Environmental enteropathy is associated with cardiometabolic risk factors in Peruvian children.

Environmental enteropathy (EE) is a syndrome of altered small intestine structure and function hypothesized to be common among individuals lacking access to improved water and sanitation. There are plausible biological mechanisms, both inflammatory and non-inflammatory, by which EE may alter the cardiometabolic profile. Here, we test the hypothesis that EE is associated with the cardiometabolic profile among young children living in an environment of intense enteropathogen exposure. In total, 156 children participating in the Peruvian cohort of a multicenter study on childhood infectious diseases, growth and development were contacted at 3-5 years of age. The urinary lactulose:mannitol ratio, and plasma antibody to endotoxin core were determined in order to assess intestinal permeability and bacterial translocation. Blood pressure, anthropometry, fasting plasma glucose, insulin, and cholesterol and apolipoprotein profiles were also assessed. Extant cohort data were also used to relate biomarkers of EE during the first 18 months of life to early child cardiometabolic profile. Lower intestinal surface area, as assessed by percent mannitol excretion, was associated with lower apolipoprotein-AI and lower high-density lipoprotein concentrations. Lower intestinal surface area was also associated with greater blood pressure. Inflammation at 7 months of age was associated with higher blood pressure in later childhood. This study supports the potential for a relationship between EE and the cardiometabolic profile.

Preoperative anxiety and fear: a comparison of assessments by patients and anesthesia and surgery residents.

We sought to compare self-assessment of preoperative anxiety levels and selection of worst fears by surgical patients with the assessments made by the anesthesia and surgery residents providing intraoperative care for those patients. One hundred inpatients at a Veterans Affairs hospital (Group 1) and 45 patients at a University hospital (Group 2) were asked to complete a brief questionnaire; the residents were asked to complete the same questionnaire. Group 1 results showed that median patient visual analog scale (VAS) scores were lower for anxiety about anesthesia compared to surgery (16 vs 22, P < or = 0.05). Anesthesia resident VAS scores were higher than patient or surgery resident scores. Neither type of resident was able to predict their individual patient's VAS score (Kendall's tau). The fear chosen with the greatest incidence by Group 1 patients and residents was "whether surgery would work". A significant number of residents (34%, anesthesia or surgery, P < or = 0.05) matched their patient's fear choice. Residents commonly chose fears related to their specialty (e.g., anesthesia residents chose anesthesia-related fears more often than surgery residents, 50% vs 28%, P < or = 0.001). In Group 2, residents demonstrated an improved ability to predict patient scores. For instance, both surgery and anesthesia residents were able to predict individual University patient VAS scores (P < or = 0.01). The fear chosen with the greatest frequency by Group 2 patients was "pain after the operation". Sixty percent of anesthesia residents matched their patients' fear choice (P < or = 0.001). This study indicates a variable ability of anesthesia and surgery residents to predict patient anxiety and fear which may be due, in part, to difficulty in understanding a Veterans Affairs hospital patient population.

The effect of cimetidine and ranitidine on the duration of action of succinylcholine.

A recent study suggested that cimetidine prolongs the duration of action of succinylcholine (SCh). We examined this reported interaction, and investigated whether it is the result of inhibition of plasma cholinesterase (PChE). We also studied the effect of ranitidine on the duration of action of succinylcholine. Thirty patients were randomly assigned to three groups to receive oral cimetidine 300 mg or ranitidine 150 mg or no H2-antagonist the night before surgery and again 1-2 hours prior to induction of anesthesia. Succinylcholine (1.5 mg/kg i.v.) was given to facilitate tracheal intubation after induction of anesthesia; neuromuscular function was monitored by evoked compound electromyogram. Pretreatment blood samples were analyzed for PChE activity. PChE activity and levels of appropriate H2-antagonists were measured in preinduction blood samples. No significant effect of either cimetidine or ranitidine on the duration of action of SCh or PChE activity was demonstrated. We conclude that H2-antagonists administered preoperatively do not prolong the duration of action of succinylcholine or alter PChE activity.