251: Numeracy and literacy in pregnant women with pregestational diabetes

women with pregestational diabetes Etoi Garrison, Cornelia Graves, Rebecca Gregory, Russell Rothman, James Slaughter, Sarah Fletcher, Kelly A. Bennett Vanderbilt University School of Medicine, Obstetrics and Gynecology, Nashville, TN, St. Thomas Health-Baptist Hospital, Obstetrics and Gynecology, Nashville, TN, Vanderbilt University Medical Center, Eskind Diabetes Center, Nashville, TN, Vanderbilt University School of Medicine, Medicine, Nashville, TN, Vanderbilt University School of Medicine, Biostatistics, Nashville, TN, Vanderbilt University School of Medicine, Obstetrics and Gynecology, Nashville, TN OBJECTIVE: Numeracy is defined as the ability to use numbers and math in daily life. Diabetes-related numeracy skills may be used to perform diabetes-related tasks for self-management of Type 1 and Type 2 diabetes. Inadequate health literacy and poor diabetes-related numeracy have been found to be independently associated with poor glycemic control among nonpregnant adult diabetics. This association in diabetes during pregnancy has not been well studied. We investigated this association in a defined pregnant diabetic population. STUDY DESIGN: Subjects were prospectively enrolled and administered validated measures of literacy (REALM), diabetes-related numeracy (DNT), and perceived self-efficacy (PDSMS). Glucose meter readings and A1C data were collected at baseline enrollment and prior to delivery. Univariate analyses were conducted. RESULTS: Fifty-eight subjects were recruited, 52% (n 30) with Type 1 and 48 % (n 28) with Type 2 diabetes. Subjects were high school educated, but 8% had less than 9th grade literacy skills. Mean baseline A1C was 7.0%, mean DNT score was 84 out of 100. Thirty-three percent could not use a food label to determine caloric content based upon serving size. Seventy-one percent of the Type 2 diabetics and 41 % of the Type 1 diabetics were unable to use a nutrition label to calculate carbohydrate grams based upon serving size. Eighteen percent of the Type 2 diabetics could not use numerical hierarchy to determine which glucose values were above or below a normal reference range. Health literacy and DNT scores were negatively and significantly associated with HgBA1C (r2 0.08 p 0.04; r2 0.11, p 0.01), respectively. Every 14% increase in DNT score was associated with a 0.35 (Type I) and 0.52 (Type II) decrease in HgBA1C (p 0.04). CONCLUSION: In this defined group, health literacy and numeracy-dependent diabetes self-management skills were significantly associated with better glycemic control. This data may be useful in the development of targeted diabetes education tools in pregnancy. 252 TNF alpha has a direct inhibitory effect on Ca2 responses necessary for eNOS activation in primary HUVEC Heather Bankowski, Fu Xian Yi, Derek Boeldt, Dinesh Shah, Ian Bird University of Wisconsin, Obstetrics and Gynecology, Maternal Fetal Medicine, Madison, WI, University of Wisconsin, Obstetrics and Gynecology, Madison, WI, University of WI School of Medicine and Public Health, Obstetrics and Gynecology, Madison, WI, University of WI School of Medicine and Public Health, Obstetrics and Gynecology, Maternal Fetal Medicine, Madison, WI, University of WI School of Medicine and Public Health, Obstetrics and Gynecology & Pediatrics, Madison, WI OBJECTIVE: Evidence suggests that the pathologic metabolic state of diabetes mellitus(DM)results in oxidative stress. Tumor necrosis factor alpha (TNF ) has been shown to induce intracellular reactive oxygen species formation and is proposed to be a significant perpetrator of insulin resistance in gestational diabetes mellitus (GDM). Previously we have shown in DM HUVEC in vivo ROS damage to eNOS protein. Even in GDM patients, there is a overall decrease in NO production consistent with ROS damage of functional eNOS protein, despite maintenance of eNOS protein levels. It is known that sustained Ca2 elevation is also required for eNOS activity. Could TNF also inhibit NO production at the level of Ca2 signaling? Hypothesis: The decrease in agonist stimulated NO production due to TNF stimulated ROS production may not only occur through damage to eNOS protein in DM HUVEC but may also involve direct impairment of Ca2 signaling mechanisms necessary for eNOS activation. STUDY DESIGN: HUVEC cells from a combined pool of control patients were prepared at a density of 95%. HUVEC underwent acute (30 minutes)and chronic (16 hours) treatments with 50, 10 or 1 ng/ml TNF prior to imaging using Fura-2 to detect Ca2 in real time in response to 30 minute stimulation with ATP (100 uM). RESULTS: There were statistically significant reductions (P 0.05) in burst numbers in cells in the acute and chronic TNF treatment groups (Fig. 1). The decrease in Ca2 bursts was dose dependent in each case. In addition to the damaged eNOS protein itself, there is an acute, direct effect of TNF to directly inhibit eNOS activation by also impairing sustained Ca2 signaling in the form of repetitive bursts. These in vitro findings compliment our prior observations on in vivo ROS damage to eNOS in DM HUVEC. CONCLUSION: Ultimately, such improved understanding of the inhibitory role of TNF and other inflammatory cytokines will lead to a therapeutic strategy to reduce oxidative stress and development of macro and micro-vascular complications in pregnancies complicated by DM. www.AJOG.org Diabetes, Labor, Medical-Surgical-Disease, Obstetric Quality & Safety, Prematurity, Ultrasound-Imaging Poster Session II