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: The neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) are novel biomarkers that provide insight into systemic inflammation and how the immune system responds to stress or infection. These ratios have been associated with predicting clinical outcomes in various diseases, including COVID-19. This study aims to evaluate the prognostic value of NLR and PLR in anticipating ICU admission, acute respiratory failure, and disease severity in COVID-19 patients. Materials and Methods: We conducted a retrospective, observational study that included 536 patients diagnosed with COVID-19. We analyzed the NLR and PLR values at admission and correlated them with ICU admission, the onset of acute respiratory failure, and clinical outcomes. Results: Statistical correlations were identified between elevated NLR and PLR values and the development of complications during hospitalization (p = 0.04 and p = 0.00), acute hypoxemic respiratory failure (p = 0.00), and admission to the intensive care unit (ICU) (p = 0.04). No correlations were found between the values of these ratios and mortality (p = 0.46 and p = 0.32) nor with the development of hepatic cytolysis (p = 0.79 and p = 0.87). Conclusions: NLR and PLR are reliable, easily obtainable biomarkers that can aid in the early prediction of ICU admission and disease severity in COVID-19 patients, offering valuable insights for risk stratification and clinical management. Further prospective studies are needed to validate these biomarkers as part of a broader predictive model for critical care in COVID-19.

Background: Insulin resistance is frequent in human immunodeficiency virus (HIV) infection and may be related to antiretroviral therapy. Cytokines secreted by adipose tissue (adipokines) are linked to insulin sensitivity. The present study is aimed to assess the prevalence of insulin resistance (IR) and its association with several adipokines, in a non-diabetic Romanian cohort of men and women with HIV-1 infection, undergoing combination antiretroviral therapy (cART).Methods: A cross-sectional study was conducted in an unselected sample of 89 HIV-1-positive, non-diabetic patients undergoing stable cART for at least 6 months. Metabolic parameters were measured, including fasting plasma insulin, and circulating adiponectin, leptin, resistin, tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) levels. Insulin resistance was estimated by measuring the Quantitative Insulin Sensitivity Check Index (QUICKI), using a cut-off value of 0.33. A linear regression model was fitted to QUICKI to test the association of IR and adipokines levels.Results: A total of 89 patients (aged 18–65, median: 28 years) including 51 men (57.3%) and 38 women (42.7%) were included in the study. Fifty nine patients (66.3%) were diagnosed with IR based on QUICKI values lower than the cut-off point. IR prevalence was 72.5% in men and 57.6% in women. The presence of the IR was not influenced by either the time of the HIV diagnosis or by the duration of cART. Decreased adiponectin and increased serum triglycerides were associated with increased IR in men (R=0.43, p=0.007). Hyperleptinemia in women was demonstrated to be associated with the presence of IR (R=0.33, p=0.03).Conclusions: Given the significant prevalence of the IR in our young non-diabetic cohort with HIV infection undergoing antiretroviral therapy reported in our study and the consecutive risk of diabetes and cardiovascular events, we suggest that the IR management should be a central component of HIV-infection therapeutic strategy. As adipokines play major roles in regulating glucose homeostasis with levels varying according to the sex, we suggest that further studies investigating adipokines should base their analyses on gender differences.

Leptin is an adipokine with complex metabolic, neuroendocrine and immune functions. Our objective was to evaluate leptin serum levels in a cohort of Romanian HIV-infected patients undergoing antiretroviral therapy in relation to their immune-virological status, lipid and glucose metabolic abnormalities and the presence of metabolic syndrome (MS). We enrolled consecutive non-diabetic HIV-infected patients aged 18 and over on stable cART for at least 6 months. Blood samples were tested for: leptin, CD4 T cells count, HIV viral load and lipid panel. A total of 90 HIV-infected patients were included in the study: 50 males (55.6%) with a mean age of 33.3 years and 40 females with a mean age of 30.4 years. Most patients (74.4%) had HIV viral load below the limit of detection and the median CD4 count for the cohort was 476 (410) cells/cmm. More than one third of the patients (41.1%) had hypoleptinemia. The prevalence of MS was 13.3%. Hypoleptinemia was significantly more frequent in men. In a subset of patients with undetectable HIV viral load, the median leptin value was 0.6 (6.07) ng/mL in patients with poor immune recovery (CD4 count ≤ 200/cmm) compared to 2 (3.07) ng/mL for those with better immune response (CD4 count > 200/cmm), without statistical significance. The median values of leptin were similar for persons with and without MS criteria. HDL-cholesterol values were positively correlated to leptin values in a linear regression model. A significant proportion of patients in our study presented low levels of leptin; this finding was not associated with immune and virological parameters or the presence of MS. Hypoleptinemia was significantly correlated with lower levels of HDL-cholesterol, a key cardiovascular risk factor.

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.

Urinary tract infections are a public health problem exacerbated by the rising concern of antibiotic resistance. Carbapenem-resistant Enterobacterales