Background: Severe COVID-19 is frequently complicated by hyperinflammation and is associated with a high mortality rate. Objectives: Adjunctive hemoperfusion (HP) aims to remove inflammatory mediators; however, its clinical benefits remain controversial. Methods: This retrospective 1:1 propensity score-matched case-control study included 70 patients with severe COVID-19 who were admitted to the intensive care unit (ICU) at Dr. Gharazi Hospital, Malayer, Iran, from March 2020 to September 2022. Patients received adjunctive HP using Jafron cartridges plus standard care (n = 35) or standard care alone (n = 35). Results: After matching, baseline characteristics were well balanced. Adjunctive hemoperfusion was associated with a significantly greater reduction in C-reactive protein (46% ± 14% vs. 18% ± 9%; P < 0.001), a greater improvement in peripheral oxygen saturation (SpO2; +7% ± 2% vs. +2% ± 1%; P = 0.01), a shorter ICU length of stay (11.2 ± 4.1 vs. 16.5 ± 5.8 days; P = 0.03), and a lower need for mechanical ventilation (40.0% vs. 62.9%; P = 0.04). Mortality in the intensive care unit was numerically lower in the HP group (20.0% vs. 34.3%; P = 0.08) but did not reach statistical significance. No procedure-related deaths occurred. Conclusions: In this propensity-matched cohort, adjunctive hemoperfusion was associated with attenuated systemic inflammation, improved oxygenation, a reduced need for mechanical ventilation, and a shorter ICU stay. These findings should be interpreted cautiously given the retrospective design.
Background: Mental health problems are common among people living with HIV and may adversely affect treatment adherence, disease progression, and quality of life. Objectives: This study compared depressive symptoms, quality of life, and worry among adults living with HIV and community controls in Tehran, Iran. Methods: We conducted a cross-sectional comparative study of 48 adults living with HIV and 71 community controls recruited through convenience sampling in Tehran, Iran. Participants completed the Depression subscale of the Depression Anxiety Stress Scales–21, the World Health Organization Quality of Life–BREF, and the Penn State Worry Questionnaire. Between-group differences were assessed using independent-samples t tests and Pearson's chi-square tests. Binary logistic regression was used to examine cross-sectional associations of age and psychological variables with group membership (0 = HIV, 1 = community controls), with a sensitivity analysis additionally adjusting for education. Results: Compared with community controls, adults living with HIV reported significantly higher depressive symptoms (P = 0.013, Cohen's d = 0.50) and lower quality of life (P = 0.015, d = −0.50), whereas worry did not differ significantly (P = 0.355, d = 0.17). Educational attainment also differed significantly between the groups (χ2(2) = 27.50, P < 0.001). In the complete-case logistic model (n = 108), older age (odds ratio [OR] = 0.94, 95% confidence interval [CI], 0.90 - 0.98, P = 0.002) and higher depressive symptom scores (OR = 0.84, 95% CI, 0.74 - 0.96, P = 0.008) were associated with lower odds of community-control membership, corresponding to higher odds of HIV-group membership. Quality of life and worry were not independently associated with group membership. When education was added (n = 105), university-level education was strongly associated with control membership (OR = 5.63, 95% CI, 2.10 - 15.10), the depressive-symptom association was attenuated (OR = 0.86, 95% CI, 0.75 - 1.00, P = 0.047), and age was no longer significant (P = 0.069). Conclusions: In this sample, adults living with HIV reported higher depressive symptoms and lower quality of life than community controls. Depressive symptoms were the only measured psychological variable associated with group membership in the primary model, although this association was attenuated after adjustment for education. These findings support further evaluation of mental health assessment and psychosocial support within HIV care; however, causal inferences and the effectiveness of specific screening or intervention strategies require longitudinal and interventional research.
Background: Mycobacterium simiae, a slow-growing nontuberculous mycobacterium (NTM), poses diagnostic and therapeutic challenges because of its clinical similarity to Mycobacterium tuberculosis and its resistance to standard antituberculosis drugs. Accurate and rapid identification is critical, particularly in immunocompromised individuals. Therefore, species-specific diagnostic targets are essential for differentiating among Mycobacterium species. Objectives: To identify and evaluate a novel species-specific genetic target for the detection of Mycobacterium simiae. Methods: An innovative approach was used to identify a unique and conserved genetic target specific to M. simiae. Two complete genomes were evaluated in silico using a modified genome-comparison approach to detect conserved coding sequences. A specific gene, G6N33_RS00430, encoding an alpha/beta hydrolase (ABH), was selected. Specific primers were designed, assessed for secondary structures, and screened against human and mycobacterial genomes to confirm their specificity. The ABH-PCR assay was validated using genomic DNA from various mycobacterial species and clinical isolates. Results: The ABH gene was confirmed to be unique to M. simiae, with minimal similarity to closely related species. The PCR assay demonstrated high analytical specificity, with amplification observed exclusively in M. simiae. Sensitivity testing indicated a detection limit of 5 fg of genomic DNA. All 10 clinical isolates yielded positive results, and 5 were confirmed by sequencing. Conclusions: This study identifies a novel species-specific genetic target for M. simiae, enabling rapid, accurate, and cost-effective PCR-based identification. The ABH-PCR assay shows strong potential for routine diagnostic use, particularly in resource-limited settings, and helps address a critical gap in NTM diagnostics.
Context: Tuberculosis is an airborne infectious disease influenced by multiple factors. Exposure to air pollutants may aggravate pulmonary tuberculosis. This systematic review examined the increased risk of tuberculosis and its exacerbation associated with exposure to air pollutants. Evidence Acquisition: The review searched PubMed, ScienceDirect, Web of Science, the Cochrane Library, and Google Scholar for studies published from 1995 through 2024 using terms related to air pollution, ambient air, Mycobacterium tuberculosis, the respiratory system, and tuberculosis. The initial search retrieved 404 records. Results: The main symptoms of pulmonary tuberculosis include chills, night sweats, fatigue, fever, chronic hemoptysis, lymphadenopathy, and weight loss. Tuberculosis most commonly affects the lungs, although other organs may also be involved. Environmental agents, including gases and airborne particles, may delay treatment and further damage lung tissue. The reviewed evidence indicates that exposure to certain air pollutants may increase the risk or severity of tuberculosis by impairing immune function and lung health, highlighting air pollution as an important public health concern. Discussion: The findings indicate an association between ambient air pollutant levels and tuberculosis. Air pollutants can damage healthy lung tissue through multiple mechanisms and impair pulmonary defenses against disease, thereby exacerbating conditions such as tuberculosis. Therefore, reducing air pollution may help to lessen the severity of symptoms of respiratory diseases, including tuberculosis.
