID-19 include fever, dry cough, shortness of breath (dyspnea), muscle aches (myalgia), confusion, headache, sore throat, rhinorrhea, chest pain, diarrhea, nausea / vomiting, conjunctival congestion, nose. congestion, sputum production, fatigue (malaise), hemoptysis, and shivering. However, the spread of COVID-19 infection has shown new symptoms of the disease: patients with dysfunction of smell, taste and indigestion. Methods: Literature review by taking libraries from 34 journals and 2 textbook. The journal obtained from the Google, NCBI and Pubmed search engine, as well as processing research materials into new information related to the research objectives. Results: One hypothesis currently developing is that SARS-CoV-2 will cause olfactory changes through direct access and damage to the CNS through its penetration by the cribriform plate. Another hypothesis that is also developing suggests direct viral damage to olfactory cells and taste receptors. Glial cells, neurons, and the oral cavity present the ACE-2 receptor which appears to be a mechanism of cell invasion by viruses. Conclusion: People who have lost their smell or taste are six times more likely to become positive for COVID-19. Likewise, people who have anosmia have a 10-fold higher chance of being diagnosed with COVID-19. Taste and smell disorders with ageusia have a 10 times higher chance of catching COVID-19.

Chronic and delayed neurological manifestations of persistent infections.

Persistent infections capable of causing central nervous system (CNS) complications months or years after the initial infection represent a major public health concern. This concern is particularly relevant considering the ongoing coronavirus disease 2019 pandemic, where the long-term neurological effects are still being recognized. Viral infections are a risk factor for the development of neurodegenerative diseases. In this paper, we provide an in-depth exploration of the prevalent known and suspected persistent pathogens and their epidemiological and mechanistic links to later development of CNS disease. We examine the pathogenic mechanisms involved, including direct viral damage and indirect immune dysregulation, while also addressing the challenges associated with detecting persistent pathogens. Viral encephalitis has been closely associated with the later development of neurodegenerative diseases and persistent viral infections of the CNS can result in severe and debilitating symptoms. Further, persistent infections may result in the development of autoreactive lymphocytes and autoimmune mediated tissue damage. Diagnosis of persistent viral infections of the CNS remains challenging and treatment options are limited. The development of additional testing modalities as well as novel antiviral agents and vaccines against these persistent infections remains a crucial research goal.

Mechanisms of atrial fibrillation in COVID-19

Atrial fibrillation (AF) is the most frequent form of cardiac arrhythmia in COVID-19 infected patients. The occurrence of AF paroxysms is often associated with the acute period of infection in time. At the same time, the pathophysiological mechanisms of the occurrence of AF associated with COVID-19 remain insufficiently studied. The review considers the available literature data on the influence of factors such as reduced availability of angiotensin-converting enzyme 2 re- ceptors, interaction of the virus with the cluster of differentiation 147 and sialic acid, increased inflammatory signaling, “cytokine storm”, direct viral damage to the endothelium, electrolyte and acid-alkaline balance in the acute phase of severe illness and increased sympathetic activity.

Case Report: Recurrence of Acute Respiratory Distress Syndrome After Bilateral Lung Transplantation

The main causes of early respiratory failure after lung transplantation include primary graft dysfunction (PGD), acute rejection, and infection. This report describes a case of unclear early respiratory failure after bilateral lung transplantation for extensive COVID-19-induced acute respiratory distress syndrome (ARDS). We reviewed the patient file to investigate the course of the functional decline and evaluate reasons for early graft failure. Analyzed data included crossmatching results, biopsy results, HLA antibodies testing, bronchoalveolar lavages, respiratory parameters, and medications. After an initial excellent early postoperative course, the patient developed progressive respiratory failure, making re-implantation of extracorporeal membrane oxygenation (ECMO) support necessary. An extensive diagnostic workup revealed no signs of infection or rejection. Because the patient showed no signs of improvement with any treatment, lung-protective ventilation with the intermittent prone position was initiated. The patient's respiratory situation and bilateral opacities slowly improved over the next few weeks, and ECMO support was eventually discontinued. With no evidence of PGD, rejection, or infection, recurrent ARDS caused by a systemic immunologic process was seen as the only plausible cause for the patient's respiratory failure after lung transplantation. The fact that ARDS can develop extrapulmonarily, without direct viral or bacterial damage, makes us conclude that the preceding systemic activation and recruitment of immune cells by the primarily injured lung could potentially lead to the recurrence of ARDS even if the injured organ is removed.

Патогенетические и структурно-функциональные изменения в почках после перенесенного COVID-19

There is now a growing evidence of the long-term effects of COVID-19, affecting almost all human systems and organs, including the kidneys. The objective of this paper was to study pathogenetic and structural and functional changes in the kidneys in patients with COVID-19 infection. Materials and methods. Articles were searched in PubMed, Medline, Google Scholar, E-library, Clinical Trial databases using the keywords "post-COVID syndrome," "renal damage (kidney disease)," "COVID-19," "SARS-CoV-2," and "glomerulonephritis" in Russian and English. Databases reporting cases of detectable renal damage following a prior coronavirus infection published by September 28, 2022 were used. This review includes literature reviews, clinical cases, and original studies reporting the confirmed cases of detectable renal damage after confirmed prior COVID-19. The sources that focus only on renal damage during the acute period of coronavirus infection have been excluded. Results. Primary viral damage is carried out through the effect on the receptors of angiotensin-converting enzyme-2 (ACE-2). No less important mechanisms of viral damage are immunological and inflammatory reactions, dysfunctions of the complement system, leading to multiple organ failure. The long-term consequences of coronavirus infection on the kidneys were manifested in a decrease in the estimated glomerular filtration rate (eGFR), an increase in creatinine levels, proteinuria, and microhematuria. Dickkopf-3 protein (uDKK-3) may become a promising marker of kidney damage. Post-COVID renal disease can occur both de novo and with a previous renal complication of COVID-19. The most common morphological variants of kidney damage were tubular lesions and various morphological variants of glomerulonephritis. Conclusion. The association of COVID-19 and kidney damage in the post-COVID period is supported by common mechanisms of pathogenesis, including direct viral damage through ACE-2, inflammatory and immune reactions of the body. These data are confirmed by detectable markers of inflammation and damage to the renal tissue, the morphological picture of necrosis, fibrosis of the renal parenchyma in patients with COVID-19 infection.

Alzheimer's disease and COVID-19

In elderly patients with COVID-19 cognitive functions decline; it has been suggested that SARS-CoV-2 infection may lead to the development of Alzheimer's disease (AD) and other long-term neurological consequences. We review several parallels between AD and COVID-19 in terms of pathogenetic mechanisms and risk factors. Possible mechanisms through which COVID-19 can initiate AD are discussed. These include systemic inflammation, hyperactivation of the renin-angiotensin system, innate immune activation, oxidative stress, and direct viral damage. It has been shown that increased expression of angiotensin-renin receptors (ACE2) may be a risk factor for COVID-19 in patients with AD. When entering the central nervous system, the SARS-CoV-2 virus can directly activate glial cell-mediated immune responses, which in turn can lead to the accumulation of beta-amyloid and the subsequent onset or progression of current AD. The involvement of inflammatory biomarkers, including interleukins (IL): IL6, IL1, as well as galectin-3, as a link between COVID-19 and AD is discussed. The rationale for the use of memantine (akatinol memantine) in patients with COVID-19 in order to prevent the development of cognitive deficits is discussed. Memantine has been shown to have a positive effect on neuroinflammatory processes in the onset or exacerbation of cognitive deficits, in reducing cerebral vasospasm and endothelial dysfunction in viral infections. Memantine therapy may improve everyday activity and reduce the risk of severe SARS-CoV-2 infection.

238. Acalculous Cholecystitis: A Novel and Lethal Unrecognized Complication in Severe CoVID 19

Abstract Background SARS-COV-2 infection is known to cause tissue damage in several organs outside of the respiratory tract. The pathogenesis of tissue damage is hypothesized to be caused by direct viral damage, endothelial injury, and ischemic or thrombotic events. Gastrointestinal symptoms were first characterized mainly as diarrhea and diffuse abdominal pain and discomfort, which can be hard to interpret in the setting of a generalized inflammatory response; gallbladder injury and inflammation causing acute acalculous cholecystitis has been scarcely reported Methods Here we discuss five cases of patients presenting with symptoms of cholecystitis. All five patients underwent multiple imaging studies, and all of them were compatible with acute cholecystitis; some of them had an imaging report of lithiasic cholecystitis, while the rest were reported with microlithiasis or biliary sludge. Four out of the five patients underwent laparoscopic cholecystectomy; biopsies were taken, consistently those reported with acalculous cholecystitis. The remaining patient died of CoVID 19 complications prior to surgery, but after a percutaneous cholecystostomy tube was placed. Results All these patients have in common the prolonged fasting, because they all required invasive mechanical ventilation, consequently, they all developed multiple focal pneumonia and respiratory distress syndrome. This fast is related to the development of gangrenous ischemia in the gallbladder, which manifests as a late complication due to SARS-CoV-2 infection, in addition to being related to angiotensin-2 converting receptors and virus replication proteins, as well as the pro-inflammatory and hypoxia state that in itself causes the infection (9). All showed a cholestatic pattern, highlighting that this complication developed in an average time of 3 weeks after the onset of SARS-CoV2 symptoms, in addition to the fact that in most cases a negative test was already shown at the time of the complication. Conclusion Acalculous cholecystitis is one of the extrapulmonary complications that has been seen in patients with this infection, not being the most common, but one of those that has generated a higher mortality rate in patients due to its late diagnosis and non-specific clinical picture in certain occasions (9). Disclosures All Authors: No reported disclosures.