Current Issue : January-March Volume : 2026 Issue Number : 1 Articles : 5 Articles
Background/Objectives: This study was designed to investigate the potential clinical, biochemical, haematological, and pathological associations of carpal tunnel syndrome through a multidisciplinary approach encompassing the fields of internal medicine, gastroenterology, and neurology. Methods: The study group (CTS-positive) comprised 265 patients who presented with dyspeptic complaints and underwent upper gastrointestinal endoscopy, gastric antrum biopsy, electromyography, and comprehensive biochemical and haematological analyses. A control group of 265 patients with similar symptoms but without CTS was selected for comparison. A comparative analysis was conducted on clinical findings, gastric biopsy results, and biochemical and haematological parameters. Results: There were no significant differences in age, gender distribution, or gastric biopsy findings (Helicobacter pylori, intestinal metaplasia, atrophy, and dysplasia) between the CTS-positive and CTSnegative groups. However, significant biochemical differences were identified, including elevated calcium and reduced magnesium levels in CTS-positive patients. Haematological evaluations revealed higher lymphocyte, eosinophil, basophil, erythrocyte, haemoglobin, and haematocrit levels, along with reduced neutrophil-to-lymphocyte ratios and red blood cell distribution widths in the CTS-positive group. Further analysis in the form of correlation and logistic regression analyses provided further confirmation of the association of elevated calcium, haemoglobin, and lymphocyte levels with increased risk of CTS. Conclusions: This multidisciplinary study identifies significant associations between CTS and specific biochemical and haematological parameters, notably calcium-magnesium imbalance and erythrocyte indices. These findings suggest underlying biological interactions that may guide future diagnostic and therapeutic strategies for patients with carpal tunnel syndrome....
Background: This study aimed to evaluate the clinical effectiveness of dupilumab and its impact on CRSwNP and type 2 inflammatory biomarkers in patients with severe uncontrolled asthma, with or without comorbidities, within a real-life cohort. Methods: This was a single-center, prospective, and observational real-life study conducted at the Severe Asthma Unit of Germans Trias i Pujol University Hospital. The objective of this study was to assess the real-world response to dupilumab treatment in patients with severe asthma, with or without nasal polyposis, bronchiectasis, obesity, or switching from another biologic drug for their asthma. Results: The ACT score significantly increased (13.7 vs. 20.6; p = 0.001), while the number of exacerbations decreased (3.1 vs. 0.7; p = 0.005). Patients with CRSwNP showed an increase in the ACT score (13.1 vs. 19.8; p = 0.011) and a decrease in the number of exacerbations (3.0 vs. 1.3; p = 0.217). Patients with nasal polyps showed an increase in both SNOT22 (78.3 vs. 38.3; p = 0.013) and global VAS (8 vs. 4.2; p = 0.028). Patients with bronchiectasis receiving dupilumab showed an increase in the ACT score (12.7 vs. 21.3; p = 0.039) and a marked decrease in the number of exacerbations (2.8 vs. 0; p = 0.025). Obese patients treated with dupilumab showed an improvement in the ACT score (14.1 vs. 21.3; p = 0.044) and a decrease in the rate of exacerbations (3.2 vs. 1.3; p = 0.030). Patients with rhinoconjunctivitis receiving dupilumab showed an increase in the ACT score (13.4 vs. 19.1; p = 0.017) and a decrease in the number of exacerbations (3.3 vs. 0.8; p = 0.024). Conclusions: Dupilumab is a highly effective treatment for severe asthma, showing significant improvements in lung function, reductions in exacerbations, and enhanced quality of life for patients with and without nasal polyps. The results of this real-life study support dupilumab as a valuable addition to the therapeutic armamentarium for asthma, particularly for those with type 2 inflammation despite the presence of comorbidities such as bronchiectasis or obesity, or for patients in whom a previous biologic treatment failed....
The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has brought to light unexpected complications beyond respiratory illness, including effects on kidney function and a potential link to kidney stone disease (KSD). This review proposes a novel framework connecting COVID-19-induced epigenetic reprogramming to disruptions in mitochondrial sulfur metabolism and the pathogenesis of kidney stones. We examine how SARS-CoV-2 interferes with host methylation processes, leading to elevated homocysteine (Hcy) levels and impairment of the trans-sulfuration pathway mechanisms particularly relevant in metabolic disorders such as homocystinuria. These epigenetic and metabolic alterations may promote specific kidney stone subtypes through disrupted sulfur and oxalate handling. Additionally, we explore the role of COVID-19-associated gut dysbiosis in increasing oxalate production and driving calcium oxalate stone formation. Together, these pathways may accelerate the transition from acute kidney injury (AKI) to chronic KSD, linking viral methylation interference, sulfur amino acid imbalance, mitochondrial dysfunction, and microbiota changes. Unlike earlier reviews that address these mechanisms separately, this work offers an integrated hypothesis to explain post-viral renal lithogenesis and highlights the potential of targeting sulfur metabolism and redox pathways as therapeutic strategies for KSD triggered or aggravated by viral infections such as COVID-19....
Primary ciliary dyskinesia (PCD) is a rare, genetically heterogeneous disorder that impairs mucociliary clearance and leads to progressive lung disease. This study aimed to characterize lung function decline in a genetically homogeneous cohort of Puerto Rican patients with RSPH4A-associated PCD and to develop a clinical tool to predict lung function decline and support transplant referral decisions. We conducted a retrospective chart review of patients (n = 25) with a confirmed RSPH4A [c.921+3_6delAAGT] genetic variant, collecting longitudinal spirometry data and applying linear regressions to calculate each patient’s individual FEV1 decline. The median FEV1 at diagnosis was 55%, with a median annual decline of −0.75% predicted. Adults exhibited significantly lower lung function compared to pediatric patients, while no difference was seen between males and females. Based on this observed decline, we developed the Predicted Capacity Decline Index (PCDx), an index that estimates the age and time until a patient reaches the 30% FEV1 threshold, the point at which lung transplant referral is typically considered. Our findings underscore the need for early intervention and suggest that genotype-specific tools like the PCDx may enhance clinical decision-making in managing progressive lung disease in PCD....
The three pathological hallmarks of multiple sclerosis (MS) are inflammation, demyelination, and progressive neurodegeneration. None of the approved disease-modifying therapies for MS counters all three pathologies, and, more specifically, none is approved for neuroprotection. Axonal loss is the most significant contributor to chronic and irreversible disability in MS. A tantalizing molecular target has emerged to uniquely counter all three MS pathologies: tumor necrosis factor receptor 2 (TNFR2). Agonism or activation of TNFR2 has been shown in MS models to induce immunosuppression, oligodendrocyte precursor differentiation, and neuroprotection. Further, in basic science studies stemming from the past 15 years, TNFR2 agonism is known to be a strong inducer of T-regulatory cells (Tregs). Treg cells, and especially those expressing TNFR2, are known to confer the strongest suppression per cell type. TNFR2 is even more attractive as a therapeutic target because of its restricted expression by only a handful of CNS and immune cell subsets, thereby minimizing the likelihood of systemic and other adverse effects. Recent antibody design work suggests many of the hurdles of Treg agonism may have been overcome. This review covers the current treatment landscape for MS, the basic science of TNFR2, the rationale for and evidence behind TNFR2 agonism to treat multiple sclerosis, the design of potent TNFR2 agonist antibodies, and the treatment applications for other neurological, autoimmune, or inflammatory diseases....
Loading....