Diana Patraș

The global elimination of hepatitis C virus (HCV) has been prioritized by the World Health Organization (WHO) as a key public health target, with a deadline set for 2030. This initiative aims to significantly reduce both new infection rates and HCV-associated mortality. A major breakthrough in achieving this goal has been the development of direct-acting antiviral agents (DAAs), which offer cure rates exceeding 95%, along with excellent safety and tolerability. Nevertheless, transmission via parenteral routes continues to be the dominant pathway, particularly among high-risk groups, such as individuals who inject drugs, incarcerated populations, those exposed to unsafe medical practices, and healthcare professionals. Identifying, monitoring, and delivering tailored interventions to these groups is crucial to interrupt ongoing transmission and to reduce the burden of chronic liver disease. On a global scale, several nations have demonstrated measurable progress toward HCV elimination, with some nearing the targets set by WHO. These achievements have largely resulted from context-adapted policies that enhanced diagnostic and therapeutic access while emphasizing outreach to vulnerable communities. This review synthesizes current advancements in HCV prevention and control and proposes strategic frameworks to expedite global elimination efforts.

Psychiatric disorders, chronic obstructive pulmonary disease (COPD), and type 2 diabetes (T2D) share common mechanisms, including neuroinflammation, oxidative stress, systemic inflammation, and gut microbiota alterations. This literature review evaluates key molecular and clinical intersections across these diseases. Analyzing peer-reviewed studies (2020–2025) from databases like PubMed and Scopus, our findings highlight oxidative stress and systemic inflammation as major drivers of disease progression, with hypoxia-induced neuroinflammation and gut dysbiosis emerging as critical factors. Early psychiatric screening in COPD and T2D patients is essential, alongside precision medicine approaches such as biomarker diagnostics and microbiome-based therapies. Addressing inflammation and autonomic dysfunction could help break the cycle of disease progression. This study advocates for a multidisciplinary healthcare approach, emphasising integrated, patient-centered management strategies.

Iron deficiency (ID) is a common comorbidity in heart failure (HF), affecting nearly 50% of patients and worsening symptoms, exercise capacity, and prognosis. This review summarizes recent evidence from meta-analyses, clinical trials, and guidelines on the pathophysiology, diagnosis, and treatment of ID in HF. ID in HF results from chronic inflammation, intestinal congestion, and impaired iron metabolism. Diagnosis is based on serum ferritin and transferrin saturation (TSAT) levels. While oral iron therapy has limited efficacy, intravenous iron, particularly ferric carboxymaltose and ferric derisomaltose, improves symptoms and exercise tolerance and reduces hospitalizations. Timely diagnosis and treatment of ID in HF are essential. Intravenous iron is the preferred therapeutic approach, but further research is needed to optimize long-term management.

Chronic obstructive pulmonary disease (COPD) and type 2 diabetes mellitus (T2DM) are highly prevalent chronic conditions, frequently coexisting due to their shared pathophysiological mechanisms and risk factors. Epidemiological studies estimate that up to 30% of COPD patients have comorbid T2DM, contributing to worsened disease progression, more hospitalizations, and higher mortality rates. Systemic inflammation in COPD contributes to insulin resistance by increasing pro-inflammatory cytokines (TNF-α, IL-6, and CRP), which impair glucose metabolism and beta-cell function. Conversely, hyperglycemia in T2DM exacerbates oxidative stress, leading to endothelial dysfunction, reduced lung function, and impaired pulmonary repair mechanisms. A comprehensive narrative review was conducted to evaluate the interplay between COPD and T2DM, examining shared pathophysiological mechanisms, clinical consequences, and management strategies. The co-occurrence of COPD and T2DM accelerates disease development, elevates hospitalization rates, and deteriorates overall prognosis. Pharmacological interactions complicate illness treatment, requiring a multidisciplinary therapy strategy. Recent data underscore the need to integrate palliative care, facilitate shared decision-making, and provide psychological support to enhance patient outcomes. Efficient therapy of COPD-T2DM comorbidity necessitates a customized, interdisciplinary strategy that targets both respiratory and metabolic health. Preliminary prognostic dialogues, palliative care, and holistic lifestyle modifications can improve patient quality of life and clinical results.