Worldwide, chronic hepatitis B and C infections remain a significant public health challenge, causing millions of cases of liver disease globally.
The objective of this article is to highlight the need for testing and monitoring hepatitis B and C virus infections using Real-Time PCR, as well as to analyze the implementation of strategies for the eradication of hepatitis in accordance with WHO targets for 2030.
This narrative review highlights the necessity, performance, advantages, limitations, and challenges of implementing Real-Time PCR testing in clinical practice and public health policies for hepatitis B and C.
The results show that Real-Time PCR has superior sensitivity and specificity in the early detection of active infection and monitoring of viral load, facilitating optimal therapeutic management. Serological testing retains its essential role in initial screening, identifying exposure to viruses. Vulnerable groups, including hemodialysis patients, people who inject drugs, HIV-positive patients, healthcare workers, and marginalized populations, have increased prevalence and require prioritization in testing. The main limitations reported include unequal access to PCR technology and potential technical errors. Proposed strategies for improving testing include expanding access to molecular techniques, awareness campaigns, standardization of protocols, and international collaborations to support screening and treatment.
The conclusions emphasize that integrating serological testing with Real-Time PCR and focusing on vulnerable groups are crucial for achieving the objectives.
Category Archives: Review
Polycystic ovary syndrome and infertility: A narrative review of diagnostic and therapeutic approaches
Objective: To synthesize current evidence on mechanisms, diagnostic evaluation, and treatment of infertility in PCOS, with emphasis on phenotype-specific implications and integrative management.
Methods: A narrative review was conducted using PubMed, Scopus, and Web of Science from January 2015 to March 2024. Search terms included “PCOS,” “infertility,” “phenotype,” “letrozole,” “metformin,” “gonadotropins,” and “ART.” Eligible studies involved human females aged 18–45 years, written in English, and focused on PCOS-related infertility. Randomized trials, meta-analyses, and international guidelines were critically assessed for methodological rigor and clinical relevance.
Results: PCOS accounts for 70–80% of anovulatory infertility, with marked variability across phenotypes. Phenotype A, combining hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology, carries the greatest reproductive and metabolic burden. Biomarkers such as AMH, testosterone, DHEAS, fasting insulin, and HOMA-IR improve risk stratification. Lifestyle modification restores ovulation in up to 60% of overweight patients. Letrozole is superior to clomiphene, while gonadotropins and ART are effective in resistant cases. Metformin enhances ovulatory and pregnancy outcomes in insulin-resistant women. IVF protocols using antagonists and agonist triggers improve safety by reducing ovarian hyperstimulation syndrome. Psychological comorbidities, particularly anxiety and depression, are frequent and negatively affect fertility outcomes.
Conclusion: PCOS-related infertility requires a personalized, multidisciplinary approach. Integration of phenotype-based assessment, biomarker evaluation, lifestyle intervention, and tailored reproductive strategies optimizes outcomes. Addressing metabolic and psychological dimensions further improves reproductive success and long-term health.
Sodium-glucose transporter 2 inhibitors and their antiarrhythmic role: New insights and future perspective
Sodium-glucose transporter 2 inhibitors have been identified as pleiotropic pharmacological agents with demonstrated efficacy in a wide range of pathologies. Given the strong association between arrhythmias and significant comorbidities, exploring the potential antiarrhythmic effects of sodium-glucose transporter 2 inhibitors represents a critical therapeutic opportunity, particularly considering the limited efficacy and adverse profile of current antiarrhythmic drugs. The antiarrhythmic mechanisms of sodium-glucose transporter 2 inhibitors operate through direct cardiac ion channel modulation. Along with the ion channel effects, sodium-glucose transporter 2 inhibitors improve gap junction coupling by modulating connexin-43, lower sympathetic tone, maximize mitochondrial function, and induce metabolic reprogramming through adenosine monophosphate-activated protein kinase/sirtuin 1 activation and autophagy enhancement. Translating these encouraging mechanisms into focused antiarrhythmic strategies still requires establishing clear cause-and-effect links between sodium-glucose transporter 2 inhibitor therapy and arrhythmia prevention. Nevertheless, the current evidence regarding these effects remains inconsistent, underscoring the necessity for further research to elucidate the underlying mechanisms and resolve existing controversies.
Autonomic modulation in ventricular arrhythmias: Clinical insights and therapeutic opportunities
Recent evidence establishes robust causal relationships between autonomic nervous system dysfunction and ventricular arrhythmias through multiple converging mechanisms. Direct neural recording studies demonstrate that sympathetic discharge from the left stellate ganglion immediately precedes ventricular fibrillation. At the same time, mechanistic investigations reveal that nerve growth factor-mediated sympathetic sprouting creates heterogeneous innervation patterns, directly triggering arrhythmogenesis. Although genetic syndromes like Brugada syndrome show opposing patterns with parasympathetic dominance driving arrhythmic events, disease-specific autonomic patterns have emerged, with heart failure and post-myocardial infarction displaying sympathetic overactivation and parasympathetic withdrawal. Current predictive tools show significant advances, but implementation challenges persist. The most clinically validated method is meta-iodobenzylguanidine imaging, and when using standardized protocols, heart rate variability analysis shows dependable prognostic value. Therapeutic interventions reveal mixed clinical outcomes. While beta-blockers remain effective in reduced ejection fraction populations, questions regarding benefits in preserved ejection fraction patients persist. Stellate ganglion blocks show promise for managing electrical storms, achieving a 62% reduction in ventricular arrhythmias. However, major clinical trials have yielded disappointing results for spinal cord stimulation and cardiac sympathetic denervation. Future directions emphasize personalized medicine approaches integrating genetic data, advanced imaging, and artificial intelligence for biomarker-guided therapy selection, representing the next frontier in precision cardiology for arrhythmia management.
Pharmacological management of intraoperative hypertensive crises in pheochromocytoma: A narrative review of esmolol, nicardipine, and sodium nitroprusside
Management of pheochromocytoma, particularly in the perioperative period, requires a tailored pharmacological approach to address hemodynamic instability and hypertensive crises. This review evaluates the safety, efficacy, and clinical context of esmolol, nicardipine, and sodium nitroprusside in managing blood pressure and heart rate during pheochromocytoma resection. Esmolol, an ultra-short-acting β1-adrenergic antagonist, is essential in controlling tachyarrhythmias and myocardial stress in the perioperative period. Its rapid onset and short half-life enable precise titration, though continuous monitoring is required to mitigate the risk of bradycardia and hypotension. Nicardipine, a dihydropyridine calcium channel blocker, is effective in controlling acute hypertensive episodes and maintaining coronary perfusion. Its selectivity for vascular smooth muscle makes it an ideal agent for patients with low ejection fraction, minimizing cardiac depression. In contrast, sodium nitroprusside, a direct nitric oxide donor, provides immediate and reversible vasodilation, which is crucial for managing hypertensive crises during surgery. However, its use necessitates close monitoring due to the risk of cyanide and thiocyanate toxicity with prolonged use.
Choosing the most appropriate antihypertensive therapy depends on patient-specific factors such as comorbidities and the severity of hemodynamic changes. Each medication’s therapeutic effect, side effects, and risk profiles should be carefully considered to optimize clinical outcomes in high-risk patients undergoing pheochromocytoma surgery. This review highlights the importance of understanding the pharmacodynamics and appropriate use of these agents in clinical practice to improve patient management and outcomes.
Point-of-care ultrasound in palliative care management of malignant pleural effusion in outpatients and nursing home residents: A narrative review
Early integration of palliative care for patients with malignant pleural effusion (MPE) significantly improves symptom control, quality of life, and reduces healthcare costs. Despite well-developed palliative care services in Romania, timely access to multidisciplinary care remains challenging, particularly in outpatient settings and nursing homes. Point-of-Care Ultrasound (POCUS) has emerged as a valuable diagnostic and therapeutic tool in managing malignant pleural effusions within various clinical settings, including hospitals, outpatient clinics, home care, and nursing homes. Its diagnostic advantages include high accuracy in identifying small effusions and differentiating malignant from benign conditions. Therapeutically, POCUS significantly enhances the safety and effectiveness of procedures such as thoracentesis, reducing complications and the need for hospital transfers.
This review highlights how POCUS aligns with key palliative care principles by alleviating patient burden and enhancing comfort. We advocate for its adoption as standard practice in both inpatient and outpatient palliative care, supported by targeted training and standardized protocols. Further studies should assess the long-term clinical benefits and economic implications of routine POCUS use in palliative care.
The impact of pharmacological agents on neuroinflammation in neurodegenerative diseases
Neuroinflammation plays a crucial role in the progression of age-related and chronic neurological diseases, including Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. This review examines the mechanisms of neuroinflammation by focusing on microglial and astrocyte activation, key signaling pathways such as NFκB and JAK/STAT, and metabolic disturbances that modulate inflammatory processes. Pharmacological treatments, including NSAIDs, minocycline, and statins, have demonstrated some efficacy; however, their therapeutic potential is often limited by suboptimal drug delivery to the target regions and variability in patient response. The review further highlights innovative pharmacologic strategies that modulate microglial function, moving beyond the outdated M1/M2 polarization models and embracing a more dynamic view of microglial plasticity, where activation depends on the local environment and disease context. Furthermore, state-of-the-art computational and experimental drug discovery techniques are leveraged to explore novel therapies. Additionally, natural compounds such as curcumin, resveratrol, and nootropics have shown potential in modulating neuroinflammation through diverse molecular pathways. Compounds were selected based on their demonstrated clinical relevance and ability to modulate neuroinflammation through well-defined molecular mechanisms. Excluded compounds like melatonin and cannabidiol were omitted due to limited clinical data on their efficacy and concerns about off-target effects.
Despite these promising advances, significant challenges remain, particularly in crossing the blood-brain barrier (BBB), which hinders drug bioavailability. Novel strategies, including nanoparticle-based delivery systems, receptor-mediated transcytosis, and focused ultrasound, are being explored to enhance drug bioavailability and cross the blood-brain barrier. Furthermore, the development of reliable biomarkers is essential for tracking treatment response in neurodegenerative diseases. Integrating biomarker-driven therapeutic strategies with emerging drug delivery technologies can lead to more precise, personalized treatment approaches tailored to individual patient needs. These efforts are particularly crucial, as neurodegenerative diseases are heterogeneous in their pathogenesis and progression. Future research should focus on these multidisciplinary approaches to bridge existing gaps in treatment and improve patient outcomes.
Utilization of lipoxins and other specialised pro-resolving mediators in the prevention and treatment of diabetic nephropathy and diabetic cardiovascular disease
Diabetes mellitus type 2 is a chronic disease caused by insulin resistance. Whilst first originating in the adipose tissue, this pathophysiological process later affects the muscles and the liver as well. This induces high plasma levels of glucose and fatty acids, leading to the inflammatory-related chronic complications of diabetes, such as diabetic nephropathy and diabetic cardiovascular disease. Specialized pro-resolving mediators are lipid mediators responsible for resolving inflammation and could therefore be beneficial in the management of chronic diabetes complications. The aim of this review is to assess if specialised pro-resolving mediators have the potential to attenuate the chronic complications of diabetes. Specialised pro-resolving mediators, especially lipoxins, can modulate both diabetic nephropathy and diabetic cardiovascular disease. In mice it was demonstrated that, at the glomerular level, lipoxins reduced collagen deposition and expression of pro-inflammatory markers. In human saphenous vein smooth muscle cells instead, lipoxins were able to reduce collagen deposition and vascular smooth muscle cells proliferation and chemotaxis. Aspirin is a medication that could be used to modulate specialised pro-resolving mediator levels, as aspirin triggered-specialised pro-resolving mediators exist. Aspirin triggered-specialised pro-resolving mediators are pro-resolving substances with similar effects, but synthetised in a different way, requiring the partial blockage of the cyclooxygenase 2 enzyme. These results demonstrate how such substances could be useful in the treatment of diabetic patients and why further research is needed to create efficient and economical medications.
The genetic landscape of early and late-onset Alzheimer’s disease: A review
Alzheimer’s disease(AD) is a multifactorial neurodegenerative disorder characterized by the progressive loss of neurons and synaptic dysfunction, primarily affecting the cortex and hippocampus. The etiology of AD is complex, involving the continuous and intricate interaction between genetic and non-genetic environmental factors. Genetic predisposition plays a significant role, with approximately 60-80% of AD risk attributed to hereditary factors. Familial early-onset AD(EOAD), with autosomal-dominant mutations in APP, PSEN1, and PSEN2, represents about 1-5% of cases and typically manifests before age 65. Rare autosomal-recessive mutations, like A673V(APP gene), are also implicated. Late-onset AD(LOAD), more common, is influenced by a combination of genetic and environmental factors, with the APOE ε4 allele being a major risk factor. Protective factors, such as the APOE ε2 allele and rare mutations like Ala673Thr, can reduce AD risk. The interplay between genetic variants, environmental influences, and pathological processes underpins the disease’s progression. This study highlights the importance of understanding the genetic and non-genetic determinants of AD to advance personalized treatment and early detection strategies. Future research and personalized medicine approaches are essential for mitigating AD risks and improving management outcomes.
The gut-skin axis: Investigating gut microbiota
dysbiosis in pemphigus and bullous pemphigoid
Gut microbiota dysbiosis has been linked with numerous autoimmune disorders and inflammatory skin pathologies. The present study is a narrative review aiming to examine dysregulations in the gut microbiota of patients with pemphigus and bullous pemphigoid, exploring how these alterations may contribute to diseases’ development and/or progression. Significant alterations in the composition of intestinal microbiota were identified in patients with pemphigus and bullous pemphigoid: reduction in short-chain fatty acid-producing bacteria: Faecalibacterium prausnitzii, Lachnospiraceae and Coprococcus spp., which are known for their anti-inflammatory effects, and increased abundance of Escherichia coli, Shigella spp., Klebsiella spp., Bacteroides fragilis and Flavonifractor spp., which are recognized for their pro-inflammatory impact. The composition of gut microbiota might influence the pathogenesis of autoimmune bullous diseases. Modified levels of bacteria could become innovative biomarkers for the detection of high-risk individuals, monitoring disease progression and predicting response to treatment. Furthermore, regulating bacterial levels might have therapeutic effects in diminishing inflammation and disease advancement, potentially serving as future therapeutic strategies.