author's response

DIABETIC

Medicine

© 2008 The Authors.Journal compilation © 2008 Diabetes UK.

Diabetic Medicine

,

25

, 1125–1131

1125

Blackwell Publishing Ltd

Letters: Correspondence

DOI: 10.1111/j.1464-5491.2008.02555.x

Can we predict future improvement in glycaemic control? Response to Singh and Press, 2008

I was pleased to read the recent study reported by Singh andPress, which identified patient-related factors associated withsustained poor glycaemic control [1]. Their prospective cohortstudy followed 130 patients with poorly controlled diabetesat a clinic in the UK. Glycated haemoglobin (HbA

1c

) wasrecorded at the start of the study (all HbA

1c

levels

≥

10.0%)and again at 12-month follow-up. The investigators allocateda principal cause for each patient’s poor glycaemic control,based on interviews and clinical notes. Fifteen separate causeswere identified, with eight of these being associated with asignificant improvement in HbA

1c

at 12 months, suggestingthat the cause had either been addressed or resolved withstandard care. However, six additional causes were associatedwith continuing poor glycaemic control after 12 months,implying that they were not addressed sufficiently by standardcare. Factors associated with sustained poor glycaemic controlcentred around treatment adherence and included refusal totake oral glucose-lowering agents or insulin, refusal to increasethe insulin dose and a failure to self-monitor blood glucose.The study indicates that additional steps, over and abovestandard care for diabetes, may be needed to tackle these issuesif levels of glycaemic control are to be improved.

The Global Task Force (GTF) on Glycaemic Control wasestablished over a year ago and comprises 14 clinicians fromeight countries (China, Canada, India, Poland, Russia, Swedenand the UK). As chairman of the GTF, I and my fellowmembers aim to investigate and implement practical solutionsto try to help tackle the problem of poor glycaemic control. In2007, we conducted a survey review of over 2000 physiciansand patients with Type 2 diabetes from the eight countries,which was designed to canvass their opinion on the barriers togood glycaemic control. The survey revealed a consistency inresponses from each country, despite their markedly differenthealthcare systems. Patients considered adherence to diet andexercise programmes, medication regimens and glucosemonitoring as the most difficult aspects of managing theirdiabetes. Physicians cited patients’ lack of motivation totackle their condition and failure to adhere to treatment as keyreasons for elevated HbA

1c

levels. The findings of Singh andPress are consistent with the international barriers identifiedby patients and physicians in our survey and show that theseissues associated with elevated HbA

1c

are sustained for atleast 12 months.

Clearly, practical solutions are required to tackle theproblem of patient motivation and analysis by the GTF hasagain revealed uniformity between countries in identifyingthat further education has the potential to play a significantrole. Consequently, we, in collaboration with Novo Nordisk,are currently developing an educational toolkit for healthcareprofessionals (HCPs) treating patients with Type 2 diabetes,adaptable for local needs. The toolkit aims to provideadditional skills to ensure effective communication with patientsand to promote ongoing patient motivation, especially whenpatients undergo ‘life events’ in relation to their diabetestreatment. The aim is to encourage greater understanding ofthe potential barriers to good glycaemic control experiencedby patients and how best to overcome these challenges.

Improving glycaemic control significantly is a difficultenough challenge in developed countries, never mind in thoseless affluent ones where the burden of Type 2 diabetes is set torise fastest. We hope that implementation of initiatives, such asthe educational toolkit, will go some way towards tackling thebarriers identified by Singh and Press.

Competing interests

Professor Kilpatrick has received remuneration fromNovoNordisk for time spent developing the GTF project. Heis Chairman of the Global Task Force on Glycaemic Control.

Eric S. Kilpatrick

Chairman of the Global Task Force on Glycaemic Control,Department of Clinical Biochemistry, Hull Royal

Infirmary, Hull, UK

Reference

1 Singh R, Press M. Can we predict future improvement in glycaemiccontrol?

Diabet Med

2008;

25

: 170–173.

DOI: 10.1111/j.1464-5491.2008.02551.x

Author’s response

We welcome and wholeheartedly endorse the comments byKilpatrick. Recently, it seems that increased importance isbeing given to studies into compliance and behavioural factorsin glycaemic control with correlation to various patient andtreatment characteristics [1–3]. Particular focus has beenplaced on whether self-monitoring is of any use in Type 2diabetic patients not using insulin [4].

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DIABETIC

Medicine Letters

© 2008 The Authors.

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Journal compilation © 2008 Diabetes UK.

Diabetic Medicine

,

25

, 1125–1131

It would be useful to know more about the educationaltoolkit. Will more resources or staff be needed for implementa-tion? As Kilpatrick confirms, in at least half of individuals,glycated haemoglobin (HbA

1c

) will not improve and additionalstrategies will be needed. We have suggested more counsellingand psychology input, which anecdotally does seem to beincreasing across diabetes services. It is interesting thatKilpatrick found no difference between factors causingpoor compliance in developed vs. developing countries. Againanecdotally and from personal experience, we often believe,perhaps wrongly, that patients in developing countries aremore likely to comply with health professional advice.

It will be interesting to see whether the educational toolkitmakes a difference to diabetes control and if results varybetween different countries. Barely a year goes by without anew drug target for diabetes treatment being launched andour therapeutic armamentarium is becoming impressive.It would be a shame if our efforts to improve outcomes indiabetes are rendered ineffective because of our limited under-standing of the behavioural and compliance barriers thatindividuals face.

Competing interests

Nothing to declare.

Rajiv Singh

Rehabilitation Medicine, Northern General Hospital,Sheffield, UK

References

1 Bebb C, Kendrick D, Stewart J, Coupland C, Madeley R, Brown K

et al

. Inequalities in glycaemic control in patients with Type 2 diabetesin primary care.

Diabet Med

2005;

22

: 1364–1371.2 Ng TP, Goh LG, Tan Y, Tan E, Leong H, Tay EG

et al

. Ethnic differ-ences in glycaemic control in adult Type 2 diabetic patients in primarycare: a 3-year follow-up study.

Diabet Med

2005;

22

: 1598–1604.3 Davis WA, Bruce DG, Davis TM. Does self-monitoring of blood

glucose improve outcome in Type 2 diabetes? The Fremantle DiabetesStudy.

Diabetologia

2007;

50

: 510–515.4 Farmer A, Wade A, Goyder E, Yudkin P, French D, Craven A

et al

.Impact of self-monitoring of blood glucose in the management ofpatients with non-insulin-treated diabetes: open parallel group ran-domised trial.

Br Med J

2007;

335

: 105–106.

XXX LetterLettersLettersLetters

DOI: 10.1111/j.1464-5491.2008.02528.x

Methodology problems in using eGFR to investigate the prevalence of renal anaemia

In a recent study, New

et al

. [1] described the prevalence ofanaemia in patients with diabetes and chronic kidney disease(CKD). The study sampled diabetes patients using data fromprimary, secondary and tertiary care services over 6 weeks forall values of estimated glomerular filtration rate (eGFR). The

results suggested 25% (95% confidence interval 20, 31) ofpeople with diabetes with an eGFR < 60 ml/min per 1.73 m

2

are anaemic with Hb < 110 g/l.We produced similar results in a previous study, but with a

prevalence of 16% in diabetic CKD patients in primary care[2,3]. Our study simultaneously raised a number of issuesregarding the use of eGFR.

The four-variable Modification of Diet in Renal Disease(MDRD) equation [4] is currently the best estimator of kidneyfunction, but has some inaccuracies. As a result, using onesingle eGFR has a degree of variability. To produce a moreaccurate result, we have used two consecutive eGFRs separatedby a minimum of 3 months [2,3]. This helps to tease outwhether CKD exists and to which stage a patient truly belongs.

As the MDRD equation becomes more inaccurate aboveeGFR > 60 ml/min per 1.73 m

2

, Kidney Disease OutcomesQuality Initiative guidelines [5], the Royal College of Physicians,Royal College of General Practitioners and the Renal Associa-tion [6] all suggest that another form of renal impairment, suchas persistent proteinuria or haematuria, must be present.Without this added information, an isolated value of eGFR> 60 ml/min per 1.73 m

2

is harder to relate directly to kidneydisease. As interpretation can be problematic, we excludedanybody with eGFR > 60 ml/min per 1.73 m

2

[2,3].The source of data is also important. Using tertiary care data

may be influenced by those with acute renal impairment, notthe intended stable chronic renal impairment. The issue ofacute haemoglobin loss is then also raised. We have previouslyused primary care data [2,3], which are less likely to beinfluenced by acutely ill patients. A major disadvantage of usingprimary care data is that a smaller proportion of patients haveCKD stage 4 and 5, perhaps explaining why our estimationwas lower. Out-patient secondary care data may be the bestoption, and we have used these for determining requirementsof i.v. iron in anaemic CKD patients [7].

New

et al

. [1] end by mentioning the limitation of notperforming investigations such as haematinics to excludenon-renal causes of anaemia. Other studies have mentioneddiabetes-related influences such as autonomic neuropathy [8],use of angiotensin-converting enzyme inhibitors [9] andlow-grade systemic inflammation, all of which influenceanaemia. Although we found the former difficult to assess inall patients, the latter could be investigated by measuringinflammatory markers such as C-reactive protein and erythro-cyte sedimentation rate.

The eGFR is only an approximate value, and its accuracyshould be considered in clinical and research contexts. Theprinciples raised in this letter also apply to any study usingeGFR.

S. Mostafa and A. Burden*

Academic Clinical Fellow/SHO in Medicine, LeicesterGeneral Hospital, Leicester and

*

Diabetes Care,Heart of Birmingham Teaching Primary Care Trust,

Birmingham, UK

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