Recent research indicates that the microbiome has a significant impact on the progression of inflammatory bowel disease (IBD) and that creating therapies that change its composition could positively impact the outcomes of IBD treatment. This review summarizes the results of extensive studies that examined IBD patients undergoing several therapies, including anti-TNF medication, vedolizumab, ustekinumab, probiotics, and fecal microbiota transplantation (FMT), and the alterations in their gut microbiota’s composition and function. The objective was to investigate the variety and effectiveness of microbial species in order to discover new biomarkers or therapeutic targets that could improve the outcome of treatment for these patients. This research aimed to offer useful insights into personalized medicine techniques for managing IBD. Beneficial bacteria such as Faecalibacterium prausnitzii and Roseburia have been consistently linked to favorable clinical outcomes, whereas pathogenic bacteria such as Escherichia coli and Clostridioides difficile are associated with worsening disease conditions. Although many studies have examined the role of gut microbiota in IBD, there is still a need for more targeted research on the connection between specific microbial communities and treatment outcomes. This study sought to address this gap by exploring the intricate relationship between the gut microbiota composition and the effectiveness of IBD medications.

Background and Objectives: Ward-level risk in pulmonary tuberculosis (TB) is often estimated from static admission data. This study evaluated a pragmatic composite—TRIAD-TB—integrating physiology (SpO₂, respiratory rate), inflammation (systemic immune-inflammation index [SII], C-reactive protein [CRP]), and nutrition (BMI, albumin), augmented by 72 h changes in CRP and albumin, to predict 30-day mortality and hospital length of stay (LOS). Methods: A pooled prospective cohort of 126 HIV-negative adults without chronic systemic immunosuppression hospitalized with culture-confirmed pulmonary TB at two Romanian tertiary centers was analyzed. TRIAD-TB combined z-scored admission markers and 72 h deltas. The primary outcome was 30-day all-cause mortality; secondary outcomes included LOS. Associations were estimated using Firth logistic regression (mortality) and quasi-Poisson regression (LOS). Discrimination and overall performance were summarized by AUC and Brier score; internal performance used bootstrap optimism-correction. Results: Across TRIAD-TB tertiles, 30-day mortality increased from 2.4% to 16.7%, and mean LOS rose from 24.7 ± 5.8 to 32.1 ± 7.3 days. Each SD increase in TRIAD-TB was associated with higher odds of death (adjusted OR 2.4, 95% CI 1.3–4.8; p = 0.006) and longer hospitalization (adjusted IRR 1.19, 95% CI 1.09–1.30; p < 0.001). The full model discriminated mortality well (AUC 0.84; Brier 0.067) and explained 21.8% of LOS deviance. Early dynamics were informative: higher CRP ratio (72 h/0 h) and albumin decline tracked with adverse outcomes. An admission-only “mini-TRIAD” retained strong discrimination (AUC 0.79). Conclusions: A dynamic composite leveraging routine vitals and laboratory tests—plus 72 h trajectories—accurately stratified short-term risk in hospitalized pulmonary TB, while an admission-only “mini-TRIAD” retained strong discrimination. Together, these tools may support early escalation, targeted monitoring, and capacity planning. TRIAD-TB may support early escalation, targeted monitoring, and capacity planning; however, because it was derived in HIV-negative, non-immunosuppressed adults in an Eastern European setting, TRIAD-TB and the admission-only “mini-TRIAD” require external validation, including in cohorts with substantial HIV co-infection and different comorbidity profiles, before any broader implementation.

Background and Objectives: Blood-borne inflammatory ratios have been proposed as inexpensive prognostic tools across a range of diseases, but their role in pulmonary tuberculosis (TB) remains uncertain. In this retrospective case–control analysis, we explored whether composite indices derived from routine haematology—namely the neutrophil-to-lymphocyte ratio (NLR), the platelet-to-lymphocyte ratio (PLR), the systemic immune–inflammation index (SII) and a novel CRP–Fibrinogen Index (CFI)—could enhance risk stratification beyond established cytokine measurements among Romanian adults with culture-confirmed pulmonary T. Materials and Methods: Data were drawn from 80 consecutive TB in-patients and 50 community controls. Full blood counts, C-reactive protein, fibrinogen, and four multiplex cytokines were extracted from electronic records, and composite indices were calculated according to standard formulas. The primary outcomes were in-hospital mortality within 90 days and length of stay (LOS). Results: Among TB patients, the median NLR was 3.70 (IQR 2.54–6.14), PLR was 200 (140–277) and SII was 1.36 × 10⁶ µL⁻¹ (0.74–2.34 × 10⁶), compared with 1.8 (1.4–2.3), 117 (95–140) and 0.46 × 10⁶ µL⁻¹ (0.30–0.60 × 10⁶) in controls. Those with SII above the cohort median exhibited more pronounced acute-phase responses (median CRP 96 vs. 12 mg L⁻¹; fibrinogen 578 vs. 458 mg dL⁻¹), yet median LOS remained virtually identical (29 vs. 28 days) and early mortality was low in both groups (8% vs. 2%). The CFI showed no clear gradient in hospital stay across its quartiles, and composite ratios—while tightly inter-correlated—demonstrated only minimal association with cytokine levels and LOS. Conclusions: Composite cell-count indices were markedly elevated but did not predict early death or prolonged admission. In low-event European cohorts, their chief value may lie in serving as cost-free gatekeepers, flagging those who should proceed to more advanced cytokine or genomic testing. Although routine reporting of NLR and SII may support low-cost surveillance, validation in larger, multicentre cohorts with serial sampling is needed before these indices can be integrated into clinical decision-making.

Pulmonary complications are an important yet underappreciated aspect of inflammatory bowel disease (IBD), which includes Crohn’s disease (CD) and ulcerative colitis (UC). These conditions often manifest with extraintestinal symptoms that can significantly influence the clinical trajectory of the disease. Pulmonary involvement in IBD can range from mild symptoms, such as a persistent cough, to severe conditions, including interstitial lung disease or pulmonary embolism. This systematic review aims to assess the prevalence, clinical presentations, and implications of pulmonary involvement in IBD patients. A comprehensive literature search was conducted using PubMed database up to the 1st of May 2024. Inclusion criteria focused on studies involving adult IBD patients with documented pulmonary symptoms, evaluated through clinical, radiological, and histopathological approaches. Of the 463 studies identified, 27 met the inclusion criteria, consisting of 36,264 patients. Pulmonary manifestations were classified into airway diseases and parenchymal involvement. Airway diseases, including bronchiectasis and chronic bronchitis, were the most common, followed by parenchymal conditions such as organizing pneumonia and interstitial lung disease (ILD). Smoking was identified as a significant risk factor for pulmonary involvement. Pulmonary involvement in IBD is diverse and often underdiagnosed. Early recognition and management are crucial to improving patient outcomes.

Background: Chronic ethanol consumption is a major global health concern traditionally associated with liver disease. Ethanol disrupts gut microbial communities, compromises intestinal barrier function, and contributes to hepatic, metabolic, and neurocognitive disorders. Methods: We conducted a systematic PubMed search and meta-analysis of 11 human and 19 animal studies evaluating ethanol-induced gut microbiota alterations. Studies were assessed for microbial diversity, taxonomic shifts, barrier integrity, and systemic effects. Effect sizes were calculated where possible, and interventional outcomes were examined. Results: Across species, ethanol exposure was consistently associated with reduced microbial diversity and depletion of beneficial commensals such as Faecalibacterium, Lactobacillus, Akkermansia, and Bifidobacterium, alongside an expansion of proinflammatory taxa (Proteobacteria, Enterococcus, Veillonella). Our analysis uniquely highlights discrepancies between human and animal studies, including opposite trends in specific genera (e.g., Akkermansia and Bifidobacterium) and the impact of confounders such as antibiotic exposure in human cohorts. We also demonstrate that microbiota-targeted interventions can partially restore diversity and improve clinical or behavioral outcomes. Conclusions: This meta-analysis highlights reproducible patterns of ethanol-induced gut dysbiosis across both human and animal studies.

Background/Objectives: Romania remains a tuberculosis (TB) hotspot in the European Union, yet host-derived factors of poor outcomes are poorly characterised. We quantified circulating pro-inflammatory cytokines and examined their interplay with behavioural risk factors, the nutritional status, and the clinical course in adults hospitalised with pulmonary TB. We analysed 80 adults with microbiologically confirmed pulmonary TB and 40 respiratory symptom controls; four TB patients (5%) died during hospitalisation, all within 10 days of admission. Methods: A retrospective analytical case–control study was conducted at the Constanța regional TB referral centre (October 2020—October 2023). Patients with smear- or culture-confirmed TB were frequency-matched by sex, 10-year age band, and BMI class to culture-negative respiratory controls at a 2:1 ratio. The patients’ serum interferon-γ (IFN-γ), interleukin-1α (IL-1α), interleukin-1β (IL-1β), and tumour-necrosis-factor-α (TNF-α) were quantified within 24 h of admission; the neutrophil/lymphocyte ratio (NLR) was extracted from full blood counts. Independent predictors of in-hospital mortality were identified by multivariable logistic regression; factors associated with the length of stay (LOS) were modelled with quasi-Poisson regression. Results: The median TNF-α (24.1 pg mL⁻¹ vs. 16.2 pg mL⁻¹; p = 0.009) and IL-1β (5.34 pg mL⁻¹ vs. 3.67 pg mL⁻¹; p = 0.008) were significantly higher in the TB cases than in controls. TNF-α was strongly correlated with IL-1β (ρ = 0.80; p < 0.001), while NLR showed weak concordance with multiplex cytokine patterns. Among the patients with TB, four early deaths (5%) exhibited a tripling of TNF-α (71.4 pg mL⁻¹) and a doubling of NLR (7.8) compared with the survivors. Each 10 pg mL⁻¹ rise in TNF-α independently increased the odds of in-hospital death by 1.8-fold (95% CI 1.1–3.0; p = 0.02). The LOS (median 29 days) was unrelated to the smoking, alcohol, or comorbidity load, but varied across BMI strata: underweight, 27 days; normal weight, 30 days; overweight, 23 days (Kruskal–Wallis p = 0.03). In a multivariable analysis, under-nutrition (BMI < 18.5 kg m⁻²) prolonged the LOS by 19% (IRR 1.19; 95% CI 1.05–1.34; p = 0.004) independently of the disease severity. Conclusions: A hyper-TNF-α/IL-1β systemic signature correlates with early mortality in Romanian pulmonary TB, while under-nutrition is the dominant modifiable determinant of prolonged hospitalisation. Admission algorithms that pair rapid TNF-α testing with systematic nutritional assessment could enable targeted host-directed therapy trials and optimise bed utilisation in high-burden settings.