Endodiabology 2007; Issue 3 (October)
Endodiabology.blogspot.com
NORTHEAST NEWSLETTER FOR SPRs AND BOSSES TRAPPED IN THE NORTHERN DEANERY
OCTOBER 2007
Editors: Shaz Wahid and Petros Perros
Associate Editors: Freda Razvi, Akheel Syed, Arut Vijayaraman
RVI- Andrew Advani (5), Arutchelvan Vijayaraman (4), Jeevan Mettayil (3), Muthu Jayapaul(5), Khaled Mansur-Dukhan (4)
Freeman- Chandima Idampitiya (3), Ravikumar Balasubramanian (5), Kerry Livingstone (2)
South Tyneside- Kathryn Stewart (1)
Gateshead- Asgar Madathil (4)
Sunderland- Shafie Kamarrudin (2), LAT
North Tees/Hartlepool-
Middlesbrough- Srikanth Mada(1),
Carlisle- Sudeep Manohar
Bishop Auckland /
NGH/QEH- Freda Razvi (3)
Research with numbers (supervisor)- Eelin Lim(4-Prof
28th November 2007 Northern Endocrine Region Research and Audit Group annual meeting, Lumley Castle, Durham 2pm-8pm. Contact Shaz Wahid
5th-7th March 2008 DUK Annual Professional Conference,
Endocrinology & Diabetes section of the RSM website offers the following meetings beginning at
TRAINING ISSUES
DIABETES & ENDOCRINOLOGY PIMD WEBSITE Our specialty website has been redesigned and is now available on PIMD website . Click onto the specialty training tab then follow to Diabetes & Endocrinology. This site is essential reading, especially for RITA preparation.
Registering with PMETB It is essential that all new SpRs/StRs (even LATs) register with the PMETB through the newly created Joint Royal Colleges of Physicians Training Board (formally the JCHMT) on JRCPTB website. Not doing so means your training is not counted.
Log Book/Portfolio Documentation It is a trainee’s responsibility to make sure their portfolio/log book is prospectively completed and the necessary signatures obtained. Any experience that is not signed off by your educational supervisor at the time cannot be counted towards training.
Assessment tools Please see JRCPTB website. It is the trainee’s responsibility to give all the appropriate forms to their Educational or Clinical Supervisor. It is the trainee’s responsibility to make sure that the appropriate assessment summaries are available in their portfolio for RITA purposes, e.g. MSF Summary Form.
Laboratory Training Following SpR feedback, the STC has prepared a document providing guidance for training units and SpRs on the minimum training to be provided in relation to this important subject. It can be accessed on PIMD website.
ANOTHER CURRICULUM!!! Trainees who have been recently appointed now have a new curriculum for both the specialty, Acute Medicine to Level 2 and a generic curriculum. Essentially there is no difference other than the sections being reorganised into the subsections of OBJECTIVE/COMPETENCY, KNOWLEDGE, SKILLS, ATTITUDE. They are essential reading and can be accessed on JRCPTB website.
The GOLD Guide This replaces the
REPLACING RITA MMC/PMETB/JRCPTB has produced new guidance on assessing trainees’ progression. The RITA will be replaced with the Annual Review of Competence Progression. ARCP for short. Our region already fulfils the majority of the guidance as the RITAs were revamped 2-yrs ago. Further guidance will be issued in early 2008, once the TPD has been on the course!
ARCP (RITAs 2008) Next year they will be held on Weds 14th, Thursday 15th and
PERSONAL DEVELOPMENT PLANS One of the recommendations of the new Gold Guide is for each trainee to document a PDP at the beginning of each new post. This is something the STC will provide future guidance on, but it would do no harm for trainees to develop one at the start of their current training unit. A suggested template: What development needs have I? How will I address them? Date by which I plan to achieve development goal? Outcome? Completed? Another suggested template: What do I need to learn? How am I going to learn this? What resources do I need to achieve the learning? How will I measure when I have achieved this? How long will this take?
Training Committee Chair – Jola Weaver; Regional Speciality Advisor – Richard Quinton; Programme Director – Shaz Wahid; Consultant members – Jean Macleod, Simon Pearce (Research Advisor), Simon Eaton, and Nicky Leech ; SpR representatives – Arutchelvam Vijayaraman and Andrew Advani.
NEW FACES ON THE SCENE
Welcome to Kathryn Stewart, Anjali Santhakumar, Arif Ullah and Sudeep Manohar as new SpRs (now called StRs (Specialty Trainees) to the region.
Welcome to Chris Strey as Consultant Endocrinologist at Wansbeck. Since graduation from medical school in
NEWS FROM THE NORTHEAST
It may be a little early to officially announce, but unofficially then!, congratulations to Professor Simon Pearce on his Chair.
Congratulations to Peter Carey on obtaining the Consultant post at Sunderland Royal. Also, our congratulations to Pete and family on the birth of his daughter Maebh which occurred just after the last newsletter was published.
Congratulations to Salman Razvi on obtaining the Consultant post at
Congratulations to Sony Anthony on obtaining the Consultant post at
Reena Thomas will be undertaking a Locum Consultant post at
Congratulations to Srikanth Mada on obtaining his NTN at the recent interviews.
Nicky Leech has joined the STC as a Consultant member.
Our best wishes to Ebaa Al-Ozairi as she returns to
Freda Razvi has returned from her period of career break in a part-time capacity.
Richard Quinton has joined the Specialist Advisory Committee for Diabetes & Endocrinology, representing the Northern Deanery.
Kerry Livingstone has joined the NED CME committee with Arut.
Congratulations to Arut on his recent oral presentation at EASD titled “changes in plasma glucose following exercice:comparison of three basal insulins, V. Arutchelvam , T. Heise, S. Dellweg, B. Elbroend, I. Minns, P. D. Home”.
Congratulations to Simon Eaton on being selected as Lead Clinician for Care Planning in Diabetes leading the national engagement and implementation of Care Planning with the National Diabetes Support Team and the Department of Health.
Contributions for this section can include meeting reports, research experiences, book reviews, experiences abroad, and anything else you feel may benefit trainees and trainers around the region. The success of this section really does depend on YOU.
Is Management for me?-Shaz Wahid
Having been a Consultant for 4-years I am now asked whether I would like to develop “formal” management skills by a number of individuals at the Trust and attend some regional/national events. Basically, it is a “code” for do you want to join “The Management”? There are 2 courses I could attend, the Kings Fund Development Programme for Diabetologists or the regional NHS course supported by the StHA and the PIMD (I was nominated by Nancy Redfern and my MD). Having looked at the course objectives both of them have a number of objectives which I have already obtained. This is backed up in my portfolio with reflection and via the BMJ Learning website with completed modules and practical examples from my working practice. My activities over the last 4-yrs in relation to Programme Director, Specialty service redesign and more recently Leading the clinical input into redesigning Acute Medicine at the Trust have required obvious managerial skills. If it had not been for this activity I certainly would have booked up on either of the latter courses for my own professional development. However, I personally at this point in time can not see myself wishing to reduce my clinical activities in the future to take on a formal management role. I still enjoy the “coal” face both when delivering a clinical service or an educational “service”. Joining “Management” at the moment is not right for me. My advice to those Consultants recently appointed is that trying to get onto a formal management course (the Kings Fund Course is probably the best one) would be worthwhile for professional development and is certainly a stepping stone to joining “The Management” in the future.
Laboratory Training-Shaz Wahid
As specialists we are frequently asked to comment on investigation that seems out of the “box”, e.g. funny TFTs. Having a working knowledge as to what the Labs do” is therefore essential and helps in test interpretation. It is part of being a specialist! Following SpR feedback the STC have produced the following guidance:
It is important to arrange exposure to laboratory medicine during each unit attachment backed up by background reading. It is important to cover the following topics:
HbA1c assay measurement, cv, standardisation
Glucose measurements in the lab and meters with causes of errors
Hormone assay methods
Immunometric; RIA, ELISA
Chromatography
Reasons for variability+errors, eg hook effect, protein binding
Pitfalls in autoAb measuring, e.g. TBII, thyroid, adrenal
Pitfalls in measuring or assessing the following hormones or endocrine axis
TSH, fT4, fT4, thyroglobulin, total thyroid hormones
Prolactin
Cortisol, ACTH
PTH, calcitonin, calcium, vitamin D
Water & electrolyte handling; electrolytes, osmolality, ADH
GH, IGF1
LH, FSH, Testosterone, SHBG, E2
Renin, aldosterone, PRA
Catecholamines
The domains of a Consultant Diabetologist/Endocrinologist-Shaz Wahid
“A review of job satisfaction and current practice of consultant diabetologists in England-barriers and successes, MacLeod K, et al. Diabetic Medicine September 2007;24:946-954” is essential reading for ALL, including Endocrinologists! It is a wonderful collection of thoughts on what a Consultant in Diabetes&Endocrinology truly is in practice. There are 3 basic overlapping domains to being a specialist in our specialty: clinical specialist skills, leadership skills across boundaries and clinical education skills. Each of the domains overlap and pertain to clinical activity, management activity, research activity, governance activity, etc. It is essential for trainees to develop these domains during their training. We far too often concentrate on the clinical skills development that is guided by the curriculum, but it is important to bear in mind that there is ample opportunity for the development of subspecialty skills (diabetic foot, transitional care, etc). It is important to develop leadership skills (eminently demonstrated by Simon Eaton in the letter below) and to undertake activity during training demonstrating these skills, e.g. rota leader, audit resulting in service change that is implemented by the trainee. It is important to demonstrate effective activity as a clinical educator of patients, students, junior Drs, allied health professionals, peers in the hospital and community. When undertaking PYAs one can get a sense of which domains have been developed by the trainee. I highly recommend reading this important piece of work.
The Diabetes Year of Care Pilot Project-Simon Eaton
Year of Care is about people with diabetes taking charge of their condition and working in partnership with healthcare professionals to plan their care. Year of Care describes all the planned care that a person with diabetes should expect to receive, usually over the course of a year. This includes support for self management in line with national standards and, where appropriate, planned specialist referrals.
This national pilot project, backed by Diabetes
RECENT PUBLICATIONS FROM THE NORTHEAST
Please send us your recent publication for inclusion in the next newsletter.
Dashora
Al-Ozairi E, Sibal L, Home PD. Counterpoint: ADOPT; good for sulfonylureas? Diabetes Care 2007; Jun;30(6):1677-80.
Advani A, Kelly DJ, Advani SL, Cox AJ, Thai K, Zhang Y, White KE, Gow RM, Marshall SM, Steer BM, Marsden PA, Gilbert RE (2007) Role of VEGF in maintaining renal structure and function under normotensive and hypertensive conditions. Proc Natl Acad Sci
Raivio T, Falardeau J, Dwyer AA, Quinton R, Hayes FJ, Hughes VA, Cole LW, Pearce SHS, Lee H, Boepple P, Crowley WF, Jr, Pitteloud N. 2007 Reversal of congenital idiopathic hypogonadotropic hypogonadism.
Maggi M, Schulman C, Quinton R, Langham S, Uhl-Hochgräber K. 2007 The burden of testosterone deficiency in adult men: economic and quality-of-life impact. Journal of Sexual Medicine. 4: 1056-1069.
Rossor AM, Pearce SH, Adams PC. Left ventricular apical ballooning (takotsubo cardiomyopathy) in thyrotoxicosis. Thyroid. 2007; 17:181-2.
Fanciulli M, Norsworthy PJ, Petretto E, Dong R, Harper L, Kamesh L, Heward JM, Gough SC, Froguel P, Owen CJ, Pearce SHS, Teixeira L, Guillevin L, Cunningham Graham DS, Pusey CD, Cook HT, Vyse TJ, Aitman TJ. FCGR3B copy number variation is associated with susceptibility to systemic but not organ-specific autoimmunity. Nature Genetics. 2007; 39: 721-3.
Donaldson P, Veeramani S, Baragiotta A, Floreani A, Venturi C, Pearce S, Wilson V, Jones D, James O, Taylor J, Newton J, Bassendine M. Cytotoxic T-Lymphocyte-Associated Antigen-4 Single Nucleotide Polymorphisms and Haplotypes in Primary Biliary Cirrhosis. Clin Gastroenterol Hepatol. 2007; 5: 755-60.
Sutherland A, Davies J, Owen CJ, Vaikkakara S, Cheetham TD, James RA, Perros P, Cordell HJ, Donaldson PT, Quinton R, Pearce SHS. Genomic polymorphism at the interferon-induced helicase (IFIH1) locus is associated with Graves’ disease. J Clin Endocrinol Metab 2007: 92(8):3338-41.
Razvi S, Pearce SHS. Do antithyroid drugs influence outcome after radioiodine therapy for hyperthyroidism? Nat Clin Pract Endocrinol Metab 2007; 3: 628-9.
RECENT PUBLICATIONS IN DIABETES & ENDOCRINOLOGY THAT HIT THE NEWS OR THAT MAY HAVE A SIGNIFICANT IMPACT ON MANAGEMENT
Clinical update:adverse effects of antiretroviral therapy. Calmy A, et al. Lancet 2007;370:12-14. An excellent article summarising the metabolic problems associated with antiretroviral therapy. Essential reading for trainees.
Vitamin D Deficiency. Michael Holick. NEJM 2007;357:266-281. An excellent review and essential reading for trainees.
Clinical update: new treatments for hot flushes. Vered Stearns. Lancet 2007;369:2062-2064. A symptom we often come across as Endocrinologists which can be very difficult to treat. This update is well worth a read.
Polycystic Ovary Syndrome.
Diagnosis and management of chronic fatigue syndrome or myalgic encephalomyelitis (or encephalopathy); Summary of NICE guidance. Baker R, Shaw EJ. BMJ 2007;335:446-448. Editorial White P, et al. BMJ 2007:411-412. Well worth a read for those of you have to deal with the common referral of “lethargy”.
Hypertriglyceridaemia. John Brunzell. NEJM 2007;357:1009-1017. An excellent practical review.
Gynecomastia. Glenn Braunstein. NEJM 2007;357:1229-1237. Mandatory reading for trainees. An excellent practical account. After reading it, I had a referral in clinic the next day. I had found this article useful.
Reversal of idiopathic hypogonadotropic hypogonadism. Raivio T, Falardeau J, Dwyer A, Quinton R, Hayes FJ, Hughes VA, Cole LW, Pearce SH, et al. N Engl J Med. 2007 Aug 30;357(9):863-73. The authors describe 15 men in whom reversal of idiopathic hypogonadotropic hypogonadism was sustained after discontinuation of hormonal therapy. Sustained reversal of idiopathic hypogonadotropic hypogonadism was defined as the presence of normal adult testosterone levels after hormonal therapy was discontinued. Ten sustained reversals were identified retrospectively. Five sustained reversal were identified prospectively among 50 men with idiopathic hypogonadotropic hypogonadism after a mean (+/-SD) duration of treatment interruption of 6+/-3 weeks. Of the 15 men who had a sustained reversal, 4 had anosmia. At initial evaluation, 6 men had absent puberty, 9 had partial puberty, and all had abnormal secretion of GnRH-induced luteinising hormone. All 15 men had received previous hormonal therapy. Among those whose hypogonadism was reversed, the mean serum level of endogenous testosterone increased from 1.9+/-1.0 nmol/l to 13.4+/-3.2 nmol/l (P less than 0.001), the luteinising hormone level increased from 2.7+/-2.0 to 8.5+/-4.6 IU/L (P less than 0.001), the level of follicle-stimulating hormone increased from 2.5+/-1.7 to 9.5+/-12.2 IU/L (P less than 0.01), and testicular volume increased from 8+/-5 to 16+/-7 ml (P less than 0.001).This study has shown sustained reversal of normosmic idiopathic hypogonadotropic hypogonadism and the Kallmann syndrome after discontinuation of treatment in about 10% of patients with either absent or partial puberty. The authors hypothesise the cause of this reversal as improved plasticity of the neuronal system with time, whilst the accompanying editorial by Shalender Bhasin (NEJM 2007;357:929-932) favours the pubertal clock hypothesis (delayed activation of the GnRH pulse generator) and uses the study by Adriano Lorano-Porto, et al (NEJM 2007;357:897-904) in the same issue to back this up. Whatever the hypothesized mechanism, this study has certainly influenced my own clinical practice.
Efficacy and safety of combined use of aliskiren and valsartan in patients with hypertension: a randomised, double-blind trial. Oparil S, Yarows SA, et al. Lancet 2007;370:221-229. This double-blind study assessed dual renin system intervention with the maximum recommended doses of aliskiren and valsartan, compared with each drug alone in patients with hypertension. 1797 patients with hypertension (mean sitting diastolic blood pressure 95-109 mm Hg and 8-h daytime ambulatory diastolic blood pressure > or =90 mm Hg) were randomly assigned to receive once-daily aliskiren 150 mg (n=437), valsartan 160 mg (455), a combination of aliskiren 150 mg and valsartan 160 mg (446), or placebo (459) for 4 weeks, followed by forced titration to double the dose to the maximum recommended dose for another 4 weeks. The primary endpoint was change in mean sitting diastolic blood pressure from baseline to week 8 endpoint. Analyses were done by intention to treat. 196 (11%) patients discontinued study treatment before the end of the trial (63 in the placebo group, 53 in the aliskiren group, 43 in the valsartan group, and 37 in the aliskiren/valsartan group), mainly due to lack of therapeutic effect. At week 8 endpoint, the combination of aliskiren 300 mg and valsartan 320 mg lowered mean sitting diastolic blood pressure from baseline by 12.2 mm Hg, significantly more than either monotherapy (aliskiren 300 mg 9.0 mm Hg decrease, p less than 0.0001; valsartan 320 mg, 9.7 mm Hg decrease, p less than 0.0001), or with placebo (4.1 mm Hg decrease, p less than 0.0001). Rates of adverse events and laboratory abnormalities were similar in all groups. In conclusion, the combination of aliskiren and valsartan at maximum recommended doses provides significantly greater reductions in blood pressure than does monotherapy with either agent in patients with hypertension, with a tolerability profile similar to that with aliskiren and valsartan alone. This study uses a new class of antihypertensive drugs that are active oral inhibitors of rennin. The accompanying editorial provides an excellent summary (Birkenhager W, Staessen JA Lancet 2007;320:195-196).
Impact of self monitoring of blood glucose in the management of patients with non-insulin treated diabetes: open parallel group randomised trial. Farmer A, et al. BMJ 2007;335:132-136. This Three arm, open, parallel group randomised trial set in 48 general practices in Oxfordshire and South Yorkshire recruited 453 patients with non-insulin treated type 2 diabetes (mean age 65.7 years) for a median duration of three years and a mean HbA1c level of 7.5%. The patients were randomized into either of the following 3 treatments arms: standardised usual care with measurements of HbA1c every three months as the control group (n=152); blood glucose self monitoring with advice for patients to contact their doctor for interpretation of results, in addition to usual care (n=150); blood glucose self monitoring with additional training of patients in interpretation and application of the results to enhance motivation and maintain adherence to a healthy lifestyle (n=151). At 12 months the differences in HbA1c level between the three groups (adjusted for baseline HbA1c level) were not statistically significant (P=0.12). The difference in unadjusted mean change in HbA1c level from baseline to 12 months between the control and less intensive self monitoring groups was -0.14% (95% confidence interval -0.35% to 0.07%) and between the control and more intensive self monitoring groups was -0.17% (-0.37% to 0.03%). This trial’s evidence is not convincing of an effect of self monitoring blood glucose, with or without instruction in incorporating findings into self care, in improving glycaemic control compared with usual care in reasonably well controlled non-insulin treated patients with type 2 diabetes. This is a very emotive subject and Simon Heller’s accompanying editorial (BMJ 2007;335:105-106) provides excellent “advice”. The bottom line is that we as clinicians should discuss the value of blood monitoring in our patients and only advocate its use and continued use in patients who utilize the results to self-manage their diabetes. However, this fact is lost in primary care with Type 2 Diabetic patients on insulin being advised to test twice a week if that! Furthermore, the special group of pregnant diabetic patients often need to jump through hoops to get glucose monitoring strips. Who said type 2 diabetes is easy!
Estrogen therapy and coronary-artery calcification. Manson JE, Allison MA, et al. NEJM 2007;356:2591-2602. This sub study of the Women's Health Initiative trial of conjugated equine oestrogens (0.625 mg per day) as compared with placebo in women who had undergone hysterectomy, computed tomography of the heart was performed in 1064 women aged 50 to 59 years at randomisation. Imaging was conducted at 28 of 40 centres after a mean of 7.4 years of treatment and 1.3 years after the trial was completed (8.7years after randomization). Coronary-artery calcium (or Agatston) scores were measured at a central reading centre without knowledge of randomization status. The mean coronary-artery calcium score after trial completion was lower among women receiving oestrogen (83.1) than among those receiving placebo (123.1) (P=0.02 by rank test). After adjustment for coronary risk factors, the multivariate odds ratios for coronary-artery calcium scores of more than 0, 10 or more, and 100 or more in the group receiving oestrogen as compared with placebo were 0.78 (95% confidence interval, 0.58 to 1.04), 0.74 (0.55 to 0.99), and 0.69 (0.48 to 0.98), respectively. The corresponding odds ratios among women with at least 80% adherence to the study oestrogen or placebo were 0.64 (P=0.01), 0.55 (P less than 0.001), and 0.46 (P=0.001). For coronary-artery calcium scores of more than 300 (vs. less than 10), the multivariate odds ratio was 0.58 (P=0.03) in an intention-to-treat analysis and 0.39 (P=0.004) among women with at least 80% adherence. In conclusion, among women 50 to 59 years old at enrolment, the calcified-plaque burden in the coronary arteries after trial completion was lower in women assigned to oestrogen than in those assigned to placebo. This study lends support to the timing hypothesis that oestrogen has differing effects on blood vessels in younger women than in women long after the menopause.
Main morbidities recorded in the women's international study of long duration oestrogen after menopause (WISDOM): a randomised controlled trial of hormone replacement therapy in postmenopausal women. Vickers MR, MacLennan AH, et al. BMJ 2007;335:239-244. This multicentre, randomised, placebo controlled, double blind trial assessed the long term risks and benefits of hormone replacement therapy (combined hormone therapy versus placebo, and oestrogen alone versus combined hormone) by recruiting postmenopausal women aged 50-69 years from General practices in the UK (384), Australia (91), and New Zealand (24). At early closure of the trial, 56,583 had been screened, 8980 entered run-in, and 5692 (26% of target of 22,300) started treatment. The trial was prematurely closed during recruitment, after a median follow-up of 11.9 months (interquartile range 7.1-19.6, total 6498 women years) in those enrolled, after the publication of early results from the women's health initiative study. The mean age of randomised women was 62.8 (SD 4.8) years. When combined hormone therapy (n=2196) was compared with placebo (n=2189), there was a significant increase in the number of major cardiovascular events (7 v 0, P=0.016) and venous thromboembolisms (22 v 3, hazard ratio 7.36 (95% CI 2.20 to 24.60)). There were no statistically significant differences in numbers of breast or other cancers (22 v 25, hazard ratio 0.88 (0.49 to 1.56)), cerebrovascular events (14 v 19, 0.73 (0.37 to 1.46)), fractures (40 v 58, 0.69 (0.46 to 1.03)), and overall deaths (8 v 5, 1.60 (0.52 to 4.89)). Comparison of combined hormone therapy (n=815) versus oestrogen therapy (n=826) outcomes revealed no significant differences. The results of this trial are consistent with the findings of the women's health initiative study and secondary prevention studies in that hormone replacement therapy increases cardiovascular and thromboembolic risk when started many years after the menopause. The Kronos Early Estrogen Prevention Study (KEEPS) and the Early Versus Late Intervention Trial with Estradiol (ELITE) trials should answer whether the effect HRT is different early in the menopause than later on.
Incidence of new-onset diabetes and impaired fasting glucose in patients with recent myocardial infarction and the effect of clinical and lifestyle risk factors. Mozaffarian D, et al. Lancet. 2007 Aug 25;370(9588):667-75. The authors prospectively obtained data for 8291 Italian patients with a myocardial infarction within the previous 3 months, who were free of diabetes(determined by medication use, a physician-reported diagnosis, or fasting glucose > or =7 mmol/L) at baseline. Incidence of new-onset diabetes (new diabetes medication or fasting glucose > or =7 mmol/L) and impaired fasting glucose (fasting glucose > or =6.1 mmol/L and less than 7 mmol/L) were assessed at follow-up at 0.5, 1.0, 1.5, 2.5, and 3.5 years. Baseline data for body-mass index (BMI), other risk factors, dietary habits, and medications were updated during follow-up. A Mediterranean diet score was assigned according to consumption of cooked and raw vegetables, fruit, fish, and olive oil. Associations of demographic, clinical, and lifestyle risk-factors with incidence of diabetes and impaired fasting glucose were assessed with multivariable Cox proportional hazards. During 26 795 person-years (mean follow-up 3.2 years [SD 0.9]), 998 individuals (12%) developed new-onset diabetes. Of the 7533 without impaired fasting glucose at baseline, 2514 (33%) developed new-onset impaired fasting glucose or diabetes rising to 3859 (62%) of 6229 with the lower cut-off for impaired fasting glucose of 5.6 mmol/L. Independent risk factors for new-onset diabetes or impaired fasting glucose included older age, hypertension, use of beta-blockers, lipid-lowering medications (protective), and diuretic use. Independent lifestyle risk-factors included higher BMI, greater BMI gain during follow-up, current smoking, a lower Mediterranean dietary score, and wine consumption of more than 1 L/day. Data for physical activity were unavailable, but inability to perform exercise testing was associated with higher incidence of diabetes and impaired fasting glucose. In conclusion, this study has shown that compared with population-based cohorts, patients with a recent myocardial infarction had a higher annual incidence rate of impaired fasting glucose (1.8 vs 27.5%) and diabetes (0.8-1.6% compared with 3.7%). Thus, indicating that myocardial infarction could be a prediabetes risk equivalent. This makes the case for screening all patients who have had an MI for dysglycaemia. Each service should develop local protocols. The questions to answer are: fasting glucose vs OGTT and frequency of screening. As an example it would not be unreasonable to undertake an OGTT on all patients 6-weeks post MI initially followed by fasting blood glucose on annual basis via their GP. Any one disagree?
ROSIGLITAZONE Do not moan! As Rudy Bilous aptly stated in his excellent editorial in Diabetic Medicine on the issue of Rosiglitazone and MI risk “you must have been practicing Diabetes in Mars if have not heard about this”.
NEXT NEWSLETTER Due out beginning of February 2008 so keep the gossip coming.
posted by Arutchelvam at 11:53 PM
