Background: Privacy restrictions limit access to protected patient-derived health information for research purposes. Consequently, data anonymization is required to allow researchers data access for initial analysis before granting institutional review board approval. A system installed and activated at our institution enables synthetic data generation that mimics data from real electronic medical records, wherein only fictitious patients are listed. Objective: This paper aimed to validate the results obtained when analyzing synthetic structured data for medical research. A comprehensive validation process concerning meaningful clinical questions and various types of data was conducted to assess the accuracy and precision of statistical estimates derived from synthetic patient data. Methods: A cross-hospital project was conducted to validate results obtained from synthetic data produced for five contemporary studies on various topics. For each study, results derived from synthetic data were compared with those based on real data. In addition, repeatedly generated synthetic datasets were used to estimate the bias and stability of results obtained from synthetic data. Results: This study demonstrated that results derived from synthetic data were predictive of results from real data. When the number of patients was large relative to the number of variables used, highly accurate and strongly consistent results were observed between synthetic and real data. For studies based on smaller populations that accounted for confounders and modifiers by multivariate models, predictions were of moderate accuracy, yet clear trends were correctly observed. Conclusions: The use of synthetic structured data provides a close estimate to real data results and is thus a powerful tool in shaping research hypotheses and accessing estimated analyses, without risking patient privacy. Synthetic data enable broad access to data (eg, for out-of-organization researchers), and rapid, safe, and repeatable analysis of data in hospitals or other health organizations where patient privacy is a primary value.

Introduction: Community acquired pneumonia (CAP) is a major cause of morbidity and mortality. While there is much data about risk factors for severe outcome in the general population, there is less focus on younger group of patients. Therefore, we aimed to detect simple prognostic factors for severe morbidity and mortality in young patients with CAP. Methods: Patients of 60 years old or younger, who were diagnosed with CAP (defined as pneumonia identified 48 hours or less from hospitalization) between March 1, 2005 and December 31, 2008 were retrospectively analyzed for risk factors for complicated hospitalization and 90-day mortality. Results: The cohort included 637 patients. 90-day mortality rate was 6.6% and the median length of stay was 5 days. In univariate analysis, male patients and those with co-morbid conditions tended to have complicated disease. In multivariate analysis, variables associated with complicated hospitalization included post chest radiation state, prior neurologic damage, blood urea nitrogen (BUN) > 10.7 mmol/L and red cell distribution width (RDW) > 14.5%; whereas, variables associated with an increased risk of 90-day mortality included age ≥ 51 years, prior neurologic damage, immunosuppression, and the combination of abnormal white blood cells (WBC) and elevated RDW. Complicated hospitalization and mortality rate were significantly higher among patients with increased RDW regardless of the white blood cell count. Elevated RDW was associated with a significant increase in complicated hospitalization and 90-day mortality rates irrespective to hemoglobin levels. Conclusions: In young patients with CAP, elevated RDW levels are associated with significantly higher rates of mortality and severe morbidity. RDW as a prognostic marker was unrelated with hemoglobin levels. Trial registration: ClinicalTrials.Gov NCT00845312

Aims Heart failure (HF) is one of the leading causes for hospitalization and mortality. After first admission with acute decompensated HF, some patients are in high risk for short‐term and long‐term mortality. These patients should be identified, closely followed up, and treated. It has been observed that blood urea nitrogen (BUN) on admission is a predictive marker for short‐term mortality. Recently, it has been shown that higher BUN levels on discharge are also a bad prognostic predictor. However, the prognostic value of BUN alteration during hospital stay was not investigated; therefore, we aimed to investigate the effect of BUN variation during hospitalization on mortality. Methods and results A retrospective study included patients with first hospitalization with the primary diagnosis of HF. The patients were divided into four groups on the basis of the values of BUN on admission and discharge, respectively: normal‐normal, elevated‐normal, normal‐elevated, and elevated‐elevated. Four thousand seven hundred sixty‐eight patients were included; 2567 were male (53.8%); the mean age was 74.7 ± 12.7 years. The 90 day mortality rate in the normal‐normal group was 7% lower than that in the elevated‐normal (14.6%) and normal‐elevated (19.3%) groups; P value < 0.01. The 90 day mortality in the elevated‐elevated group (28.8%) was significantly higher than that in the other groups; P < 0.001. During the 36 month follow‐up, these results are maintained. While sub‐dividing BUN levels into 40 mg/dL, higher BUN levels correlated with higher 90 day mortality rate regardless of creatinine levels, brain natriuretic peptide, or age. Moreover, BUN on admission and on discharge correlated better with mortality than did creatinine and glomerular filtration rate at the same points. Conclusions The BUN both on admission and on discharge is a prognostic predictor in patients with HF; however, patients with elevated levels both on admission and on discharge have the worst prognosis. Moreover, worsening or lack of improvement in BUN during hospitalization is a worse prognostic predictor. To the best of our knowledge, this is the first trial to discuss the BUN change during hospitalization in HF.

Widespread vascular endothelial injury is the major mechanism for multiorgan dysfunction in sepsis. Following this process, the permeability of the alveolar capillaries is augmented with subsequent increase in water content and acute respiratory distress syndrome (ARDS). Nevertheless, the role of alveolar epithelium is less known. Therefore, we examined alveolar fluid clearance (AFC) using isolated perfused rat lung model in septic rats without ARDS. Sepsis was induced by ligating and puncturing the cecum with a 21-gauge needle. AFC was examined 24 and 48 h later. The expression of Na-K-ATPase proteins was examined in type II alveolar epithelial cells (ATII) and basolateral membrane (BLM). The rate of AFC in control rats was 0.51 ± 0.02 ml/h (means ± SE) and decreased to 0.3 ± 0.02 and 0.33 ± 0.03 ml/h in 24 and 48 h after sepsis induction, respectively (P < 0.0001). Amiloride, significantly decreased AFC in sepsis; conversely, isoproterenol reversed the inhibitory effect of sepsis. The alveolar-capillary barrier in septic rats was intact; therefore the finding of increased extravascular lung water in early sepsis could be attributed to accumulation of protein-poor fluid. The expression of epithelial sodium channel and Na-K-ATPase proteins in whole ATII cells was not different in both cecal ligation and puncture and control groups; however, the abundance of Na-K-ATPase proteins was significantly decreased in BLMs of ATII cells in sepsis. Early decrease in AFC in remote sepsis is probably related to endocytosis of the Na-K-ATPase proteins from the cell plasma membrane into intracellular pools, with resultant inhibition of active sodium transport in ATII cells.

Community acquired pneumonia (CAP) is a common illness affecting hundreds of millions worldwide. Few studies have investigated the relationship between serum magnesium levels and outcomes of these patients. We aimed to study the association between serum magnesium levels and 30-day mortality among patients with CAP. Retrospective overview of patients hospitalized with CAP between January 1, 2010 and December 31, 2016. Participants were analyzed retrospectively in order to identify the risk factors for a primary endpoint of 30-day mortality. Normal levels of magnesium levels in our laboratory varies between 1.35 and 2.4 mg/dl. 3851 patients were included in our cohort. Age > 75 years, blood urea nitrogen (BUN) > 20 mg/dl, hypoalbuminemia, and abnormal levels of magnesium were all associated with increased risk of 30-day mortality. Normal magnesium levels were associated with the lowest mortality rate (14.7%). Notably, within the normal levels, high normal magnesium levels (2–2.4 mg/dl) were correlated with higher mortality rates (30.3%) as compared to levels that ranged between 1.35–2 mg/dl (12.9%). Hypomagnesemia and hypermagnesemia were both associated with excess of 30-day mortality, 18.4 and 50%, respectively. Hypomagnesemia and hypermagnesemia on admission were associated with an increased rate of 30-day mortality among adult patients hospitalized with CAP. Interestingly, magnesium levels within the upper normal limits were associated with higher mortality.