Background: Non-alcoholic fatty liver disease (NAFLD), now termed metabolic dysfunction-associated steatotic liver disease (MASLD), is a common chronic liver condition with significant metabolic and cardiovascular implications. Although sodium-glucose cotransporter 2 inhibitors (SGLT2i) have demonstrated hepatic benefits in diabetic populations, their role in non-diabetic individuals with NAFLD remains unclear. Objective: This meta-analysis aimed to evaluate the effects of SGLT2 inhibitors in non-diabetic NAFLD/MASLD patients. Methods: PubMed, Embase, and CENTRAL were searched up to May 2025 for randomized controlled trials (RCTs) comparing SGLT2i with placebo or other pharmacologic agents in non-diabetic adults with NAFLD. Primary outcomes included changes in hepatic function; secondary outcomes assessed anthropometric, metabolic, and imaging-based markers of hepatic steatosis and fibrosis. A random-effects model was applied to estimate pooled mean differences (MDs) and 95% confidence intervals (CIs). Results: Five RCTs comprising 273 non-diabetic patients (142 in the SGLT2i group) were included. SGLT2i significantly improved liver enzymes: AST (MD = -2.03; 95% CI: -3.24 to -0.82; p < 0.01), ALT (MD = -4.50; 95% CI: -6.89 to -2.10; p < 0.01), and GGT (MD = -4.12; 95% CI: -6.87 to -1.37; p < 0.01). Modest but significant reductions were also observed in body weight (MD = -3.24 kg), BMI (MD = -1.02 kg/m²), and waist circumference (MD = -3.12 cm). However, SGLT2i did not significantly affect triglycerides, HbA1c, fasting glucose, liver stiffness, CAP scores, or FIB-4 index. Conclusion: SGLT2i significantly improves liver enzyme levels and anthropometric markers in non-diabetic individuals with NAFLD/MASLD, suggesting potential therapeutic benefits. However, their effects on hepatic steatosis resolution and fibrosis progression remain inconclusive. Graphical

The current therapy for resistant hypertension is often limited by hyperkalemia, renal decline, and a failure to prevent compensatory increases in circulating aldosterone. The aldosterone synthase inhibitors (ASIs) address these limitations by directly suppressing aldosterone biosynthesis sparing other steroid pathways. To evaluate the safety and efficacy of ASIs in resistant hypertension. Databases searched through March 2026 to find relevant studies, following PRISMA guidelines. Data analysis was performed using R-Software. Primary outcome analyzed was reduction in systolic and diastolic blood pressures. A total of 8 RCTs were analyzed which showed that Aldosterone Synthase Inhibitors (ASI) significantly reduced systolic blood pressure (MD:8.0; 95% CI:10.53, -5.47, p < 0.01) and diastolic blood pressure (MD:3.44; 95% CI:5.03, -1.86, p < 0.01) and with double the likelihood of achieving target SBP < 130 mmHg (RR: 2.26; 95% CI: 1.73, 2.95, p = 0.002). ASI were associated with significant risk of any adverse events (RR: 1.23; 95% CI: 1.08, 1.41, p = 0.02), hyponatremia (RR: 2.04; 95% CI: 1.10, 3.80, p = 0.024), hypotension (RR: 2.47; 95% CI: 1.14,5.33, p = 0.02), and notably seven-fold increase risk of hyperkalemia (RR: 7.18; 95% CI: 3.20, 16.12, p < 0.001). Despite these risks, there was no statistically significant increase in serious adverse events (RR: 1.26; 95% CI: 0.68, 2.34, p = 0.47) and drug discontinuation rate (RR: 1.84; 95% CI: 0.41, 8.12, p = 0.28) with ASIs compared to placebo. Mechanistically, ASI was associated with a significant reduction in aldosterone (SMD:1.12; 95% CI:1.25, -1.0; p < 0.01), reduction in eGFR (MD:6.48; 95% CI:9.02, -3.94, p < 0.01) and an increase in plasma renin activity (SMD: 0.53; 95% CI: 0.37, 0.68, p < 0.01) associated with significant increase in serum potassium level(MD:0.47; 95% CI:0.34, 0.61; p < 0.01). Aldosterone synthase inhibitors (ASI) provide clinically meaningful reductions in systolic and diastolic blood pressure in uncontrolled or resistant hypertension, doubling the likelihood of achieving target blood pressure levels, with treatable safety concerns which is evidenced by non-significant trend in serious adverse events and drug discontinuation rate.

Acne vulgaris is a chronic inflammatory disease and is one of the leading causes of dermatological morbidities among young adults. Doxycycline is widely recommended as first-line therapy for moderate to severe acne; however, its use is limited. To systematically compare the efficacy and safety of oral azithromycin pulse therapy versus doxycycline in patients with moderate to severe acne vulgaris. This systematic review and meta-analysis followed PRISMA guidelines. A comprehensive literature search on different databases was performed. Two reviewers independently screened studies, extracted data, and assessed risk of bias. Mean differences (MDs) and risk ratios (RRs) with 95% confidence intervals (CIs) were pooled using random-effects models based on heterogeneity. A total of 23 comparative studies comprising 2,769 patients were included. Pooled analysis demonstrated a statistically significant improvement in global acne severity favoring azithromycin (GAGS reduction: MD 1.81; 95% CI 1.28-2.34; I² = 0%). Azithromycin achieved a significantly greater reduction in non-inflammatory lesion counts (MD -7.56; 95% CI -14.33 to -0.79). No significant differences were observed in inflammatory lesion reduction (MD 1.08; 95% CI -0.03 to 2.18). Oral azithromycin pulse therapy appears to have similar efficacy, better tolerability, and fewer side effects as compared to doxycycline.

Background: Chagas disease (CD) remains a significant public health problem and may progress to Chagas cardiomyopathy (ChCM), a distinct inflammatory–fibrotic myocardial phenotype characterized by a high burden of atrial fibrillation (AF) and conduction system abnormalities. Updated estimates of the prevalence of these electrical disturbances are essential to inform clinical risk stratification and guideline development. Objective: This updated meta-analysis aimed to evaluate the prevalence of AF and Conduction Abnormalities in ChCM. Methods: We conducted a comprehensive systematic review and meta-analysis of 33 studies published through February 2025, comprising 17,100 participants, of whom 6,644 had ChCM. The prevalence of AF and conduction abnormalities was evaluated in individuals with ChCM compared with non-Chagas controls, including healthy individuals and patients with CD and non-ChCM. Pooled estimates were generated using random-effects models, with formal assessment of between-study heterogeneity and publication bias. The review protocol was prospectively registered in PROSPERO (CRD420251005184). Results: AF was significantly more prevalent in ChCM (9.9%) than in controls (6.6%; OR = 1.88, 95% CI: 1.46–2.42). Among patients with cardiomyopathy, AF was more frequent in CD patients (12.1% vs. 9.5%; OR = 1.31, 95% CI: 1.07–1.60). Compared with ischemic cardiomyopathy, ChCM was associated with a higher AF risk (OR = 1.55; 95% CI: 1.13–2.12), whereas no difference was observed with dilated cardiomyopathy. Other conduction abnormalities were markedly more common in ChCM: first-degree atrioventricular block (OR = 2.71, 95% CI: 1.66–4.44), right bundle branch block (isolated or with left anterior fascicular block), and second-degree atrioventricular block. Conclusions: This updated meta-analysis demonstrates that Chagas cardiomyopathy is associated with a higher prevalence of atrial fibrillation and conduction abnormalities compared with other cardiomyopathy subtypes. These findings highlight the distinctive arrhythmogenic profile of Chagas cardiomyopathy and support the need for systematic electrocardiographic surveillance and heightened clinical awareness in affected patients. Future studies are warranted to define thromboembolic risk better, optimize rhythm management, and inform disease-specific strategies to reduce morbidity and mortality in populations affected by Chagas disease.

Atherosclerotic cardiovascular disease remains a leading cause of death globally. Cholesteryl ester transfer protein (CETP) inhibitors have been proposed as a novel strategy for cardiovascular risk reduction, yet evidence remains inconsistent. PubMed, EMBASE, and Scopus were searched for randomized controlled trials comparing CETP inhibitors with placebo in patients with atherosclerotic cardiovascular disease. Random-effects models were used to pool risk ratios (RRs) and mean differences (MDs) with 95% confidence intervals (CIs). Heterogeneity was assessed using I ² statistics. Statistical analysis was performed using R software version 4.3.3. We included 5 RCTs involving 62,565 participants, of whom 31,698 (50.7%) received CETP inhibitors. Compared with placebo, CETP inhibitors showed no significant reduction in death from coronary heart disease (RR: 0.91; 95% CI, 0.82 to 1.01), unplanned coronary revascularization (RR: 0.91; 95% CI, 0.79–1.05), nonfatal myocardial infarction (RR: 0.94; 95% CI, 0.87–1.02), and stroke (RR: 1.02; 95% CI, 0.93–1.12). In addition, no excess risk of adverse events was observed (RR: 1.00; 95% CI, 0.99–1.02). Conversely, HDL-C (MD: +130.82%; 95% CI, 121.49–140.15), LDL-C (MD: −32.68%; 95% CI, −40.73 to −24.63), ApoA1 (MD: +45.04%; 95% CI, 40.51–49.57), and Apo B (MD: −17.26%; 95% CI, −20.51 to −14.00) showed significant improvement. CETP inhibitors produce substantial lipid modifications but do not reduce major adverse cardiovascular events, underscoring the limitations of surrogate lipid markers and the need for outcome-based validation of lipid-modifying therapies.