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Q J Med 2003; 96: 833-836
© 2003 Association of Physicians

Intensified treatment of type 2 diabetes—positive effects on blood pressure, but not glycaemic control

G.V. Gill, A. Woodward, S. Pradhan, M. Wallymahmed, T. Groves, P. English and J.P. Wilding

From the Department of Diabetes and Endocrinology, University Hospital Aintree, Liverpool, UK

Received 9 April 2003 and in revised form 21 May 2003


    Summary
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 Summary
 Introduction
 Methods
 Results
 Discussion
 References
 
Background: Since publication of the UK Prospective Diabetes Study (UKPDS) in 1998, there has been a clear evidence base for tight glycaemic (HBA1c < 7.0%) and blood pressure (BP < 140/85 mmHg) control.

Aim: To determine the effect of UKPDS–based intensified glycaemic and BP targets on the care of type 2 diabetic patients attending a routine diabetes clinic.

Design: Two surveys, each of 500 consecutively attending type 2 diabetic patients.

Methods: The first survey was in a 3-month period in 1999, shortly after publication of the UKPDS study. The second was identical, but 2 years later. Glycaemic control (by DCCT-aligned HBA1c), BP and treatment details were recorded in both.

Results: BP control was significantly improved in the second survey (mean ± SD systolic BP from 151 ± 25 to 146 ± 26 mmHg, p = 0.001; diastolic from 77 ± 13 to 72 ± 12 mmHg, p < 0.0001) and the proportion of patients on anti-hypertensive treatment increased from 33% to 60% (p < 0.0001). Mean HbA1c however remained unchanged (8.7 ± 1.8% in 1999 vs. 8.5 ± 1.8% in 2001), although there was evidence of more intensive treatment patterns, with declining numbers on diet alone and more on oral agents and/or insulin.

Discussion: Intensified BP control may be achievable within the confines of routine diabetes care, but achievement of optimal glycaemic targets remains problematic.


    Introduction
 Top
 Summary
 Introduction
 Methods
 Results
 Discussion
 References
 
Type 2 diabetes is associated with a high risk of cardiovascular mortality and morbidity, accounting for almost two-thirds of all deaths in diabetic patients, with up to 75% of cardiovascular disease in diabetic subjects being attributed to hypertension.1–3 Tight glycaemic and blood pressure (BP) control reduces the risk of microvascular and macrovascular complications.4,5 International management guidelines have been developed to help achieve targets6 and improve cardiovascular status, but attaining such standards in type 2 diabetes is difficult. Evidence from the UK Prospective Diabetes Study (UKPDS)4,5 has been used to set targets for glycaemic (HbA1c) and BP control that are associated with significantly reduced mortality and morbidity. Since this study reported in 1998, diabetic clinics have been greatly increasing efforts to intensify glycaemic and BP control, but it remains uncertain how effective such efforts have been.7 We report two detailed assessments of HbA1c and BP control in a large number of type 2 patients attending our clinic—the first in 19998 just after publication of the UKPDS, and the second 2 years later in 2001.


    Methods
 Top
 Summary
 Introduction
 Methods
 Results
 Discussion
 References
 
The Walton Diabetes Centre at the University Hospital Aintree provides specialist diabetic care for the population of north Liverpool, UK. The Diabetes Centre caseload of more than 5000 patients includes patients with type 1 and type 2 diabetes, many with complex problems. For the purpose of this study, we defined type 2 diabetes as any person developing the disease after the age of 30 years, and not requiring insulin at diagnosis. Patients within one year of diagnosis were excluded from the study.

The initial audit of 500 type 2 patients attending the Diabetes Centre follow-up clinics during a 3-month period in 1999, was done by consecutive case-note extraction onto proforma, and has been reported previously.8 At the time of the second audit (2 years later), hospital and out-patient activity was computerized, and we used data extraction of consecutive type 2 patients attending clinics during a similar 3-month period in 2001.

Our criteria for ‘control’ of HbA1c and BP levels were based on UKPDS data.4,5 HbA1c was measured by high pressure liquid chromatography (HPLC). The assay was aligned to the Diabetes Control and Complications Trial9 (‘DCCT aligned‘), and was identical in both studies. An HbA1c level < 7.0% was regarded as good control and > 8.0% as poor control. BP was also measured by the same method in both studies with a Dynamap Compact T monitor. A BP level < 140/85 was used to define ‘controlled’ BP, and above this level for ‘uncontrolled’ BP.

Data recording and analysis used StatsDirect biomedical software. Values in the text are expressed as mean ± SD or n(%). Continuous variables were analysed by unpaired t-tests and the {chi}2 test was used for categorical variables. Data recorded included age, sex, duration of diabetes, diabetes treatment, most recent HbA1c, blood pressure (BP), and anti-hypertensive medication. For HbA1c and BP, ‘most recent’ was regarded as within the last 12 months. Regarding diabetes treatment; the ‘insulin’ category included those on insulin alone, and those on insulin plus oral agents.


    Results
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 Summary
 Introduction
 Methods
 Results
 Discussion
 References
 
The 1999 and 2001 studies both comprised 500 patients. Demographic characteristics were similar between groups: age 64 ± 11 years in 1999, 65 ± 11 years in 2001; duration of diabetes 7 ± 6 years in 1999, 7 ± 6 years in 2001; male:female ratio 51:49 in 1999 and 52:48 in 2001. Glycaemic control showed no significant change (Table 1), and in both studies a significant proportion of patients (58% in 1999 and 56% in 2001) had poor glycaemic control. Fewer patients however, were treated with diet only (10%) in 2001, with significant increases in the number of patients treated with oral hypoglycaemic agents (Table 2) (59% to 68%) and insulin (14% to 20%). Analysis of the HbA1c data by treatment modality showed that in the diet-only treated group, control was better in 2001 compared with 1999 (Table 1).


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Table 1 Treatment and glycaemic control of type 2 diabetic patients in 1999 and 2001

 

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Table 2 Diabetes treatment of type 2 patients in 1999 and 2001

 
Unlike HbA1c levels, however, BP levels were highly significantly improved between 1999 and 2001. This included analysis of systolic and diastolic BP, proportion of patients with uncontrolled hypertension (BP > 140/85), and proportion of patients on antihypertensive treatment (Table 3). Multiple drug treatment was also more common, and in 2001 only 17% of patients with a BP level > 140/85 were not on antihypertensive medication, compared with 45% in 1999 (p < 0.0001).


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Table 3 Blood pressure (BP) levels in relation to treatment of type 2 diabetic patients in 1999 and 2001

 

    Discussion
 Top
 Summary
 Introduction
 Methods
 Results
 Discussion
 References
 
This study describes and compares two separate audits of type 2 diabetic patients attending a single diabetic clinic, 2 years apart. A possible limitation of the study is that patient cohorts were different at the two study times. However, the numbers were large and the groups well-matched. In fact, there are also significant problems in assessing treatment efficacy in the same type 2 diabetic patients sequentially over time, as the UKPDS study has clearly shown that glycaemic control deteriorates significantly as diabetes duration prolongs.4,10 Even a 2-year excess in diabetes duration would therefore mean that glycaemic control could not be validly compared.

The striking finding of this study is that we were able to ‘close the audit loop’ and greatly improve the shortfalls in hypertensive control. Mean BP fell highly significantly from 151/77 in 1999 to 146/72 in 2001. There was clearly more liberal use of anti-hypertensive drugs, the proportion of hypertensive patients on drugs almost doubling from 33% to 60% (p < 0.0001). This change in treatment philosophy was probably driven by the remarkable outcome improvements in strict BP control reported in the UKPDS,5 and we believe that a general ‘BP awareness’ amongst clinic doctors was the major factor driving these dramatic improvements. We did not evaluate complication prevalence in the two groups, but have no reason to believe that rates were significantly different, or that this may have affected treatment practices. In our clinic we have always aimed to treat patients to current evidence-based targets, regardless of co-morbidity or complications.

In contrast, our findings on glycaemic control are less encouraging. Mean HbA1c was unchanged at 8.7% in 1999 and 8.5% in 2001. However, there was evidence that the case-mix of patients had changed. The population on diet-only decreased from 27% to 12%, those on oral agents increased from 59% to 68% and those on insulin increased from 14% to 20%. This was partly due to increased use of oral agents and insulin, but also to a clinic policy of discharging stable diet-controlled patients to community care. Thus, the 2001 cohort may represent a more problematic group. Nevertheless, it remains of concern that over half of patients in both studies (58% in 1999 and 56% in 2001) undoubtedly had poor glycaemic control (HbA1c > 8.0%). Interestingly, a recent Danish intervention study in type 2 diabetes has shown that even with intensive management, target HbA1c levels are hard to achieve in significant numbers of patients.11 As with our findings, BP targets were more attainable.

In conclusion, our study shows that hypertension control can be significantly improved in type 2 diabetic patients within the structure of routine hospital clinic care. Achieving glycaemic targets, however, appears to remain a ‘holy grail’, so far unobtainable.


    Acknowledgments
 
We thank Michelle Morgan and the staff in the Clinical Audit Department, and Julie Powell and Alan Peate in the Information Systems and Services Department, both at University Hospital Aintree, Liverpool, UK.


    Footnotes
 

Address correspondence to: Dr G.V. Gill, Department of Diabetes and Endocrinology, University Hospital Aintree, Liverpool L9 1AE. e-mail: g.gill{at}liv.ac.uk


    References
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 Summary
 Introduction
 Methods
 Results
 Discussion
 References
 
1. Harris MI. Health care and health status and outcomes for patients with type 2 diabetes. Diabetes Care 2000; 23:754–8.[Abstract/Free Full Text]

2. Panzram G. Mortality and survival in type 2 diabetes mellitus. Diabetologia 1987; 30:123–31.[CrossRef][Web of Science][Medline]

3. Sowers JR, Epstein M, Frohlich ED. Diabetes, hypertension and cardiovascular disease: an update. Hypertension 2001; 37:1053–9.[Abstract/Free Full Text]

4. United Kingdom Prospective Diabetes Study Group. Intensive blood glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet 1998; 352:837–53.[CrossRef][Web of Science][Medline]

5. United Kingdom Prospective Diabetes Study Group: Tight blood pressure control and risk of macrovascular and microvascular complications in type 2 diabetes (UKPDS 38). Br Med J 1998; 317:703–13.[Abstract/Free Full Text]

6. European Diabetes Policy Group. A desktop guide to type 2 diabetes mellitus. Diabet Med 1999; 16:716–73.[CrossRef][Web of Science][Medline]

7. Berlowitz DR, Glickman M, Ash AS, Friedman R, Hickey EC, Kader B. Hypertension management in patients with diabetes. Diabetes Care 2003; 26:355–9.[Abstract/Free Full Text]

8. Woodward A, Groves T, Wallymahamed M, Wilding JP, Gill GV. Attaining UKPDS management targets in type 2 diabetes: failures and difficulties. Practical Diabetes Int 2001; 18:307–10.[CrossRef]

9. The Diabetes Control and Complications Trial (DCCT) Research Group. The effect of intensive treatment of diabetes on the development and progression of long term complications in insulin dependent diabetes mellitus. N Engl J Med 1993; 329:977–86.[Abstract/Free Full Text]

10. United Kingdom Prospective Diabetes Study Group. Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35). Br Med J 2000; 321:405–12.[Abstract/Free Full Text]

11. Gaede P, Vedel P, Larsen N, Jensen GVH, Parving HH, Pedersen O. Multifactorial intervention and cardiovascular disease in patients with type 2 diabetes. N Engl J Med 2003; 348:383–93.[Abstract/Free Full Text]


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