Hamad Medical Corporation

Synthesised evidence on the formal recognition of advanced community pharmacists (ACPs) and their practice is limited. This review aims to explore global evidence on the practice of formally recognised ACPs. This scoping review followed the JBI Manual for Evidence Synthesis and PRISMA guidelines. Advanced practice was determined using the International Pharmaceutical Federation framework encompassing four pillars: professional practice, leadership, research, and education. Formal recognition referred to post-registration acknowledgement by authorised bodies. Twelve databases and Google Scholar were searched between 2004 and 2024, without country or language restrictions. Findings were thematically analysed using NVivo 14. Sixty-three studies from six high-income countries were included, predominantly from Canada (n=18) and the United States (n=16). Formally recognised ACPs provided clinical services including prescribing (n=27), vaccination (n=22), and medication review (n=20). Few studies reported ACPs practice within the research and education pillars. There was variation in the definition and formal recognition mechanisms of ACPs between studies. In addition, many studies reported practice corresponding to advanced services but did not describe prerequisite training or formal recognition. Reported challenges included inadequate remuneration, limited access to patient records, and low stakeholder awareness. Key facilitators were availability of formal recognition, interprofessional relationships, and appropriate training. ACPs have expanded public access to clinical services. However, formal recognition and practice of ACPs from low-middle-income-countries are underrepresented in the literature. More work is needed to recognise ACPs' practice in education and research. Future research should clearly operationalise advanced practice within existing frameworks, explicitly report recognition mechanisms, and engage broader stakeholders in the implementation, evaluation, and role development of ACPs.

Introduction: Emotional abuse and neglect are among the most underestimated forms of child maltreatment, carrying serious long-term mental health consequences. This meta-analysis synthesizes evidence on the prevalence, risk factors, and outcomes of emotional abuse and neglect among children in Arab countries. Methods: We systematically searched PubMed, Scopus, Web of Science, and the Cochrane Library, from inception to May 2025, for studies reporting emotional abuse or neglect in Arabian children. Eligibility criteria included studies reporting prevalence, risk factors, or consequences in participants <20 years; studies not assessing emotional abuse or neglect or conducted in conflict settings were excluded. Risk of bias was assessed using the Newcastle–Ottawa Scale. Synthesis of results was performed using random-effects meta-analysis. Results: A total of 41 studies, predominantly cross-sectional and mainly from Saudi Arabia and Egypt, were included, representing 50,862 individuals. Lebanon (64%) and Yemen (63%) reported the highest rates of emotional abuse, with a pooled prevalence of 46% (95% confidence interval [CI]: 35%–56%; I 2 = 99.9%). Emotional neglect was most common in Tunisia (61%), with a pooled prevalence of 42% (95% CI: 33%–51%). Significantly identified risk factors included parental divorce, low parental education levels, and exposure to violence. Behavioral disorders, suicidal ideation, and physical harm were frequently reported outcomes. Conclusion: The prevalence of emotional abuse and neglect among children in Arab countries is high, comparable to or exceeding that of other global regions. Culturally grounded preventive strategies, including parent education and strengthening protective systems, are needed to safeguard children’s well-being.

Background: Statins are central to primary and secondary prevention of atherosclerotic cardiovascular disease but are often underutilized due to myopathy and intolerance. While individual pharmacogenetic (PGx) variants, particularly in SLCO1B1, are linked to statin-associated muscle symptoms, the real-world impact of both clinical and cumulative PGx burden on regimen modification and adverse outcomes remains unclear. We aimed to evaluate the existing uncertainty regarding whether combined PGx scores can effectively guide statin dose titration and regimen modification, thereby filling a key clinical gap. Methods: A retrospective cohort study of 911 statin-treated patients with coronary artery disease was conducted from the Qatar Cardiovascular Biorepository with available whole-genome sequencing data. Variants in SLCO1B1, ABCG2, and CYP2C9 were combined into a functional PGx burden score, and their associations with statin regimen modification, intolerance, myopathy, liver injury, adherence, and composite adverse events were evaluated. The composite adverse events were defined as the occurrence of any statin-related adverse event, including statin-associated myopathy, liver injury, or poor medication adherence, during the follow-up period. Patients were classified as having experienced the composite outcome if at least one of these events occurred. Results: Over 12 months following statin initiation, 10.2% of patients underwent dose escalation, 11.4% de-escalation, and 78.4% remained on the same regimen. PGx burden is not statistically significantly associated with statin intolerance (OR 1.14; 95% CI: 0.73-1.76), composite adverse outcome (OR 1.08; 95% CI 0.82-1.42), or time to regimen change (HR 1.02; 95% CI 0.77-1.35). However, higher PGx burden showed a directional tendency toward dose de-escalation (RRR 1.18, 95% CI 0.76-1.84) and lower likelihood of escalation (RRR 0.93, 95% CI 0.56-1.54). Conclusions: Clinical factors, particularly statin intensity and myopathy, were the primary determinants of regimen modification. The PGx burden contributes to vulnerability to statin-related adverse effects in a context-dependent manner but does not independently drive statin regimen modification in routine clinical practice. Prospective studies are warranted to assess the clinical utility of PGx-guided workflows in statin therapy.

Acute respiratory distress syndrome (ARDS) remains a leading cause of mortality among critically ill patients with COVID-19. Inhaled nitric oxide (iNO), a selective pulmonary vasodilator, is often used as rescue therapy to improve oxygenation; however, its impact on survival remains uncertain. To evaluate the clinical outcomes of iNO therapy in patients with COVID-19-related ARDS and to stratify patients into Early, Delayed, and Non-Responder groups based on the timing of their oxygenation response. A retrospective cohort study of 99 patients with COVID-19-related ARDS who received iNO was conducted. Patients were categorized as. ≥20% improvement in the PaO2/FiO2 ratio within 8 h. ≥20% improvement in the PaO2/FiO2 ratio between 8 and 24 h. <20% improvement in the PaO2/FiO2 ratio within 24 h, including those who showed in their PaO2/FiO2 ratio within 24 h of iNO initiation.Baseline demographics, comorbidities, and outcomes, including duration of mechanical ventilation, ICU and hospital length of stay, and mortality, were compared. Early and Delayed Responders showed significant improvement in oxygenation (mean PaO2/FiO2: 137.3 vs. 126.9 vs. 106.4; p = 0.004), with mean percentage increases of 65.3%, 56.6%, and 8.2%, respectively (p < 0.001). However, this did not translate into differences in ICU mortality (64.8%, 62.5%, and 71.4%, respectively; p = 0.81) or other hospital outcomes. Rates of acute kidney injury (AKI), methemoglobinemia, and other complications were comparable among the groups. iNO improved oxygenation in a subset of patients with COVID-19-related ARDS but did not reduce mortality. Stratification by timing of response highlights patient heterogeneity and supports response-guided, time-limited use of iNO in critical care.

Atopic dermatitis (AD) is a common, relapsing inflammatory skin disease driven by an immune imbalance, microbial dysbiosis, and skin barrier impairment, culminating in (neurogenic) inflammation and itch. We hypothesized that the neuropeptide and pruritogen endothelin-1 (ET-1) contributes to AD pathology by impeding skin barrier formation via its cognate receptor ETAR and TRPA1, a cation channel involved in neurogenic inflammation, pain, and itch. We utilized differentiated human keratinocytes and exvivo human skin organ cultures invitro to evaluate the impact of ET-1 on human skin barrier function. ET-1 effects were assessed at the RNA level by RT-qPCR and at the protein level by quantitative immunofluorescence microscopy. Barrier integrity was monitored using real-time cell analysis and transwell permeability assays. ET-1 markedly reduced cell resistance in differentiated keratinocytes, an effect abrogated by the ETAR antagonist bosentan. ET-1 significantly decreased expression of skin differentiation markers filaggrin and loricrin, and tight junction proteins occludin, claudin-1, and claudin-4, at mRNA and protein levels. ETAR-specific siRNA in combination with ET-1, rescued ET-1-mediated downregulation of filaggrin. Furthermore, TRPA1 antagonist HC-030031 abrogated the impairing effect of ET-1 on the skin barrier. We observed increased inflammatory responses of ET-1-stimulated keratinocytes, suggesting that the ET-1-initiated barrier disruption could be mediated by IL-6 and IL-1β and induced by TNF-α. Our findings suggest that a neurogenic inflammation axis ET-1/ETAR/TRPA1 contributes to skin barrier impairment in AD by repressing differentiation markers and tight junction proteins. Additionally, we demonstrate ETAR-blockage as a rational therapeutic modality for patients with AD.

Abdominal aortic aneurysms (AAAs) are a serious medical condition that may culminate in internal bleeding and death. Clinicians are expected to assess the rupture risk of AAAs accurately to determine the mode and timing of intervention. In general practice, AAA diameter and growth rate are used as rupture risk indicators. However, numerous cases have been reported where relying solely on these two AAA characteristics has proven insufficient, suggesting that other biomechanical factors deserve further consideration. This paper aims to investigate the involvement of disturbed hemodynamics in AAA rupture. Twenty-two AAA cases that had progressed to the point where surgical intervention was necessitated were assessed to examine the flow dynamics around the rupture sites. Using computational fluid dynamics (CFD), four key wall shear stress (WSS)-related hemodynamic parameters were calculated for each studied case, namely the time-averaged wall shear stress (TAWSS), oscillatory shear index (OSI), endothelial cell activation potential (ECAP), and relative residence time (RRT). CFD geometries were developed exclusively using patient computed tomography images, and simulations were run with general physiological boundary conditions to demonstrate a clinically practical, low-input CFD pipeline. The study found that analyzing the spatial distribution of the WSS-related hemodynamic parameters can be a powerful approach for predicting the site of rupture in AAAs. Low TAWSS and high OSI/ECAP/RRT regions (specifically within the ranges: TAWSS 0-0.5 Pa, OSI 0.35-0.5, ECAP 1.6-2.0 Pa-1, RRT 24-30) were found to be high-risk locations for rupture. Additionally, the simultaneous analysis of all four parameters was critical for rupture risk assessment.