Point-of-Care Gastric Ultrasound in a Pediatric Patient After Bowel Preparation: A Case Report.

Polyethylene glycol electrolyte solutions (PEG, NuLYTELY®) are widely used to prepare the GI tract before colonoscopy or barium enema examinations. Although PEG appears as a clear liquid, the optimal interval for sedation or general anesthesia after the last administration of these solutions is unclear and controversial in the anesthetic literature. We present a 3-year-old patient with intermittent bloody stools who required anesthetic care for esophagogastroduodenoscopy (EGD) and colonoscopy. Given the controversial nil per os time with the use of PEG-containing solutions, point-of-care gastric ultrasound was performed to evaluate gastric contents and gastric volume before the induction of anesthesia.

Using Serum IgE Antibodies to Predict Esophageal Eosinophilia in Children.

OBJECTIVES: Symptoms of eosinophilic esophagitis are variable and can be nonspecific. Food-specific serum immunoglobulin E (IgE) antibodies are frequently found in patients with eosinophilic esophagitis and are obtained using a widely available blood test. Our objective was to evaluate the ability of food-specific IgE antibodies to predict the presence of esophageal eosinophilia. METHODS: We reviewed 144 medical records for pediatric patients having esophageal biopsy and serum analysis for IgE antibodies to food (exploratory group). We performed logistic regression using sex and number of positive food-specific IgE tests to develop a model that predicts ≥15 eosinophils/high-power field (hpf) in the esophagus. We tested the model using 142 additional patients (validation group). RESULTS: The probability of having ≥15 eosinophils/hpf in the esophagus was higher in boys and increased with the number of positive food-specific IgE tests from 12% (95% confidence interval 4.8-26) in girls with 0 foods positive to 86% (95% confidence interval 71-94) for boys with 4 or 5 foods positive. The statistical model using sex and number of positive IgE tests to predict patients having ≥15 eosinophils/hpf showed acceptable discriminative ability (area under the receiver operating characteristic curve 0.80). The performance metrics for the model to predict ≥15 eosinophils/hpf in the validation group were similar (area under the receiver operating characteristic curve 0.75). CONCLUSIONS: Requiring only a blood test and a simple algorithm, analysis for IgE antibodies to food may expedite an esophagogastroduodenoscopy and decrease delays in the diagnosis and treatment of patients with nonspecific gastrointestinal symptoms who have increased eosinophils in the esophagus.

Serum IgE measurement and detection of food allergy in pediatric patients with eosinophilic esophagitis.

BACKGROUND: Although associated allergies are common and the mechanism may include long-term exposure to allergens, measurement of serum specific IgE levels has not been studied in pediatric eosinophilic esophagitis (EE). OBJECTIVE: To compare the results of serum IgE testing, patch testing, and epicutaneous skin testing to measure allergic sensitization in pediatric patients with EE. METHODS: In a cross-sectional study of 53 pediatric patients with EE, relevant history was obtained by questionnaire, and patch testing to foods was performed. Food and inhalant sensitivities were also assessed using skin prick testing and serum specific IgE measurement. Streptavidin CAP was used to measure specific IgE to cross-reactive carbohydrate determinants and Helicobacter pylori. RESULTS: The overall prevalence of food and inhalant sensitization was 80%, with higher total IgE levels in sensitized vs nonsensitized patients (median, 150 vs 13 IU/mL; P < .001). For foods, serum IgE measurement detected more positive results than did skin prick testing. Specific IgE to milk was most common (43%). Inhalants were implicated as frequently as were foods. In keeping with this, 32% of patients had a cluster of multiple sensitivities that included pollens, soy, grains, peanut, and tree nuts and had higher total IgE levels (P = .001). Patch test results were interpreted as positive in 39% of patients (rye, wheat, and soy were the most common). CONCLUSIONS: Most, but not all, patients with EE are highly atopic individuals with frequent allergic sensitivities. Thus, serum IgE measurement of low-titer IgE antibody may be useful in identifying relevant food sensitivities and in distinguishing subgroups of patients with EE, making a more directed approach to food avoidance possible.

Effects of a potent and selective PPAR-alpha agonist in patients with atherogenic dyslipidemia or hypercholesterolemia: two randomized controlled trials.

CONTEXT: Fibrates are weak agonists of peroxisome proliferator-activated receptor alpha (PPAR-alpha). No trials have reported effects of more potent and selective agents. OBJECTIVES: To examine the safety and efficacy of LY518674, a PPAR-alpha agonist. DESIGN, SETTING, AND PARTICIPANTS: Two multicenter, randomized, double-blind, placebo-controlled trials: 1 in patients with elevated triglycerides and low HDL-C (atherogenic dyslipidemia), the other in patients with elevated LDL-C (hypercholesterolemia). Between August 2005 and August 2006, the dyslipidemia study randomized 309 patients at US centers; the hypercholesterolemia study, 304 patients. INTERVENTIONS: Dyslipidemia study: placebo, fenofibrate (200 mg), or LY518674 (10, 25, 50, or 100 microg) for 12 weeks. Hypercholesterolemia study: placebo or atorvastatin (10 or 40 mg) for 4 weeks, then placebo or LY518674 (10 or 50 microg) for 12 more weeks. MAIN OUTCOME MEASURES: Dyslipidemia study: percentage change in levels of HDL-C and triglycerides. Hypercholesterolemia study: percentage change in levels of LDL-C. RESULTS: Dyslipidemia study: LY518674 (25 mug) and fenofibrate increased HDL-C by 5.9 and 5.5 mg/dL (15.8% and 14.4%) (both P< or =.001 vs placebo, P = .79 between treatments). Higher LY518674 doses yielded smaller increases. LY518674 decreased triglycerides by 97.3 to 114.5 mg/dL (34.9% to 41.7%) but was similar to fenofibrate. LY518674 produced a dose-dependent increase in LDL-C, reaching 20.4 mg/dL (19.5%) for the 100-mug dose vs 0.3 mg/dL (2.3%) for fenofibrate (P< or =.01). Fenofibrate and LY518674 (50 microg and 100 microg) increased serum creatinine (P< or =.001 vs placebo), with 38% and 37.3% of patients exceeding the normal range. Fenofibrate, but not LY518674, increased creatine phosphokinase (P = .004 vs placebo). Hypercholesterolemia study: LY518674 (10 mug or 50 microg) decreased LDL-C by 21.4 to 26.0 mg/dL (13.2%-15.8%) and triglycerides approximately 37% for both doses, and increased HDL-C by 6.3 to 6.7 mg/dL (12.5%-15.0%). When added to atorvastatin, LY518674 changed HDL-C by -0.7 to 6.2 mg/dL (-0.6% to 11.9%) and significantly decreased triglycerides but had no additional effect on LDL-C. CONCLUSIONS: In patients with dyslipidemia, LY518674 and fenofibrate decreased triglycerides and increased HDL-C but also increased serum creatinine. LY518674, but not fenofibrate, increased LDL-C. In those with hypercholesterolemia, LY518674 reduced triglycerides and increased HDL-C, but did not further reduce LDL-C in combination with atorvastatin. Fenofibrate and LY518674 both raised safety concerns. TRIAL REGISTRATION: clinicaltrials.gov Identifiers: NCT00133380 and NCT00116519

Distinct temporal-spatial roles for rho kinase and myosin light chain kinase in epithelial purse-string wound closure.

BACKGROUND & AIMS: Small epithelial wounds heal by purse-string contraction of an actomyosin ring that is regulated by myosin light chain (MLC) kinase (MLCK) and rho kinase (ROCK). These studies aimed to define the roles of these kinases in purse-string wound closure. METHODS: Oligocellular and single-cell wounds were created in intestinal epithelial monolayers. Fluorescence imaging and electrophysiologic data were collected during wound closure. Human biopsies were studied immunohistochemically. RESULTS: Live-cell imaging of enhanced green fluorescent protein-beta-actin defined rapid actin ring assembly within 2 minutes after wounding. This progressed to a circumferential ring within 8 minutes that subsequently contracted and closed the wound. We therefore divided this process into 2 phases: ring assembly and wound contraction. Activated rho and ROCK localized to the wound edge during ring assembly. Consistent with a primary role in the assembly phase, ROCK inhibition prevented actin ring assembly and wound closure. ROCK inhibition after ring assembly was complete had no effect. Recruitment and activation of MLCK occurred after ring assembly was complete and coincided with ring contraction. MLCK inhibition slowed and then stopped contraction but did not prevent ring assembly. MLCK inhibition also delayed barrier function recovery. Studies of human colonic biopsy specimens suggest that purse-string wound closure also occurs in vivo, because MLC phosphorylation was enhanced surrounding oligocellular wounds. CONCLUSIONS: These results suggest complementary roles for these kinases in purse-string closure of experimental and in vivo oligocellular epithelial wounds; rho and ROCK are critical for actin ring assembly, while the activity of MLCK drives contraction.

An opioid basis for early-phase isoflurane-induced hypotension in rats.

This study was conducted to more clearly delineate the possible role of endogenous opioid receptors and opioid peptides in general anesthesia-associated hypotension in rats. Exposure to 2% isoflurane in oxygen produced a triphasic change in mean arterial pressure (MAP), including an early phase in which MAP fell by -28.4 +/- 2.2%. The magnitude of this early-phase hypotension was attenuated in rats pretreated with intravenous (i.v.) mu-subtype-selective doses of either naloxone or methylnaloxone but not central doses of the selective mu-opioid antagonist beta-funaltrexamine. This early hypotensive phase was also reduced following i.v. pretreatment with antiserum against methionine-enkephalin but not beta-endorphin. These findings suggest that early-phase isoflurane-induced hypotension may be due to activation of peripheral mu-opioid receptors by an endogenous opioid peptide, possibly related to methionine-enkephalin.