Concomitant 5-Aminosalicylate Therapy in Moderate-to-Severe Ulcerative Colitis Patients Escalated to Infliximab Is Not Beneficial

Digestive Diseases and Sciences - While there is recent literature to support the discontinuation of 5-aminosalicylate (5-ASA) upon the initiation of biologics, continuing 5-ASA after treatment...     

Too Big to Fail: Successful Resection of a Large Hepatocellular Carcinoma with Portal Tumor Thrombus

Digestive Diseases and Sciences -     

Adverse consequences of immediate thrombolysis-related complications: a multi-centre registry-based cohort study of acute stroke

Journal of Thrombosis and Thrombolysis - Complications following thrombolysis for stroke are well documented, and mostly concentrated on haemorrhage. However, the consequences of patients who...     

Effects of obesity on the association between long‐term sleep apnea treatment and changes in interleukin‐6 levels: the Icelandic Sleep Apnea Cohort

The aim of this study was to evaluate changes in interleukin (IL)‐6 and soluble IL‐6 receptor levels in obstructive sleep apnea patients and assess the role of positive airway pressure treatment and obesity on these changes. A total of 309 newly diagnosed subjects with sleep apnea from the Icelandic Sleep Apnea Cohort were referred for treatment and reassessed at a 2‐year follow‐up. Full treatment was defined objectively as use ≥4 h day^?1 and ≥20 days month^?1. At the 2‐year follow‐up, there were 177 full users, 44 partial users and 88 non‐users. The mean change in biomarker levels from baseline to the 2‐year follow‐up was assessed in a primary model that included adjustment for baseline biomarker levels, baseline body mass index and change in body mass index, as well as after adjustment for numerous relevant covariates. No significant overall difference in IL‐6 level change was found among full, partial and non‐users. However, in severely obese patients (body mass index ≥35), a significant increase in IL‐6 levels during the 2‐year period was found in partial and non‐users, compared to no change in full users. Results were attenuated in a smaller propensity score matched subsample, although similar trends were observed. No differences were found in soluble IL‐6 receptor levels between full users and non‐users, after adjustment for confounders. In conclusion, among untreated obese sleep apnea patients, IL‐6 levels increase substantially during 2 years, while adherence to positive airway pressure treatment may prevent further increases in this inflammatory biomarker.     

Interactions between vagal afferent nerve subtypes mediating cough

The cough reflex is initiated through activation of vagal afferent nerves. Rapidly adapting receptors fulfill all criteria for the afferents subserving the cough reflex. Bronchopulmonary C-fibres may also initiate cough when activated. C-fibre-mediated cough may depend upon ongoing or initiated activity in rapidly adapting receptors. The interaction between airways C-fibres and rapidly adapting receptors may occur at sites in the periphery or in the brainstem. C-fibre mediated cough must also overcome a coincident inhibitory effect of C-fibre activation on cough, an inhibitory effect that becomes prominent under general anesthaesia.     

Leptin distribution and metabolism in the pregnant rat: transplacental leptin passage increases in late gestation but is reduced by excess glucocorticoids

Leptin is essential for the establishment of pregnancy and appears to promote fetal growth, but the mechanisms regulating fetal leptin exposure remain unclear. In rodents, indirect evidence suggests that fetal leptin is partly derived from the maternal circulation via transplacental passage. Indeed, the placenta expresses mRNA for Ob-Ra, one of the short forms of the leptin receptor (Ob-R(S)) important in leptin transport, and this expression increases markedly in late pregnancy. Therefore, we determined the transplacental passage of maternal leptin to the fetus in the rat and whether this transport increases near term in association with a rise in placental expression of Ob-R(S) protein. Because of the proposed role of leptin in promoting fetal growth, we also assessed the effect of glucocorticoid-induced fetal growth retardation on placental leptin transport. Anesthetized rats received a constant infusion of (125)I-leptin via a jugular cannula before and at d 16 and 22 of pregnancy (term = d 23); plasma samples were obtained at 10, 20, 40, 60, 80, and 100 min, and fetuses and placentas were collected at the time of the final sample. The metabolic clearance rate of leptin fell (P < 0.01) from 3.08 +/- 0.23 ml/min per kg in nonpregnant rats to 2.36 +/- 0.13 ml/min per kg by d 22. Transplacental passage of (125)I-leptin, estimated from its concentration in the whole fetus relative to maternal plasma, increased 10-fold (P < 0.005) between d 16 and d 22 of pregnancy. Over this same period, Ob-R(S) protein expression in the placental labyrinth zone increased by almost 2-fold. Transplacental leptin passage was reduced (P < 0.05) by 77% after maternal dexamethasone treatment, whereas suppression of endogenous glucocorticoid synthesis (by metyrapone) increased (P < 0.05) the transfer of maternal leptin to the fetus by 55%. These data show that transplacental passage of maternal leptin is a significant source of fetal leptin and increases markedly during late pregnancy. Consistent with the proposed role of leptin as a fetal growth factor, transplacental leptin passage is reduced in association with glucocorticoid-induced fetal growth retardation.     

Measuring Emergency Care Survival: The Implications of Risk Adjusting for Race and Poverty

Objectives

We determined the impact of including race, ethnicity, and poverty in risk adjustment models for emergency care–sensitive conditions mortality that could be used for hospital pay‐for‐performance initiatives. We hypothesized that adjusting for race, ethnicity, and poverty would bolster rankings for hospitals that cared for a disproportionate share of nonwhite, Hispanic, or poor patients.

Methods

We performed a cross‐sectional analysis of patients admitted from the emergency department to 157 hospitals in Pennsylvania with trauma, sepsis, stroke, cardiac arrest, and ST‐elevation myocardial infarction. We used multivariable logistic regression models to predict in‐hospital mortality. We determined the predictive accuracy of adding patient race and ethnicity (dichotomized as non‐Hispanic white vs. all other Hispanic or nonwhite patients) and poverty (uninsured, on Medicaid, or lowest income quartile zip code vs. all others) to other patient‐level covariates. We then ranked each hospital on observed‐to‐expected mortality, with and without race, ethnicity, and poverty in the model, and examined characteristics of hospitals with large changes between models.

Results

The overall mortality rate among 170,750 inpatients was 6.9%. Mortality was significantly higher for nonwhite and Hispanic patients (adjusted odds ratio [aOR] = 1.27, 95% confidence interval [CI] = 1.19–1.36) and poor patients (aOR = 1.21, 95% CI = 1.12–1.31). Adding race, ethnicity, and poverty to the risk adjustment model resulted in a small increase in C‐statistic (0.8260 to 0.8265, p = 0.002). No hospitals moved into or out of the highest‐performing decile when adjustment for race, ethnicity, and poverty was added, but the three hospitals that moved out of the lowest‐performing decile, relative to other hospitals, had significantly more nonwhite and Hispanic patients (68% vs. 11%, p < 0.001) and poor patients (56% vs. 10%, p < 0.001).

Conclusions

Sociodemographic risk adjustment of emergency care–sensitive mortality improves apparent performance of some hospitals treating a large number of nonwhite, Hispanic, or poor patients. This may help these hospitals avoid financial penalties in pay‐for‐performance programs.