Background The number of medication related hospital admissions and readmissions are increasing over the years due to the ageing population. Medication related hospital admissions and readmissions lead to decreased quality of life and high healthcare costs. Aim of the review To assess what is currently known about medication related hospital admissions, medication related hospital readmissions, their risk factors, and possible interventions which reduce medication related hospital readmissions. Method We searched PubMed for articles about the topic medication related hospital admissions and readmissions. Overall 54 studies were selected for the overview of literature. Results Between the different selected studies there was much heterogeneity in definitions for medication related admission and readmissions, in study population and the way studies were performed. Multiple risk factors are found in the studies for example: polypharmacy, comorbidities, therapy non adherence, cognitive impairment, depending living situation, high risk medications and higher age. Different interventions are studied to reduce the number of medication related readmission, some of these interventions may reduce the readmissions like the participation of a pharmacist, education programmes and transition-of-care interventions and the use of digital assistance in the form of Clinical Decision Support Systems. However the methods and the results of these interventions show heterogeneity in the different researches. Conclusion There is much heterogeneity in incidence and definitions for both medication related hospital admissions and readmissions. Some risk factors are known for medication related admissions and readmissions such as polypharmacy, older age and additional diseases. Known interventions that could possibly lead to a decrease in medication related hospital readmissions are spare being the involvement of a pharmacist, education programs and transition-care interventions the most mentioned ones although controversial results have been reported. More research is needed to gather more information on this topic.

The severe acute respiratory distress syndrome coronavirus-2 (SARS-CoV-2) Omicron variant (B.1.1.529) is spreading rapidly, even in vaccinated individuals, raising concerns about immune escape. Here, we studied neutralizing antibodies and T-cell responses to SARS-CoV-2 D614G (wildtype, WT), and the B.1.351 (Beta), B.1.617.2 (Delta), and B.1.1.529 (Omicron) variants of concern (VOC) in a cohort of 60 health care workers (HCW) after immunization with ChAdOx-1 S, Ad26.COV2.S, mRNA-1273 or BNT162b2. High binding antibody levels against WT SARS-CoV-2 spike (S) were detected 28 days after vaccination with both mRNA vaccines (mRNA-1273 or BNT162b2), which significantly decreased after 6 months. In contrast, antibody levels were lower after Ad26.COV2.S vaccination but did not wane. Neutralization assays with authentic virus showed consistent cross-neutralization of the Beta and Delta variants in study participants, but Omicron-specific responses were significantly lower or absent (up to a 34-fold decrease compared to D614G). Notably, BNT162b2 booster vaccination after either two mRNA-1273 immunizations or Ad26.COV.2 priming partially restored neutralization of the Omicron variant, but responses were still up to-17-fold decreased compared to D614G. CD4+ T-cell responses were detected up to 6 months after all vaccination regimens; S-specific T-cell responses were highest after mRNA-1273 vaccination. No significant differences were detected between D614G- and variant-specific T-cell responses, including Omicron, indicating minimal escape at the T-cell level. This study shows that vaccinated individuals retain T-cell immunity to the SARS-CoV-2 Omicron variant, potentially balancing the lack of neutralizing antibodies in preventing or limiting severe COVID-19. Booster vaccinations may be needed to further restore Omicron cross-neutralization by antibodies.

From the case history, as well as use of the Naranjo scale, we concluded that fluconazole was the highly probable cause of the development of torsade de pointes in our patient.

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