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The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection represented a disruptive pathology that emerged in late 2019 with profound implications ranging from individual health to health systems and world economy. Our study aimed to evaluate clinical, biochemical and computerized tomography (CT) parameters values in determining the severity of pulmonary embolism (PE) associated with COVID-19.

Background/objectives: We aimed to characterize the fibrosis following COVID-19 pneumonia, using quantitative analysis, after three months and subsequently, after two years of patients' release from the hospital, and to identify the risk factors for pulmonary fibrosis., Methods: We performed a retrospective, observational cohort study on 420 patients with severe forms of COVID-19. For all patients, we registered demographic, inflammatory and biochemical parameters, complete blood count and D-dimers; all patients underwent three computed tomography scans (at admittance, at 3 months and at 2 years)., Results: We found fibrosis in 67.9% of patients at the 3-month evaluation and in 42.4% of patients at the 2-year evaluation, registering a significant decrease in the severe and moderate fibrosis cases, with a slight increase in the mild fibrosis cases. The risk of fibrosis was found to be proportional to the values of age, duration of hospital stay, inflammatory markers (ESR, fibrinogen), cytolytic markers (LDH, AST) and D-dimers. The highest correlations with lung fibrosis were registered for interstitial pulmonary involvement (for the 3-month evaluation) and total pulmonary involvement (for the 2-year evaluation)., Conclusions: Lung fibrosis represents a significant post-COVID-19 complication found in 42% of patients with severe forms of pneumonia at the 2-year evaluation. A significant overall decrease in the severity of lung fibrosis was registered at the 2-year evaluation compared to the 3-month evaluation. We consider that the amount of interstitial pulmonary involvement represents the optimal parameter to estimate the risk of lung fibrosis following SARS-CoV-2 pneumonia.

Background/Objectives : This review aims to provide a comprehensive understanding of how HIV alters normal aging trajectories in the brain, presenting the HIV-related molecular mechanisms and pathophysiological pathways involved in brain aging. The review explores the roles of inflammation, oxidative stress, and viral persistence in the brain, highlighting how these factors contribute to neuronal damage and cognitive impairment and accelerate normal brain aging. Additionally, it also addresses the impact of antiretroviral therapy on brain aging and the biological markers associated with its occurrence. Methods : We extensively searched PubMed for English-language articles published from 2000 to 2024. The following keywords were used in the search: "HIV", "brain", "brain aging", "neuroinflammation", "HAART", and "HAND". This strategy yielded 250 articles for inclusion in our review. Results: A combination of blood-brain barrier dysfunction, with the direct effects of HIV on the central nervous system, chronic neuroinflammation, telomere shortening, neurogenesis impairments, and neurotoxicity associated with antiretroviral treatment (ART), alters and amplifies the mechanisms of normal brain aging. Conclusions: Current evidence suggests that HIV infection accelerates neurodegenerative processes of normal brain aging, leading to cognitive decline and structural brain changes at an earlier age than typically observed in the general population.

Cytopenias or coagulation deficiencies can occur in people living with HIV (PLWH). The severity of these disorders is influenced by the low levels of CD4+ lymphocytes, viral load, and the stage of viral infection. The aim of our retrospective observational study was to determine the frequency of cytopenias and coagulation deficiencies in PLWH as well as the need for replacement therapy with blood products. We sought to determine whether there is an association between severe anemia or thrombocytopenia (requiring replacement therapy) and CD4+T lymphocyte levels. All 29 patients were critically ill, with 27 out of 29 (93%) in advanced stages of HIV disease and 23 out of 29 (79%) having CD4+ lymphocyte counts below 200 cells/microL. Most patients were either late presenters (45%) or had been lost to follow-up (41%). In addition to HIV infection, various conditions that could alter hematologic parameters were associated, including co-infections with hepatitis viruses, tuberculosis at various sites, malignant diseases, sepsis, SARS-CoV-2 infection, or other opportunistic infections. No significant correlation was found between severe anemia or severe thrombocytopenia or coagulation deficiencies and the CD4+T lymphocyte count. Our data suggest that these hematological disorders in patients with advanced HIV infection are more likely to be associated comorbidities rather than the HIV infection per se.

Esophageal lesions are common findings in disorders of the digestive tract in patients living with HIV, the most typical symptoms being odynophagia and/or dysphagia. This article provides a narrative review of the spectrum of esophagitis in patients living with HIV, focusing on fungal, viral, bacterial and non-infectious etiologies, as well as co-infections with viral hepatitis viruses. The article provides a comprehensive approach to the strategy of diagnosis and the role of upper digestive endoscopy and histopathological examination in the evaluation of esophageal pathology in patients living with HIV., Competing Interests: Conflicts of interest: All authors – none to declare., (GERMS.)

SARS-CoV-2 infection is a significant health concern that needs to be addressed not only during the initial phase of infection but also after hospitalization. This is the consequence of the various pathologies associated with long COVID-19, which are still being studied and researched. Lung fibrosis is an important complication after COVID-19, found in up to 71% of patients after discharge. Our research is based on scientific articles indexed in PubMed; in the selection process, we used the following keywords: "lung fibrosis", "fibrosis mediators", "fibrosis predictors", "COVID-19", "SARS-CoV-2 infection", and "long COVID-19". In this narrative review, we aimed to discuss the current understanding of the mechanisms of initiation and progression of post-COVID-19 lung fibrosis (PC-19-LF) and the risk factors for its occurrence. The pathogenesis of pulmonary fibrosis involves various mediators such as TGF-β, legumain, osteopontin, IL-4, IL-6, IL-13, IL-17, TNF-α, Gal-1, Gal-3, PDGF, and FGFR-1. The key cellular effectors involved in COVID-19 lung fibrosis are macrophages, epithelial alveolar cells, neutrophils, and fibroblasts. The main fibrosis pathways in SARS-CoV-2 infection include hypoxemia-induced fibrosis, macrophage-induced fibrosis, and viral-fibroblast interaction-induced fibrosis.

Introduction: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is a viral disease with primary pulmonary involvement and systemic impact. This article aims to assess the importance of clinical, biological, demographic and radioimaging parameters in COVID-19 patients in characterizing the incidence and severity of the hepatobiliary involvement., Methods: We performed an observational cohort study on 132 consecutive patients, evaluating their demographics, hospitalization period, peripheral oxygen saturation (SpO 2 ) in the ambient air, as well as biochemical markers of hepatobiliary involvement: aspartate aminotransferase (AST), alanine aminotransferase (ALT), total bilirubin (TB), direct bilirubin (DB), gamma-glutamyl transferase (GGT), serum albumin, total serum proteins, D-dimers; coagulation tests such as prothrombin time (PT), activated partial thromboplastin time (aPTT), and international normalized ratio (INR); inflammatory markers: fibrinogen, serum ferritin, C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis alpha (TNF-α). Hepatobiliary involvement was further stratified by type of affection pattern: hepatocytolysis, cholestasis or mixed type. All patients received a computerized tomography (CT) chest scan in the first or second day of hospital admission., Results: We observed lower SaO 2 and longer hospitalization days in patients with hepatobiliary involvement, as well as longer coagulation times (PT and INR), lower serum albumin and higher serum ferritin (p<0.05). No significant correlations have been found between the degree or type of pattern of lung involvement as seen on CT scans performed and biochemical liver changes., Conclusions: Hepatobiliary involvement occurred in 72% of patients in the study group, associated with longer hospitalization period, prolonged coagulation parameters, lower serum albumin levels, raised serum ferritin and CRP levels. Cholestatic and mixed types of injury were associated with higher ferritin levels, while mixed type alone presented higher D-dimers levels compared with the cholestatic or hepatocytolysis groups. No significant correlation was found between lung involvement by CT evaluation and hepatobiliary involvement., Competing Interests: Conflicts of interest: All authors – none to declare., (GERMS.)

Sepsis is a major cause of morbidity and mortality worldwide. Sepsis-associated coagulation disorders are involved in the pathogenesis of multiorgan failure and lead to a subsequently worsening prognosis. Alongside the global impact of the COVID-19 pandemic, a great number of research papers have focused on SARS-CoV-2 pathogenesis and treatment. Significant progress has been made in this regard and coagulation disturbances were once again found to underlie some of the most serious adverse outcomes of SARS-CoV-2 infection, such as acute lung injury and multiorgan dysfunction. In the attempt of untangling the mechanisms behind COVID-19-associated coagulopathy (CAC), a series of similarities with sepsis-induced coagulopathy (SIC) became apparent. Whether they are, in fact, the same disease has not been established yet. The clinical picture of CAC shows the unique feature of an initial phase of intravascular coagulation confined to the respiratory system. Only later on, patients can develop a clinically significant form of systemic coagulopathy, possibly with a consumptive pattern, but, unlike SIC, it is not a key feature. Deepening our understanding of CAC pathogenesis has to remain a major goal for the research community, in order to design and validate accurate definitions and classification criteria.

Background and Objectives : SARS-CoV-2 infection is frequently associated with pneumonia but has a broad tissue tropism also leading to systemic complications (hematologic, gastro-intestinal, cardiac, neurologic, etc.). In this study, we aim to evaluate the impact of COVID-19 infection on the liver and to identify the risk factors/predictors for liver injury at admission to the hospital. Materials and Methods : We performed a retrospective cohort study on 249 patients, divided into two Group A (157 patients with liver involvement) and Group B (92 patients without liver involvement). We recorded demographic and lifestyle parameters, anthropometric parameters, comorbidities, clinical parameters, inflammation markers, complete blood count, coagulation, and biochemical parameters. Lung parenchyma, liver dimensions, and morphology were evaluated by computer tomography (CT) scans. Results : Patients with liver involvement had higher heart and respiratory rates, lower oxygen saturation (SO 2 ), and necessitated higher oxygen flow at admittance. We found higher serum levels of C-reactive protein, fibrinogen, ferritin, creatine kinase, lactate dehydrogenase (LDH), serum triglycerides, and lower values for serum albumin in Group A patients. The patients with liver involvement presented more extensive lung injury with higher percentages of alveolar, mixed, and interstitial lesions, an increase in liver dimensions, and lower density ranges for the liver parenchyma. The patients presented hepatocytolytic involvement in 26 cases (10.4% from the entire study population), cholestatic involvement in 63 cases (37.7% from the entire study population), and mixed liver involvement in 68 cases (37.7% from the entire study population). Conclusions : Liver involvement in COVID-19 patients is frequent, usually mild, and occurs mostly in male patients over 50 years old. Cholestatic and mixed liver injuries are more frequent than hepatocytolytic injuries. The severity of lung injury evaluated by CT scan, increased values of inflammatory markers, LDH, and low values of SO 2 can be considered risk factors/predictors for liver injury at admission to the hospital., Competing Interests: The authors declare that they have no conflict of interest.

Background and Objectives : Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection represents a pathology with primary pulmonary involvement and multisystemic impact, including cardiovascular injuries. The present study aimed to assess the value of clinical, biochemical, and imaging factors in COVID-19 patients in determining the severity of myocardial involvement, and to create a model that can be used toevaluate myocardial injury risk based on clinical, biochemical and imaging factors. Materials and Methods : We performed an observational cohort study on 150 consecutive patients, evaluating their age, sex, hospitalization period, peripheral oxygen saturation (SpO 2 ) in ambient air, systolic and diastolic blood pressure, heart rate, respiratory rate, biochemical markers of cardiac dysfunction (TnI, and NT-proBNP), inflammatory markers (C reactive protein (CRP), fibrinogen, serum ferritin, interleukin-6 (IL-6), tumor necrosis factor alpha (TNFα)), D-dimers, lactate dehydrogenase (LDH), myoglobin and radio-imaging parameters. All patients underwent computerized tomography chest scan in the first two days following admission. Results : We observed elevated heart and respiratory rates, higher systolic blood pressure, and a lower diastolic blood pressure in the patients with cardiac injury; significant differences between groups were registered in TnI, NT-proBNP, LDH, CRP, and D-dimers. For the radiological parameters, we found proportional correlations with the myocardial injury for the severity of lung disease, number of pulmonary segments with alveolar consolidation, number of pulmonary lobes with pneumonia, crazy paving pattern, type of lung involvement, the extent of fibroatelectatic lesions and the mediastinal adenopathies. Conclusions : Myocardial injury occurred in 12% of patients in the study group. Ground glass opacities, interstitial interlobular septal thickening (crazy paving pattern), fibroatelectasic lesions and alveolar consolidations on CT scan were correlated with myocardial injury. Routine lung sectional imaging along with non-specific biomarkers (LDH, D-dimers, and CRP) can be further valuable in the characterization of the disease burden, thus impacting patient care., Competing Interests: The authors declare that they have no conflict of interest.

Context: Both human immunodeficiency virus (HIV) infection and hepatitis C virus (HCV) infection represent systemic diseases that may develop metabolic complications, thus HIV/HCV coinfection metabolic changes need to be depicted., Objective: We aimed to evaluate the body composition changes in patients with either HIV and HCV monoinfections or HIV/HCV coinfection., Methods: 123 young men divided into three groups: 41 with HIV/HCV coinfection, 42 with HIV-monoinfection, and 40 with HCV-monoinfection were evaluated for total and regional bone and soft tissue body composition assessments using a Dual-energy X-ray absorptiometry (DXA) and were compared with 40 healthy men with age and body mass index similar to the study groups. To detect sarcopenia, we calculated the appendicular limbs' lean mass index (ALMI), for obesity, we used the percent of body fat, and for lipodystrophy, we calculated the trunk/limbs index., Results: HIV/HCV coinfection is associated with a significant higher bone demineralization in all regions of interest compared to HCV or HIV monoinfections and to controls. The prevalence of bone demineralization in HIV/HCV patients was 31.7%, more frequently at lumbar spine. Fat mass and lean mass were significantly lower in HIV/HCV-coinfected patients than in controls. Lipodystrophy was found in similar percentages in all three evaluated groups (80.4% in HIV/HCV, 92.5% in HIV, and 95% in the HCV group). Sarcopenia was higher in HIV/HCV group (43.9%) and important in HCV-monoinfection group (30%)., Conclusions: HIV/HCV-coinfected patients had the highest prevalence of bone demineralization, fat mass, and lean mass loss, compared to controls and to HIV and HCV monoinfections., Competing Interests: The authors declare that they have no conflict of interest., (©2022 Acta Endocrinologica (Buc).)

Background and Objectives: Pulmonary fibrosis represents a stage of normal physiologic response to inflammatory aggression, mostly self-limiting and reversible; however, numerous patients treated for SARS-CoV-2 pneumonia present after release from hospital residual lung fibrosis. In this article, we aim to present an optimization method for evaluating pulmonary fibrosis by quantitative analysis, to identify the risk factors/predictors for pulmonary fibrosis in patients with SARS-CoV-2 infection, and to characterize the impact of pulmonary fibrosis on the symptomatology of patients after release from the hospital. Materials and Methods: We performed a prospective observational study on 100 patients with severe forms of pneumonia, with a control group of 61 non-COVID normal patients. Results: We found persistent interstitial changes consistent with fibrotic changes in 69% of patients. The risk of fibrosis was proportional to the values of erythrocyte sedimentation rate (ESR), C reactive protein (CRP), and lactate dehydrogenase (LDH), and to the duration of hospitalization. The imaging parameters correlated with increased risk for interstitial fibrosis were the number of affected pulmonary lobes and the percent of interstitial pulmonary fibrosis. Conclusions: The main risk factors for pulmonary fibrosis post-COVID-19 identified in our study are increased ESR, CRP, LDH, duration of hospitalization and the severity of pneumonia.

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.

Background and Objectives : The severe forms of SARS-CoV-2 pneumonia are associated with acute hypoxic respiratory failure and high mortality rates, raising significant challenges for the medical community. The objective of this paper is to present the importance of early quantitative evaluation of radiological changes in SARS-CoV-2 pneumonia, including an alternative way to evaluate lung involvement using normal density clusters. Based on these elements we have developed a more accurate new predictive score which includes quantitative radiological parameters. The current evolution models used in the evaluation of severe cases of COVID-19 only include qualitative or semi-quantitative evaluations of pulmonary lesions which lead to a less accurate prognosis and assessment of pulmonary involvement. Materials and Methods: We performed a retrospective observational cohort study that included 100 adult patients admitted with confirmed severe COVID-19. The patients were divided into two groups: group A (76 survivors) and group B (24 non-survivors). All patients were evaluated by CT scan upon admission in to the hospital. Results : We found a low percentage of normal lung densities, PaO 2 /FiO 2 ratio, lymphocytes, platelets, hemoglobin and serum albumin associated with higher mortality; a high percentage of interstitial lesions, oxygen flow, FiO 2 , Neutrophils/lymphocytes ratio, lactate dehydrogenase, creatine kinase MB, myoglobin, and serum creatinine were also associated with higher mortality. The most accurate regression model included the predictors of age, lymphocytes, PaO 2 /FiO 2 ratio, percent of lung involvement, lactate dehydrogenase, serum albumin, D-dimers, oxygen flow, and myoglobin. Based on these parameters we developed a new score (COV-Score). Conclusions : Quantitative assessment of lung lesions improves the prediction algorithms compared to the semi-quantitative parameters. The cluster evaluation algorithm increases the non-survivor and overall prediction accuracy.COV-Score represents a viable alternative to current prediction scores, demonstrating improved sensitivity and specificity in predicting mortality at the time of admission.

Introduction: Nowadays, chronic viral hepatitis represents one of the most common pathological entities with over 400 million cases worldwide, with high diagnosis and treatment cost, severe complications in late stages and an annual death-rate around 1 million. The purpose of this study was to identify noninvasive ultrasound markers in order to establish an early diagnosis in asymptomatic chronic hepatitis., Methods: We enrolled in a prospective study 111 patients diagnosed with asymptomatic chronic hepatitis: 53 patients with hepatitis B (group A) and 58 patients with hepatitis C (group B). All patients underwent ultrasound exam; we evaluated the dimensions of the left hepatic lobe, right hepatic lobe, caudate lobe, portal vein, liver stiffness, presence of hepatic hilar lymph nodes, number and dimensions of the adenopathies., Results: Increased liver size was found in over 16% of patients in group A and over 20% of patients in group B. We registered an enlarged portal vein in 3.77% of patients in group A and in 3.45% of patients in group B. Adenopathies were found in 64.16% of group A and 82.76% of group B. Using long adenopathic axis as marker, we obtained a NPV over 0.9, PPV of 0.5 in the detection of chronic hepatitis B and a PPV of 0.9 in the detection of chronic hepatitis C in asymptomatic patients, a specificity of 0.98 for both chronic hepatitis B and C, a sensitivity of 0.81 for group B and 0.64 for group A., Conclusions: The presence of hilar liver adenopathies represents an important marker in detecting asymptomatic chronic viral hepatitis., Competing Interests: Conflicts of interest: All authors – none to declare., (GERMS.)