Clinical Efficacy and Safety Profile of Prucalopride in Chronic Idiopathic Constipation

Chronic idiopathic constipation (CIC) can be defined as bowel movements that are difficult to pass, are not occurring frequently, or have incomplete evacuation during defecation. A high-fiber diet and laxatives are the commonly used treatments, but in many cases, they do not produce satisfactory results. The first line of treatment is osmotic laxatives. If there is no improvement, the second line is guanylate cyclase-C (GCC) agonists like linaclotide or prokinetic agents such as prucalopride. On December 14, 2018, the United States Food and Drug Administration (US FDA) approved prucalopride for treating chronic idiopathic constipation. Prucalopride is a prokinetic agent which works at the 5-hydroxytryptamine receptor 4 (5-HT4) as an agonist with greater receptor selectivity. Patients on prucalopride reported improved symptoms, quality of life and satisfaction. The most frequent adverse events were headaches and problems related to the gastrointestinal tract. Caution should be taken when using prucalopride in patients with impaired liver and renal function. In Canada, prucalopride has been approved for treatment of female patients with chronic idiopathic constipation who have failed therapy with at least two laxatives from different classes over a six-month period.Open access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

Clinical outcomes in patients with heart failure with and without cirrhosis: an analysis from the national inpatient sample.

Outcomes of heart failure (HF) hospitalization are driven by the presence or absence of comorbid conditions. Cirrhosis is associated with worse outcomes in patients with HF, and both HF and cirrhosis are associated with worse renal outcomes. Using a nationally representative sample we describe inpatient outcomes of all-cause mortality and length of stay (LOS) among patients with and without cirrhosis hospitalized for decompensated with HF. We conducted a cross sectional analysis using Nationwide Inpatient Sample (2010-2014) data including patients hospitalized for decompensated HF, with or without cirrhosis. We calculated the adjusted odds of all-cause mortality, acute kidney injury (AKI), and target LOS after adjusting for potential confounders. Out of the 2,487,445 hospitalized for decompensated HF 39,950 had cirrhosis of which majority (75.1%) were non-alcoholic cirrhosis. Patients with comorbid cirrhosis were more likely to die (OR, 1.26; 95% CI, 1.11 to 1.43) and develop AKI (OR, 1.26; 95% CI, 1.16 to 1.36) as compared to those without cirrhosis. Underlying CKD was associated with a greater odds of AKI (OR, 4.99; 95% CI, 4.90 to 5.08), and the presence of cirrhosis amplified this risk (OR, 6.03; 95% CI, 5.59 to 6.51). There was approximately a 40% decrease in the relative odds of lower HF hospitalization length of stay among those with both CKD and cirrhosis, relative to those without either comorbidities. Cirrhosis in patients with hospitalizations for decompensated HF is associated with higher odds of mortality, decreased likelihood of discharge by the targeted LOS, and AKI. Among patients with HF the presence of cirrhosis increases the risk of AKI, which in turn is associated with poor clinical outcomes

Treating iron deficiency (ID) anemia in heart failure (HF) patients with IV iron: A meta-analysis

Findings on the effects of iron on heart failure (HF) hospitalizations and mortality among patients with iron deficiency (ID) and HF remain conflicting across different studies. We performed a meta-analysis of clinical trials assessing the clinical, hematic and cardiovascular benefits of treating ID in HF patients. We completed a systematic search for studies comparing IV iron to placebo in HF patients with ID. The primary outcomes were rates of HF hospitalization and all-cause mortality. Secondary outcomes included change in hematic values, New York Heart Association (NYHA) class and ejection fraction. We applied a random-effects model with planned sensitivity analyses of studies with skewed effect sizes. Nine studies were included with a total of 2,261 patients. Analysis revealed that treatment of HF patients with IV iron replacement significantly reduced the odds of HF hospitalization (odds ratio (OR): 0.44; 95% confidence interval (CI): 0.24 to 0.78; p=0.005, I2=67%),) but did not significantly impact all-cause mortality compared to placebo (OR: 0.89; 95%, CI: 0.67 to 1.19; p=0.44, I2: 0%). Analysis showed that IV iron treatment group had significantly higher serum ferritin, transferrin saturation and hemoglobin (Hb) levels. They also had lower NYHA class -1.90 (95% CI (-2.91 to -0.89); p\u3c0.001, I2:89%) with higher ejection fraction 0.50 (95% CI (0.09 to 0.90) p=0.016, I2:86%). Treatment with IV iron in HF patients with ID is associated with a significant reduction of HF hospitalization but no effects on all-cause mortality. There were also significant increases in hematic values and ejection fraction with a reduction in NYHA class

Cumulative Social Disadvantage and All-Cause Mortality in the United States: Findings from a National Study

The extent to which cumulative social disadvantage-defined as aggregate social risk resulting from multiple co-occurring adverse social determinants of health (SDOH)-affects the risk of all-cause mortality, independent of demographic and clinical risk factors, is not well understood. The objective of this study was to examine the association between cumulative social disadvantage, measured using a comprehensive 47-factor SDOH framework, and mortality in a nationally representative sample of adults in the United States. The authors conducted secondary analysis of pooled data for 63,540 adult participants of the 2013-2015 National Death Index-linked National Health Interview Survey. Age-adjusted mortality rates (AAMRs) were reported by quintiles of aggregate SDOH burden, with higher quintiles denoting greater social disadvantage. Cox proportional hazards models were used to examine the association between cumulative social disadvantage and risk of all-cause mortality. AAMR increased significantly with greater SDOH burden, ranging from 631 per 100,000 person-years (PYs) for participants in SDOH-Q1 to 1490 per 100,000 PYs for those in SDOH-Q5. In regression models adjusted for demographics, being in SDOH-Q5 was associated with 2.5-fold higher risk of mortality, relative to Q1 (adjusted hazard ratio [aHR] = 2.57 [95% confidence interval, CI = 1.94-3.41]); the observed association persisted after adjusting for comorbidities, with over 2-fold increased risk of mortality for SDOH-Q5 versus Q1 (aHR = 2.02 [95% CI = 1.52-2.67]). These findings indicate that cumulative social disadvantage is associated with increased risk of all-cause mortality, independent of demographic and clinical factors. Population level interventions focused on improving individuals\u27 social, economic, and environmental conditions may help reduce the burden of mortality and mitigate persistent disparities

Cumulative social disadvantage and all-cause mortality in the United States: findings from a national study

The extent to which cumulative social disadvantage-defined as aggregate social risk resulting from multiple co-occurring adverse social determinants of health (SDOH)-affects the risk of all-cause mortality, independent of demographic and clinical risk factors, is not well understood. The objective of this study was to examine the association between cumulative social disadvantage, measured using a comprehensive 47-factor SDOH framework, and mortality in a nationally representative sample of adults in the United States. The authors conducted secondary analysis of pooled data for 63,540 adult participants of the 2013-2015 National Death Index-linked National Health Interview Survey. Age-adjusted mortality rates (AAMRs) were reported by quintiles of aggregate SDOH burden, with higher quintiles denoting greater social disadvantage. Cox proportional hazards models were used to examine the association between cumulative social disadvantage and risk of all-cause mortality. AAMR increased significantly with greater SDOH burden, ranging from 631 per 100,000 person-years (PYs) for participants in SDOH-Q1 to 1490 per 100,000 PYs for those in SDOH-Q5. In regression models adjusted for demographics, being in SDOH-Q5 was associated with 2.5-fold higher risk of mortality, relative to Q1 (adjusted hazard ratio [aHR] = 2.57 [95% confidence interval, CI = 1.94-3.41]); the observed association persisted after adjusting for comorbidities, with over 2-fold increased risk of mortality for SDOH-Q5 versus Q1 (aHR = 2.02 [95% CI = 1.52-2.67]). These findings indicate that cumulative social disadvantage is associated with increased risk of all-cause mortality, independent of demographic and clinical factors. Population level interventions focused on improving individuals' social, economic, and environmental conditions may help reduce the burden of mortality and mitigate persistent disparities

Social determinants of health and obesity: Findings from a national study of US adults

Objective: This study examined the association between social determinants of health (SDOH) burden and overweight/obesity in a nationally representative sample of adults in the United States.Methods: Data for 161,795 adults aged ≥18 years from the 2013 to 2017 National Health Interview Survey were used. A total of 38 SDOH were aggregated to create a cumulative SDOH score, which was divided into quartiles (Q1-Q4) to denote levels of SDOH burden. Prevalence of overweight and obesity was examined across SDOH quartiles in the total population and by age, sex, and race/ethnicity. Multinomial logistic regression models were used to analyze the association between SDOH quartiles and overweight/obesity, adjusting for relevant covariates.Results: There was a graded increase in obesity prevalence with increasing SDOH burden. At nearly each quartile, overweight and obesity rates were higher for middle-aged and non-Hispanic Black adults compared with their counterparts; additional differences were observed by sex. In fully adjusted models, SDOH-Q4 was associated with 15%, 50%, and 70% higher relative prevalence of overweight, obesity class 1 and 2, and obesity class 3, respectively, relative to SDOH-Q1.Conclusions: Cumulative social disadvantage, denoted by higher SDOH burden, was associated with increased odds of obesity, independent of clinical and demographic factors