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1.
J Diabetes Complications ; 36(11): 108336, 2022 11.
Article in English | MEDLINE | ID: covidwho-2117652

ABSTRACT

The raging COVID-19 pandemic is in its third year of global impact. The SARS CoV 2 virus has a high rate of spread, protean manifestations, and a high morbidity and mortality in individuals with predisposing risk factors. The pathophysiologic mechanisms involve a heightened systemic inflammatory state, cardiometabolic derangements, and varying degrees of glucose intolerance. The latter can be evident as significant hyperglycemia leading to new-onset diabetes or worsening of preexisting disease. Unfortunately, the clinical course beyond the acute phase of the illness may persist in the form of a variety of symptoms that together form the so-called "Long COVID" or "Post-COVID Syndrome". It is thought that a chronic, low-grade inflammatory and immunologic state persists during this phase, which may last for weeks or months. Although numerous insights have been gained into COVID-related hyperglycemia and diabetes, its prediction, course, and management remain to be fully elucidated.


Subject(s)
COVID-19 , Diabetes Mellitus , Hyperglycemia , Humans , SARS-CoV-2 , Pandemics , COVID-19/complications , RNA, Viral , Diabetes Mellitus/epidemiology , Diabetes Mellitus/therapy , Hyperglycemia/complications , Inflammation/complications
2.
Leg Med (Tokyo) ; 59: 102154, 2022 Nov.
Article in English | MEDLINE | ID: covidwho-2105536

ABSTRACT

A male in his 90 s consulted a doctor because he experienced several days of general fatigue and dyspnea. He was diagnosed with heart failure, and diuretic medications taken for 3 days relieved his symptoms. However, he was found dead on the morning of the fourth day after consultation. He had received a third dose of coronavirus disease 2019 (COVID-19) vaccine approximately 2 weeks before death. An autopsy revealed dissection of the ascending aorta and pericardial hemotamponade. The heart showed a white villous surface, and the pericardium was fibrously thick. Microscopic examination revealed pericarditis with predominantly macrophage and lymphocyte infiltration. These histological findings were compatible with those of post-vaccination myocarditis. To the best of our knowledge, histopathologically proven pericarditis after COVID-19 vaccination has not been reported. In the present case, extended inflammation of the aortic adventitia was a possible cause of aortic wall fragility followed by dissection.


Subject(s)
Aneurysm, Dissecting , COVID-19 , Myocarditis , Pericarditis , Male , Humans , COVID-19/complications , COVID-19 Vaccines/adverse effects , Autopsy , RNA, Messenger , Pericarditis/etiology , Pericarditis/pathology , Aneurysm, Dissecting/etiology , Aorta/pathology , Myocarditis/complications , Inflammation/complications , Inflammation/pathology , Vaccination , Diuretics
3.
World J Gastroenterol ; 28(39): 5735-5749, 2022 Oct 21.
Article in English | MEDLINE | ID: covidwho-2099935

ABSTRACT

BACKGROUND: The coronavirus disease 2019 (COVID-19) was perhaps the most severe global health crisis in living memory. Alongside respiratory symptoms, elevated liver enzymes, abnormal liver function, and even acute liver failure were reported in patients suffering from severe acute respiratory disease coronavirus 2 pneumonia. However, the precise triggers of these forms of liver damage and how they affect the course and outcomes of COVID-19 itself remain unclear. AIM: To analyze the impact of liver enzyme abnormalities on the severity and outcomes of COVID-19 in hospitalized patients. METHODS: In this study, 684 depersonalized medical records from patients hospitalized with COVID-19 during the 2020-2021 period were analyzed. COVID-19 was diagnosed according to the guidelines of the National Institutes of Health (2021). Patients were assigned to two groups: those with elevated liver enzymes (Group 1: 603 patients), where at least one out of four liver enzymes were elevated (following the norm of hospital laboratory tests: alanine aminotransferase (ALT) ≥ 40, aspartate aminotransferase (AST) ≥ 40, gamma-glutamyl transferase ≥ 36, or alkaline phosphatase ≥ 150) at any point of hospitalization, from admission to discharge; and the control group (Group 2: 81 patients), with normal liver enzymes during hospitalization. COVID-19 severity was assessed according to the interim World Health Organization guidance (2022). Data on viral pneumonia complications, laboratory tests, and underlying diseases were also collected and analyzed. RESULTS: In total, 603 (88.2%) patients produced abnormal liver test results. ALT and AST levels were elevated by a factor of less than 3 in 54.9% and 74.8% of cases with increased enzyme levels, respectively. Patients in Group 1 had almost double the chance of bacterial viral pneumonia complications [odds ratio (OR) = 1.73, P = 0.0217], required oxygen supply more often, and displayed higher biochemical inflammation indices than those in Group 2. No differences in other COVID-19 complications or underlying diseases were observed between groups. Preexisting hepatitis of a different etiology was rarely documented (in only 3.5% of patients), and had no impact on the severity of COVID-19. Only 5 (0.73%) patients experienced acute liver failure, 4 of whom died. Overall, the majority of the deceased patients (17 out of 20) had elevated liver enzymes, and most were male. All deceased patients had at least one underlying disease or combination thereof, and the deceased suffered significantly more often from heart diseases, hypertension, and urinary tract infections than those who made recoveries. Alongside male gender (OR = 1.72, P = 0.0161) and older age (OR = 1.02, P = 0.0234), diabetes (OR = 3.22, P = 0.0016) and hyperlipidemia (OR = 2.67, P = 0.0238), but not obesity, were confirmed as independent factors associated with more a severe COVID-19 infection in our cohort. CONCLUSION: In our study, the presence of liver impairment allows us to predict a more severe inflammation with a higher risk of bacterial complication and worse outcomes of COVID-19. Therefore, patients with severe disease forms should have their liver tests monitored regularly and their results should be considered when selecting treatment to avoid further liver damage or even insufficiency.


Subject(s)
COVID-19 , Liver Failure, Acute , Pneumonia, Viral , United States , Humans , Male , Female , COVID-19/complications , COVID-19/epidemiology , SARS-CoV-2 , Pneumonia, Viral/complications , Liver Failure, Acute/complications , Inflammation/complications
4.
Nutrients ; 14(20)2022 Oct 13.
Article in English | MEDLINE | ID: covidwho-2071661

ABSTRACT

Overweight and obesity are associated with chronic low-grade inflammation and represent risk factors for various diseases, including COVID-19. However, most published studies on COVID-19 defined obesity by the body mass index (BMI), which does not encounter adipose tissue distribution, thus neglecting immunometabolic high-risk patterns. Therefore, we comprehensively analyzed baseline anthropometry (BMI, waist-to-height-ratio (WtHR), visceral (VAT), epicardial (EAT), subcutaneous (SAT) adipose tissue masses and liver fat, inflammation markers (CRP, ferritin, interleukin-6), and immunonutritional scores (CRP-to-albumin ratio (CAR), modified Glasgow prognostic score, neutrophile-to-lymphocyte ratio, prognostic nutritional index)) in 58 consecutive COVID-19 patients of the early pandemic phase with regard to the necessity of invasive mechanical ventilation (IMV). Here, metabolically high-risk adipose tissues represented by increased VAT, liver fat, and WtHR strongly correlated with higher levels of inflammation, pathologic immunonutritional scores, and the need for IMV. In contrast, the prognostic value of BMI was inferior and absent with regard to SAT. Multivariable logistic regression analysis identified an optimized IMV risk prediction model employing liver fat, WtHR, and CAR. In summary, we suggest an immunometabolically risk-adjusted model to predict COVID-19-induced respiratory failure better than BMI-based stratification, which warrants prospective validation.


Subject(s)
COVID-19 , Respiratory Insufficiency , Humans , Body Mass Index , Interleukin-6 , Obesity/complications , Obesity/pathology , Inflammation/complications , Respiratory Insufficiency/complications , Albumins , Ferritins , Risk Assessment , Intra-Abdominal Fat/pathology , Risk Factors
5.
Front Immunol ; 13: 991256, 2022.
Article in English | MEDLINE | ID: covidwho-2065519

ABSTRACT

Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a group of diseases characterized by inflammation and destruction of small and medium-sized blood vessels. Clinical disease phenotypes include microscopic polyangiitis (MPA), granulomatosis with polyangiitis (GPA), and eosinophilic granulomatosis with polyangiitis (EGPA). The incidence of AAV has been on the rise in recent years with advances in ANCA testing. The etiology and pathogenesis of AAV are multifactorial and influenced by both genetic and environmental factors, as well as innate and adaptive immune system responses. Multiple case reports have shown that sustained exposure to silica in an occupational environment resulted in a significantly increased risk of ANCA positivity. A meta-analysis involving six case-control studies showed that silica exposure was positively associated with AAV incidence. Additionally, exposure to air pollutants, such as carbon monoxide (CO), is a risk factor for AAV. AAV has seasonal trends. Studies have shown that various environmental factors stimulate the body to activate neutrophils and expose their own antigens, resulting in the release of proteases and neutrophil extracellular traps, which damage vascular endothelial cells. Additionally, the activation of complement replacement pathways may exacerbate vascular inflammation. However, the role of environmental factors in the etiology of AAV remains unclear and has received little attention. In this review, we summarized the recent literature on the study of environmental factors, such as seasons, air pollution, latitude, silica, and microbial infection, in AAV with the aim of exploring the relationship between environmental factors and AAV and possible mechanisms of action to provide a scientific basis for the prevention and treatment of AAV.


Subject(s)
Air Pollutants , Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis , Churg-Strauss Syndrome , Granulomatosis with Polyangiitis , Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis/drug therapy , Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis/epidemiology , Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis/etiology , Antibodies, Antineutrophil Cytoplasmic , Carbon Monoxide/therapeutic use , Churg-Strauss Syndrome/complications , Endothelial Cells/pathology , Humans , Inflammation/complications , Peptide Hydrolases , Silicon Dioxide
6.
Eur J Gastroenterol Hepatol ; 34(11): 1165-1171, 2022 11 01.
Article in English | MEDLINE | ID: covidwho-2051710

ABSTRACT

BACKGROUND: Although several liver- and inflammation-based scores to predict the clinical course of patients with coronavirus disease 2019 (COVID-19) have been evaluated, no direct comparison regarding their predictive ability has been performed. METHODS: 1038 patients (608 males, age 63.5 ± 17 years) hospitalized with documented COVID-19 infection to the non-ICU ward, were included retrospectively. Clinical and laboratory characteristics on admission including evaluation of Fibrosis-4 (FIB-4) score and C-Reactive Protein (CRP) to albumin ratio (CAR) were recorded. RESULTS: One hundred and twenty-four patients (11.9%) died during hospitalization after 8 (3-72) days. In multivariate analysis, FIB-4 (hazard ratio, 1.11; 95% confidence interval (CI), 1.034-1.19; P = 0.004), was independently associated with mortality, with very good discriminative ability (area under the receiver operating characteristic curve curve, 0.76). The patients with FIB-4 >2.67 (n = 377), compared to those with ≤2.67 (n = 661), had worse survival (log-rank 32.6; P < 0.001). Twenty-four (6.8%) of 352 patients with possible nonalcoholic fatty liver disease (NAFLD) (defined as Hepatic Steatosis Index >36) died during hospitalization. In multivariate analysis, CAR was an independent risk factor (1) for mortality (hazard ratio, 1.014; 95% CI, 1.002-1.025; P = 0.021), (2) the need for high-flow nasal cannula with or without intubation (hazard ratio, 1.016; 95% CI, 1.004-1.027; P = 0.007) and (3) development of acute kidney injury (hazard ratio, 1.017; 95% CI, 1.006-1.028; P = 0.002). In addition, the patients with possible NAFLD and CAR >12 (n = 154), compared to those with CAR ≤12 (n = 198), had worse survival (log-rank 5.1; P = 0.024). CONCLUSIONS: FIB-4 was an independent factor for mortality with better performance compared to other liver function test- and inflammation-based scores in patients with COVID-19, while CAR was the only score independently associated with the clinical course in COVID-19 patients with possible NAFLD.


Subject(s)
COVID-19 , Non-alcoholic Fatty Liver Disease , Aged , Aged, 80 and over , Albumins , C-Reactive Protein , Fibrosis , Humans , Inflammation/complications , Liver Cirrhosis/complications , Liver Function Tests , Male , Middle Aged , Non-alcoholic Fatty Liver Disease/complications , Prognosis , Retrospective Studies
7.
Life Sci ; 310: 121018, 2022 Dec 01.
Article in English | MEDLINE | ID: covidwho-2049616

ABSTRACT

Since the very beginning of the coronavirus disease 2019 (COVID-19) pandemic in early 2020, it was evident that patients with cardiovascular disease (CVD) were at an increased risk of developing severe illness, and complications spanning cerebrovascular disorders, dysrhythmias, acute coronary syndrome, ischemic and non-ischemic heart disease, pericarditis, myocarditis, heart failure, thromboembolic disease, stroke, and death. Underlying these was excessive systemic inflammation and coagulopathy due to SARS-COV-2 infection, the effects of which also continued long-term as evidenced by post-COVID-19 cardiovascular complications. The acute and chronic cardiovascular effects of COVID-19 occurred even among those who were not hospitalized and had no previous CVD or those with mild symptoms. This comprehensive review summarizes the current understanding of molecular mechanisms triggered by the SARS-CoV-2 virus on various cells that express the angiotensin-converting enzyme 2, leading to endothelial dysfunction, inflammation, myocarditis, impaired coagulation, myocardial infarction, arrhythmia and a multisystem inflammatory syndrome in children or Kawasaki-like disease.


Subject(s)
COVID-19 , Cardiovascular Diseases , Myocarditis , Child , Humans , COVID-19/complications , SARS-CoV-2 , Myocarditis/complications , Cardiovascular Diseases/complications , Inflammation/complications
8.
Front Immunol ; 13: 885029, 2022.
Article in English | MEDLINE | ID: covidwho-2039674

ABSTRACT

Periodontitis was an inflammatory disease associated with a dysbiosis of the oral flora characterized by a chronic sustained inflammation inducing the resorption of alveolar bone and leading to tooth loss. Type 2 diabetes mellitus (T2D) was a metabolic disease caused by impaired insulin action. The oral microbiome played a crucial role in modulating both the innate and adaptive immune system during the trigger and exacerbation of periodontitis and T2D. The bidirectional relationship of T2D and periodontitis had been the focus of intensive research, but those were not well explored. In this commentary, an in-depth analysis of the changes of microbiome and bacterial metabolites in periodontitis with or without diabetes was described. The promotion of periodontitis to T2D might involve inflammatory factors/receptors, oxidative stress, microRNA and so on. The effect of diabetes on periodontitis might involve adipose factor pathway, AGE/RAGE and RANK/RANKL pathway etc. Generally, periodontitis and diabetes are closely related to the microecological-epithelial interaction, soft tissue degradation, bone coupling disorder, immune regulation and gene transcription. The viruses, including HBV, HCV, HSV-1, Coronavirus, HCMV, EBV, HIV, phageome and so on, played an important role in the development of T2D and periodontitis. An in-depth understanding of the relationship between microbiome and host was of great significance to clarify the bidirectional mechanisms, suggesting that the periodontitis or T2D remission will have a positive impact on the other.


Subject(s)
Diabetes Mellitus, Type 2 , Insulins , MicroRNAs , Microbiota , Periodontitis , Viruses , Bacteria/genetics , Humans , Inflammation/complications , Microbiota/genetics , Viruses/genetics
9.
Int Immunopharmacol ; 110: 109040, 2022 Sep.
Article in English | MEDLINE | ID: covidwho-1991087

ABSTRACT

Known as a pivotal immunohemostatic response, immunothrombosis is activated to restrict the diffusion of pathogens. This beneficial intravascular defensive mechanism represents the close interaction between the immune and coagulation systems. However, its uncontrolled form can be life-threatening to patients with the critical coronavirus disease 2019 (COVID-19). Hyperinflammation and ensuing cytokine storm underlie the activation of the coagulation system, something which results in the provocation of more immune-inflammatory responses by the thrombotic mediators. This vicious cycle causes grave clinical complications and higher risks of mortality. Classified as an evolutionarily conserved family of the small non-coding RNAs, microRNAs (miRNAs) serve as the fine-tuners of genes expression and play a key role in balancing the pro/anticoagulant and pro-/anti-inflammatory factors maintaining homeostasis. Therefore, any deviation from their optimal expression levels or efficient functions can lead to severe complications. Despite their extensive effects on the molecules and processes involved in uncontrolled immunothrombosis, some genetic agents and uncontrolled immunothrombosis-induced interfering factors (e.g., miRNA-single nucleotide polymorphysms (miR-SNPs), the complement system components, nicotinamide adenine dinucleotide phosphate (NADPH) oxidases, and reactive oxygen species (ROS)) have apparently disrupted their expressions/functions. This review study aims to give an overview of the role of miRNAs in the context of uncontrolled immunothrombosis/thromboinflammation accompanied by some presumptive interfering factors affecting their expressions/functions in the critical COVID-19. Detecting, monitoring, and resolving these interfering agents mafy facilitate the design and development of the novel miRNAs-based therapeutic approaches to the reduction of complications incidence and mortality in patients with the critical COVID-19.


Subject(s)
COVID-19 , MicroRNAs , Thrombosis , Humans , Immunologic Factors , Inflammation/complications , Inflammation/genetics , MicroRNAs/genetics , MicroRNAs/metabolism , SARS-CoV-2 , Thromboinflammation , Thrombosis/genetics
10.
Medicina (Kaunas) ; 58(8)2022 Aug 12.
Article in English | MEDLINE | ID: covidwho-1987886

ABSTRACT

Background and Objectives: SARS-CoV-2 has an extensive tissue tropism due to its ability to attach to the surfaces of cells through different receptors, leading to systemic complications. In this article, we aim to present the prevalence of pericardial effusions in patients with severe COVID-19, to identify the risk factors/predictors for pericardial involvement, and to evaluate its impact on overall mortality. Materials and Methods: We enrolled 100 patients with severe COVID-19 in our observational cohort study and divided them in two groups: Group A (27 patients with pericardial effusion) and Group B (73 patients without pericardial effusion). We recorded demographic and lifestyle parameters, anthropometric parameters, clinical parameters, inflammation markers, respiratory function parameters, complete blood count, coagulation parameters, and biochemical serum parameters. All patients were evaluated by computer tomography scans within 48 h of admission. Results: The median age was 61 years in both groups and the male/female ratio was 3.5 vs. 2.8 in Group A vs. Group B. We identified mild pericardial effusion (3-4 mm) in 62.9% patients and moderate pericardial effusion (5-9 mm) in 37.1% patients, with a median value of 4 [3;6] mm. The patients with pericardial effusion presented with higher percentages of obesity, type-2 diabetes mellitus, arterial hypertension, and congestive heart failure, without statistical significance. Increased values in cardiac enzymes (myoglobin, CK, CK-MB) and LDH were statistically associated with pericardial effusion. The overall mortality among the participants of the study was 24% (24 patients), 33.3% in Group A and 20.8% in Group B. Conclusions: Pericardial effusion has a high prevalence (27%) among patients with severe forms of COVID-19 and was associated with higher mortality. Pericardial effusion in our study was not associated with the presence of comorbidities or the extent of lung involvement. Overall mortality was 60% higher in patients with pericardial effusion.


Subject(s)
COVID-19 , Pericardial Effusion , COVID-19/complications , Comorbidity , Female , Humans , Inflammation/complications , Male , Middle Aged , Pericardial Effusion/epidemiology , Pericardial Effusion/etiology , SARS-CoV-2
11.
PLoS One ; 17(8): e0272608, 2022.
Article in English | MEDLINE | ID: covidwho-1974329

ABSTRACT

PURPOSE: We describe the rationale for and design of an innovative, nested, tripartite prospective observational cohort study examining whether relative estrogen insufficiency-induced inflammation amplifies HIV-induced inflammation to cause end organ damage and worsen age-related co-morbidities affecting the neuro-hypothalamic-pituitary-adrenal axis (Brain), skeletal (Bone), and cardiovascular (Heart/vessels) organ systems (BBH Study). METHODS: The BBH parent study is the Multicenter AIDS Cohort/Women's Interagency HIV Study Combined Cohort Study (MWCCS) with participants drawn from the Atlanta MWCCS site. BBH will enroll a single cohort of n = 120 women living with HIV and n = 60 HIV-negative women, equally distributed by menopausal status. The innovative multipart nested study design of BBH, which draws on data collected by the parent study, efficiently leverages resources for maximum research impact and requires extensive oversight and management in addition to careful implementation. The presence of strong infrastructure minimized BBH study disruptions due to changes in the parent study and the COVID-19 pandemic. CONCLUSION: BBH is poised to provide insight into sex and HIV associations with the neuro-hypothalamic-pituitary-adrenal axis, skeletal, and cardiovascular systems despite several major, unexpected challenges.


Subject(s)
COVID-19 , HIV Infections , Cohort Studies , Estrogens , Female , HIV Infections/complications , HIV Infections/epidemiology , Humans , Hypothalamo-Hypophyseal System , Inflammation/complications , Multicenter Studies as Topic , Observational Studies as Topic , Pandemics , Pituitary-Adrenal System , Prospective Studies
12.
Transl Psychiatry ; 12(1): 314, 2022 08 05.
Article in English | MEDLINE | ID: covidwho-1972576

ABSTRACT

Olfactory impairments contribute to the psychopathology of mental illnesses such as schizophrenia and depression. Recent neuroscience research has shed light on the previously underappreciated olfactory neural circuits involved in regulation of higher brain functions. Although environmental factors such as air pollutants and respiratory viral infections are known to contribute to the risk for psychiatric disorders, the role of nasal inflammation in neurobehavioral outcomes and disease pathophysiology remains poorly understood. Here, we will first provide an overview of published findings on the impact of nasal inflammation in the olfactory system. We will then summarize clinical studies on olfactory impairments in schizophrenia and depression, followed by preclinical evidence on the neurobehavioral outcomes produced by olfactory dysfunction. Lastly, we will discuss the potential impact of nasal inflammation on brain development and function, as well as how we can address the role of nasal inflammation in the pathophysiological mechanisms underlying psychiatric disorders. Considering the current outbreak of Coronavirus Disease 2019 (COVID-19), which often causes nasal inflammation and serious adverse effects for olfactory function that might result in long-lasting neuropsychiatric sequelae, this line of research is particularly critical to understanding of the potential significance of nasal inflammation in the pathophysiology of psychiatric disorders.


Subject(s)
COVID-19 , Mental Disorders , Olfaction Disorders , Humans , Inflammation/complications , Mental Disorders/psychology , Olfaction Disorders/etiology , Psychophysiology
13.
Int J Mol Sci ; 23(14)2022 Jul 20.
Article in English | MEDLINE | ID: covidwho-1964013

ABSTRACT

Iron is a crucial element for mammalian cells, considering its intervention in several physiologic processes. Its homeostasis is finely regulated, and its alteration could be responsible for the onset of several disorders. Iron is closely related to inflammation; indeed, during inflammation high levels of interleukin-6 cause an increased production of hepcidin which induces a degradation of ferroportin. Ferroportin degradation leads to decreased iron efflux that culminates in elevated intracellular iron concentration and consequently iron toxicity in cells and tissues. Therefore, iron chelation could be considered a novel and useful therapeutic strategy in order to counteract the inflammation in several autoimmune and inflammatory diseases. Several iron chelators are already known to have anti-inflammatory effects, among them deferiprone, deferoxamine, deferasirox, and Dp44mT are noteworthy. Recently, eltrombopag has been reported to have an important role in reducing inflammation, acting both directly by chelating iron, and indirectly by modulating iron efflux. This review offers an overview of the possible novel biological effects of the iron chelators in inflammation, suggesting them as novel anti-inflammatory molecules.


Subject(s)
Iron Overload , Animals , Benzoates/therapeutic use , Deferasirox/therapeutic use , Deferiprone , Deferoxamine/therapeutic use , Inflammation/complications , Inflammation/drug therapy , Iron/therapeutic use , Iron Chelating Agents/pharmacology , Iron Chelating Agents/therapeutic use , Iron Overload/drug therapy , Iron Overload/etiology , Mammals , Pyridones/therapeutic use
14.
BMJ Case Rep ; 15(5)2022 May 31.
Article in English | MEDLINE | ID: covidwho-1923167

ABSTRACT

Temporal arteritis is usually caused by giant cell arteritis (GCA). However, inflammation of the temporal artery can also occur secondary to autoimmune diseases or infections.We present a remarkable case of a man in his 70s with biopsy proven temporal arteritis, who was later diagnosed with meningovascular neurosyphilis. The presentation of an acute onset monocular vision loss with inflammation of the temporal artery on biopsy appeared a GCA, misleading the physicians, as it turned out to be a manifestation of neurosyphilis.


Subject(s)
Giant Cell Arteritis , Neurosyphilis , Biopsy , Giant Cell Arteritis/complications , Humans , Inflammation/complications , Male , Neurosyphilis/complications , Neurosyphilis/diagnosis , Neurosyphilis/drug therapy , Temporal Arteries/pathology
15.
Curr Opin Pharmacol ; 63: 102181, 2022 04.
Article in English | MEDLINE | ID: covidwho-1920791

ABSTRACT

Peripheral inflammation and neuroinflammation are host-mounted to eliminate injury, infection, or toxin to restore homeostasis. However, when inflammation persists, it may promote collateral tissue damage that ultimately culminates in pathological peripheral damage or neurodegeneration. Since the beginning of the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) pandemic, responsible of Coronavirus disease 2019 (COVID-19), accumulating evidence describes neurological manifestations and complications worldwide particularly in approximately one-third of patients with COVID-19 particularly in those affected with the severe forms of the disease. Different access routes to the central nervous system have been identified. One immediately used is the entrance by the olfactory and trigeminus nervous affecting olfactory and sensory nerve endings when individuals get the infection by the intranasal route. It can also reach the central nervous system through the choroid plexuses and periventricular areas that lack blood-brain barrier or by its disruption by the exacerbated peripheral inflammation. Until now, the long-term sequelae of SARS-CoV-2 infection is still under research and the post-COVID syndrome. This review focuses on the consequences of the neuroinflammatory response in patients with COVID-19 considering its potential relevance in the appearance of neurological sequelae including neurodegenerative disorders.


Subject(s)
COVID-19 , Nervous System Diseases , COVID-19/complications , Humans , Inflammation/complications , Neuroinflammatory Diseases , Pandemics , SARS-CoV-2
16.
Front Endocrinol (Lausanne) ; 13: 877010, 2022.
Article in English | MEDLINE | ID: covidwho-1902948

ABSTRACT

Background: The coronavirus disease 2019 (COVID-19) pandemic has caused substantial threats to people's physical health and lives, claiming the lives of over 5 million people worldwide. It is imperative to identify the disease severity and intervene with effective therapy as early as possible. Previous studies have shown that low free triiodothyronine (FT3) may possess the predictive value on COVID-19 prognosis. Methods: In this retrospective cohort study, 15-day clinical and laboratory data of 186 hospitalized patients of COVID-19 after admission were analyzed. Groups were based on the disease severity of COVID-19, survival or non-survival, and presence or absence of euthyroid sick syndrome (ESS). Categorical variables were compared with the chi-square test or Fisher's exact test. Continuous variables were tested by Wilcoxon rank-sum test for the non-normal distribution. Spearman correlations were used to assess the correlations between FT3 with clinic parameters of multiple time points. Results: The non-survival patients had significant lower levels of FT3 (3.24 ± 0.42 vs. 4.19 ± 0.08 pmol/L, p < 0.05) and thyroid-stimulating hormone (TSH) (0.69 ± 0.19 vs. 2.32 ± 0.2 uIU/ml, p < 0.05), and the FT3 of severe patients was significantly lower than that of non-severe patients (3.67 ± 0.14 vs. 4.33 ± 0.09 pmol/L, p < 0.05). Fifty-nine cases of COVID-19 patients were diagnosed with ESS. Compared with non-ESS patients, those with ESS were older and had higher proportions of fever, shortness of breath, hypertension, diabetes, severe disease, and mortality. In addition, the correlation analysis between FT3 and clinical parameters showed that FT3 were positively related to the lymphocyte count and albumin and negatively correlated with C-reactive protein, erythrocyte sedimentation rate, and D-dimer at all time points in the first 15 days after admission. Conclusion: Low FT3 had a significant predictive value on the prognosis of COVID-19 patients, and FT3 was significantly related with clinic parameters of inflammation/coagulopathy/fibrinolysis.


Subject(s)
COVID-19 , Euthyroid Sick Syndromes , COVID-19/complications , Fibrinolysis , Humans , Inflammation/complications , Retrospective Studies
17.
Int J Mol Sci ; 23(11)2022 May 24.
Article in English | MEDLINE | ID: covidwho-1884204

ABSTRACT

Alzheimer's disease (AD) is a complex chronic disease of the brain characterized by several neurodegenerative mechanisms and is responsible for most dementia cases in the elderly. Declining immunity during ageing is often associated with peripheral chronic inflammation, and chronic neuroinflammation is a constant component of AD brain pathology. In the Special Issue published in 2021 eight papers were collected regarding different aspects of neurodegeneration associated with AD. Five papers presented and discussed infectious agents involved in brain AD pathology and three discussed data regarding receptors regulation and possible treatment of the disease. Below I will discuss and further elaborate on topics related to infections, inflammation, and neurodegenerative pathways in AD and brain senescence. The topic presented here may contribute to early intervention protocols for preventing or slowing the progression of cognitive deterioration in the elderly.


Subject(s)
Alzheimer Disease , Cognition Disorders , Aged , Alzheimer Disease/metabolism , Brain/metabolism , Humans , Inflammation/complications , Neurons/metabolism
18.
Dtsch Med Wochenschr ; 147(11): 704-710, 2022 06.
Article in German | MEDLINE | ID: covidwho-1873574

ABSTRACT

Pericardial disease represents a large diversity of inflammation related injury of the pericardium. Multifactorial causes may contribute to acute and recurrent pericarditis, pericardial effusion without major hemodynamic compromise, cardiac tamponade or constrictive pericarditis. Currently, inflammatory pericardial pathologies are observed in cases of SARS-CoV-2-infection or after vaccination. Beside established anti-inflammatory therapeutic strategies with NSAID, corticosteroids and colchicine, auto-inflammation and inflammasomes seam to offer more specific targets for advanced treatment options.


Subject(s)
COVID-19 , Cardiac Tamponade , Pericardial Effusion , Cardiac Tamponade/diagnosis , Cardiac Tamponade/etiology , Cardiac Tamponade/therapy , Humans , Inflammation/complications , Pericardial Effusion/therapy , SARS-CoV-2
19.
Int J Infect Dis ; 122: 285-294, 2022 Sep.
Article in English | MEDLINE | ID: covidwho-1867239

ABSTRACT

OBJECTIVES: The aim of this study was to investigate the dose-response relationship of admission fasting glucose (FBG) with corona virus disease 2019 (COVID-19) mortality and to further evaluate potential interactions of hyperglycemia with inflammation and hypercoagulation on COVID-19 outcomes. METHODS: This retrospective study included 2555 consecutively hospitalized patients with COVID-19, until death or discharge, in Wuhan Union hospital between January 1 and April 9, 2020. The poor early outcomes included admission to intensive care unit, intubation, and deaths occurring within 28 days. We used splines nested in Cox regression to visualize dose-response associations and generalized additive models to fit three-dimensional (3D) trend plots for joint effects of FBG with markers of inflammation and coagulation. RESULTS: J-shaped associations existed between hospitalized mortality or poor early outcomes and FBG with a nadir at 5 mmol/L, which were more evident in women. 3D plots demonstrated significant joint effect trends, and patients with hyperglycemia and high neutrophil-lymphocyte ratio, C-reactive protein, lactate dehydrogenase, procalcitonin, d-dimer, and interleukin-6 had 7.4-25.3-fold risks; the proportions of joint associations attributed to additive interactions reached 30% to 54%. CONCLUSIONS: FBG was associated with hospitalized mortality and poor early outcomes in a J-shaped manner, and a combination of hyperglycemia, inflammation, hypercoagulation, and cytokines conferred a dramatically higher risk.


Subject(s)
COVID-19 , Hyperglycemia , Blood Glucose/metabolism , COVID-19/complications , Cytokines , Fasting , Female , Glucose , Humans , Hyperglycemia/complications , Inflammation/complications , Prognosis , Retrospective Studies , Risk Factors , SARS-CoV-2
20.
BMJ Case Rep ; 15(4)2022 Apr 29.
Article in English | MEDLINE | ID: covidwho-1854262

ABSTRACT

Calciphylaxis also known as calcific uraemic arteriolopathy is a rare condition mostly seen in patients with end-stage kidney disease. We report a case of a simultaneous-kidney-pancreas transplant patient with functioning grafts developing biopsy-proven calciphylaxis in the setting of chronic inflammation. Despite several modalities of management, the patient developed progression of her disease leading to multiple amputations. This case illustrates chronic inflammation driven by persistent infection as a probable contributing factor to the development and progression of calciphylaxis in a simultaneous kidney-pancreas recipient. Calciphylaxis should be considered in the differential for a painful, non-healing ulcer even in the absence of common risk factors.


Subject(s)
Calciphylaxis , Kidney Failure, Chronic , Calciphylaxis/complications , Calciphylaxis/diagnosis , Female , Humans , Inflammation/complications , Kidney Failure, Chronic/complications , Kidney Failure, Chronic/therapy , Male , Risk Factors
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