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Background: Severe acute pain is still commonly treated with opioid analgesics in the United States, but this practice could prolong the duration of pain.Objectives: Estimate the risk of experiencing persistent pain after opioid analgesic use after emergency department (ED) discharge among patients with suspected urolithiasis.Methods: We analyzed data collected for a longitudinal, multicenter clinical trial of ED patients with suspected urolithiasis. We constructed multilevel models to estimate the odds ratios (ORs) of reporting pain at 3, 7, 30, or 90 days after ED discharge, using multiple imputation to account for missing outcome data. We controlled for clinical, demographic, and institutional factors and used weighting to account for the propensity to be prescribed an opioid analgesic at ED discharge.Results: Among 2413 adult ED patients with suspected urolithiasis, 62% reported persistent pain 3 days after discharge. Participants prescribed an opioid analgesic at discharge were OR 2.51 (95% confidence interval [CI] 1.82-3.46) more likely to report persistent pain than those without a prescription. Those who reported using opioid analgesics 3 days after discharge were OR 2.24 (95% CI 1.77-2.84) more likely to report pain at day 7 than those not using opioid analgesics at day 3, and those using opioid analgesics at day 30 had OR 3.25 (95% CI 1.96-5.40) greater odds of pain at day 90.Conclusions: Opioid analgesic prescription doubled the odds of persistent pain among ED patients with suspected urolithiasis. Limiting opioid analgesic prescribing at ED discharge for these patients might prevent persistent pain in addition to limiting access to these medications. [ABSTRACT FROM AUTHOR]

Objective: Previous research has suggested caution about opioid analgesic usage in the emergency department (ED) setting and raised concerns about variations in prescription opioid analgesic usage, both across institutions and for whom they are prescribed. We examined opioid analgesic usage in ED patients with suspected urolithiasis across fifteen participating hospitals.Methods: This is a secondary analysis of a clinical trial including adult ED patients with suspected urolithiasis. In multilevel models accounting for clustering by hospital, we assessed demographic, clinical, state-level, and hospital-level factors associated with opioid analgesic administration during the ED visit and prescription at discharge.Results: Of 2352 participants, 67% received an opioid analgesic during the ED visit and 61% were prescribed one at discharge. Opioid analgesic usage varied greatly across hospitals, ranging from 46% to 88% (during visit) and 34% to 85% (at discharge). Hispanic patients were less likely than non-Hispanic white patients to receive opioid analgesics during the ED visit (OR 0.72, 95% CI 0.55-0.94). Patients with higher education (OR 1.29, 95% CI 1.05-1.59), health insurance coverage (OR 1.27, 95% CI 1.02-1.60), or receiving care in states with a prescription drug monitoring program (OR 1.64, 95% CI 1.06-2.53) were more likely to receive an opioid analgesic prescription at ED discharge.Conclusion: We found marked hospital-level differences in opioid analgesic administration and prescribing, as well as associations with education, healthcare insurance, and race/ethnicity groups. These data might compel clinicians and hospitals to examine their opioid use practices to ensure it is congruent with accepted medical practice. [ABSTRACT FROM AUTHOR]

Neighborhood deprivation is consistently associated with greater risk of low birthweight. However, large birth size is increasingly relevant but overlooked in neighborhood health research, and proximity within which neighborhood deprivation may affect birth outcomes is unknown. We estimated race/ethnic-specific effects of neighborhood deprivation index (NDI) within 1, 3, 5, and 8 km buffers around Oregon Pregnancy Risk Assessment Monitoring System ( n =3716; 2004–2007) respondents׳ homes on small and large for gestational age (SGA, LGA). NDI was positively associated with LGA and SGA in most race/ethnic groups. The results varied little across the four buffer sizes. [ABSTRACT FROM AUTHOR]

Heart muscle is metabolically versatile, converting energy stored in fatty acids, glucose, lactate, amino acids, and ketone bodies. Here, we use mouse models in ketotic nutritional states (24 h of fasting and a very low carbohydrate ketogenic diet) to demonstrate that heart muscle engages a metabolic response that limits ketone body utilization. Pathway reconstruction from microarray data sets, gene expression analysis, protein immunoblotting, and immunohistochemical analysis of myocardial tissue from nutritionally modified mouse models reveal that ketotic states promote transcriptional suppression of the key ketolytic enzyme, succinyl-CoA:3-oxoacid CoA transferase (SCOT; encoded by Oxct1), as well as peroxisome proliferatoractivated receptor a-dependent induction of the key ketogenic enzyme HMGCS2. Consistent with reduction of SCOT, NMR profiling demonstrates that maintenance on a ketogenic diet causes a 25% reduction of myocardial 13C enrichment of glutamate when 13C-labeled ketone bodies are delivered in vivo or ex vivo, indicating reduced procession of ketones through oxidative metabolism. Accordingly, unmetabolized substrate concentrations are higher within the hearts of ketogenic diet-fed mice challenged with ketones compared with those of chow-fed controls. Furthermore, reduced ketone body oxidation correlates with failure of ketone bodies to inhibit fatty acid oxidation. These results indicate that ketotic nutrient environments engage mechanisms that curtail ketolytic capacity, controlling the utlization of ketone bodies in ketotic states. [ABSTRACT FROM AUTHOR]

To compensate for the energetic deficit elicited by reduced carbohydrate intake, mammals convert energy stored in ketone bodies to high energy phosphates. Ketone bodies provide fuel particularly to brain, heart, and skeletal muscle in states that include starvation, adherence to low carbohydrate diets, and the neonatal period. Here, we use novel Oxct1-/- mice, which lack the ketolytic enzyme succinyl-CoA:3-oxo-acid CoA-transferase (SCOT), to demonstrate that ketone body oxidation is required for postnatal survival in mice. Although Oxct1-/- mice exhibit normal prenatal development, all develop ketoacidosis, hypoglycemia, and reduced plasma lactate concentrations within the first 48 h of birth. In vivo oxidation of 13C-labeled β-hydroxybutyrate in neonatal Oxct1-/- mice, measured using NMR, reveals intact oxidation to acetoacetate but no contribution of ketone bodies to the tricarboxylic acid cycle. Accumulation of acetoacetate yields a markedly reduced β-hydroxybutyrate:acetoacetate ratio of 1:3, compared with 3:1 in Oxct1+ littermates. Frequent exogenous glucose administration to actively suckling Oxct1-/- mice delayed, but could not prevent, lethality. Brains of newborn SCOT-deficient mice demonstrate evidence of adaptive energy acquisition, with increased phosphorylation of AMP-activated protein kinase a, increased autophagy, and 2.4-fold increased in vivo oxidative metabolism of [13C]glucose. Furthermore, [13C]lactate oxidation is increased 1.7-fold in skeletal muscle of Oxct1-/- mice but not in brain. These results indicate the critical metabolic roles of ketone bodies in neonatal metabolism and suggest that distinct tissues exhibit specific metabolic responses to loss of ketone body oxidation. [ABSTRACT FROM AUTHOR]