editorial

© 2002 Diabetes UK.

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Blackwell Science Ltd

Continuing education

EDITORIAL

Continuing educationContinuing education

Admission to hospital is a crisis in a diabetic person’s life.Hospital life is very different from normal routine, and well-intentioned (if ill-informed) clinical staff can cause mayhem bytaking over control. Although up to 10% of bed-days in theUK National Health Service are directly related to diabetes andits complications, in-patient diabetes care is very much thepoor relation in diabetes research and practice. However, it isa major focus of this issue of

Continuing Education

. ArpanBhattacharya and Kalpana Kaushall mix pragmatism,experience, and available evidence in their review of themanagement of hospitalized patients. Sue Roberts picks up thetheme of in-patient care, commenting on a critically appraisedpaper that provides much-needed evidence of the efficacy ofspecialist nursing support of diabetic in-patients. The involve-ment of a specialist nurse, it would seem, can improve satisfac-tion, and shorten length of stay.

Carl Montague discusses the chemistry and physiology ofthiazolidinediones, exploring the bridge between laboratoryscience and clinical practice. The short citations provide addi-tional evidence of the efficacy of thiazolidinediones and providethe usual eclectic mix of diagnostic and therapeutic aspects ofdiabetes practice, with a slant towards cardiovascular preven-tion. The ‘Learning and Teaching Skills’ article considers howbest to obtain and respond to feedback on your educationalactivities, treading a middle path between theory, empiricismand pragmatism.

Word counts in this issue have been a major editorial concern.Practical aspects of in-patient management have been givenmore space than a critical appraisal of evidence on the sametopic. Concerned that this article was too long, we asked ourhouse officers to take a look at it. Their answer was that,

for the person at the sharp end of care, none of the text wasdispensable. Likewise, the article on evaluation of educationis longer than either the citations, or a scientific review ofthiazolidinediones. We could argue that education evaluationis more unfamiliar, less well documented in the ‘home ground’of the biomedical literature, and less clear-cut so it needs moreexplanation and discussion. However, to be true to the messageof the article, we can draw no conclusions without yourfeedback, since evaluation exists in the eye of you, the reader.


is now in its third year of publication.We hope sincerely we are serving your needs. We remain asopen as ever to suggestions on content, structure or style, andlook forward to correspondence, criticism and comment.

A point for the future. Our diet of editorials, learning andteaching skills articles, clinical practice questions, and shortcitations will continue. We have struggled in our journalscreening and commentary commissioning to strike a balancebetween reliable and valid evidence and exciting advanceswhose practical implementation may yet be a little way off. Weare keen to avoid the reductionism of pure evidence-basedpractice and wish to give basic and clinical science their say.From the next issue, our journal screening will present majorchanges in the empirical evidence-base of diabetes care underthe title ‘Today’s Evidence’, and advances that we judge to bepromising, but whose time to enter the mainstream has not yetcome, under the heading ‘Horizons’.

Any reactions to this Editorial, or the contents of this issue,will be gladly received at [email protected]

Tim Dornan

LEARNING AND TEACHING SKILLS


Was the education I provided effective?

T. Dornan

Hope Hospital, Salford, UK

Question

As newly appointed CPD lead, you inherit feedback on previousevents. On a 1–5 Likert scale (1 worst, 5 best), the medianresults are as follows:• Quality of information prior to the event 3• Quality of catering 4• Ease of car parking 2

• Choice of topics 4• Educational value of the events 3How should you respond to that information?

This article considers, in relation to education evaluation:why?; what?; when?; by whom?; and how?

Why evaluate?

To prove that education is of quality, it requires standardsand a process of measurement. Governance of education,

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like clinical governance, is a cyclical process [1], with fourstages:1 Plan the objectives and methods2 Deliver the education3 Measure the outcome4 Interpret the measurements and feed your analysis intofuture planning.

‘Evaluation’ is the third and fourth of those steps. When youread the literature on this topic, remember George BernardShaw’s words that England and America are divided by a com-mon language. US English uses the term ‘evaluation’ to meanexaminations as well as governance. While it is true that per-formance in examinations is a quality measure of sorts, BritishEnglish is more specific in its use of the word ‘evaluation’.Accordingly, this article uses ‘evaluation’ to mean quality meas-urement, and ‘assessment’ to mean examination. The catch-phrases ‘programme evaluation’ and ‘student assessment’make that distinction easy to remember. ‘Evaluation’ describesand interprets the experiences of learners and teachers, andplaces a value on them that can help guide future action [1].

The need for objectives

There are several reasons why the Likert results above are hardto interpret. One is that you do not know against what standardsthe judgements were made. An appropriately worded item canrepresent a standard. For example, I would take a score of 3more seriously for an item worded ‘The speaker encouragedme to appraise my clinical practice’ than for ‘The speaker usedclear visual aids’. The thought that goes into planning educa-tion often stops at choosing titles and speakers withoutconsidering what the learners are supposed to learn, so it isunsurprising that events are so often evaluated on car parkingand lunch. Depending on the specificity of educational objec-tives, an evaluation item may be as broad as the appraisal ques-tion above, or as narrow as ‘I will prescribe statins to diabeticpatients with greater confidence’. I will use the jargon term‘global’ to refer to broad items, and ‘specific’ to more narrowlyfocused ones.

What should you evaluate?

Consider, for example, evaluating one session in a monthly,half-day release course for specialist registrars.

Structure

As event organizer, you will be interested in feedback on the time-table of the event and how it fitted with events before and after it.

Process

You might, for example, want to know whether the balance ofdidactic input and group discussion was appropriate, and howeffective your speakers and group facilitators were.

Outcome

When all is said and done, structure and process are of no valueunless they achieve an outcome. One approach is to view out-comes along a continuum. From the lowliest to the mostimportant, outcomes may be:• Reactions to the event• Learning: what participants took away from the event• Behaviour: how the event influenced their on-the-jobperformance• Results: how patients and colleagues ultimately benefited.

The heading ‘learning’ has three major subcategories:knowledge (what new understandings the event leads to); ‘skills’(what participants were able to do as a result of attending); and‘attitudes’ (in what way participants felt differently towardsthemselves, others, or their job as a result of attending). Theoutcomes of greatest interest are the hardest to measure, sothere is a ‘trade-off’ between desirability and feasibility, particu-larly between short-term and long-term outcomes.

When?

The sooner feedback is given after an event, the greater itsimpact will be [2]. The only reason for delay is if participantsneed time to judge how valuable an event has been to theirnormal professional activities, but even then you should ana-lyse feedback and distribute your analysis as fast as possible.

By whom?

A glib answer would be ‘by everyone, including yourself’.

The importance of multiple perspectives

In a clinical trial, you would probably be satisfied with a deathcertificate as evidence that a patient had died. For myocardialinfarction, you would seek more than one piece of evidence(cardiac enzymes, ECG, typical symptoms). Education evalua-tion, because of its inherent subjectivity, has to go even further.It requires evidence from as many personal perspectives aspossible, and ideally of more than one type (e.g. numerical andtextual). It is through comparing and contrasting perspectivesthat the most valid conclusions can be drawn. Not all pieces ofevidence must, or can, have the objectivity even of cardiacpain. Personal impressions, discussions and casual commentscan be valid evidence to put beside written evidence. One rewardfor collating this information is that consistency betweenobservations makes pieces of evidence much more persuasiveto anyone who might otherwise dismiss them as ‘soft data’ [2].

Sources

You would be well advised to debrief with any co-leaders and jotdown impressions while they are fresh in your mind. People aremost receptive to feedback from someone who is knowledgeable,



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well intended and equal or lower in status [2], so you shouldconsider asking a trusted learner to observe and pass backcomments. A key message of this article, particularly to readerswhose major concern is objectivity, is that evaluation bylearners is valid and useful. Ratings of perceived educationalvalue correlate well with seemingly more robust measures ofeducational outcome [2]. Although more personal and lessreliable, your own evaluation of an activity you have organizedalso has validity in that it is part of the reflective process thatwill make you a more effective educator [3].

How? Questionnaires

Quantitative vs. qualitative measures

Another reason the feedback at the head of this article is mean-ingless is that, apart from one another, the numbers have nocomparators to give them meaning. Moreover, they give noclue what changes are needed. If you had, for example, thescores from the same learners for other events in the sameprogramme, the quantitative evaluation could answer the ques-tion: ‘Do I need to make a change?’, but it still does not answerthe question: ‘How?’ True, you could find out where improve-ments should be made by obtaining numerical scores formultiple specific items, but how would you know what itemsto include? Compared with global items, a battery of specificitems adds complexity to the instrument and reduces reliability.Textual evaluation, on the other hand, allows the learners todefine the strengths and weaknesses, and points you towardsappropriate improvements more efficiently and effectively. So,a second key message of this article is that textual commentsare a crucial guide to education improvement [2]. They canusefully be combined with quantitative evaluation to provide both‘formative’ (textual) and ‘summative’ (numerical) data. Anonym-ity should be assured unless there is some clear reason why youneed to know who said what; even then, consider carefullywhether accountability for comments will inhibit respondents.

Quantitative measures

Your rating scale could offer three to seven alternative responses,for example on a continuum between ‘strongly agree’ to ‘stronglydisagree’, or ‘not at all important’ to ‘very important’. Theknack is to word the stems appropriately. They may consist ofstatements for the person to agree or disagree with, or requeststo evaluate against a stated standard. A point of statisticalimportance is that ratings on Likert scales, even with sevenpoints, should not be treated as continuous variables, at leastunless scores are very evenly distributed across the breadth ofthe scale. It is better to report results as percentages above andbelow a ‘breakpoint’ such as the median value.

Qualitative measures

Feedback is most effective when it is accurate, concrete,

specific and descriptive rather than evaluative. When it concernsa person, it should be focused on behaviour, rather than on thequalities of the persons themselves [2]. Thus, the wording ofthe stem again needs careful consideration. Learners should besteered towards identifying what they have (or have not)learned, and on making constructive suggestions for change.As with quantitative measures, stems may be broad or narrowin scope. They may direct the learner towards specific points ofinterest to the evaluator, or take a ‘critical incident’ approachwhere the content of the comments is left entirely to the learner.Learners are most likely to give constructive criticism if theyare asked to state what was good about the education beforecriticising it, and to phrase the request ‘Please make sugges-tions for change’, rather than ‘What was bad\unsatisfactory’.

Allowing time for evaluation

The most certain way of ensuring that you get valid responsesis to allocate time for evaluation within the event itself. Textualquestions, in particular, take time to answer.

How? Other forms of evaluation

I have already suggested using a peer or trainee as reviewer.Individual and group discussions are other sources of evalua-tion. Time within an event can be allocated for a facilitated dis-cussion of its strengths and weaknesses. This has an education,as well as evaluation, rationale, because putting learning intowords helps consolidate it. The ‘Minute Paper’ is a simple tech-nique whereby every learner is given a card on which to write,for example, one thing they have learned, and something aboutwhich they are still unclear [4]. This helps clarify their ownminds, and tells you how well you have achieved your objectives.

How? Activities other than group events

Most of this article refers to large group events, but the sameprinciples can be applied to a traineeship, distance learningevent, or one-to-one tutorial.

From description to evaluation

Obtaining feedback is only half the battle. The challenge nowis to draw conclusions. This is a process of analysis (findingmeaning in the data) and synthesis (making inferences fromyour analysis). If you have data from more than one perspective,the analysis should seek commonalities and patterns. Theremay also be inconsistencies that require you to make valuejudgements before you draw final conclusions.

Summary and conclusion

Key points in this article have been:• You cannot evaluate unless you know what you set out toteach



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• Learners’ evaluation is valid because learning exists in theeye of the learner• The best evaluation is from multiple perspectives, includingsuch ‘soft’ sources as your own impressions• Promptness is of the essence• The content of your evaluation may include structure,process and outcome• Numerical scores, if there are reference standards forcomparison, can answer the question ‘Does my educationalactivity need to change?’• Textual comments answer the question ‘How should itchange?’• Time devoted to evaluation within educational activity istime well spent

Your task as an evaluator was nicely encapsulated by aliterature review of the factors that make evaluation effective [5].It should show insight into local conditions and circumstances,be straightforward, relevant, broadly framed, prompt,

comprehensive and fed back in jargon-free language. Recipientsof feedback are most receptive to the feedback they expect toreceive [5]. It is important to make evaluation very focused andbuild up a culture of receptivity to criticism so that unanticipatedor unwanted findings will be given the attention they deservein subsequent quality development.

References

1 Wilkes M, Bligh J. Evaluating educational interventions.

BMJ

1999;

318

: 1269–1272.2 Braskamp LA, Ory JC.

Assessing Faculty Work. Enhancing Individualand Institutional Performance

. San Francisco: Jossey-Bass, 1994.3 Boud D, Keogh R, Walker D eds.

Reflection: Turning Experience IntoLearning

. London: Kogan Page, 1985.4 Angelo TA, Cross KP.

Classroom Assessment Techniques. A Hand-book For College Teachers

, 2nd edn San Francisco: Jossey-Bass, 1993.5 Cousins JB, Leithwood KA. Current empirical research on evaluation

utilisation.

Rev Educat Res

1986;

56

: 331–364.

CLINICAL PRACTICE QUESTION


Glucose control in in-patients

A. Bhattacharyya, K. Kaushal and T. L. Dornan

Department of Diabetes, Hope Hospital, Salford, Manchester, UK

Consider the following

The house staff who have recently joined your diabetes unitask you for a ‘teach-in’ on the management of in-patients withdiabetes. What concerns might they have and what key messageswould you want them to take away?

Introduction

We would suggest to our house staff that they approach anin-patient with diabetes by thinking of:• the impact of the underlying medical condition, its treatment,and the stress of hospitalization on glycaemic control• the impact of glycaemic control on the underlying medicalor surgical condition.

For the person with diabetes, hospitalization can be trau-matic because exercising control is central to self-care, andhospital makes that very difficult, particularly when medicaland nursing staff project their anxiety about diabetes on tothe patient.

Does good glycaemic control really matter?

There is accumulating evidence that controlling blood glucosein the hospital setting is important. Studies amongst patientswith diabetes following acute myocardial infarction [1],

coronary artery bypass surgery [2] and wound and nosocomialinfections [3] show a potential to reduce morbidity, mortality,length of stay and cost if effective measures are undertaken toachieve normoglycaemia. Malmberg [1] reported that theabsolute reduction in mortality at 3.4 years post-myocardialinfarction was 11% in the patients treated with an insulin–glucose infusion followed by an intensive subcutaneous insulinregime. Furnary

et al

. [3] found the incidence of deep sternalwound infection following open heart surgery was significantlyreduced by intensive control of perioperative blood glucoselevels from 2% in the control group to 0.8% in the studygroup. Koproski

et al

. [4] conducted a controlled prospectiverandomized study to investigate the effects of a diabetes teamon hospitalized diabetic patients. They found that a multi-disciplinary team consisting of a diabetes nurse educator andan endocrinologist could improve glycaemic control and alsosignificantly reduce the readmission rate at 3 months afterdischarge (15% of patients in intervention group vs. 32% ofpatients in control group,

P

= 0.01). We conclude that it isessential to identify hyperglycaemia at the time of hospitaladmission and probably valuable to keep glucose values below10 mmol/ l.

Our experience

Concerns expressed by our junior doctors almost all relate toinsulin treatment. Some of them are:• How do I calculate insulin doses?



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• What action do I take when I am called to see a patientbecause their blood glucose is high, or because they have hada hypo?• What level of control am I aiming for?• When do I call for help, and from whom?

Common behaviour patterns that illustrate unspokenanxieties are:• Withholding insulin from a patient with a normal bloodglucose level in case they become hypoglycaemic• Continuing sliding scale regimens and keeping patients inhospital for too long• Calling for help only after days of unsuccessful juggling withinsulin doses.

We give them several simple pieces of advice to get themstarted and anticipate or relieve unspoken concerns:• Remember that your patient is the greatest expert on theirdiabetes; listen to their views and be ready to take their advice• There is no science to calculating insulin doses; apply simplerules of thumb, pay close attention to how patients respond toyour regimens, be unafraid of making mistakes, and learn fromexperience• If you do not give insulin to patients with normal bloodglucose levels, they will not stay normal for long• More instability is caused by fear of hypoglycaemia (oftenon the part of nursing staff, projected on to a junior doctorthey summon to see their patient) than excessive insulin doses• Diabetic patients rarely achieve completely normal bloodglucose levels, especially in hospital• If there is a diabetes advisory team in your hospital, involvethem as soon as possible but learn from them, do not just passresponsibility on to them• Do not give metformin to an ‘ill’ patient in hospital (e.g. ona coronary care unit) because of the risk of lactic acidosis• There are three levels of intensity of insulin treatment forhospitalized patients:

–an iv insulin/glucose regimen for acutely ill (non-eating) patients–four times daily insulin for the patient who is unstable but

well enough to eat–a maintenance regimen (which may be two, three or four

times daily) for all other patients.We recently audited the first 100 diabetic patients admitted to

Hope Hospital in the year 2000 for reasons other than diabetes[5]. Hypoglycaemia was common, but happily there was nocase of diabetic ketoacidosis or non-ketotic hyperosmolarcoma. Only 53% of patients on surgical and 37% of patientson medical wards were well controlled (defined as four out offive preprandial glucose concentrations within our targetrange of 4–10 mmol/ l); 19% and 33%, respectively, werepoorly controlled (one or none in the target range). Strikingpatterns of behaviour were continuing a ‘standard’ insulininfusion rate/sliding scale despite recurrent hypo- or hyper-glycaemia, and prescribing subcutaneous insulin several daysahead. Key educational messages are that insulin prescriptionsneed to be reviewed daily, and that sliding scales need to bereviewed several times a day. Junior medical staff should be

encouraged to take these decisions but to seek help whenunsure about adjustments.

Monitoring

We advocate monitoring blood glucose levels up to four timesper day preprandially (before meals and before bedtimesnack), and point out to our junior staff that measuring bloodglucose ‘by the clock’, for example four-hourly, will producechaotic and uninterpretable results because some measure-ments are made before and others after meals.

What level of control am I aiming for?

We define ‘good control’ first as the avoidance of symptomatichyperglycaemia and hypoglycaemia. We know of no evidence-based standards for glucose control in hospitalized patients,but advocate a target glucose concentration between 4 and10 mmol/l, allowing an exception in 20% of measurements asin our audit definition of good control described above. Hae-moglobin A

1c

is unhelpful because it merely reflects the glycae-mic state at the time of admission, and even fructosaminechanges too slowly to be of any real value. Urine glucosemonitoring is no alternative to blood glucose monitoring, butchecking for urinary ketones, particularly when the bloodglucose concentration exceeds 17 mmol/ l, is essential to diag-nose impending or actual ketosis. An electrochemical ketonesensor that is as fast and accurate as the equivalent fingerprickglucose sensor shows considerable promise in this setting [6].

What regimen should I use?

A few factors must be taken into consideration in selecting theoptimal hypoglycaemic regimen (Box 1). As a general rule,insulin is the preferred treatment for hospitalized ‘ill’ patients.Metformin, in particular, should be avoided in such patients,because of the risk of lactic acidosis. Concomitant medicationsprescribed in hospital, commonly corticosteroids, may cause adeterioration in glycaemic control. We would remind the juniorstaff that patients who are less active in hospital than at homewill need higher treatment doses, particularly if they have anintercurrent illness that will further increase glucose levels.

Non-eating patients (acutely ill, vomiting or nil by mouth)should be treated with iv insulin according to a sliding scale,together with a constant iv infusion of 5% glucose with addedpotassium, the insulin infusion rate being altered according toblood glucose values. A ‘GKI’ (glucose potassium and insulinadded to the bag of fluid) is a perfectly satisfactory alternative.Eating but ‘unwell’ patients, whether with Type 1 or Type 2 dia-betes, are best treated with a subcutaneous (sc) basal bolus regi-men (short-acting insulin before meals and an intermediateacting insulin at bedtime). There is no place for ‘old fashioned’ scsliding scales [7,8]. Queale

et al

. [7] studied diabetic patientsadmitted to medical in-patient services for reasons other than theirdiabetes. Seventy-six percent were placed on a subcutaneous sliding



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scale insulin regimen. When used alone, i.e. without continu-ing a standing regimen of treatment, sliding scale regimens wereassociated with an increased risk of hyperglycaemic episodes.

Admission to hospital may bring to medical attention thefact that the control of a patient with Type 2 diabetes has beenpoor on oral agents prior to admission, in which case theopportunity should be taken to start insulin (Box 2). If indoubt, it is always best to treat the patient with insulin initiallyand make a later decision about a maintenance regimen. Insome patients with Type 2 diabetes who were on oral hypogly-caemic agents before admission, it may be appropriate tocontinue them. Bear in mind, however, that sulphonylureadoses must be adjusted in people with renal insufficiency sincedecreased clearance of sulphonylurea increases the risk ofhypoglycaemia. It should be drummed into junior doctors thatmetformin must never be prescribed for a patient in acute/severe heart failure, renal failure or who has liver disease.Thiazolidinediones are contraindicated in the presence ofincreased liver transaminases.

Iv insulin and transition from iv to sc insulin

Box 3 shows a standard iv insulin infusion rate. We advocatethat blood glucose values are checked one to two-hourly. Patientswith Type 1 diabetes on iv insulin should not be off insulin atany time as they are, by definition, insulinopenic. If their bloodglucose is low the insulin infusion should be continued at adecreased rate (0.5 U/h) and the glucose infusion rate increased.

The transition from iv to sc insulin can generally be madeonce the patient is well enough to eat and it should ideally beplanned so that the first sc dose is given before breakfast. Sub-cutaneous short-acting insulin should be given 30 min beforestopping iv insulin to allow the sc insulin to act before the infu-sion is stopped. If the patient was not previously on insulin, thedose can be calculated by several methods. One option is tocalculate a total daily dose by multiplying the body weight inkg by 0.6. Informal discussion within our department showedthat most of us administer 80–90% of the previous day’s iv dose.

In theory, sc insulin should be given 30 min before eating toallow the insulin’s peak effect to coincide with the post-mealglucose excursion. In practice, ward routine rarely allows suchprecise timing. Insulin analogues have a clear advantage asthey can be given immediately before meals.

When do I call for help?

Junior doctors should seek specialist advice when hyperglycaemiaor recurrent unexplained hypoglycaemia presents a problem,in all cases of diabetic ketoacidosis or hyperosmolar non-ketotic state, and in patients with foot ulceration, problematicdiabetic neuropathy, suspected nephropathy or sight-threateningretinopathy. Once called, the specialist team should encourage

Box 1 Important considerations for the treatment of diabetesin hospital.

1 What type of diabetes does the patient have? Type 1, Type 2 diabetes or stress-induced hyperglycaemia?

2 What is the influence of the other medications the patient is taking? Medications like β-blockers, cyclosporin, thiazide diuretics and narcotics can worsen glycaemic control. Corticosteroid therapy, however, poses the biggest problem, usually in the setting of patients admitted with an acute exacerbation of chronic obstructive airways disease.

3 What is the patient’s current diet? Is the patient eating? If not, how long before he/she is likely to?

4 Which anti-hyperglycaemic agents should be given? What was the therapy prior to admission? What was the level of control prior to admission? What does the present situation demand?

Box 2 Indications for insulin therapy in patients with Type2 diabetes admitted to hospital.

Patients:1 Who cannot take oral medication for a variety of

reasons.2 Admitted with acute myocardial infarction or stroke.3 With poor prior glycaemic control on maximal oral therapy.4 Admitted with significant infection.5 Undergoing surgical procedures (excluding minor surgery).6 In whom certain oral agents are contraindicated, e.g.

thiazolidinediones in patients with liver dysfunction or metformin in patients with acidosis or impaired renal function.

7 Undergoing investigation with contrast agents.

Box 3 Treatment with iv insulin.

1 Patients should be on a glucose infusion (with added potassium) unless the blood glucose is very high.

2 Blood glucose should be monitored every hour.3 Suggested rate of insulin infusion (50 unit short-acting

insulin in 50 ml saline)a Blood glucose < 4 mmol/l – 0.5 U/hb Blood glucose between 4.1 and 6 mmol/l – 1 U/hc Blood glucose between 6.1 and 9 mmol/ l – 2 U/hd Blood glucose between 9.1 and 12 mmol/l – 3 U/he Blood glucose between 12.1 and 16 mmol/l – 4 U/hf Blood glucose between 16.1 and 20 mmol/l – 6 U/h andg Blood glucose > 20 mmol/ l—to consult doctor for

review of the scale.The rate of the infusion should be modified until acceptable

glycaemic control is achieved. If the blood glucose remains high persistently, e.g. the patient is requiring 4 U/h and the blood glucose is still 14 mmol/ l, the infusion rate should be increased by 1–2 U/h.



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self-sufficiency by guiding rather than taking over. It may besufficient to be contactable by telephone. Diabetes specialistnurses and written guidelines have a valuable potential role.

Follow-up of patients not previously known to have diabetes

Newly diagnosed diabetes must be followed up, although notnecessarily by the diabetic clinic if appropriate primary care isavailable. In patients with stress-induced hyperglycaemia,treatment should be tapered as early as possible and a glucosetolerance test done at about 6 weeks on unrestricted diet.Non-specialist teams usually ask for urgent diabetic clinicfollow-up, but that is neither always possible, taking into accountclinic waiting times, nor appropriate. Active complications orunresolved glycaemic instability are the clearest indications forearly follow-up; readily accessible telephone advice from adiabetes specialist nurse is likely to achieve more than a fixed-date appointment for glycaemic difficulties.

Summary

• Good glycaemic control is an important goal in hospitalizedpatients with diabetes.• We suggest a target of preprandial blood glucose concentrationsbetween 4 and 10 mmol/ l on four out of five occasions.• Support to junior house staff should aim to help thembecome self-sufficient.• The value of written guidelines and the role of diabetesspecialist nurses should not be underestimated. (The latter isdiscussed ealier in this issue of


.)• Anxieties commonly expressed include the ‘calculation’ ofinsulin doses, the correct management of a hyper- or hypo-glycaemic episode, the target level of control and the thresholdfor seeking help.• Intravenous insulin infusions should generally be reservedfor non-eating patients.

• Both iv and sc insulin regimens need to be reviewed daily anddoses adjusted according to blood glucose results.• Take into account that the effects of a hospital diet andrelative inactivity may cause hypo- or hyperglycaemia.• Metformin should be avoided in hospitalized ‘ill’ patients.• The rationale for overlapping an insulin infusion with thefirst sc insulin injection needs to be explained clearly.

For further reading on this subject we recommend to juniordoctors that they refer to

Diabetes: Emergency and HospitalManagement

by S. R. Page and G. M. Hall (BMJ Books, 1999).

References

1 Malmberg K for the DIGAMI (Diabetes Mellitus Insulin GlucoseInfusion in Acute Myocardial Infarction) study group. Prospectiverandomized study of intensive insulin treatment on long-term survivalafter acute myocardial infarction in patients with diabetes mellitus.

BMJ

1997;

314

: 1521–1515.2 Kalin MF, Tranbaugh RF, Salas J, Zumoff B, Cohen BI, Stelzer P

et al.

Intensive intervention by a diabetes team diminishes excesshospital mortality in patients with diabetes who undergo coronaryartery bypass graft.

Diabetes

1998;

47

: A87.3 Furnary AP, Zerr KJ, Grunkemeier GL, Starr A. Continuous intrave-

nous insulin infusion reduces the incidence of deep sternal woundinfection in diabetic patients after cardiac surgical procedures.

AnnThorac Surg

1999;

67

: 352–362.4 Koproski J, Pretto Z, Poretsky L. Effects of an intervention by a diabetes

team in hospitalized patients with diabetes.

Diabetes Care

1997;

20

:1553–1555.

5 Bhattacharyya A, Christodoulides C, Kaushal K, New JP, Young RJ.Glucose control during in-patient management of diabetes.

DiabetMed

2001;

18

: P322.6 Byrne HA, Tieszen KL, Hollis S, Dornan TL, New JP. Evaluation of an

electrochemical sensor for measuring blood ketones.

Diabetes Care

2000;

23

: 500–503.7 Queale WS, Seidler AJ, Brancati FL. Glycaemic control and sliding

scale insulin use in medical inpatients with diabetes mellitus.

ArchIntern Med

1997;

157

: 545–552.8 Sawin CT. Action without benefit. The sliding scale of insulin use.

Arch Intern Med

1997;

157

: 489.

January 200219000000

SCIENCE IN CONTEXT


A treatment for Mr WP: thiazolidinediones after troglitazone

C. T. Montague

Cardiovascular & Gastrointestinal Discovery Department, AstraZeneca Pharmaceuticals, Mereside, Alderley Park, UK

Mr WP was first discussed in our May 2000 issue. At that timehe was 70 years old and had been diagnosed with Type 2diabetes in 1982 and referred to hospital care for furthermanagement in 1997. He had poor glycaemic control (HbA

1c

12%), marked central obesity (body mass index (BMI)

34.5 kg/m

2

), combined hyperlipidaemia, hypertension, micro-albuminuria, maculopathy, peripheral vascular disease andangina. Treatment with insulin (116 U/day) had not improvedhis glycaemic control and metformin was contraindicated dueto his mild renal impairment. It was then that he was started ontroglitazone in addition to insulin. There was a marked improve-ment in his home glucose monitoring and he commented that‘this is the best anyone has done for my diabetes!’ Unfortunately,



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his euphoria was curtailed by the withdrawal of troglitazone afew weeks later. In the following 2 years Mr WP required increasedinsulin dosages (240 U/day), his weight increased (BMI 36.6 kg/m

2

) and he suffered two myocardial infarctions and underwentcoronary artery bypass grafting. Would things be different forMr WP now or in the near future? Carl Montague now updatesus on the current state of play with thiazolidenediones (TZDs).

In his article entitled ‘Insulin resistance: a problem forclinicians and scientists’, Mark Walker described how Mr WP’stroglitazone treatment, in combination with his usual insulinregimen, led to a pronounced improvement in his home bloodglucose measurements [1]. However, a few weeks after Mr WPwas started on troglitazone treatment, the drug was with-drawn from the UK market because of hepatotoxicity, andMr WPs treatment was discontinued. In the 2 years since thispublication, other TZDs have reached the market for treatmentof Type 2 diabetes. Pioglitazone (Actos®; Takeda/Eli Lilly) androsiglitazone (Avandia®; GlaxoSmithKline) are thought to befree of the liver toxicity that was associated with troglitazoneand offer some hope to patients such as Mr WP for whom con-ventional therapy has not been successful. In this article I willdescribe current understanding of how TZDs mediate theirinsulin-sensitizing effects and also briefly explore the merits offuture drug development in this area.

How do thiazolidinediones work?

TZDs work by binding to and activating the nuclear hormonereceptor peroxisome proliferator-activated receptor-gamma(PPAR

γ

). PPAR

γ

is expressed at high levels in adipose tissue,kidney, heart and intestine, although it is found in many othertissues at lower levels, and activation of this receptor regulatesgene transcription within these tissues. The insulin-sensitizingeffects of TZDs are thought to result mainly from their activa-tion of PPAR

γ

activity in adipocytes [2]. TZD treatment ofadipocyte progenitor cells, preadipocytes, stimulates thedifferentiation pathway of these cells into mature lipid storingadipocytes [3]. Therefore, treatment of patients with TZDscan increase the number of adipocytes and it is commonlyobserved that patients treated with TZDs experience anincrease in their BMI [4], suggesting that the size of their fatdepots has increased. If the patient’s food intake and energyexpenditure remain the same as before, then the amount ofstorage space for the pool of fatty acids within the body willhave increased. This extra sink of adipose tissue will lead toreduced levels of fatty acid storage in skeletal muscle and theliver and, according to Randle’s cycle, lead to increased glucoseutilization by muscle, lower glucose levels and increasedinsulin sensitivity. Another consequence of a greater numberof adipocytes is that fatty acids can be redistributed from largeinsulin-resistant adipocytes to smaller, more insulin-sensitiveadipocytes, as has been observed in some rat models of diabetestreated with TZDs [5]. In consequence, insulin will act moreeffectively upon adipocytes within body fat, to inhibit lipolysisand increase trapping of fatty acids within fat cells.

The effects of PPAR

γ

activation on adipocytes are notrestricted to the differentiation pathway. TZDs also decreasethe levels of tumour necrosis factor-alpha (TNF-

α

) and leptinproduction by adipocytes. It has been suggested that TNF-

α

inhibits insulin signalling and insulin-stimulated glucose trans-port in adipocytes and skeletal muscle, and that leptin alsoinhibits insulin action in these cells. Therefore the TZD-inducedreduction of TNF-

α

and leptin production by adipocytes mightalso contribute to the insulin-sensitizing effects of these agents [2].

To complicate our understanding of the mechanism of actionof TZDs further, it has been proposed that they can also alterbody fat distribution. When total body fat is measured usingsensitive imaging techniques such as computed tomography ormagnetic resonance imaging, and divided into subcutaneousvs. visceral adipose depots, it is the size of the visceral adiposedepots that correlates closest with the incidence of Type 2diabetes and insulin resistance syndrome [6,7]. Therefore, itwould seem that storage of fatty acids within the visceralrather than the subcutaneous adipose depots is worse for anindividual’s health. One reason for this could be that thevisceral adipose depots release fatty acids directly into thehepatic portal system, where they are transported to the liverand may affect insulin sensitivity and hepatic glucose produc-tion to a far greater extent than fatty acids stored in the moreperipheral subcutaneous adipose depots [8]. In studies using

ex vivo

human adipocyte cultures, TZDs had a greater effectupon cells originating from subcutaneous compared withomental adipose depots [9]. This observation prompted cliniciansto examine the body fat distribution of patients treated withTZDs. Several studies have now shown that after 6 months to1 year of treatment with troglitazone the total body fat of thepatients, as measured by BMI, increases as does the size ofthe subcutaneous adipose depots. However, the size of thevisceral adipose depots in these patients either remains thesame as before treatment or, in the individuals treated in onestudy, was reduced [4,10]. These studies suggest that treatmentof patients with TZDs leads to increased fat storage in thesubcutaneous adipose depots—probably the safest place tostore excess fat.

The above is a description of a very indirect mechanism ofaction for TZDs, i.e. the TZD is activating a receptor in cellswhich leads to repartitioning of fatty acids that in turn leads toincreased glucose utilization and insulin sensitivity in othercells. This indirect mechanism of action of TZDs may explainwhy, although they are potent PPAR

γ

agonists, the maximalglucose-lowering effects in humans take up to 6 months oftreatment. However, there are some convincing data that castdoubt on this hypothesis. Mice in which adipose tissue wasvirtually eliminated by fat-specific expression of diphtheriatoxin developed severe hyperglycaemia and hyperinsulinaemia.Treatment of these mice with troglitazone alleviated the hyper-glycaemia and significantly decreased the raised insulin levels,thus demonstrating that in this model the antidiabetic action oftroglitazone was independent of an effect on adipose tissue [11].To date there are no convincing explanations for these results.



9


Diabetic Medicine

,

19

, 1–14

An eye to the future

It is feasible that the glucose-lowering effects of TZDs could beincreased if they not only stimulated fat storage in adipocytesbut also increased mitochondrial fatty acid oxidation. Per-oxisome proliferator-activated receptor-alpha (PPAR

α

) is asimilar nuclear hormone receptor to PPAR

γ

, but activates thefatty acid oxidation pathway instead of the preadipocytedifferentiation pathway. If drugs could be developed thatactivated both PPAR

γ

and PPAR

α

it may be possible to increasethe amount of free fatty acid incorporated into triglycerideswithin the adipocytes and also to increase their rate of oxida-tion, leading to a net decrease in fatty acids within the body.However, this approach is likely to prove difficult as, althoughsimilar, there are some differences between the ligand bindingdomains of PPAR

γ

and PPAR

α

, and a compound that is capableof binding and activating both of these receptors is likely to beless potent at each individual receptor than compoundsdeveloped as pure PPAR

γ

or pure PPAR

α

agonists. An alter-native to developing one drug with agonist activities at bothreceptors is to use a specific PPAR

γ

agonist in combinationwith a specific PPAR

α

agonist, although to date no potentPPAR

α

agonists have been approved by the regulatory authorities.A PPAR

γ

knockout mouse has recently been described withan extremely interesting, if rather surprising, phenotype. Thehomozygous knockout mouse was embryonic lethal; however,the heterozygous knockout animals, with approximately halfthe level of PPAR

γ

expression of the wild-type animals, werehealthy and viable [12]. On further study it was found that,when the mice where given a high fat diet, they did not put onas much weight as their wild-type littermates and they also hadimproved insulin sensitivity and plasma lipid profiles [12].This result suggests that reducing PPAR

γ

activity with a PPAR

γ

antagonist may have utility in treating individuals with diabetesand/or obesity. However, this work is at an early stage and ourunderstanding of the effects in humans of inhibiting PPAR

γ

activity is still very poor.In conclusion, there are already two alternative TZD treat-

ments available for patients like Mr WP for whom conven-tional therapy does not work—although as yet unlicensed incombination with insulin in the UK. Whilst undoubtedlyeffective, the exact mode of action of TZDs remains to be

completely elucidated. It is probable that the next phase will bedrugs working through similar mechanisms but with modifiedprofiles. This rapidly expanding field of research is likely toresult in the availability of new non-TZD PPAR

γ

agonists inthe near future. It is even possible in future that drugs like thesemay prevent patients like Mr WP from ever developing suchprofound insulin resistance and its dire consequences.

References

1 Walker M. Insulin resistance: a problem for clinicians and scientists.

Diabet Med

2000;

17

: 397–409.2 Reginato M, Lazar M. Mechanisms by which thiazolidinediones

enhance insulin action.

Trends Endo

1999;

10

: 9–13.3 Lehmann JM, Moore LB, Smith-Oliver TA, Wilkison WO, Willson

TM, Kliewer SA. An antidiabetic thiazolidinedione is a high affinityligand for peroxisome proliferator-activated receptor gamma.

J BiolChem

1995;

270

: 12953–12956.4 Mori Y, Murakawa Y, Okada K, Horikoshi H, Yokoyama J, Tajima

N

et al.

Effect of troglitazone on body fat distribution in type 2 dia-betic patients.

Diabetes Care

1999;

22

: 908–912.5 Okuno A, Tamemoto H, Tobe K, Ueki K, Mori Y, Iwamoto K

et al.

Troglitazone increases the number of small adipocytes without thechange of white adipose tissue mass in obese zucker rats.

J Clin Inv

1998;

101

: 1354–1361.6 Peiris AN, Hennes MI, Evans DJ, Wilson CR, Lee MB, Kissebah AH.

Relationship of anthropometric measurements of body fat distribu-tion to metabolic profile in premenopausal women.

Acta Med ScandSuppl

1988;

723: 179–188.7 Fujioka S, Matsuzawa Y, Tokunaga K, Kawamoto T, Kobatake T,

Keno Y et al. Improvement of glucose and lipid metabolism associ-ated with selective reduction of intra-abdominal visceral fat in pre-menopausal women with visceral fat obesity. Int J Obesity 1990; 15:853–859.

8 Montague C, O’Rahilly S. The perils of portliness: causes and conse-quences of visceral adiposity. Diabetes 2000; 49: 883–888.

9 Adams M, Montague CT, Prins JB, Holder JC, Smith SA, Sanders Let al. Activators of PPARγ have depot-specific effects on human pre-adipocyte differentiation. J Clin Invest 1997; 100: 3149–3153.

10 Akazawa S, Sun FY, Ito M, Kawasaki E, Eguchi K. Efficacy of trogl-itazone on body fat distribution in type 2 diabetes. Diabetes Care2000; 23: 1067–1071.

11 Burant C, Sreenan S, Hirano KI, Tai TC, Lohmiller J, Lukens J et al.Troglitazone action is independent of adipose tissue. J Clin Invest1997; 100: 2900–2908.

12 Kubota N, Terauchi Y, Miki H, Tamemoto H, Yamauchi T, Komeda Ket al. PPAR gamma mediates high-fat diet-induced adipocyte hyper-trophy and insulin resistance. Mol Cell 1999; 4: 597–609.

DIABETES JOURNAL WATCH


Effectiveness of a hospital diabetes specialist nursing service

You are seeking to fund a diabetes specialist nurse with specialresponsibility for hospital in-patients. A lay member of thepanel reviewing your bid asks why money is better spent ondiabetes than other causes such as palliative or respiratory care.

Davies M, Dixon S, Currie CJ, Davis RE, Peters JR. Evaluation of ahospital diabetes specialist nursing service: a randomized controlledtrial. Diabet Med 2001; 18: 301–307.

Objective To evaluate the effectiveness and cost implications


© 2002 Diabetes UK. Diabetic Medicine, 19, 1–14

10 Continuing education

of a diabetes specialist nursing service for hospitalin-patients.Design Randomized, controlled trial.Setting Three hundred adult in-patients with diabetes.Intervention The control group received standard care alone.Subjects in the intervention group received additional care andadvice from a diabetes specialist nurse, who also providedfeedback to ward-based staff. Four diabetes specialist nurseswere rotated into the post during the study period.Main outcome measures The primary outcomes were lengthof stay and readmission within 12 months.Main results There was an excess of subjects with Type 1 inthe intervention group (22% vs. 11%, P = 0.04). Data on theprimary outcomes were available for all subjects. Length ofstay was lower in the intervention group (8.0 vs. 11.0 days,P < 0.01). In both groups, 25% of the subjects were readmittedafter a mean of around 280 days. There was a non-significantreduction in the mean cost per admission of £436 in the inter-vention group (1997/8 prices, P = 0.19), lower than the controlgroup (P = 0.19). Satisfaction with care (91% vs. 59% satisfied,P = 0.001) and knowledge were significantly higher in theintervention group.Conclusion A diabetes specialist nursing service for hospitalin-patients can reduce length of stay and increase satisfaction.There was no evidence of any detrimental effects on the service.

Abstract prepared by S. Hollis, Lancaster University, UK.January 200219000000Continuing educationContinuing education

Commentary

S. RobertsNorth Fyneside District General Hospital, North Shields, Tyre and Wear, UK

People with diabetes have poor experiences in hospital,especially if they are admitted for unrelated conditions [1].Length of stay is also increased [2]. Since they occupy 10% ofUK beds, it seems neither patients nor the service are benefittingfrom the current arrangements. This paper shows that an in-patient diabetes specialist nurse (DSN) can reduce length of staywithout increasing readmissions. There may even be some increasein patient satisfaction and financial savings. This is importantnews, and would be of interest to patients, to hospital mangers,Local Diabetes Service Advisory Group (LDSAG) membersand commissioners of health care in the local health economy.

What would individuals with diabetes make of this study?A third of those invited chose not to take part, although it isunclear how the aims were presented to them. Did they perceivethat a trial devoted to getting then out quicker was accountant-driven? Surprisingly, and unconventionally, those who declinedto take part were all given the intervention (i.e. the nurse visit)rather than the traditional treatment. Did those who declinedhave previous good experiences of DSNs and not want to missout? Or did they feel this study was not relevant to theirparticular concerns? Patient satisfaction is multidimensional[3]. In-patients, whether they have diabetes or not, may holdnegative views towards the information they receive, their rela-

tionship with healthcare professionals and the progress theymake through the system. In diabetes there are specificproblems. ‘When in hospital for 8 days it was not until thethird or fourth day that I was given my insulin injection beforefood ... Listen to those who need insulin injections. They knowwhat insulin they need and when.’ The audit commission found‘in over the half the hospitals visited, less than 30% of wardsallowed patients to keep and control their own insulin and medi-cation. This undermines the principle of supporting individualself-management, which is so important in diabetes care [1]’.

This study used the Diabetes Care Service Questionnaire(DCSQ) [4] to study patient satisfaction. The modificationsmade by the researchers presumably removed statementsspecifically related to out-patient care, the purpose for whichthe scale was originally developed, but retained the items: ‘Thevalue to me of talking to staff’, ‘The extent to which I feltunderstood by staff’, ‘How I am treated as a person by staff’.Increase in satisfaction was probably related to these aspects ofinterpersonal communication. However, not all the difficultiesexperienced by diabetic in-patients lend themselves to addi-tional care from a diabetes specialist nurse: ‘I found it hard toget insulin doses changed quickly, as you have to have a doctorthere to get insulin changed ... you need your insulin put upright away ... if there is no doctor about this can take a longtime or sometimes not be done at all.… I feel the new diabeticis not helped enough in the ward as I have had to explain manytimes about diabetes and its effect after doctors and specialistnurses have seen them’ [5]. A satisfaction questionnairedeveloped specifically for in-patient use [6] might have beenmore sensitive to these concerns. However, diabetes patientsare thirsting for information so it is good news that knowledgeimproved, although unsurprising it translated into neitherimproved self-management nor quality of life.

The hospital manager has a lot to gain from this approach.Presented in financial terms, the savings are notional and notnecessarily significant. But length of stay is one of the largestcontributors to marginal costs of in-patient care. If the savings(3 out of 11 days) reported here were distributed evenly acrossa 500-bed hospital, it would release a notional 10 beds. Wherehospitals are running close to 100% capacity, reducingpressure from any one group of patients will help others.

How should a LDSAG view this study? The outcomes forpatients look impressive. This could be a quick and cheap wayto achieve considerable benefits. However, as advisors onspending a diabetes budget, they would want to ask if this isthe only or the best way to obtain these. The researcherspostulate that lack of confidence in managing diabetes on thepart of ward staff may be the biggest contributor to delayeddischarge. In support of that the audit commission citedfrequent problems related to insufficient staff training in theneeds of people with diabetes [1]. The LDSAG might want tocompare other schemes such as ‘Link’ nurses [1] which canbenefit a whole ward rather than individuals alone. A localaudit might identify recurring problems and lead to specificprotocol development or tailored training, thus defining a


Continuing education 11


different but valuable role for the in-patient diabetes specialistnurse. Alternatively, the LDSAG might decide that moneycould be better spent on education programmes outside hospitalto improve overall patient knowledge of what care to expect ordemand when admitted, or systems of written information forpatients and staff.

Commissioning decisions in the wider health economy areeven more difficult. Specialist teams in palliative care [7],respiratory medicine [8] and stroke [9] can all improve care,but there is no guarantee that the existence of a specialist teamwill improve satisfaction or other health outcomes, which arecontext specific and susceptible to many influences.

This paper reminds us that length of stay can be profoundlyaffected by organizational change, and that changes, like manycomplex interventions [10] in healthcare, can be broken downinto parts. Whether outcomes are beneficial will depend on howthese are put together and work in particular local environ-ments. A complex mixture of local and national priorities andimperatives will influence the decision where to directresources. Most good from the deployment of specialist nurseswill be achieved by focused interventions [8] directed at gapsin service identified by local needs assessment, and wherepatients, clinicians and managers all agree on the direction ofthe service, are committed to improve all aspects of practice,and work together to achieve it.

References1 Audit Commission. Testing Times. A review of Diabetes Services in

England and Wales. London: Audit Commission, 2000.2 Currie CJ, Kraus D, Morgan CL, Gill L, Stott NC, Peters JR. NHS

acute sector expenditure for diabetes: the present, future, and excessin-patient cost of care. Diabet Med 1997; 14: 686–692.

3 Fitzpatrick RHA. Measurement of Patients’ Satisfaction with theirCare. London: Royal College of Physicians of London, 1993.

4 Wilson AE, Home PD. A dataset to allow exchange of informationfor monitoring continuing diabetes care. The Diabetes Audit WorkingGroup. Diabet Med 1993; 10: 378–390.

5 Raleigh VS, Clifford GM. Analysis of audit commission survey dataon people with diabetes. 20001–45 ... www.doh.gov.uk/nsf/diabetes

6 Bhattacharyya A, Christodonlides C, Kaushal K, New JP, Young RJ.Assessing in-hospital management of diabetes by anonymous patientsatisfaction questionnaire. Diabet Med 2001; 18 (Suppl. 2): 134.

7 Center for Reviews and Dissemination Reviewers. Do SpecialistPalliative Care Teams Improve Outcomes for Cancer Patients: aSystematic Literature Review. Database of Abstracts of reviews ofEffectiveness. Issue 1. York UK: NHS Center for Reviews andDissemination, 2001.

8 Hobbs R, Murray ET. Specialist liaison nurses. BMJ 1999; 318: 683–684.

9 Stroke Trialists’ Collaboration. Organised inpatient (stroke unit)care for stroke. Cochrane database of Systematic reviews 2001; Issue 3.

10 Medical Research Council. A Framework for Development andEvaluation of RCTs for Complex Interventions to Improve Health.April 2000; www.mrc.ac.uk/complex_packages

January 200219000000


What’s new in the journals?

Coeliac disease

Holmes GKT. Coeliac disease and type 1 diabetes mellitus—the case forscreening. Diabet Med 2001; 19: 169–177.

This literature review reports prevalences of coeliac diseasebetween 1% and 6% in adults, and between 1% and 16% inchildren with Type 1 diabetes. Coeliac disease may come tolight in diabetic patients with vague abdominal symptoms, orhypoglycaemia due to impaired carbohydrate absorption. Nowthat a sensitive and specific immunological test is available, theauthor makes the case for screening. Whether or not oneaccepts the screening argument, this review serves to remindphysicians to be on the lookout for subtle manifestations ofmalabsorption in their Type 1 diabetic patients.

Treatment of type 1 diabetes

Cox DJ, Gonder-Frederick L, Polonsky W, Schlundt D, Kotutchev B,Clarke W. Blood glucose awareness training (BGAT-2). DiabetesCare 2001; 24: 637–642.

This study looked at the long-term effects of blood glucoseawareness training (BGAT). Seventy-three adults with Type 1diabetes were followed for 12 months from baseline to follow-up. BGAT reduced the occurrence of diabetic ketoacidosis,severe hypoglycaemia and motor vehicle violations. There wasno worsening of diabetic control. There were also observed

improvements in quality of life and diabetes knowledge. It isargued that this psychoeducational programme should becomepart of routine treatment of those at highest risk of hypoglycaemia.

Treatment of Type 2 diabetes

Raskin P, Rendell M, Riddle MC, Dole JF, Freed MI, Rosenstock J.A randomized trial of rosiglitazone therapy in patients withinadequately controlled insulin-treated type 2 diabetes. DiabetesCare 2001; 24: 1226–1232.

This study determined the efficacy and safety of rosiglitazonewhen added to insulin in the treatment of Type 2 diabeticpatients who are not well controlled on insulin alone. After arun-in period of 8 weeks, they were allocated to placebo orrosiglitazone (4 or 8 mg) for a 26-week period. Rosiglitazone(8 mg) significantly improved glycaemic control. HbA1c fell by1.2%, despite a 12% reduction in insulin dosage. Over 50% ofpatients taking rosiglitazone 8 mg recorded a ≥ 1% fall inHbA1c. No serious adverse effects were reported.

Yale J-F, Valiquete TR, Ghazzi MN, Owens Grillo JK, Whitcomb RW,Foyt HL for the Troglitazone Triple-Therapy Study Group. Theeffect of a Thiazolidinedione drug, Troglitazone, on glycemia inpatients with type 2 diabetes mellitus poorly controlled withsulphonylurea and metformin. Ann Intern Med 2001; 134: 737–745.

In the UK, the glitazones are licensed for use in combinationwith either metformin or sulphonylurea. Their place in ‘triple’




therapy (i.e. with metformin and sulphonylurea) is uncertain.This study of 200 patients with suboptimal glycaemic controlon maximum tolerated dose of metformin and sulphonylureashowed an additional drop of 1.4% in HbA1c with troglita-zone. Troglitazone is no longer available, but this study raisesthe question of whether Rosiglitazone and Proglitazone shouldbe used as an alternative to insulin therapy in patients withsuboptimal glycaemic control on maximum tolerated sulpho-nylurea and metformin.

Rosenstock J, Schwartz SL, Clark CM, Park GD, Donley DW, EdwardsMB. Basal insulin therapy in type 2 diabetes. 28-week comparison ofinsulin glargine (HOE 901) and NPH insulin. Diabetes Care 2001;24: 631–636.

Insulin glargine, a novel recombinant insulin analogue, islikely to be available for use in the UK some time in 2002. Inthis study of 518 subjects with Type 2 diabetes, once-dailybedtime insulin glargine was as effective as once or twice dailyNPH insulin in terms of glycaemic control. With glargine there wasa lower risk of nocturnal hypoglycaemia and less weight gain.

Treatment of obesity

Pinkney JH, Sjöström CD, Gale EAM. Should surgeons treat diabetes inseverely obese people? Lancet 2001; 357: 1357–1359.

Most diabetologists regard obesity as an untreatable disorder.Despite the recent introduction of drugs to treat it, success islimited and many patients quickly regain what weight theylose. In the UK, obesity surgery is rarely used, partly becauseso few centres can offer it. This short review reminds us howsuccessful surgical treatment can be. In the Swedish ObesitySubjects (SOS) study, 845 patients with a body mass index> 40 kg/m2 lost 28 kg compared with 0.5 kg/m2 in the controlgroup. Patients with diabetes lost 28 kg in 2 years, resulting inbetter glycaemic control, and less use of oral hypoglycaemicagents (OHA) and insulin (the proportion treated with dietalone increased from 59% to 73% in the treatment groupwhereas it fell from 55% to 34% in the control group). In anothergroup, the percentage of surgically treated patients requiringan OHA or insulin fell from 32% to 9%, whereas it rose in thecontrol group (56% to 88%). Perhaps diabetologists shouldremember the older methods of treating obesity before usingthe newer weight-reducing drugs?

Cardiovascular disease

Iribarren C, Karter AJ, Go AS, Ferrara A, Liu JY, Sidney S, Selby JV.Glycemic control and heart failure among adult patients withdiabetes. Circulation 2001; 103: 2668–2673.

Improved glycaemic control by therapeutic intervention hasbeen shown to reduce microvascular complications in Type 2diabetes. A cohort of 25 958 men and 22 900 women with(predominantly Type 2) diabetes aged ≥ 19 years, with noknown history of heart failure, were followed for a median2.2 years. After adjustment for other risk factors, each 1%increase in HbA1c was associated with an 8% increased risk ofheart failure (95% CI 5% to 12%). An HbA1c ≥ 10%, relativeto HbA1c < 7%, was associated with a 56% increased risk ofheart failure (95% CI 26% to 93%). Poor glycaemic controlappears to be associated with an increased risk of heart failurein diabetic patients.

Abizaid A, Costa MA, Centemero M, Abizaid AS, Legrand VMG, LimetRV et al. Clinical and economic impact of diabetes mellitus onpercutaneous and surgical treatment of multivessel coronary diseasepatients. Insights from the Arterial Revascularization Therapy Study(ARTS) Trial. Circulation 2001; 104: 533–538.

The Bypass Angioplasty Revascularization Investigation(BARI) Study demonstrated that diabetic patients with multi-vessel coronary disease had a worse outcome when treatedwith balloon angioplasty compared with coronary arterybypass graft (CABG) surgery. A subgroup analysis of theArterial Revascularization Therapy Study (ARTS) comparingCABG and the stenting of multivessel coronary disease included208 diabetic patients. After 1 year, the event-free survival ratefor death, cerebrovascular events, myocardial infarction orany repeat revascularization for diabetic patients was lowerthan those treated with CABG (63.4% vs. 84.4%, P < 0.001),and also non-diabetic patients treated with stents (76.2%,P = 0.04). However, both diabetic and non-diabetic patientshad a similar 1-year event-free survival when treated withCABG (84.4% and 88.4%).

Hunt D, Young P, Simes J, Hague W, Mann S, Dwensby D et al. for theLIPID Investigators. Benefits of Pravastatin on cardiovascular eventsand mortality in older patients with coronary heart disease are equalto or exceed those seen in younger patients: results from the LIPIDtrial. Ann Intern Med 2001; 134: 931–940.

This secondary prevention trial randomized 3514 patientsaged 65–75 years with a baseline plasma cholesterol level of4.0–7.0 mmol/ l to pravastatin or placebo. Follow-up was6 years. Compared with younger patients (31–64 years ofage), older patients were at higher risk of death, MI, unstableangina and CVA. Pravastatin reduced the risk of all events,and the reductions were similar in older and younger patients.However, numbers needed to treat were lower and thereforeabsolute benefit of treatment was significantly higher in olderpatients.

Continuing educationContinuing education


Continuing education 13


General description and methods

Aims and editorial philosophy

This section of Diabetic Medicine aims to promote good careof people with diabetes by meeting the educational needs oftrainee and trained professionals. Its goals are to:• Respect adult learning principles.• Report and comment on important changes in the evidencebase of diabetes care.• Explore problems and controversies in care and offer expertsolutions when the evidence base is weak.• Explain scientific concepts and developments that impact ondiabetes care.• Support the readers’ development of study skills.• Promote and report interaction with the readership.• Be concise.

It aims to be rigorous, always clinically relevant, and todraw on the discipline of evidence-based medicine.

Editorial panel

The contents of the Section are contributed or commissionedby a panel whose members are:Dr Melanie Davies, Leicester; Dr Tim Dornan, Salford (Co-ordinating Editor); Dr Martin Gibson, Salford; Dr Sally Hollis,Lancaster; Dr Ian Lawrence, Leicester; Dr Paul McNally,Leicester; Dr John New, Salford.

Publication details

Continuing Education is published three times per annum.Full-text and PDF versions are available to Diabetic Medicinesubscribers on the Blackwell Science Synergy website (http://www.blackwell-synergy.com). The electronic version of thesection provides an electronic link to MedLine and, wheneveravailable, to the full electronic text of any original articlecited. An electronic discussion forum will be linked to thewebsite to promote communication between readers (http://www.mediabetes.com).

Contents

Each issue contains some or all of the following types of article:

Editorial. A brief commentary on the contents of the issue andother matters relevant to continuing education and clinicalpractice in diabetes.

Learning and teaching skills. These commissioned articles ontopics related to professional development aim to help readersdevelop their learning skills.

Clinical practice question. The Editorial Panel commissionsan expert to write a short commentary around a difficult situ-ation arising in clinical practice. The article begins with self-assessment questions, and then answers them as far as existingevidence and the experience of the commentator permit. TheEditorial Panel invites readers to submit questions and nomi-nate commentators. The electronic discussion forum will, withtime, act as a source of topics.

Today’s evidence. Members of the Editorial Panel screen thefollowing journals for original articles which, in their opinion,have the potential to change clinical practice:

General journals: British Medical Journal; Journal of theAmerican Medical Association; The Lancet; New EnglandJournal of Medicine; British Journal of General Practice;Annals of Internal Medicine.

Specialist journals: Diabetes; Diabetic Medicine; Diabetes Care;Diabetes Research and Clinical Practice; Diabetologia; EndocrineReviews; Journal of Clinical Endocrinology and Metabolism.

Having identified a paper, the screener scores it for its potentialto change practice, originality, importance and strength ofevidence. At present, the journals are not second-screened. Sixmonths before an issue is due to be published, all articles identifiedin the preceding 4 months are ranked. A structured abstract ofthe highest-ranking article is prepared, prefaced by self-assessmentquestions, and an expert in the field is commissioned to writea short commentary discussing the article and putting it in thecontext of the current medical literature, and clinical practicegenerally. Other articles are cited with a short comment.

Horizons. These articles aim to give a succinct discussion of anew or evolving aspect of basic science that impacts on clinicalpractice. They are commissioned in response to importantbiomedical developments.

Correspondence. A resume of any important correspondence,electronic and on paper, may be published.

Citation

For citation purposes, each issue will be regarded as a singlearticle; citations should be in the following format: ContinuingEducation. Diabetic Med 1999; 17: 000–000.

Communication with the readership

The Editorial Panel hopes to develop two-way interaction withits readership, through;• The website, electronic discussion forum and use of e-mail.• Publication of correspondence on previously published material.




Correspondence from readers is welcomed, both electronicallyon our bulletin board and on paper. Letters should beaddressed to:

Continuing Education, c/o Diabetic Medicine, 25 JohnStreet, London WC1N 2BS, UK. E-mail: [email protected] http://www.mediabetes.com


editorial

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