This review examined study characteristics and common practices in continuous glucose monitoring (CGM)-based exercise studies. Following PRISMA guidelines, a systematic search in the PubMed database was conducted. Data were extracted from 93 publications. A minority of studies (12.9%) focused on CGM system validation. Acute exercise studies were more common (87.1%) than chronic exercise studies (12.9%). Randomized crossover designs predominated (71.0%). Participant populations varied and included 46.2% non-diabetic individuals (7.5% athletes), 36.6% individuals with type 1 diabetes mellitus, and 17.2% individuals with type 2. The upper arm was the most common sensor placement site (41.9%), although nearly one-third of studies did not report placement details. Devices were primarily from Abbott (40.9%), Medtronic (36.6%), and Dexcom (26.9%). Sample sizes were typically small, with 40.9% of studies including 10-14 participants. Reporting practices frequently deviated from the International Consensus Statement on CGM Metrics for Clinical Trials. Many studies used modified or non-standard metrics, whereas "mean sensor glucose" was reported in compliance with consensus recommendations in 58.1% of studies. Regarding data completeness, "data gaps" was the most frequently reported consensus-compliant metric (43.0%). In validation studies, accuracy metrics predominated, with "absolute relative difference" representing the most common outcome (87.5%). Overall, substantial heterogeneity limits comparability across studies, highlighting the need for standardized CGM reporting.

Functional secondary hypogonadism is frequent in men with obesity, metabolic syndrome, and type 2 diabetes mellitus (T2DM), but whether testosterone replacement therapy (TRT) produces clinically relevant metabolic benefits remains uncertain. This systematic review evaluated double-blind randomized placebo-controlled trials of TRT in obese men with functional secondary hypogonadism and either T2DM or metabolic syndrome.

PubMed and Scopus were searched up to May 2026. Eligible studies enrolled adult men with biochemical hypogonadism and T2DM or metabolic syndrome, compared TRT with placebo, and reported metabolic outcomes. Open-label, single-blind, and non-randomized studies were excluded. Risk of bias was assessed with the Cochrane RoB 2 framework and certainty of evidence with GRADE.

Eight trials were included. The most consistent signal was improvement in body composition, mainly increased lean mass and reduced fat mass. Effects on insulin resistance were favorable in several trials but heterogeneous. GRADE certainty was low for fat mass, lean mass, and Homeostatic Model Assessment for Insulin Resistance (HOMA-IR), and it was very low for clamp-derived insulin sensitivity, HbA1c, fasting glucose, lipid outcomes, inflammatory and vascular surrogate markers, and long-term safety.

Low-certainty evidence suggests that TRT may improve body composition and HOMA-IR in carefully selected men with functional secondary hypogonadism and metabolic disease, whereas effects on glycemic and lipid outcomes remain very uncertain. TRT should not be regarded as an antidiabetic or lipid-lowering intervention. Larger phenotype-specific trials with longer follow-up are needed.

Background/Objective: Chronic obstructive pulmonary disease (COPD) and tuberculosis (TB) are among the most prevalent respiratory disorders worldwide and frequently coexist in the same patient. However, the contribution of active TB and post-tuberculosis lung disease to COPD exacerbations and long-term prognosis remains incompletely defined. This paper aim to evaluate the prevalence, clinical correlates, and prognostic significance of tuberculosis and its sequelae in patients with COPD. Materials and methods: We conducted a population-based retrospective cohort study using de-identified data from the regional healthcare information system. The cohort included all adults aged 18 years or older with a recorded diagnosis of COPD (ICD-10 code J44). Tuberculosis was identified by codes A15-A19 and B90. The primary outcomes were COPD exacerbations and all-cause mortality. Group comparisons, cluster analysis, Kaplan-Meier survival analysis, Cox proportional hazards modeling, and multivariable logistic regression were performed. Results: Tuberculosis and/or its sequelae were identified in 267 of 16,714 patients (1.60%): post-TB sequelae (B90) in 197 (73.8%), active TB (A15-A19) in 22 (8.2%), and both in 48 (18.0%). Compared with patients without TB, those with COPD-TB were younger (63.5 ± 14.2 vs. 65.7 ± 14.7 years; p = 0.018), more often male (75.3% vs. 52.0%; p < 0.001), and had higher mortality (16.5% vs. 10.6%; p = 0.003). COPD-TB was associated with bronchiectasis (OR = 6.07; 95% CI, 3.03-12.16), pulmonary fibrosis (OR = 5.67; 95% CI, 3.40-9.45), and pneumonia (OR = 2.01; 95% CI, 1.50-2.71), but with lower prevalences of obesity, diabetes mellitus, and hypertension. Patients with TB experienced more COPD exacerbations, including recurrent exacerbations. In multivariable models, tuberculosis was associated with COPD exacerbations after adjustment for age and sex (adjusted OR = 1.43; 95% CI, 1.05-1.96); this association was attenuated and lost significance after further adjustment for post-tuberculosis structural lung disease, indicating that it is largely mediated by post-TB sequelae. Tuberculosis remained associated with mortality after adjustment for available covariates, both in logistic regression (adjusted OR = 1.61; 95% CI, 1.14-2.28) and in Cox analysis (hazard ratio = 1.37; 95% CI, 1.01-1.85). Conclusions: Tuberculosis and post-tuberculosis lung disease are clinically accessible risk markers associated with COPD exacerbations and mortality. These findings support recognizing patients with COPD and a history of TB as a high-risk subgroup requiring intensified follow-up, proactive exacerbation prevention, and prioritized vaccination counseling. In the context of personalized medicine, a documented history of tuberculosis and post-tuberculosis lung changes represents a clinically accessible marker that can be used to stratify individual risk and to tailor monitoring and prevention in patients with COPD.

Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have rapidly evolved from glucose-lowering agents to central players in cardiovascular risk reduction. Evidence from landmark randomized controlled trials has established their capacity to reduce major adverse cardiovascular events, promote anti-inflammatory signaling, attenuate ischemia-reperfusion injury, and improve myocardial metabolic efficiency. As the prevalence of obesity, type 2 diabetes mellitus, and heart failure in the cardiac surgical population grows, GLP-1 RAs are increasingly encountered in the perioperative setting. Yet the cardiac surgery literature has yet to synthesize their emergent role coherently. This is a narrative review; no systematic review or meta-analysis was performed. This narrative review integrates mechanistic, clinical, and translational evidence to reframe GLP-1 RAs as potential perioperative cardioprotective agents in patients undergoing cardiac surgery. We examine receptor-level biology, evidence from the GLOBE randomized trial, observational data linking GLP-1 RA use to reduced postoperative atrial fibrillation after coronary artery bypass grafting, the rationale for the forthcoming REVERSE-TAVR trial, and evolving perioperative management guidelines. Key evidence gaps are identified, including the absence of prospective data in open cardiac surgery, aortic surgery, and high-acuity populations. We propose a research agenda and conceptual framework to guide future investigation into GLP-1 RAs as a new dimension of perioperative cardioprotection. The current evidence is hypothesis-generating; a definitive perioperative cardioprotective benefit has not yet been demonstrated in cardiac surgery populations, and these agents are presented here as potential rather than proven cardioprotective tools.

Depression ranks among the most prevalent mental health disorders worldwide. Numerous studies have linked the C-1019G (rs6295) polymorphism in the serotonin 1A (5-HT1A) receptor gene to increased susceptibility to depression. In this study, sociodemographic variables and clinical characteristics were integrated with targeted genotyping of the C-1019G polymorphism to identify risk factors associated with depressive symptoms in a Mexican cohort.

Sociodemographic and clinical data were collected from 257 volunteers (202 healthy controls, 55 with depressive symptoms). Genotyping for C-1019G was performed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Sociodemographic variables, clinical characteristics, and genotype frequencies were analyzed relative to Beck Depression Inventory II (BDI-II) scores.

BDI scores were significantly lower among males, participants aged < 40 years, unmarried individuals, and those with a high school education (p < 0.05). Females were three times more likely to exhibit depressive symptoms than males (p = 0.004; OR = 3.08). Compared with participants aged < 40 years, those aged 40-65 and >65 years were two (p = 0.026; OR = 2.19) and five times (p < 0.001; OR = 5.71) more likely to report depressive symptoms, respectively. Participants with type 2 diabetes mellitus had twice the odds of depressive symptoms (p = 0.025; OR = 2.38). Odds increased twelvefold among those with diabetes plus arterial hypertension (p < 0.001; OR = 12.25). Among males, the C/C genotype was observed exclusively in controls (p = 0.010). Furthermore, the genotypic distribution of this study population differed from that of European and Asian populations.

These findings advance the understanding of depressive symptoms' multifactorial etiology and may inform targeted screening and prevention strategies.

Diabetes Mellitus (DM) is a metabolic disorder characterized by chronic hyperglycemia resulting from the body's inability to produce insulin or effectively respond to it. In this review, we summarize the cellular and molecular mechanisms involved in common clinical manifestations of DM, including neuropathy, retinopathy, nephropathy, sensorineural hearing loss, cardiovascular disease, stroke, immune dysfunction, and chronic wounds. Common pathways explored in these dysfunctions include the polyol pathway, formation of advanced glycation end products (AGEs) and their interaction with the receptor for advanced glycation end products (RAGE), mitochondrial dysfunctions leading to overproduction of reactive oxygen species (ROS), and the chronic state of inflammation and inflammatory cytokines. Furthermore, we explore current and developing treatments for DM, along with more targeted therapies for the clinical manifestations of DM. In summary, this review gives a comprehensive overview of the pathways involved in the clinical manifestations of DM, and how these pathways are targets for therapeutics and treatments.

The cardiovascular effects of sodium-glucose cotransporter-2 inhibitors and dipeptidyl peptidase-4 inhibitors have attracted increasing interest in patients with type 2 diabetes mellitus. This study aimed to compare the time-dependent effects of empagliflozin and linagliptin on left ventricular diastolic function and global longitudinal strain (GLS).

This prospective longitudinal study included 350 patients with type 2 diabetes mellitus treated with empagliflozin (n = 200) or linagliptin (n = 150). Transthoracic echocardiography and speckle-tracking strain analysis were performed at baseline, 1 month, and 6 months. Diastolic function was evaluated using septal e' velocity, E/e' ratio, isovolumetric relaxation time (IVRT), and mitral E-wave deceleration time. Longitudinal changes were analyzed using linear mixed-effects models including treatment group, time, and group × time interaction.

Diastolic function parameters improved significantly over time in both groups (all P < .001). At follow-up, HbA1c levels decreased in both groups, with comparable glycemic control achieved at 6 months. Significant group × time interactions were observed for septal e' velocity, E/e' ratio, and IVRT (all P < .001). These findings remained consistent after adjustment for baseline differences. At 6 months, empagliflozin was associated with greater improvement in septal e' velocity and IVRT, whereas linagliptin resulted in a more pronounced reduction in the E/e' ratio. Although GLS improved in both groups, its temporal pattern differed significantly between treatments (P < .001).

Empagliflozin and linagliptin exert distinct effects on left ventricular diastolic function and myocardial deformation in type 2 diabetes mellitus. Empagliflozin appears to provide earlier improvement in diastolic relaxation and GLS, whereas linagliptin may have a greater effect on filling pressures. These findings should be interpreted cautiously and considered hypothesis-generating; confirmation in randomized controlled trials is required to determine their clinical relevance.

This study evaluates the clinical outcomes of surgical excision for upper extremity neuropathies caused by benign soft tissue tumours and investigates the impact of tumour characteristics on clinical presentation and postoperative outcomes.

We retrospectively reviewed 34 patients (mean age 45 years) who underwent surgical excision for tumour-related nerve compression between 2016 and 2020. Preoperative and 6-month postoperative assessments were performed using the Disabilities of the Arm, Shoulder, and Hand questionnaire and the visual analogue scale for pain.

The most common pathologies were lipoma (n = 13) and schwannoma (n = 7). Postoperatively, the median Disabilities of the Arm, Shoulder, and Hand score improved significantly from 41 (IQR, 30 to 52) to 15 (9 to 21). Similarly, the median visual analogue scale score decreased from 6.5 (5.0 to 7.0) to 2.0 (1.0 to 2.0). Preoperative motor neuropathy (n = 9), larger tumour volume and diabetes mellitus (n = 8) were significantly associated with worse postoperative functional scores (p < 0.05). No major complications or recurrences were observed at the 6 month follow-up.

Surgical excision of benign soft tissue tumours causing upper extremity neuropathy leads to significant functional improvement and pain reduction. Preoperative motor deficits, larger tumour volume and diabetes are significant negative prognostic indicators. This study provides an evidence-based framework for managing patient expectations regarding postoperative recovery.

IV.

Serotonergic antidepressants, particularly selective serotonin reuptake inhibitors (SSRIs), are associated with an increased risk of hyponatremia, whereas mirtazapine appears to confer a lower risk. However, evidence regarding newer antidepressants, specifically agomelatine, remains limited. This study aimed to evaluate the risk of hyponatremia associated with agomelatine compared with mirtazapine, escitalopram, and venlafaxine.

This retrospective cohort study analyzed electronic medical records from Kaohsiung Veterans General Hospital. Antidepressant-naïve patients who initiated at least 2 weeks of monotherapy with agomelatine, escitalopram, venlafaxine, or mirtazapine between May 2013 and April 2023 were included. Hyponatremia was identified using serum sodium measurements. Multivariable logistic regression was performed to assess the association between antidepressant use and hyponatremia after adjusting for demographic, clinical, and medication-related factors.

The incidence rates of hyponatremia were 5.8% for mirtazapine, 6.9% for agomelatine, 8.5% for escitalopram, and 10.2% for venlafaxine. In the univariate analysis, venlafaxine was associated with a higher risk of hyponatremia than was mirtazapine (odds ratio [OR] = 1.80, 95% CI: 1.09-2.97, p = 0.021). However, after adjustment, the risk of hyponatremia did not differ significantly among the antidepressants (agomelatine: adjusted odds ratio [aOR] = 0.79, escitalopram: aOR = 1.18, venlafaxine: aOR = 0.87; all p > 0.05). Independent predictors of hyponatremia included older age (aOR = 1.02, p < 0.001), malignancy (aOR = 2.52, p < 0.001), diabetes mellitus (aOR = 1.64, p < 0.001), and concomitant use of anticancer agents (aOR = 2.72, p < 0.001).

These findings underscore the complexity of hyponatremia etiologies and highlight the need for individualized treatment strategies that account for comorbidities and potential drug interactions.

This study aimed to systematically evaluate the impact of concurrent respiratory viral infections on the acute severity of diabetic ketoacidosis (DKA), long-term glycemic control, and residual pancreatic β-cell function in children and adolescents with newly diagnosed type 1 diabetes mellitus (T1DM), so as to provide an evidence-based basis for clinical management.

A total of 113 children and adolescents with newly diagnosed T1DM complicated by DKA were enrolled and divided into an exposed group (respiratory virus-positive, n=28) and a control group (no respiratory infection symptoms, virus-negative, n=85) based on virus detection results within 48 hours of initial diagnosis. Demographic, hospitalization, pancreatic β-cell function, DKA-related indicators, and T1DM autoantibodies were collected. All participants were followed up at 3 and 6 months to record HbA1c, insulin dosage, and DKA recurrence.

Results showed that the exposed group had significantly longer hospital stays, higher ICU admission rates, lower fasting C-peptide levels, higher incidences of severe DKA and cerebral edema, more severe acid-base imbalance and hyponatremia, greater 24-hour fluid volume, and longer DKA correction time (all P<0.05). Regardless of treatment with an insulin pump (n=75) or insulin pen (n=38), the exposed group had significantly higher HbA1c and lower serum C-peptide levels at follow-ups (P<0.05). Notably, the insulin pen subgroup in the exposed group had higher insulin dosage and DKA recurrence rate.

Concurrent respiratory viral infections significantly increase DKA acute severity, exacerbate pancreatic β-cell dysfunction, and impair long-term glycemic control in newly diagnosed pediatric T1DM, highlighting the need for prioritized virus screening, prevention, and optimized individualized treatment.