Scandinavian Journal of Clinical and Laboratory Investigation
ISSN: 0036-5513 (Print) 1502-7686 (Online) Journal homepage: http://www.tandfonline.com/loi/iclb20
What causes impaired glucose tolerance to deteriorate or normalize? J. Cederholm & L. Wibell To cite this article: J. Cederholm & L. Wibell (1992) What causes impaired glucose tolerance to deteriorate or normalize?, Scandinavian Journal of Clinical and Laboratory Investigation, 52:6, 491-496, DOI: 10.3109/00365519209090126 To link to this article: http://dx.doi.org/10.3109/00365519209090126
Published online: 08 Jul 2009.
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Article views: 3
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Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=iclb20 Download by: [University of Sydney Library]
Date: 22 March 2016, At: 19:35
Scand J Clin Lab Invest 1992; 52: 491-495
What causes impaired glucose tolerance to deteriorate or normalize? J. C E D E R H O L M * ? & L. WIBELL*
Downloaded by [University of Sydney Library] at 19:35 22 March 2016
Departments of Internal Medicine,* and Family Medicine?, University Hospital, Uppsala, Sweden
Cederholm J, Wibell L. What causes impaired glucose tolerance to deteriorate or normalize? Scand J Clin Lab Invest 1992; 52: 491-495. Twenty-five middle-aged subjects with impaired glucose tolerance (IGT) were analysed 5 years later, showing normal glucose tolerance in 28% and persistent glucose deterioration in 72%. Body mass index (strongly) and 2-h glucose levels were clinically useful predictors, in the newly detected IGT-subjects, of persistent glucose deterioration (IGT or NIDDM) 5 years later. The frequency of hypertension was 36"/~in the newly-detected IGT subjects. Five years later this frequency increased to 54% in the persistently hyperglycaemic group, and decreased to none in the normalized group. Predictors of hypertension at the follow-up were baseline blood pressure and parts of the hyperinsulinaemic syndrome, such as serum triglyceride at baseline, BMI and 2-h glucose at the follow-up. Microalbuminuria (>20 mg day-') was not found at the 5-years follow-up, either if the subjects then had NIDDM, IGT or normal glucose tolerance. ECG abnormalities (ST segment and T wave changes) were two-fold more prevalent in the group with IGT or NIDDM than in the normalized group at the follow-up. Predictors were baseline BMI and incremental BMI. In conclusion, obesity and high 2-h glucose in newly-detected IGT-subjects seemed to predict the persistence of IGT 5 years later. Hypertension, but not microalbuminuria, was frequent when glucose deterioration persisted.
Key words: diabetes mellitus; impaired glucose tolerance; hypertension; cardiovascular disease Dr J . Cederholm, Department of Internal Medicine, University Hospital, S-75185 Uppsala, Sweden
Impaired glucose technique (IGT) has been independently related to increased mortality from cardiovascular disease, with a two-fold increased CVD incidence (1, 21, and with increased frequency of hypertension [2]. An important question today should be, whether newly-detected IGT subjects might later on return to normal glucose tolerance (NGT), or
if they remain glucose deteriorated as IGT or non-insulin-dependent diabetes mellitus (NIDDM). The former course should be less important regarding the risk of cardiovascular disease. It was the aim of this study to find some easily useful markers, in newly detected IGT subjects, for persistent glucose deterioration 5 years
49 1
492
J. Cederholm & L . Wibell
later. Another aim was to study the presence of hypertension, ecg abnormalities and related factors at the 5-years follow-up.
Downloaded by [University of Sydney Library] at 19:35 22 March 2016
MATERIAL AND METHODS Twenty-five subjects with newly-detected I G T were obtained from a health survey of 81Y middle-aged (47- 54-years-old) subjects in Uppsala with the aim of detecting IGT. These participants were selected consecutively according to their registration number from a register of the local County Council, and invited to attend the health survey. The participation rate was 70%. The prevalence of I G T in the survey was 6.2%. Of all 51 detected IGTsubjects, every other was invited to a follow-up 5 years later, and 25 IGT-subjects (15 females and 10 males, with mean age 57+4 at the follow-up) agreed to participate. I G T was diagnosed with two subsequent 75 g OGTTs with an interval of one week, according to WHO-criteria [3], with mean of two subsequent blood glucose values given here. The reproducibility of the IGT-diagnosis was 82% in the survey. Venous whole blood glucose was measured at 0, 1/2, 1 and 2 h levels by a glucose oxidase method (Yellow Spring Instrument Model 23AM Yellow Springs, O H , USA). Mean blood glucose was the total area under the glucose curve (mmol h I-'), divided by 2 (h). , Blood pressure (BP) was measured sitting at rest, using fifth phase sounds with a mercury manometer and a cuff size 12x25 cm. Hypertensive subjects were defined (WHO-criteria) as those with anti-hypertensive agents and those with untreated systolic B P 2160 mm Hg a n d o r diastolic BP 295 mm Hg. Body mass index (BMI), calculated as weight. height-', was expressed as Relative BMI (YO) for comparison between sexes, based on standard BMI values in females and males [4]. Serum triglyceride and total cholesterol values were measured by routine techniques at the chemical department of the hospital. All 25 IGT subjects were given advice of diet and exercise when diagnosed. They were followed up 5 years later with 75 g OGTTs and measurement of BMI, BP (mean of three measurements), and resting E C G according to the Minnesota code [ S ] . Major E C G items were
I . 1-2 and 7.1, and minor ECG abnormalities were items 1.3 (small Q-wave), 4.1-3 (STsegment) and 5.1-3 (T-wave). A family history of first-degreee relatives with diabetes was registered by a questionnaire. Those with at least one first-degree relative with diabetes had a positive family history of diabetes, and those with no diabetic first-degree relative had a negative family history. As 5 years earlier, no subject was given anti-diabetic agents, antihypertensives (mainly P-blockers) were given to five I G T subjects at baseline, and t o three NIDDM and five I G T subjects at the follow-up. Urinary albumin excretion was measured at the follow-up during 10 h from night to morning, by immunochemical turbidimetry at the chemical department. WHO-criteria [3] were used here for diagnosis of I G T (0-h glucose
ISSN: 0036-5513 (Print) 1502-7686 (Online) Journal homepage: http://www.tandfonline.com/loi/iclb20
What causes impaired glucose tolerance to deteriorate or normalize? J. Cederholm & L. Wibell To cite this article: J. Cederholm & L. Wibell (1992) What causes impaired glucose tolerance to deteriorate or normalize?, Scandinavian Journal of Clinical and Laboratory Investigation, 52:6, 491-496, DOI: 10.3109/00365519209090126 To link to this article: http://dx.doi.org/10.3109/00365519209090126
Published online: 08 Jul 2009.
Submit your article to this journal
Article views: 3
View related articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=iclb20 Download by: [University of Sydney Library]
Date: 22 March 2016, At: 19:35
Scand J Clin Lab Invest 1992; 52: 491-495
What causes impaired glucose tolerance to deteriorate or normalize? J. C E D E R H O L M * ? & L. WIBELL*
Downloaded by [University of Sydney Library] at 19:35 22 March 2016
Departments of Internal Medicine,* and Family Medicine?, University Hospital, Uppsala, Sweden
Cederholm J, Wibell L. What causes impaired glucose tolerance to deteriorate or normalize? Scand J Clin Lab Invest 1992; 52: 491-495. Twenty-five middle-aged subjects with impaired glucose tolerance (IGT) were analysed 5 years later, showing normal glucose tolerance in 28% and persistent glucose deterioration in 72%. Body mass index (strongly) and 2-h glucose levels were clinically useful predictors, in the newly detected IGT-subjects, of persistent glucose deterioration (IGT or NIDDM) 5 years later. The frequency of hypertension was 36"/~in the newly-detected IGT subjects. Five years later this frequency increased to 54% in the persistently hyperglycaemic group, and decreased to none in the normalized group. Predictors of hypertension at the follow-up were baseline blood pressure and parts of the hyperinsulinaemic syndrome, such as serum triglyceride at baseline, BMI and 2-h glucose at the follow-up. Microalbuminuria (>20 mg day-') was not found at the 5-years follow-up, either if the subjects then had NIDDM, IGT or normal glucose tolerance. ECG abnormalities (ST segment and T wave changes) were two-fold more prevalent in the group with IGT or NIDDM than in the normalized group at the follow-up. Predictors were baseline BMI and incremental BMI. In conclusion, obesity and high 2-h glucose in newly-detected IGT-subjects seemed to predict the persistence of IGT 5 years later. Hypertension, but not microalbuminuria, was frequent when glucose deterioration persisted.
Key words: diabetes mellitus; impaired glucose tolerance; hypertension; cardiovascular disease Dr J . Cederholm, Department of Internal Medicine, University Hospital, S-75185 Uppsala, Sweden
Impaired glucose technique (IGT) has been independently related to increased mortality from cardiovascular disease, with a two-fold increased CVD incidence (1, 21, and with increased frequency of hypertension [2]. An important question today should be, whether newly-detected IGT subjects might later on return to normal glucose tolerance (NGT), or
if they remain glucose deteriorated as IGT or non-insulin-dependent diabetes mellitus (NIDDM). The former course should be less important regarding the risk of cardiovascular disease. It was the aim of this study to find some easily useful markers, in newly detected IGT subjects, for persistent glucose deterioration 5 years
49 1
492
J. Cederholm & L . Wibell
later. Another aim was to study the presence of hypertension, ecg abnormalities and related factors at the 5-years follow-up.
Downloaded by [University of Sydney Library] at 19:35 22 March 2016
MATERIAL AND METHODS Twenty-five subjects with newly-detected I G T were obtained from a health survey of 81Y middle-aged (47- 54-years-old) subjects in Uppsala with the aim of detecting IGT. These participants were selected consecutively according to their registration number from a register of the local County Council, and invited to attend the health survey. The participation rate was 70%. The prevalence of I G T in the survey was 6.2%. Of all 51 detected IGTsubjects, every other was invited to a follow-up 5 years later, and 25 IGT-subjects (15 females and 10 males, with mean age 57+4 at the follow-up) agreed to participate. I G T was diagnosed with two subsequent 75 g OGTTs with an interval of one week, according to WHO-criteria [3], with mean of two subsequent blood glucose values given here. The reproducibility of the IGT-diagnosis was 82% in the survey. Venous whole blood glucose was measured at 0, 1/2, 1 and 2 h levels by a glucose oxidase method (Yellow Spring Instrument Model 23AM Yellow Springs, O H , USA). Mean blood glucose was the total area under the glucose curve (mmol h I-'), divided by 2 (h). , Blood pressure (BP) was measured sitting at rest, using fifth phase sounds with a mercury manometer and a cuff size 12x25 cm. Hypertensive subjects were defined (WHO-criteria) as those with anti-hypertensive agents and those with untreated systolic B P 2160 mm Hg a n d o r diastolic BP 295 mm Hg. Body mass index (BMI), calculated as weight. height-', was expressed as Relative BMI (YO) for comparison between sexes, based on standard BMI values in females and males [4]. Serum triglyceride and total cholesterol values were measured by routine techniques at the chemical department of the hospital. All 25 IGT subjects were given advice of diet and exercise when diagnosed. They were followed up 5 years later with 75 g OGTTs and measurement of BMI, BP (mean of three measurements), and resting E C G according to the Minnesota code [ S ] . Major E C G items were
I . 1-2 and 7.1, and minor ECG abnormalities were items 1.3 (small Q-wave), 4.1-3 (STsegment) and 5.1-3 (T-wave). A family history of first-degreee relatives with diabetes was registered by a questionnaire. Those with at least one first-degree relative with diabetes had a positive family history of diabetes, and those with no diabetic first-degree relative had a negative family history. As 5 years earlier, no subject was given anti-diabetic agents, antihypertensives (mainly P-blockers) were given to five I G T subjects at baseline, and t o three NIDDM and five I G T subjects at the follow-up. Urinary albumin excretion was measured at the follow-up during 10 h from night to morning, by immunochemical turbidimetry at the chemical department. WHO-criteria [3] were used here for diagnosis of I G T (0-h glucose
