Type II diabetic patients have significantly higher risk of PUB even after adjustments for possible confounding factors like age, sex, underlying comorbidities, and ulcerogenic medication.

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Introduction The increased prevalence of erectile dysfunction (ED) has been reported in patients with chronic obstructive pulmonary disease, and sustained systemic inflammation seems to play a central role in this linkage. Asthma is also a chronic inflammatory airway disorder, eliciting a low-grade systemic inflammation; however, the influence of asthma on ED has not been investigated. Aim Our study strived to explore the relationship of asthma and the subsequent development of ED using a nationwide, population-based database. Methods From 2000 to 2007, we identified newly diagnosed asthma cases involving male patients 18–55 years old. A control cohort without asthma, which was matched for age and comorbidities, was selected for comparison. Main Outcome Measures The two cohorts were followed up, and we observed the occurrence of ED by registry of ED diagnosis in the database. Results Of the 17,302 sampled patients (3,466 asthma patients vs. 13,836 control), 114 (0.66%) experienced ED during a mean follow-up period of 4.56 years, including 34 (0.98% of the asthma patients) from the asthma cohort and 80 (0.58%) from the control group. Subjects with asthma experienced a 1.909-fold (95% confidence interval [CI], 1.276–2.856; P =0.002) increase in incident ED, which was independent of age, the number of clinical visits for urologist, and other comorbidities. Kaplan–Meier analysis also revealed the tendency of asthma patients for ED development (log rank test, P =0.002). The risk of ED was higher in cases with more frequent clinical visits for asthma (asthma patients with clinical visits with >24 times/year vs. <12 times/year: hazard ratio [HR]: 4.154 [95% CI:1.392–12.396], P =0.011; clinical visits with 12–24 times/year vs. <12 times/year HR: 3.534 [95% CI:1.245–10.032], P =0.018). Conclusions Asthma may be an independent risk factor for ED, and risk of ED probably increases in accordance with asthma severity.

Objective: This study aimed to develop machine learning-based prediction models to predict masked hypertension and masked uncontrolled hypertension using the clinical characteristics of patients at a single outpatient visit.Methods: Data were derived from two cohorts in Taiwan. The first cohort included 970 hypertensive patients recruited from six medical centers between 2004 and 2005, which were split into a training set (n = 679), a validation set (n = 146), and a test set (n = 145) for model development and internal validation. The second cohort included 416 hypertensive patients recruited from a single medical center between 2012 and 2020, which was used for external validation. We used 33 clinical characteristics as candidate variables to develop models based on logistic regression (LR), random forest (RF), eXtreme Gradient Boosting (XGboost), and artificial neural network (ANN).Results: The four models featured high sensitivity and high negative predictive value (NPV) in internal validation (sensitivity = 0.914–1.000; NPV = 0.853–1.000) and external validation (sensitivity = 0.950–1.000; NPV = 0.875–1.000). The RF, XGboost, and ANN models showed much higher area under the receiver operating characteristic curve (AUC) (0.799–0.851 in internal validation, 0.672–0.837 in external validation) than the LR model. Among the models, the RF model, composed of 6 predictor variables, had the best overall performance in both internal and external validation (AUC = 0.851 and 0.837; sensitivity = 1.000 and 1.000; specificity = 0.609 and 0.580; NPV = 1.000 and 1.000; accuracy = 0.766 and 0.721, respectively).Conclusion: An effective machine learning-based predictive model that requires data from a single clinic visit may help to identify masked hypertension and masked uncontrolled hypertension.

SUMMARY BackgroundControversy exists regarding glucocorticoids therapy and the risk of peptic ulcer bleeding (PUB).

BackgroundCirculating endothelial progenitor cells (EPCs) reflect endothelial repair capacity and may be a significant marker for the clinical outcomes of cardiovascular disease. While some high-dose statin treatments may improve endothelial function, it is not known whether different statins may have similar effects on EPCs.This study aimed to investigate the potential class effects of different statin treatment including pitavastatin and atorvastatin on circulating EPCs in clinical setting.MethodsA pilot prospective, double-blind, randomized study was conducted to evaluate the ordinary dose of pitavastatin (2 mg daily) or atorvastatin (10 mg daily) treatment for 12 weeks on circulating EPCs in patients with cardiovascular risk such as hypercholesterolemia and type 2 diabetes mellitus (T2DM). Additional in vitro study was conducted to clarify the direct effects of both statins on EPCs from the patients.ResultsA total of 26 patients (19 with T2DM) completed the study. While the lipid-lowering effects were similar in both treatments, the counts of circulating CD34+KDR+EPCs were significantly increased (from 0.021 ± 0.015 to 0.054 ± 0.044% of gated mononuclear cells, P < 0.05) only by pitavastatin treatment. Besides, plasma asymmetric dimethylarginine level was reduced (from 0.68 ± 0.10 to 0.53 ± 0.12 μmol/L, P < 0.05) by atorvastatin, and plasma vascular endothelial growth factor (VEGF) level was increased (from 74.33 ± 32.26 to 98.65 ± 46.64 pg/mL, P < 0.05) by pitavastatin. In the in vitro study, while both statins increased endothelial nitric oxide synthase (eNOS) expression, only pitavastatin increased the phosphorylation of eNOS in EPCs. Pitavastatin but not atorvastatin ameliorated the adhesion ability of early EPCs and the migration and tube formation capacities of late EPCs.ConclusionsWhile both statins similarly reduced plasma lipids, only pitavastatin increased plasma VEGF level and circulating EPCs in high-risk patients, which is probably related to the differential pleiotropic effects of different statins.Trial registrationThis trial is registered at ClinicalTrials.gov, NCT01386853.