E S Kilpatrick

Hull and East Yorkshire Hospitals NHS Trust, Kingston upon Hull, England, United Kingdom

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Publications (157)717.47 Total impact

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    ABSTRACT: Background. Hyponatraemia, the commonest electrolyte abnormality amongst in-patients, is associated with increased mortality. Until recently, there has been a lack of international consensus management of patients with severe hyponatraemia. Aim. We performed a retrospective study in two teaching hospitals in Yorkshire, UK, to evaluate the management of patients with severe hyponatraemia (serum Na ≤ 110 mmol/L) and to assess the frequency of complications observed in this group, in particular central pontine myelinolysis (CPM) and death. Methods. Retrospective data collection was performed on all of patients admitted with severe hyponatraemia in a calendar year in two teaching hospitals in Yorkshire. A detailed case note evaluation was conducted to determine the patient clinical characteristics, aetiology, investigations performed, treatment, complications and outcome of patients. Results. We identified 39 patients in total at both sites over a calendar year. There was a notable female predominance (n = 27), with the median (range) age being 65 (45–92) years and median sodium concentration 107 (94–110) mmol/L. Hyponatraemia was classified as acute (onset < 48 h) in six patients, chronic (onset > 48 h) in 20 patients and of unknown duration in 13 patients. Iatrogenic hyponatraemia secondary to drugs, especially thiazides was the most commonly observed aetiology. The mortality rate was 48.7% (n = 19) at the end of one year after admission episode and CPM was seen in 7.6% (n = 3) of patients. Conclusions. Severe hyponatraemia is associated with significant morbidity and mortality. Drug-induced hyponatraemia was the most common aetiology observed in our group of patients.
    Scandinavian Journal of Clinical & Laboratory Investigation. 10/2014;
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    ABSTRACT: Obese patients with type two diabetes mellitus (T2DM) may have a better prognosis than patients of normal weight, but reports are limited by study size, duration and confounders.
    Heart (British Cardiac Society) 06/2014; 100(Suppl 3):A66. · 5.01 Impact Factor
  • Eric S Kilpatrick, Stephen L Atkin
    BMJ (online) 04/2014; 348:g2867. · 17.22 Impact Factor
  • Thozhukat Sathyapalan, Stephen Atkin, Eric Stephen Kilpatrick
    Annals of Clinical Biochemistry 04/2014; · 1.92 Impact Factor
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    ABSTRACT: Polycystic ovary syndrome (PCOS) is commonly associated with insulin resistance (IR), dyslipidaemia and subsequent risk of diabetes and cardiovascular (CV) disease. Lowering triglycerides by atorvastatin in PCOS was associated with improved IR and CV risk. This study investigated the effect of long-term niacin/laropiprant therapy on CV risk and IR in obese women with PCOS. In this double-blind randomized placebo-controlled trial, 13 and 12 PCOS women completed a 12 week course of niacin/laropiprant or placebo respectively. Fasted subjects had an endothelial function test (EndoPat2000) and then consumed a mixed meal with blood sampled postprandially for 6 hour before and after intervention. Changes in High density lipoprotein cholesterol (HDL-c), triglycerides, Reactive hyperaemic index (RHI), high sensitivity c reactive protein (hsCRP) and insulin sensitivity were measured. By 12 weeks, niacin/laropiprant lowered low density lipoprotein-cholesterol (13%) and increased HDL-c (17%). Despite a reduction in fasting triglycerides (21%), the drug had no effect on their postprandial rise (2.69 ±1.44 vs. 2.49 ± 1.14 mmol/L, p = 0.72). However, following the mixed meal, plasma glucose area under the curve increased from 13.1 ± 2.9 to 14.0 ±mmol/L, p = 0.05, as a consequence of both increased insulin resistance (HOMA-IR: 2.2 (1.2, 4.2) vs. 3.8(1.3, 5.5), p = 0.02) and a reduced acute insulin response to glucose (424 (211,975) vs. 257(122,418) pmol/mmoL, p = 0.04). Niacin/laropiprant did not improve RHI (1.97 ± 0.40 vs. 2.05 ± 0.58, p = 0.33) or hsCRP. In PCOS, Niacin/laropiprant had a significant negative impact on postprandial glucose and no improvement in postprandial hypertriglyceridaemia, with at least the former mediated through increased insulin resistance and reduced beta cell function. This data may help explain why the improvement in fasting lipids has not translated into improved cardiovascular risk markers in PCOS. Clinical trial registration Number (www.clinicaltrials.gov): NCT01118598.
    Diabetes Obesity and Metabolism 01/2014; · 5.18 Impact Factor
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    ABSTRACT: Atherothrombosis is associated with platelet hyperactivity. Hypertriglyceridemia and insulin resistance (IR) are features of polycystic ovary syndrome (PCOS). The effect of induced hypertriglyceridemia on IR and platelet function was examined in young women with PCOS. Following overnight fasting, 13 PCOS and 12 healthy women were infused with saline or 20% intralipid for 5 hours on separate days. Insulin sensitivity was measured using a hyperinsulinemic euglycaemic clamp in the final 2 hours of each infusion. Platelet responses to adenosine diphosphate (ADP) and prostacyclin (PGI2) were measured by flow cytometric analysis of platelet fibrinogen binding and P-selectin expression using whole blood taken during each infusion (at 2 hours) and at the end of each clamp. Lipid infusion increased triglycerides and reduced insulin sensitivity in both controls (median, interquartile range ) (5.25 [3.3, 6.48] versus 2.60 [0.88, 3.88] mg kg(-1) min(-1), P<0.001) and PCOS (3.15 [2.94, 3.85] versus 1.06 [0.72, 1.43] mg kg(-1) min(-1), P<0.001). Platelet activation by ADP was enhanced and ability to suppress platelet activation by PGI2 diminished during lipid infusion in both groups when compared to saline. Importantly, insulin infusion decreased lipid-induced platelet hyperactivity by decreasing their response to 1 μmol/L ADP (78.7% [67.9, 82.3] versus 62.8% [51.8, 73.3], P=0.02) and increasing sensitivity to 0.01 μmol/L PGI2 (67.6% [39.5, 83.8] versus 40.9% [23.8, 60.9], P=0.01) in controls, but not in PCOS. Acute hypertriglyceridemia induced IR, and increased platelet activation in both groups that was not reversed by insulin in PCOS subjects compared to controls. This suggests that platelet hyperactivity induced by acute hypertriglyceridemia and IR could contribute athero-thrombotic risk. www.isrctn.org. Unique Identifier: ISRCTN42448814.
    Journal of the American Heart Association. 01/2014; 3(1):e000706.
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    Eric S Kilpatrick, Zachary T Bloomgarden
    Diabetes care 12/2013; 36(12):e215. · 7.74 Impact Factor
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    ABSTRACT: Insulin resistance (IR) after bariatric surgery is significantly lower than controls matched for body mass index (BMI) and is indistinguishable from lean subjects however it is not known if this is the same for associated cardiovascular risk (CVR) markers (endothelial function (EF) and clot structure and function (maximum absorbance (MA) lysis potential (LT) and clot formation time (FT). We sought to determine if IR and associated CVR markers one year after bariatric surgery were comparable to post surgery age and BMI matched controls. Ten patients had before and 12 months after Roux-en-Y surgery CVR measurements compared to controls. BMI reduced after surgery to 33.3±1.7 kg/m(2) p<0.001 comparable to controls 32.6±1.6 kg/m(2) p=0.87. Fasting glucose reduced after surgery to 4.6±0.1 mmol/L, lower than controls 5.0±0.1 mmol/L p=0.03. IR (calculated using HOMA-IR) reduced 0.77±0.14 p=0.03 and was lower than controls 2.35±0.32 p= 0.02. Systolic blood pressure (BP) reduced to 114.2±3.6 mmHg which was lower than controls 127.7±4.1 mmHg p=0.04, but diastolic BP was unaffected by surgery and no different to controls. EF, hsCRP and HDL-cholesterol improved after surgery and did not differ to controls. Markers of blood clotting: MA and FT were unaffected by surgery and no different to controls, LT improved after surgery 3078±580 to 1665±330s p= 0.04) and was no different to controls (2088±556s p=0.12) CONCLUSIONS: Bariatric surgery improved cardiovascular risk parameters to that of the equivalent controls post surgery for weight including EF, hsCRP and LT supporting bariatric surgery as an effective management of obesity.
    Obesity Surgery 11/2013; · 3.10 Impact Factor
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    ABSTRACT: BACKGROUND:Many countries have implemented, or are considering, a change in hemoglobin A1c (Hb A1c) units from traditional percentage values [Diabetes Control and Complications Trial (DCCT)] to the new Système International d'Unités (SI) unit in millimoles per mole. Concern exists that such a large alteration in numeric values might lead, through confusion, to a deterioration in patients' glycemia. This study has assessed Hb A1c in the year before and after the change of units in a UK diabetes population.METHODS:The Hb A1c in the 12 months immediately before the unit change (October 2010 to September 2011) was compared with the 12 months after (October 2011 to September 2012). Also, the subsequent change in Hb A1c in patients who had poor glycemic control [Hb A1c >8% (64 mmol/mol)], either before or after the unit change, was compared.RESULTS:Over the 2 years, 44 721 Hb A1c measurements were requested on 13 197 (7247 male, 5950 female) known diabetes patients. The population Hb A1c was no different between years, with a median [interquartile range (IQR)] value of 7.5% (6.6%-8.7%) after the change and 7.5% (6.5-8.7) before (P = 0.34). The subsequent change in Hb A1c following a raised (>8%) result was the same regardless of whether the initial value reported was in DCCT or SI units [median (IQR) change in Hb A1c -0.2% (-0.9% to 0.3%), n = 4316, following a DCCT result, vs -0.2% (-0.8% to 0.3%), n = 4396, following SI; P = 0.44].CONCLUSIONS:In this UK diabetes population, a move to SI Hb A1c reporting did not lead to any marked short-term deterioration in glycemia or a different Hb A1c outcome in patients with initial poor glucose control.
    Clinical Chemistry 06/2013; · 7.15 Impact Factor
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    ABSTRACT: AIMS: HbA1c values are unreliable in patients with diabetes who have chronic kidney disease who receive iron and/or erythropoiesis stimulating agents. The study aimed to evaluate the utility of the complementary glycaemic markers glycated albumin, fructosamine and 1,5 anhydroglucitol in this group of patients. METHODS: A prospective study of patients with Type 2 diabetes and chronic kidney disease stage IIIB/IV undergoing intravenous iron or erythropoiesis-stimulating agent therapy. Glycaemic control was monitored using HbA1c , seven-point daily glucose thrice weekly, continuous glucose monitoring, glycated albumin, fructosamine and 1,5 anhydroglucitol. RESULTS: Fifteen patients [9 men; median age 72 years (interquartile range 68-74), follow-up period (16.4 ± 3.7 weeks)] received parenteral iron; 15 patients [11 men; 70 years (interquartile range 62-75), (17.3 ± 3.3 weeks)] received erythropoiesis-stimulating agent. HbA1c fell following treatment with both iron [57 mmol/mol (7.4%) to 53 mmol/mol (7.0%), P < 0.001] and erythropoiesis-stimulating agent [56 mmol/mol (7.3%) to 49 mmol/mol (6.6%), P = 0.01] despite mean blood glucose remaining unchanged (iron: 9.55 to 9.71 mmol/l, P = 0.07; erythropoiesis-stimulating agent: 8.72 to 8.78 mmol/l, P = 0.89). Unlike HbA1c , the glycated albumin, fructosamine and 1,5 anhydroglucitol levels did not change following iron [glycated albumin (16.8 to 16.3%, P = 0.10); fructosamine (259.5 to 256 μmol/l, P = 0.89); 1,5 anhydroglucitol (54.2 to 50.9 μmol/l, P = 0.89)] or erythropoiesis-stimulating agent [glycated albumin (17.9 to 17.5%, P = 0.29), fructosamine (324.3 to 306.0 μmol/l, P = 0.52), 1,5 anhydroglucitol (58.2 to 46.7 μmol/l, P = 0.35)]. Despite this, HbA1c was consistently the marker most closely related to mean blood glucose before and after each treatment (R range 0.7-0.88). CONCLUSIONS: These data indicate that HbA1c was statistically most closely related to mean blood glucose, but clinical trends in glycaemia in patients undergoing iron or erythropoiesis-stimulating agent therapy are likely best assessed by including one of these additional glycaemic markers. This article is protected by copyright. All rights reserved.
    Diabetic Medicine 06/2013; · 3.24 Impact Factor
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    ABSTRACT: BACKGROUND: Women with polycystic ovary syndrome (PCOS) have an adverse cardiovascular risk profile and an increased prevalence of non-alcoholic fatty liver disease (NAFLD) which is also associated with an adverse cardiovascular risk profile. OBJECTIVE: To compare the cardiovascular risk profile of women with PCOS alone and women with PCOS and NAFLD. DESIGN, SETTING AND PARTICIPANTS: Twenty-five oligoanovulatory women with PCOS were screened for NAFLD (including liver biopsy if appropriate) and had their cardiovascular risk factors measured which included the inflammatory marker (CRP), endothelial function (measured using endoPAT 2000 and serum markers (ICAM-1, VCAM-1, E-selectin and P-selectin)) and clot structure and function (maximum absorbance (MA), and lysis potential (LT)). RESULTS: 12 patients had confirmed PCOS without evidence of NAFLD and 13 patients had confirmed PCOS with evidence of NAFLD. The PCOS and NAFLD group were heavier (BMI 43.9±2.2 kg/m(2) ) compared to the PCOS alone group (BMI 37.6±1.4 kg/m(2) p=0.03). There was no difference in CRP (7.57±0.95 vs 6.59±1.87 mmol/L p=0.62) or endothelial function (RH-PAT 1.96±0.1 vs 1.74±0.16 p=0.25, ICAM-1 (221±48 vs 250±60 ng/ml p=0.19), VCAM-1 (2124±78 vs 2314±91 ng/ml p=0.13), E-selectin (33.9±3.3 vs 39.5±15.5 ng/ml p=0.31) and P-selectin (101.0±6.6 vs 95.9±10.2 ng/ml p=0.69)). There was no difference in clot formation or lysis. CONCLUSION: The patients with PCOS and NAFLD were heavier compared to patients with PCOS alone. Despite this we were unable to demonstrate differences in inflammatory markers, endothelial function or clot structure and function, suggesting that severity of steatosis is not the most important determinant of cardiovascular risk in PCOS. This article is protected by copyright. All rights reserved.
    Clinical Endocrinology 06/2013; · 3.40 Impact Factor
  • A J Dawson, T Sathyapalan, S L Atkin, E S Kilpatrick
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    ABSTRACT: Biological variation refers to the natural fluctuations found when repeated measurements are made in a biological system. Generally, biological variation remains within narrow boundaries in health, but may differ in pathological states, with implications for the diagnosis and monitoring of disease processes. In disease, biological variation may alter such that any subsequent measurement may need to have a greater difference compared with a healthy control to be biologically relevant. Treatments such as insulin or anti-hypertensive therapy have been shown to reduce biological variability closer to normal levels and theoretically this may help prevent complication development or progression in conditions such as diabetes. This article reviews how biological variation can influence our identification and assessment of vascular risk factors in a person with diabetes. The role of biological variation in the diagnosis of diabetes (glucose and HbA(1c) ) is then examined. Finally, the influence that common treatments in diabetes have in modifying biological variation is described. © 2013 The Authors. Diabetic Medicine © 2013 Diabetes UK.
    Diabetic Medicine 02/2013; · 3.24 Impact Factor
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    ABSTRACT: The pleiotropic effect of statins may be mediated in part through raising vitamin D (25OHD) concentrations. It has also been shown that an increase in oxidative stress and inflammatory markers are a feature of patients with type 2 diabetes (T2DM). A cross-over study of 26 patients with T2DM taking either simvastatin 40mg or atorvastatin 10mg was undertaken. After 3 months on one statin, lipids, hsCRP, 25OHD and MDA were measured repeatedly. The same procedure was then followed taking the other statin. Despite similar lipid lowering, the mean 25OHD was higher on atorvastatin compared to simvastatin and the mean MDA and hsCRP levels lower, irrespective of which statin the patients were taking before crossover. The changes in 25OHD predicted changes in CRP and MDA levels. Thus, compared to simvastatin, atorvastatin demonstrates apparently beneficial pleiotropic effects in respect of 25OHD concentrations as well as markers of oxidative stress and inflammation in patients with T2DM.
    Diabetes Obesity and Metabolism 01/2013; · 5.18 Impact Factor
  • E S Kilpatrick, A S Rigby, R E Warren, S L Atkin
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    ABSTRACT: AIMS: Recurrent severe hypoglycaemia in a patient with diabetes is strongly associated with a crash risk while driving. To help ensure road safety, recent changes were made to European Union driving regulations for patients with diabetes. These included the recommendation that more than one episode of severe hypoglycaemia within 12 months would lead to the loss of a driving licence. This study has assessed the impact of this regulation if applied to patients who participated in the Diabetes Control and Complications Trial. METHODS: All patients in the Diabetes Control and Complications Trial were assumed to be drivers. Repeated hypoglycaemic episodes within a year were determined during the mean 6.5 years of the study. RESULTS: Of the 1441 patients in the Diabetes Control and Complications Trial, 439 (30%) had more than one severe hypoglycaemic episode during a 12-month period of their study participation. Amongst the study groups, 312/711 (44%) of intensively treated and 127/730 (17%) of conventionally treated patients would have lost their licence at some point during the trial. The risk of licence loss increased with lower mean HbA(1c) , longer duration of diabetes and younger age (all P < 0.001). CONCLUSIONS: More than one episode of severe hypoglycaemia within a year was a frequent event in subjects in the Diabetes Control and Complications Trial, especially in intensively treated patients. If applied to current practice, improving road safety through these changes to European Union regulations could have a substantial impact on drivers who have Type 1 diabetes. This emphasizes the need to take into account the potential effects of severe hypoglycaemia in those who rely on a driving licence. © 2012 The Authors. Diabetic Medicine © 2012 Diabetes UK.
    Diabetic Medicine 12/2012; · 3.24 Impact Factor
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    ABSTRACT: [Box: see text] CME ACCREDITATION NEEDS ASSESSMENT/PROGRAM OVERVIEW There is a need for greater caution in interpreting glycated hemoglobin (A1C) results, which can be inaccurate in individual patients for a wide variety of reasons beyond the patient's control. In addition, A1C alone may not reflect critical aspects of glycemia. A panel of clinical experts from Europe and North America was convened to reexamine our glucose measuring tools and determine ways in which they can better be applied toward more purposeful processes of glycemic management. Among the main issues addressed were the clinical situations in which A1C should not be used, the role of alternative biomarkers in identifying aspects of glycemic dysregulation not captured by A1C, and the value of using patients' own glucose data to consolidate therapeutic, educational, and behavior-change objectives. TARGET AUDIENCE This activity has been designed to meet the educational needs of physicians and registered nurses involved in the management of patients with diabetes. ACCREDITATION AND CREDIT DESIGNATION Physician Continuing Education This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education through the joint sponsorship of Postgraduate Institute for Medicine, Mary Ann Liebert, Inc., and The Diabetes Education Group. Postgraduate Institute for Medicine is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. Postgraduate Institute for Medicine designates this journal-based CME activity for a maximum of 1.0 AMA PRA Category 1 Credit(s)™. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Nursing Continuing Education This educational activity for 1 contact hour is provided by Postgraduate Institute for Medicine. Postgraduate Institute for Medicine is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's Commission on Accreditation. Initial Release Date: October 15, 2012 Expiration Date: October 15, 2013 Estimated Time to Complete Activity: 1 hour Instructions for Receiving Credit There are no fees for participating and receiving CME credit for this activity. During the period October 15, 2012 through October 15, 2013, participants must read the learning objectives and faculty disclosures and study the educational activity. Postgraduate Institute for Medicine supports Green CME by offering your Request for Credit online. If you wish to receive acknowledgment for completing this activity, please complete the posttest and evaluation available online at www.cmeuniversity.com On the navigation menu, click on "Find Post-test/Evaluation by Course" and search by course ID 9068. Upon registering and successfully completing the posttest with a score of 70% or better and the activity evaluation, your certificate will be made available immediately. Processing credit requests online will reduce the amount of paper used by nearly 100,000 sheets per year. DISCLOSURE OF UNLABELED USE/DISCLAIMER This educational activity may contain discussion of published and/or investigational uses of agents that are not indicated by the Food and Drug Administration. Postgraduate Institute for Medicine, Mary Ann Liebert, Inc., The Diabetes Education Group, and Bayer HealthCare, Diabetes Care do not recommend the use of any agent outside of the labeled indications. The opinions expressed in the educational activity are those of the faculty and do not necessarily represent the views of Postgraduate Institute for Medicine, Mary Ann Liebert, Inc., The Diabetes Education Group, and Bayer HealthCare, Diabetes Care. Please refer to the official prescribing information for each product for discussion of approved indications, contraindications, and warnings. Participants have an implied responsibility to use the newly acquired information to enhance patient outcomes and their own professional development. The information presented in this activity is not meant to serve as a guideline for patient management. Any procedures, medications, or other courses of diagnosis or treatment discussed or suggested in this activity should not be used by clinicians without evaluation of their patient's conditions and possible contraindications on dangers in use, review of any applicable manufacturer's product information, and comparison with recommendations of other authorities. DISCLOSURE OF CONFLICTS OF INTEREST Postgraduate Institute for Medicine assesses conflict of interest with its instructors, planners, managers, and other individuals who are in a position to control the content of CME activities. All relevant conflicts of interest that are identified are thoroughly vetted by Postgraduate Institute for Medicine for fair balance, scientific objectivity of studies utilized in this activity, and patient care recommendations. Postgraduate Institute for Medicine is committed to providing its learners with high-quality CME activities and related materials that promote improvements or quality in healthcare and not a specific proprietary business interest of a commercial interest. FACULTY DISCLOSURES Irl B. Hirsch, MD Consulting: Roche Diagnostics, Johnson & Johnson, Abbott Diabetes Care Contracted Research: sanofi-aventis, Halozyme Therapeutics Stephanie A. Amiel, BSc, MD Consulting: Roche Diagnostics, Medtronic, Janssen Pharmaceuticals Ian R. Blumer, MD Consulting: AstraZeneca, Bayer Diabetes Care, Bristol Myers Squibb, Eli Lilly, GlaxoSmithKline, Novo Nordisk, Medtronic, sanofi-aventis Bruce W. Bode, MD Consulting: Bayer HealthCare Pharmaceuticals Steven V. Edelman, MD Consulting: Bayer HealthCare Pharmaceuticals, LifeScan, Abbott Laboratories, DexCom, Roche Diagnostics Jane J. Seley, DNP, MPH, MSN, BC-ADM, CDE Consulting: Abbott Diabetes Care, Bayer HealthCare Pharmaceuticals Carol A. Verderese, BA No relevant financial relationships to disclose Eric S. Kilpatrick, MD Consulting: Bayer HealthCare Pharmaceuticals STAFF DISCLOSURES The following Postgraduate Institute for Medicine planners and managers-Trace Hutchison, PharmD; Samantha Mattiucci, PharmD; Jan Schultz, RN, MSN, CCMEP; Laura Excell, ND, NP, MS, MA, LPC, NCC; and Patricia Staples, MSN, NP-C, CCRN-hereby state that they or their spouse/life partner do not have any financial relationships or relationships to products or devices with any commercial interest related to the content of this activity of any amount during the past 12 months. The staff at Mary Ann Liebert, Inc. and The Diabetes Education Group hereby state that they or their spouse/life partner do not have any financial relationships or relationships to products or devices with any commercial interest related to the content of this activity of any amount during the past 12 months. JOINT SPONSORSHIP STATEMENT This activity is jointly sponsored/co-provided by Postgraduate Institute for Medicine, Mary Ann Liebert, Inc., and the Diabetes Education Group. COMMERCIAL SUPPORT This activity is supported by an unrestricted educational grant from Bayer HealthCare, Diabetes Care. EDUCATIONAL OBJECTIVES After completing this activity, the participant should be better able to: • Recognize the potential limitations of A1C when evaluating individual patients • Identify nonglycemic factors, other than methodical inaccuracies, that can falsely raise or lower A1C levels • Enumerate current methods for measuring short-term variations in blood glucose • Utilize patients' own self-monitoring of blood glucose data as a tool for diabetes education • Provide appropriate care and counsel for patients and their families   Media: Online and Print Journal article.
    Diabetes Technology &amp Therapeutics 10/2012; · 2.21 Impact Factor
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    ABSTRACT: AIMS: To investigate the effects of high-polyphenol chocolate upon endothelial function and oxidative stress in Type 2 diabetes mellitus during acute transient hyperglycaemia induced following a 75-g oral glucose challenge. METHODS: Ten subjects with Type 2 diabetes underwent a double-blinded randomized controlled crossover study. A 75-g oral glucose load was used to induce hyperglycaemia, which was administered to participants 60 min after they had ingested either low (control) or high-polyphenol chocolate. Participants undertook testing at weekly intervals, following an initial cocoa-free period. Endothelial function was assessed by both functional [reactive hyperaemia peripheral artery tonometry (EndoPAT-2000) and serum markers (including intercellular adhesion molecule 1, P-selectin and P-selectin glycoprotein ligand 1]. Urinary 15-F2t-isoprostane adjusted for creatinine was used as an oxidative stress marker. Measurements were made at baseline and 2 h post-ingestion of the glucose load. RESULTS: Prior consumption of high-polyphenol chocolate before a glucose load improved endothelial function (1.7 ± 0.1 vs. 2.3 ± 0.1%, P = 0.01), whereas prior consumption of control chocolate resulted in a significant increase in intercellular adhesion molecule 1 (321.1 ± 7.6 vs. 373.6 ± 10.5 ng/ml, P = 0.04) and 15-F2t-isoprostane (116.8 ± 5.7 vs. 207.1 ± 5.7 mg/mol, P = 0.02). Analysis of percentage changes from baseline comparing control and high-polyphenol chocolate showed a significant improvement for high-polyphenol chocolate in both measures of endothelial function (P < 0.05) and for urinary 15-F2t-isoprostane (P = 0.04). CONCLUSION: High-polyphenol chocolate protected against acute hyperglycaemia-induced endothelial dysfunction and oxidative stress in individuals with Type 2 diabetes mellitus. © 2012 The Authors. Diabetic Medicine © 2012 Diabetes UK.
    Diabetic Medicine 10/2012; · 3.24 Impact Factor
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    ABSTRACT: Background:It has been shown that there is an increase in oxidative stress in polycystic ovary syndrome (PCOS). Statins are considered to have a pleiotropic effect other than their lipid-lowering effect. These effects may be mediated in part by reducing oxidative stress.Methods:This randomized, double-blind, placebo-controlled study was conducted to assess the effect of atorvastatin on serum malondialdehyde (MDA) concentrations as a marker of oxidative stress in patients with PCOS. Forty medication-naïve patients with PCOS were randomized to either atorvastatin 20 mg daily or placebo for 3 months. A 3-month extension study for both groups of patients was undertaken with metformin 1500 mg daily after completing initial 3 months of atorvastatin or placebo.Results:There was a significant decrease of MDA concentrations with atorvastatin [mean (sem)] [0.29 (0.04) vs. 0.25 (0.02) μmol/liter; P < 0.01] compared with placebo [0.28 (0.02) vs. 0.29 (0.12) μmol/liter; P = 0.52]. Three months treatment with metformin resulted in further reduction of MDA levels with atorvastatin compared with baseline [0.25 (0.02) baseline vs. 0.23 (0.03) μmol/liter for atorvastatin treated; P = 0.02]. There was also a significant correlation between the reduction in MDA with a reduction in high-sensitivity C-reactive protein (r = 0.71, P < 0.01), an increase in 25-hydroxyvitamin D (25OHD; r = -0.68, P = 0.02), and a reduction in testosterone levels (r = 0.63, P = 0.01). Multiple linear regression analysis revealed Δ25OHD, ΔC-reactive protein, and Δtestosterone were independent predictors of changes in MDA after atorvastatin treatment. No correlation was observed between the reductions in serum MDA concentrations with changes in the lipid parameters.Conclusions:Twelve weeks of atorvastatin led to a significant reduction in oxidative stress as determined by MDA concentrations among patients with polycystic ovary syndrome that was independently predicted by changes in testosterone, 25OHD, and high-sensitivity C-reactive protein.
    The Journal of Clinical Endocrinology and Metabolism 08/2012; · 6.31 Impact Factor
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    E S Kilpatrick
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    ABSTRACT: It is still unclear whether short-term, within-day, variability in glycaemic control is contributory to the development of diabetes micro- or macrovascular complications. However, consistent and compelling data are emerging that longer term fluctuations in glucose, as evidenced by increases in HbA(1c) variability, do indeed add to the mean HbA(1c) value in predicting the risk of microvascular disease. Until now, studies have found this to be the case mainly in type 1 diabetes, but in this issue of Diabetologia (DOI: 10.1007/s00125-012-2572-7 ) an analysis of the Tsukuba Kawai Diabetes Registry in Japan has found that HbA(1c) variability also predicts the risk of nephropathy in type 2 diabetic patients. These observations raise the possibility that reducing rises and falls in HbA(1c) may help avoid hyperglycaemia-related vascular disease without running the same risk of hypoglycaemia that a strategy focusing purely on lower HbA(1c) might incur.
    Diabetologia 06/2012; 55(8):2089-91. · 6.49 Impact Factor
  • A Wakil, K A Smith, S L Atkin, E S Kilpatrick
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    ABSTRACT: It is unknown whether glycaemic variability adds to the risk of microvascular complications of diabetes over and above the mean glucose value for a patient. We examined the effect of purposefully induced short-term glycaemic variability on oxidative stress markers. Eleven healthy subjects underwent three sequential glycaemic states; sustained hyperglycaemia, sustained euglycaemia and variable glycaemia, using glycaemic clamps for 3 h. Twenty-four hours urinary 8-isoprostane-PGF2α was measured before and after each glycaemic state to assess oxidative stress. The median and interquartile range of the urinary 8-iso-PGF2α in ng/24 h were (1373, 513), (996, 298) and (1227, 472) for the euglycaemic, hyperglycaemic and variable states, respectively. There was no significant difference in urinary isoprostanes between the three different states; mean ranks 20.9, 11.9 and 18.2 for the euglycaemic state, hyperglycaemic state and glycaemic variability state, respectively, p = 0.083. In conclusion, we did not see a significant increase in the urinary isoprostanes when glycaemic variability was induced under controlled conditions in healthy individuals.
    Diabetes Obesity and Metabolism 05/2012; 14(11):1047-9. · 5.18 Impact Factor
  • E S Kilpatrick, A S Rigby, S L Atkin, B M Frier
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    ABSTRACT: Severe hypoglycaemia may have a role in aggravating micro- and macrovascular disease in diabetes. Data from the Diabetes Control and Complication Trial have been reanalysed to ascertain whether the frequency of severe hypoglycaemia exerted an influence on the development and progression of retinopathy or nephropathy in people with Type 1 diabetes. Using binary longitudinal multiple logistic regression, HbA(1c) at study baseline, mean HbA(1c) throughout the study and the number of severe hypoglycaemic episodes during the trial were compared to examine the risk of development/progression of retinopathy and nephropathy. Average HbA(1c) during the study and/or HbA(1c) at baseline were independently predictive of retinopathy and nephropathy both in the intensively and the conventionally treated patients (all P ≤ 0.001). However, the number of hypoglycaemic episodes did not add to HbA(1c) in predicting retinopathy [odds ratio (95% CI) 0.99 (0.96-1.01), P = 0.51 in intensively treated patients, 0.94 (0.89-1.00), P = 0.05, conventional] or nephropathy [odds ratio (95% CI) 0.98 (0.95-1.01), P = 0.48 intensive, 1.03 (0.98-1.10), P = 0.17 conventional]. The frequency of exposure to severe hypoglycaemia did not predict a different risk of developing retinopathy or nephropathy in either treatment group of the Diabetes Control and Complications Trial at any given HbA(1c) .
    Diabetic Medicine 02/2012; 29(9):1195-8. · 3.24 Impact Factor

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  • 2005–2014
    • Hull and East Yorkshire Hospitals NHS Trust
      Kingston upon Hull, England, United Kingdom
  • 2002–2014
    • University of Hull
      • Diabetes and Endocrinology
      Kingston upon Hull, England, United Kingdom
  • 2009–2013
    • Hull York Medical School
      York, England, United Kingdom
    • University of Glasgow
      Glasgow, Scotland, United Kingdom
  • 2006–2013
    • The Bracton Centre, Oxleas NHS Trust
      Дартфорде, England, United Kingdom
  • 2012
    • San Diego Zoo
      San Diego, California, United States
    • Bradford Teaching Hospitals NHS Foundation Trust
      Bradford, England, United Kingdom
    • University of Washington Seattle
      Seattle, Washington, United States
    • University of Chester
      • Clinical Sciences
      Chester, ENG, United Kingdom
  • 1998
    • University Hospital Of South Manchester NHS Foundation Trust
      Manchester, England, United Kingdom