Medicine最新文献

This retrospective study aimed to investigate differences in clinical characteristics between different antibody phenotypes in patients with dermatomyositis (DM). Two hundred and ninety-three patients with DM were included in this study from September 2018 to September 2023. We collected basic clinical data from the patients, using statistical methods to analyze the clinical characteristics, and used survival analysis and COX regression to assess the prognosis of the patients. In the 293 patients, the antibody distribution was as follows: antibody negative (50, 20.3%), anti-melanoma differentiation-associated gene 5 (MDA5) antibody (104, 42.3%), anti-transcription intermediary factor γ (TIF-γ) antibody (41, 16.7%), anti-complex nucleosome remodeling histone deacetylase (Mi2) antibody (28, 11.4%), anti-nuclear matrix protein 2 (NXP2) antibody (19, 7.7%), anti-small ubiquitin-like modifier activating enzyme (SAE) antibody (4, 1.6%). Interstitial pneumonia (P < .001), lung infection (P < .001), respiratory symptoms (P < .001), arthralgia (P < .001), and fever (P < .001) were more likely to be seen in patients with anti-MDA5 antibody. Malignancy (P < .001) and V-sign (P = .017) were more likely to occur in anti-TIF1-γ antibody positive patients. Anti-NXP2 antibody-positive patients showed more symptoms of muscle involvement, such as myasthenia (P = .002), myalgia (P = .003) and dysphagia (P = .001). In the analysis of prognosis, age at onset (hazard ratio = 1.096, 95% CI: 1.064-1.129, P < .001), fever (hazard ratio = 2.449, 95% CI: 1.183-5.066, P = .016), γ-glutamyl transferase level (hazard ratio = 1.005, 95% CI: 1.002-1.008, P < .001), eosinophil level (hazard ratio = 0.000, 95% CI: 0.000-0.324, P = .024), and complement 3 (C3) level (hazard ratio = 0.115, 95% CI: 0.023-0.575, P = .008) had a statistically significant effect on survival time. The clinical features of DM are associated with myositis-specific antibodies. At the same time, advanced age, fever, elevated γ-glutamyl transferase levels, and reduced C3 and eosinophil levels may be associated with poor prognosis in patients with DM. These data may provide useful information for clinical management of patients with DM.

Background: Carcinoembryonic antigen (CEA) and carbohydrate antigen 19-9 (CA19-9) are currently 2 major diagnostic biomarkers for gastric cancer (GC). The aims of study were to detect the expression of long intergenic nonprotein coding RNA 1133 (LINC01133), and to evaluate its diagnostic and prognostic value in GC. Furthermore, the clinical performance of the joint detection of LINC01133, CEA and CA19-9 was also evaluate in GC.

Methods: The data were collected from 156 GC, 96 chronic superficial gastritis, 77 chronic atrophic gastritis patients and 89 healthy controls. LINC01133 expression was determined by quantitative real-time PCR. Receiver operating characteristics analysis was used to evaluate the diagnostic value of LINC01133, CEA, CA19-9 individually and jointly. Kaplan-Meier method and log-rank test were used to conduct survival comparison analysis. Cox regression was used to screen the independent prognostic factors for GC.

Results: Serum LINC01133 expression was decreased in GC patients compared with chronic superficial gastritis, chronic atrophic gastritis and healthy controls, and had considerable diagnostic potential, and notably, the joint detection of LINC01133, CEA, and CA19-9 showed the highest diagnostic accuracy in distinguishing GC patients from healthy or gastritis patients. LINC01133 expression was associated with GC patients' CEA and CA19-9 levels, tumor size, differentiation, lymph node metastasis and tumor node metastasis stage. Low LINC01133 was associated with poor GC survival, and was an independent prognostic factor for GC.

Conclusion: Decreased serum LINC01133 had considerable diagnostic potential, and the joint detection of LINC01133, CEA, and CA19-9 might be a more efficient diagnostic strategy for GC patients. Reduced LINC01133 served as a prognostic biomarker to predict poor GC survival.

Diverticular disease is a common condition that has numerous complications. Understanding the impact of diabetes mellitus (DM) on these complications, especially diverticulitis, is crucial for optimizing patient care. This study aimed to determine the relationship between type II DM and the complications of colonic diverticulitis. A retrospective cohort study was conducted on 158 patients complaining of diverticulitis at Asir Central Hospital, Abha, Saudi Arabia, between January 2013 and December 2023. Data on gender, age, and chronic diseases, especially DM, were collected. Data retrieved regarding diverticulitis included the involved segment, complications, Hinchey classification, and management. We classified the patients into groups A for nondiabetics and B for diabetics. We analyzed the data using descriptive statistics, chi-square tests, t tests, and analysis of variance. Diabetic patients were significantly older than their nondiabetic counterparts. Diabetic patients showed a significantly higher complication rate (62.5%) and a higher degree of Hinchey classification compared to nondiabetic patients (43.7%). Furthermore, in comparison to individuals without diabetes, they were hospitalized for a considerably extended period (8.06 ± 7.38 days vs 5.26 ± 5.90 days, respectively). In addition, surgical intervention was observed to be considerably more common in patients with diabetes (46.9%) than in those without diabetes (16.5%). The study showed that DM adversely affected patients with diverticulitis. A greater incidence of complications and a higher category of Hinchey classification were associated with DM compared to nondiabetics. Additionally, diabetics underwent more surgical interventions and had longer hospital stays. Diabetics with diverticulitis require particular care to prevent severe complications.

While there is ample evidence indicating an increased occurrence of general neurological conditions among individuals with diabetes, there has been limited exploration into the cause-and-effect connection between type 2 diabetes (T2D) and specific neurological disorders, including conditions like carpal tunnel syndrome and Bell's palsy. We used Mendelian randomization (MR) approach to investigate the causal effects of T2D on 67 neurological diseases. We primarily utilized the inverse-variance weighted method for the analysis, and also employed the weighted median and MR-Egger methods in our study. To detect and correct potential outliers, MR-PRESSO analysis was used. Heterogeneity was assessed using Cochrane Q-values. The MR analyses found a possible relationship between T2D and a risk increase of 8 diseases at suggestive level of evidence (P < .05). Notably, among the positive findings that met the false discovery rate threshold, nerve, nerve root, and plexus disorders (odds ratio [OR] = 1.11; 95% confidence interval [CI] = 1.08-1.15); neurological diseases (OR = 1.05; 95% CI = 1.03-1.07) and carpal tunnel syndrome (OR = 1.10; 95% CI = 1.05-1.16) were identified. Our findings affirm a cause-and-effect association between T2D and certain neurological disorders.

Cardiovascular disease has become to the main cause of death in the patients with end-stage renal disease (ESRD), and anemia is associated with increased cardiovascular morbidity and mortality in these patients. This study aimed to explore the impact of anemia on myocardial fibrosis using T1 mapping technique in patients with ESRD. A total of 128 subjects including 98 ESRD patients (65 with anemia, 33 without anemia) and 30 normal controls were enrolled. All subjects were underwent cardiovascular magnetic resonance to obtain cardiac cine and T1 mapping images. As potential markers of fibrosis, native T1 values and global longitudinal strain derived by feature-tracking technique were compared. Differences between 3 groups were analyzed using one-way analysis of variance. Associations between variables were assessed by Pearson and Spearman correlation coefficient appropriately. An independent association was identified by the multiple stepwise linear regression analysis. Intraclass correlation was applied to assess observer variability. In all ESRD patients, native T1 values were significantly longer than those of normal controls (global T1, 1357 ± 42 ms vs 1275 ± 48 ms, P < .001). Global T1 value in ESRD patients with anemia was significantly higher (1375 ± 36 ms) compared to that in ESRD patients without anemia (1322 ± 25 ms) and normal controls (1275 ± 48 ms), respectively (all P < .001). Global T1 correlated with hemoglobin negatively (R= -0.499, P < .001). Multiple stepwise linear regression analysis presented the anemia is independently associated with global T1 (R = 0.607, P < .001). Global longitudinal strain was remarkably reduced in ESRD patients with anemia in comparison to those without anemia (P < .001). Diffuse myocardial fibrosis could be detected by native T1 mapping in ESRD patients with long-term anemia. Anemia is an important factor in myocardial fibrosis in ESRD patients, and the evaluation of myocardial involvement is worth considering for clinical management.

Bioinformatics analysis of genes and immune cells that influence prostate cancer (PCa) bone metastases. Using the gene expression omnibus database, we analyzed a PCa bone metastasis dataset. Differentially expressed genes were identified through the utilization of GEO2R and weighted gene co-expression network analysis. Gene set enrichment analysis software was used to identify important pathways. In addition to creating a network of protein-protein interactions, functional enrichment analyses were conducted using Kyoto encyclopedia of genes databases. To screen hub genes, Cytoscape software was used with the CytoHubba plug-in and performed mRNA and survival curve validation analysis of key genes using the cBioPortal website and GEPIA2 database. Immune infiltration analysis was performed using the CIBERSORTx website, and finally, immune cell correlation analysis was performed for key genes according to the TIMER database. A total of 197 PCa bone metastasis risk genes were screened, "G2M_CHECKPOINT" was significantly enriched in PCa bone metastasis samples according to genomic enrichment analysis. Based on the protein interactions network, we have identified 10 alternative hub genes, and 3 hub genes, CCNA2, NUSAP1, and PBK, were validated by the cBioPortal website and the GEPIA2 database. T cells regulatory and macrophages M0 may influence PCa to metastasize to bones, according to CIBERSORTx immune cell infiltration analysis. TIMER database analysis found different degrees of correlation between 3 key genes and major immune cells. PCa bone metastasis has been associated with CCNA2, NUSAP1, and PBK. T cells regulatory and macrophages (M0) may also be involved.

Background: Previous researches have revealed some links between thyroid function and sleep characteristics, however it remains unclear which one causes the other. The purpose of this study was to investigate the potential causal relationship between hyperthyroidism, hypothyroidism, and sleep characteristics.

Methods: We utilized aggregated data from published genome-wide association studies (GWAS) to select genetic instruments for sleep variables. The 5 sleep-related traits (chronotype, short sleep duration, long sleep duration, daytime sleepiness, and insomnia) were associated with distinct genetic variants chosen as instrumental factors. Employing MR Egger's analysis of Mendelian randomization (MR), weighted median, weighted mode, and inverse variance weighted (IVW) methods to assess the 5 sleep traits in relation to hyperthyroidism and hypothyroidism, we subsequently conducted inverse MR analysis to examine the causal relationship between thyroid function and the 5 sleep characteristics.

Results: The IVW technique did not reveal a causal association between chronotype, short sleep duration, long sleep duration, daytime sleepiness, or insomnia and the risk of abnormal thyroid function in the study investigating the influence of sleep characteristics on this risk. The outcomes of the IVW approach were consistent with the remaining 3 methods. The IVW, weighted median, MR Egger, and weighted mode methods in the reverse magnetic resonance imaging investigation did not yield evidence of a causative association between the risk of time type, long sleep duration, and insomnia and abnormal thyroid function. In contrast, the weighted median and weighted mode methods showed a possible causal relationship between hypothyroidism and short sleep duration and daytime sleepiness. Sensitivity analyses showed that the results were robust and no pleiotropy or heterogeneity was detected.

Conclusion: More precisely, our analysis did not uncover any indication of a reciprocal causal link between thyroid function and genetically predicted sleep characteristics.

This retrospective cohort study aimed to examine changes in coronary blood flow before and after post-dilation following primary percutaneous coronary intervention (PPCI) in patients with ST-segment elevation myocardial infarction (STEMI). 419 eligible patients who underwent PPCI due to STEMI between January 2019 and September 2023 were enrolled. The corrected thrombolysis in myocardial infarction frame count (CTFC), final quantitative coronary angiography, and the incidence of no-reflow and slow-flow during different procedure moments were assayed. The changes in coronary blood flow before and after post-dilation in the post-dilation group were analyzed. Among the 419 patients enrolled, 259 patients underwent post-dilation. The post-dilation procedure was more frequently performed in patients with calcium plaque present, longer stents, bigger-diameter stents, and overlapping stents. The incidence of final no-reflow and slow-flow in the post-dilation group was not significantly higher than that observed in the non-post-dilation group. In contrast post-dilation patients had significantly increased CTFC values by 3.54 ± 10.54 frames (P < .001) and the rate of no-reflow/slow-flow increased on average by 114% (P < .001) in comparison to patients not undergoing post-dilation. The receiver operating characteristic curve showed that if post-dilation was performed in patients when their after-stent CTFC was smaller than 23.25, no-reflow/slow-flow was less likely to occur (63.5% sensitivity, 88.8% specificity, [AUC]: 0.817, 95% CI: 0.749-0.886, P < .001). Post-dilation exacerbates the coronary blood flow and increases the incidence of no-reflow/slow-flow during PPCI for STEMI patients, except where after-stend CTFC values were <23.25.

This study aimed to develop and validate a clinical risk model based on clinical factors to predict prognosis in patients with wake-up stroke (WUS) after multimodal magnetic resonance imaging combined with recombinant tissue plasminogen activator intravenous thrombolysis. The study enrolled 263 patients with WUS, who were divided into the training (n = 162) and validation cohorts (n = 101). In the training cohort, patients were stratified based on modified Rankin Scale (mRS) score at 90 days after thrombolysis, with mRS ≤ 2 indicating a good prognosis (n = 117), and mRS > 2 indicating a poor prognosis (n = 45). Multivariate regression analyses were employed to identify independent risk factors and develop clinical risk models. The performance and stability of the clinical risk model were evaluated using receiver operating characteristic analysis and Hosmer-Lemeshow test. The clinical risk nomogram was constructed based on this model, and evaluated using decision curve analyses. Patients with poor prognosis showed a higher proportion of hyperlipidemia and diabetes and showed a higher levels of National Institute of Health Stroke Scale (NIHSS) at admission, NIHSS at 24 hours, triglyceride, and total cholesterol. Diabetes (odds ratio [OR] = 3.823), hyperlipidemia (OR = 7.361), NIHSS at admission (OR = 5.399), NIHSS at 24 hours (OR = 2.869), triglyceride (OR = 13.790), and total cholesterol (OR = 9.719) were independent predictors of poor prognosis in patients with WUS. Hosmer-Lemeshow test showed that the clinical risk model had a good fit in the training (χ2 = 19.573, P = .726) and validation cohorts (χ2 = 19.573, P = .726). The clinical risk model had an area under the curve value of 0.929 (95% confidence interval, 0.886-0.978) in the training cohort and 0.948 (0.906-0.989) in the validation cohort. The decision curve analysis indicated clinical risk nomogram has application value. The clinical risk model can effectively predict WUS prognosis outcomes.

Background: Bisphosphonates are effective in the treatment of postmenopausal osteoporosis. However, their prolonged use induces adverse events and may lead to a rapid decline in bone mineral density (BMD) after discontinuation. Denosumab, a human monoclonal antibody, is a widely used antiresorptive agent that is more effective than bisphosphonates in improving bone density. Whether sequential treatment with denosumab after bisphosphonate therapy can maintain or further increase BMD at all sites has not been conclusively demonstrated. Thus, we performed a meta-analysis of randomized controlled trials (RCTs) to assess the effects of this sequential therapy on BMD.

Methods: We searched the PubMed, Embase, and Cochrane Library databases from December 1, 1986, to May 2, 2024, for all RCTs that assessed the efficacy of sequential therapy of bisphosphonate transition to denosumab in postmenopausal women with osteoporosis. BMD changes at the lumbar spine, femoral neck, and total hip were used as outcomes. We assessed methodological quality, extracted relevant data according to the Cochrane Handbook for Systematic Reviews of Interventions, applied random-effects models for meta-analyses, performed heterogeneity analyses, and assessed publication bias.

Results: A total of 3290 patients from 4 RCTs were included in the meta-analysis. Forest plot analysis showed that sequential treatment with bisphosphonate-denosumab was associated with higher lumbar spine BMD gain than continuous bisphosphonate treatment [mean difference (MD) = 5.50, 95% confidence interval (CI) = 5.26-5.75, I2 = 32.88%). No risk of bias was observed for the 4 trials, but there was an increase in femoral neck and total hip BMD. Moreover, analyses could not be performed because of high heterogeneity (femoral neck BMD: MD = 3.85, 95% CI = 2.84-4.85, I2 = 97.88%; total hip BMD: MD = 5.65, 95% CI = 4.28-7.02, I2 = 97.91%).

Conclusion: Sequential therapy that involves a transition from bisphosphonates to denosumab had a positive effect on lumbar spine bone density, and this type of therapy may be a potential treatment option for increasing lumbar spine bone density in postmenopausal women.