International Journal of Clinical Practice最新文献

Aims: Medication discrepancies during transitions of care pose substantial risks, particularly in older patients receiving complex medication regimens. Obtaining the best possible medication history (BPMH) is crucial to minimize this risk. This study aimed to evaluate the effectiveness of a pharmacist-led BPMH using various information sources including a nationwide medication history sharing program compared to conventional interviews in a tertiary hospital setting. In addition, we identified factors contributing to medication inaccuracies.

Methods: A single-center prospective study involving older patients scheduled for thoracic surgery at a tertiary hospital was conducted. Medication histories obtained through conventional interviews during the initial assessment on admission were compared with those obtained through BPMH by pharmacist-led interviews. Logistic regression analysis was used to identify factors associated with medication inaccuracies.

Results: This study included 216 patients, a significant proportion of whom were experiencing polypharmacy. The pharmacist-led BPMH approach demonstrated superior accuracy in documenting medication histories, with conventional methods showing inaccuracies in over 70% of the cases. Factors that significantly increased the likelihood of inaccuracies included the number of medications and number of prescribers. Nonoral and as-needed medications are particularly prone to inaccuracies.

Conclusions: Pharmacist-led BPMH significantly improved medication history accuracy compared to conventional methods, which had inaccuracies in over 70%. It is important to be careful when obtaining BPMH for older adults, particularly those with complex medication regimens, nonoral medications, or PRN medications, to enhance patient safety and reduce medication-related risks.

Trial Registration: Clinical Trial Registry identifier: KCT-006813.

Clostridium innocuum (CI) is an emerging pathogen associated with a diverse range of diseases. This review primarily delves into clinical studies pertaining to CI and its potential pathogenic mechanisms, aiming to provide guidance for future research endeavors on this topic.

Objective: To assess the association between polycystic ovary syndrome and pancreatic cancer in Taiwan.

Methods: We used the 2013–2020 claims data of Taiwan National Health Insurance Program. A case-control study was performed, including female subjects 20 years or older with and without pancreatic cancer. Cases comprised female subjects diagnosed with pancreatic cancer, identified based on diagnosis codes. Controls were selected from female subjects without pancreatic cancer and matched to cases on age and comorbidities. Polycystic ovary syndrome was identified through diagnosis codes. A conditional logistic regression model was used to assess the association between polycystic ovary syndrome and pancreatic cancer, with results presented as odds ratio (OR) and 95% confidence interval (CI).

Results: This case-control study included 12,466 cases with pancreatic cancer and 49,864 matched controls. The proportions of polycystic ovary syndrome were 2.6% among cases with pancreatic cancer and 1.4% among controls without pancreatic cancer (p < 0.001). After controlling for confounding factors, the conditional logistical regression model revealed a statistically significant association between polycystic ovary syndrome and pancreatic cancer, with an OR of 1.38 (95% CI = 1.21–1.59, p < 0.001).

Conclusion: This case-control study reveals that there is a statistically significant association between polycystic ovary syndrome and pancreatic cancer. More studies are needed to provide robust evidence.

Background and Aims: The impact of thiazide diuretics on cardiac remodeling and prognosis in heart failure remains uncertain. This study aims to investigate whether hydrochlorothiazide can improve cardiac function and remodeling by inhibiting oxidative stress.

Methods: The rat model of heart failure was established by ligating the left anterior descending branch of the coronary artery, and hydrochlorothiazide (12.5 mg/kg, ig, Qd) was administered by gavage for 6 weeks. The cardiac function was evaluated using echocardiography and hemodynamics. Various methodologies were used to evaluate the effects of hydrochlorothiazide on myocardial fibrosis, inflammation, oxidative stress, and apoptosis. The effects of hydrochlorothiazide were validated in vitro using H9c2 cell cultures. The binding mechanism of hydrochlorothiazide to carbonic anhydrase 2 (CAII) was investigated using molecular docking and dynamics simulations.

Results: The decreases in ejection fraction, fractional shortening, and left ventricular end-systolic pressure and the increases in left ventricular end-diastolic diameter, left ventricular end-diastolic pressure, and B-type natriuretic peptide in heart failure rats were improved by hydrochlorothiazide. Hydrochlorothiazide can reduce the expression of myocardial collagen I. In terms of oxidative stress, hydrochlorothiazide can decrease MDA, p47phox, and p67phox while increasing SOD2, total oxidation capacity, and mitochondrial respiratory chain complexes I and IV. Additionally, hydrochlorothiazide can inhibit the p38MAPK/JNK signaling pathway, leading to reduced expression of inflammatory markers (NF-ĸB p65) and apoptotic markers (Bax, caspase3, and cytochrome C). The possible mechanism involves hydrochlorothiazide inhibiting the expression of sodium hydrogen exchanger 1 (NHE1), which is an upstream molecule involved in oxidative stress. H9c2 cell culture further confirmed the effects of hydrochlorothiazide on oxidative stress, inflammation, and apoptosis. Molecular docking and dynamics simulation results demonstrated that hydrochlorothiazide directly binds to CAII forming an unstable conformation. Gene knockout studies showed that CAII knockout reduces the expression of NHE1, NCX1, p67phox, Bax, and NF-ĸB p65.

Conclusions: Hydrochlorothiazide can enhance cardiac function and mitigate cardiac fibrosis remodeling in rats with heart failure by reducing the oxidative stress and inhibiting the p38MAPK/JNK signaling pathway, wherein CAII and NHE1 play a crucial role.

Introduction: It is now known that the microbiota is far beyond the microbial communities living in certain parts of our body and functions like a metabolic organ. In addition, the microbiota, through its metabolites, is involved in the pathophysiology or progression of a wide range of diseases, from atherosclerotic diseases to metabolic diseases and even neurological diseases. Among these metabolites, trimethylamine n-oxide metabolite has been shown to be particularly effective in atherosclerotic heart diseases.

Materials and Methods: A total of 155 patients, who underwent coroner angiography for stable angina were included in the study. Of these patients, 81 patients with coronary artery ectasia (patient group) and 74 patients without coronary artery ectasia (control group) were evaluated for trimethylamine n-oxide metabolite.

Results: Statistically significantly higher trimethylamine n-oxide metabolite levels were observed in the coronary artery ectasia group compared to the control group.

Conclusion: The significantly higher trimethylamine n-oxide levels in patients with coronary artery ectasia without coronary artery disease suggest that the microbiota and its metabolites independently play a role in the pathophysiology or progression of vascular remodeling or endothelial dysfunctions. Also, its effect on the endothelial surface may depend on the threshold value.

Background: Recent evidence increasingly acknowledges the close interrelationship between immunity and gut microbiota (GM) in humans. Furthermore, previous studies have demonstrated a strong correlation between GM and gastroesophageal reflux disease (GERD). However, the specific impact of GM on immune factors in GERD remains largely unexplored. Therefore, we conducted the Mendelian randomization (MR) analysis to investigate the precise causal relationships and underlying mechanisms linking GM, immunity, and GERD.

Method: We employed the mediation MR utilizing summary statistics derived from Genome-Wide Association Study (GWAS) data to investigate the causal effects of 207 taxa and 205 bacterial pathways on GERD. The analysis concentrated on 731 immune cell traits as potential mediators. The inverse variance weighted (IVW) approach was the primary analytical method. To ensure robustness, we employed additional MR methods, including Bayesian weighted MR (BWMR), MR-Egger, Weighted Median, Weighted Mode, and Simple Mode. Furthermore, a series of sensitivity analyses, such as the Cochran’s Q test, leave-one-out test, MR-Egger intercept analysis, and MR-PRESSO test, were conducted to ensure the reliability and consistency of the findings.

Results: The study identified three taxa and eight bacterial pathways that exhibited a negative correlation with GERD. Mediation MR analyses indicated that four bacterial pathways influence GERD through four immune cell types acting as mediators. For instance, the “arginine, ornithine, and proline interconversion” pathway was implicated in reducing the risk of GERD via “PDL-1 on CD14- CD16+ monocyte” cells, with a total effect of −0.0484 and a mediation effect of −0.0093. Sensitivity analyses provided additional validation for the reliability of the MR findings.

Conclusion: Our study contributes evidence to the close causal relationship between the GM and GERD, emphasizing the possible role of immune cells as mediators. Future research should focus on developing microbiome-oriented therapeutic approaches for managing GERD.

Objective: Cardiovascular complications associated with COVID-19 are being increasingly recognized. They include potential long-term effects on the heart, although how these complications manifest in patients with stroke who are already vulnerable to cardiovascular issues is lacking. This study addressed this gap by investigating the influence of SARS-CoV-2 infection on cardiac hemodynamic changes in inpatients with stroke, thereby providing valuable insights into the management of cardiac complications in this population.

Methods: This retrospective cohort study enrolled inpatients with stroke who did or did not experience SARS-CoV-2 infection in Shenzhen Second People’s Hospital. Clinical information, hemodynamics data, serum myocardial enzyme levels, functional levels, including Barthel index, and Longshi scale assessment (bedridden, domestic, and community) were extracted from clinical records. An independent sample t-test and the Mann–Whitney U test were used for comparison between groups. Multiple logistic regression analysis was used to identify indicators associated with decline in cardiac function in patients with stroke post-COVID-19.

Results: Eighty-three patients with stroke (average age of 66.0 ± 15.5 years) were recruited (42 patients in the study group and 41 in the control group). No significant difference in general characteristics was observed between the groups. The ejection fraction (EF, 56.45 ± 12.46 vs. 47.64 ± 14.76, p = 0.04) was decreased, and the end-diastolic volume (EDV, 142.74 ± 80.00 vs. 193.34 ± 140.17, p = 0.001) was increased significantly in patients infected with SARS-CoV-2 compared with the noninfected participants. SARS-CoV-2 infection was an independent risk factor for EF (−10%) decrease (OR: 5.205, 95% CI: 1.621–16.720, p = 0.006). The risk of cardiac function decline among bedridden infected patients was 15.43 times higher than that of uninfected nonbedridden patients (OR: 15.430, 95% CI: 1.402–169.805, p = 0.025).

Conclusion: Patients who are bedridden after stroke face a higher potential risk of cardiac hemodynamic impairment following SARS-CoV-2 infection, emphasizing the need for meticulous hemodynamic monitoring during treatment and rehabilitation of these patients to prevent any potential cardiovascular complications.

Trial Registration: ClinicalTrials.gov identifier: ChiCTR2300071376.

Objective: Recent trends involving increased screening have led to broad populations being diagnosed with atypical ductal hyperplasia (ADH) or ductal carcinoma in situ (DCIS); as a result, many patients have had to receive surgery followed by standard treatment for ADH or DCIS. The common interest in reducing the use of superfluous invasive treatment has led us to question the necessity of surgical treatment for ADH or DCIS patients in a retrospective review. This work is expected to be a particularly useful reference as there have yet to be any studies describing the outcomes of initial treatment with tamoxifen without curative surgery in Korea.

Methods: The clinicopathological characteristics and oncologic outcomes of 36 patients with DCIS or ADH diagnosis who received initial treatment with tamoxifen between 2013 and 2019 were investigated.

Results: Among 36 patients enrolled, 30 were diagnosed with DCIS and six were diagnosed with ADH. The median age in the included cohort was 47 years old (range, 26–81 years). There was a change in the follow-up strategy including the need for surgery in 13.9% of cases. The median time to surgery in those patients was 32 months (IQR, 17.5–63.5 months). Only one patient had upgraded to a higher nuclear grade, which was a case of ADH upgrading to intermediate DCIS. Three (8.3%) of 36 patients were upstaged to an invasive disease. Of them, two patients were upstaged to microinvasive ductal carcinoma, whereas one patient was diagnosed with metastatic invasive ductal carcinoma.

Conclusion: The use of endocrine therapy without surgery could be a potential treatment strategy in patients with DCIS or ADH. Further validation in larger cohorts and in the context of clinical trials is needed.

Introduction: The aim of this study was to evaluate the potential biomarkers of bacterial translocation: lipopolysaccharide-binding protein (LBP) and soluble CD14 subtype (sCD14-ST), and intestinal wall damage: intestinal fatty acid binding protein (I-FABP), zonulin, and regenerating islet-derived protein-3α (REG3α), in the patients with multiple organ dysfunction syndrome (MODS).

Methods: The study involved 78 patients over the age of 18 with MODS set according to the Sequential Organ Failure Assessment (SOFA) scale. Venous blood was sampled during diagnostics of MODS, on the 3rd and on the 7th day of its development. The sCD14-ST, LBP, I-FABP, REG3α, and zonulin in blood serum were determined by enzyme-linked immunosorbent assay (ELISA).

Results: Out of 78 patients with MODS, 43 patients survived (55.1%) and 35 patients died (44.9%). Levels of sCD14-ST on Day 1, I-FABP on Day 3, and REG3α on Days 3 and 7 and SOFA scores on Days 1, 3, and 7, Acute Physiology and Chronic Health Evaluation II (APACHE II) scores on Days 1, 3, and 7, and Modified Nutrition Risk in Critically Ill (mNUTRIC) scores on Days 1, 3, and 7 were statistically significantly higher in deceased patients (p < 0.05).

Conclusion: In patients with MODS, an increase in sCD14-ST, I-FABP, and REG3α in blood serum can indicate the violation of intestinal barrier function and increased bacterial translocation, which ultimately may aggravate the severity of MODS and increase the risk of death. It is required to further study the factors leading to intestinal wall permeability disorders in order to screen for timely intensive care measures that can help reduce the stay of patients in the intensive care unit (ICU) as well as mortality.

Trial Registration: ClinicalTrials.gov identifier: NCT06221293

Background. Extracellular vesicles, particularly those derived from stem cells, have demonstrated promising potential in osteoarthritis in recent years. However, there has been no bibliometric analysis focusing on the relationship between extracellular vesicles and osteoarthritis. This study aimed to investigate trends and hotpots of publications on extracellular vesicles in osteoarthritis. Methods. This study collected publications on extracellular vesicles in osteoarthritis from the Web of Science Core Collection database, focusing on English-language articles and reviews. Quantitative and visual analysis was performed using Microsoft Excel, R shiny, SCImago Graphica, VOS Viewer, and CiteSpace. The data set comprised information on keywords, authors, institutions, journals, and the country or region of the included literature. Journal impact factors and H-index values were obtained from the 2021 Journal Citation Reports and SJR-International Science Ranking. Furthermore, we conducted a frequency analysis of annual publications number and fitting curves of the growth trends in the publications. Moreover, we conducted a citation burst analysis of the top 20 keywords and a related bibliometric analysis (word frequency analysis and cocitation analysis) using CiteSpace. Results. A total of 715 documents were analyzed. The number of publications increased annually from 2012 to 2022. China had the highest number (n = 394, 55.1%) of publications and total citations during the decade, followed by the United States (n = 105, 14.7%). Shanghai JiaoTong University contributed the highest number of publications (n = 28, 3.9%). Wang Y has the highest number of publications (n = 40, 5.6%), and Stem Cell Research & Therapy is the journal with the highest number of publications (n = 64, 9.0%). The hotspots of extracellular vesicle research in recent years are umbilical cord blood, drug delivery, and scaffolds. Conclusion. Our findings indicate an increase in publications on the topic in utilizing extracellular vesicles in the context of osteoarthritis. Extracellular vesicle therapy for cartilage regeneration and repair of bone defects in osteoarthritis holds significant potential. Future research will focus on the development of novel drug delivery systems that utilize extracellular vesicles, the creation of novel biomaterials that incorporate extracellular vesicles, and the potential of extracellular vesicles as early diagnostic markers of disease.