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.

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.

Acute pancreatitis (AP) has emerged as a notable complication in patients with COVID-19, yet the interplay between viral infection, systemic inflammation, and pancreatic injury remains incompletely understood. This study aimed to evaluatethe characteristics and risk factors of APin patients with severe COVID-19 pneumonia. We conducted a retrospective, single-center analysis of 405 hospitalized COVID-19 patients with and without AP. Laboratory markers, including CRP, ESR, fibrinogen, LDH, D-dimers, WBC, neutrophils, serum potassium, and serum glucose, alongside imaging and clinical parameters, were analyzed for associations with AP occurrence. Our results indicate that elevated inflammatory and coagulation markers, leukocytosis with neutrophilia, hyperglycemia, hypokalemia, and more severe pulmonary involvement were significantly associated with AP in COVID-19. LDH and inflammatory markers demonstrated particularly strong predictive value, while D-dimers and lung injury severity also contributed to risk stratification. These findings suggest that systemic inflammation, endothelial dysfunction, immunothrombosis, and metabolic impairments converge to increase pancreatic vulnerability in COVID-19 patients. Early recognition of these risk factors may guide monitoring and therapeutic interventions, although prospective validation is needed.

Background/Objectives: Coronavirus disease 2019 (COVID-19) has emerged as a multisystem disorder, with acute kidney injury (AKI) representing a frequent and severe complication associated with poor outcomes. This study assessed the incidence, risk factors, and outcomes of AKI in patients with severe COVID-19 across three pandemic waves. Methods: We retrospectively analyzed 561 patients with severe COVID-19 admitted to a tertiary hospital between March 2020 and December 2021. AKI was defined and staged according to KDIGO 2012 criteria. Demographic, clinical, laboratory, and imaging data were evaluated using univariate and multivariable logistic regression and ROC curve analyses to identify predictors of AKI. Results: AKI occurred in 71 patients (12.65%), most frequently during the third wave (40.9%). Stage 1 accounted for 62% of cases, while 23.9% progressed to stage 3 and 10% required dialysis. Compared with patients without AKI, those with AKI had longer hospital stays (15 vs. 11 days), more intense inflammatory responses (CRP 91.7 vs. 63.3 mg/L, p = 0.002), and higher mortality (35.2% vs. 10.2%, p < 0.001). Multivariable analysis identified elevated serum myoglobin (OR = 1.010, p = 0.001), prolonged corticosteroid therapy (OR = 1.096, p = 0.035), and lower hemoglobin (OR = 0.375, p < 0.001) as independent factors of AKI. Conclusions: AKI in severe COVID-19 is multifactorial, reflecting the interplay of systemic inflammation, cytolysis, coagulopathy, and renal microvascular dysfunction. The risk increases with higher myoglobin levels, longer corticosteroid exposure, and lower hemoglobin, highlighting the need for early identification and preventive strategies in high-risk patients.

Background/Objectives: This study aims to investigate the influence of demographic, behavioral, anthropometric, and comorbid factors on brain atrophy in people living with HIV (PLWH). Methods: We conducted a cross-sectional study involving 121 HIV-positive patients, stratified into two groups, those with and without brain atrophy (BA). For each participant, we recorded demographic data, smoking status, physical activity levels, disease and treatment duration, and comorbidities. BA was quantitatively assessed using MRI-derived volumetric measurements of 47 cerebral substructures. Results: Patients with BA exhibited significantly reduced gray matter (GM) and white matter (WM) volumes alongside increased cerebrospinal fluid volumes, both in absolute and percentage measurements. WM atrophy was most pronounced in the frontal, parietal, and temporal lobes, with relative sparing of the occipital lobe. GM atrophy predominantly affected the basal ganglia (notably, the thalamus and putamen) and cortical regions, including the hippocampus, frontal, and parietal lobes. Significant positive correlations were observed between BA and both smoking status (pack–years) and disease duration, while physical activity demonstrated an inverse relationship (higher atrophy risk in those with less than 30 min of daily continuous walking). Non-adherence to antiretroviral therapy (ART) was also associated with BA. Among comorbidities, type 2 diabetes and HIV-associated neurocognitive disorders (HAND) showed the strongest associations with BA. Conclusions: Brain atrophy in PWH is correlated with smoking, physical inactivity, and the duration of HIV infection. Comorbid conditions, such as type II diabetes and HAND, amplify the risk for BA. We consider that early lifestyle interventions and optimized ART may mitigate the neurodegeneration process.

Background: Chronic hepatitis C (CHC) is associated with persistent inflammation, metabolic dysfunction, and body composition abnormalities that extend beyond liver disease. However, the coexistence of reduced muscle mass, occult obesity, and altered fat distribution remains poorly characterized. This study evaluated DXA-derived body composition phenotypes in men with CHC and their associations with inflammatory markers, liver fibrosis, and lifestyle factors. Methods: In this retrospective cross-sectional study, 70 men with CHC and 70 age-, sex-, and BMI-matched healthy controls underwent whole-body dual-energy X-ray absorptiometry (DXA). Appendicular lean mass index (ALMI), total and regional fat mass, body fat percentage, and fat distribution were assessed. Associations with inflammatory markers, liver fibrosis, and lifestyle factors were analyzed using non-parametric tests, ROC analysis, and multivariable logistic regression. Results: Patients with CHC had significantly lower ALMI, total limb lean mass, trunk fat mass, body fat percentage, and android/gynoid fat ratio than controls. Low muscle mass was present in 24.3% of patients, while 48.6% met DXA criteria for obesity, including 12.9% with occult obesity and 20.0% with BMI–BFP discordance. Overall, 61.4% exhibited abnormal body composition phenotypes. Low muscle mass was associated with higher erythrocyte sedimentation rate, fibrinogen, neutrophil and leukocyte counts, and more advanced liver fibrosis. Conclusions: Men with CHC frequently exhibit reduced muscle mass, altered fat distribution, occult obesity, and obesity with low muscle mass that are not reliably detected by BMI. DXA-based body composition assessment may improve identification of high-risk metabolic phenotypes and support individualized management.