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ORIGINAL ARTICLE
Year : 2012  |  Volume : 16  |  Issue : 4  |  Page : 604-608

Isolated postprandial hyperglycemia in type 2 diabetic patients in a Nigerian Tertiary Health Center


Department of Internal Medicine, University of Port Harcourt Teaching Hospital, Port Harcourt, Nigeria

Date of Web Publication5-Jul-2012

Correspondence Address:
Sunday Chinenye
Department of Internal Medicine, University of Port Harcourt Teaching Hospital, Port Harcourt
Nigeria
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2230-8210.98019

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   Abstract 

Background: Postprandial hyperglycemia has been shown to be an independent cardiovascular risk factor. Some studies have reported that postprandial hyperglycemia is common and can occur even in patients with normal fasting glucose levels. This has been referred to as isolated postprandial hyperglycemia. Objectives: This study sets out to estimate the prevalence of isolated postprandial hyperglycemia in a cohort of patients with type 2 diabetes and to identify their clinical characteristics. Materials and Methods: Ninety patients being managed for type 2 diabetes were recruited consecutively as they attended the diabetes clinic for follow-up. The patients were assessed with questionnaires, to obtain the demographic data. Their body mass index (BMI) was calculated. Fasting blood samples were collected for analysis of fasting plasma glucose (FPG). Patients were given their usual drugs and then served a standard meal calculated to contain 50 g of carbohydrate, providing 500 kcal. Blood samples were collected two hours after the start of the meal for postprandial glucose levels. Results: The mean age of the patients was 57.7 ± 10.8 years with a male : female ratio of 2 : 3. The mean duration of diabetes was 6.77 ± 6.53 years. The mean BMI was 27.54 ± 6.01 kg / m 2 . The mean FPG and two hour postprandial glucose were 7.51 ± 3.39 mmol / l and 11.02 ± 4.03 mmol / L, respectively, and the mean HBA1c was 9.0 ± 2.5%. The prevalence of isolated postprandial hyperglycemia was 24.4%. Elevated postprandial glucose was seen in 41.7% of the patients at target glycated hemoglobin levels. The patients with isolated postprandial hyperglycemia tended to be older and less obese. Conclusion: There was poor glycemic control in the patients generally; however, a significant proportion of patients, with apparently good glycemic control, had isolated postprandial hyperglycemia.

Keywords: Cardiovascular risk, glycemic, hyperglycemia, postprandial, type 2 diabetes


How to cite this article:
Chinenye S, Young EE. Isolated postprandial hyperglycemia in type 2 diabetic patients in a Nigerian Tertiary Health Center. Indian J Endocr Metab 2012;16:604-8

How to cite this URL:
Chinenye S, Young EE. Isolated postprandial hyperglycemia in type 2 diabetic patients in a Nigerian Tertiary Health Center. Indian J Endocr Metab [serial online] 2012 [cited 2019 Jul 23];16:604-8. Available from: http://www.ijem.in/text.asp?2012/16/4/604/98019


   Introduction Top


Various modalities are used to assess glycemic control in patients with type 2 diabetes. The most common method is the use of fasting blood glucose, as it is cheap, reproducible, and widely available. [1] It is also the most convenient in a busy clinic. Glycated hemoglobin (HBA1c) levels are usually assessed two to three times yearly in most patients. In developing countries, this is not always done, as the test is expensive and not widely available. Postprandial blood glucose is commonly measured two hours after the onset of a meal as this generally approximates the peak value in patients with diabetes, and provides a reasonable assessment of postprandial hyperglycemia. [2] There is an ongoing interest in specifically measuring and treating, to target postprandial hyperglycemia. This is because recent studies indicate that elevated postprandial plasma glucose levels are an independent and clinically significant risk factor for cardiovascular disease in non-diabetic and diabetic individuals. [3] Isolated post-challenge hyperglycemia in the presence of normal fasting plasma glucose and HbA1c levels is associated with a two-fold increase in cardiovascular risk. [4] Acute hyperglycemia experienced after a meal results in endothelial dysfunction and oxidative stress. [5] Studies have shown an association between postprandial glucose levels and the development of atherosclerosis. [6] Although postprandial glucose is significantly related to fasting plasma glucose and HbA1c, some studies have shown that quite a significant percentage of patients experience excessive post-meal glycemic surges and elevated postprandial glucose. [7] Elevated postprandial glucose has been defined by various bodies. The American Diabetes Association (ADA) recommends a cut-off value of 10 mmol / L 2 . The International Diabetes Federation (IDF) recommends a postprandial glucose level of less than 7.8 mmol / L. [8] The European Association for the study of diabetes (EASD) recommends less than 7.5 mmol / L. [9] The American Association of Clinical Endocrinologists (AACE) recommends less than 7.8 mmol / L. [10] This study aims to evaluate the prevalence of isolated postprandial hyperglycemia in our patients and to identify their clinical characteristics.


   Ethical Approval Top


Ethical approval for the study was obtained from the Ethics Committee of the hospital and only patients who gave informed consent were recruited.


   Materials and Methods Top


Setting

The study was carried out in the weekly diabetes clinic of the University of Port Harcourt Teaching Hospital. This hospital is the main tertiary / referral center for Rivers State, Nigeria, and the neighboring Bayelsa State. The Rivers State has a heterogeneous population, consisting of several local tribes such as Ikwerre, Ijaw, Kalabari, and so on.There are also a lot of people from other parts of Nigeria and expatriates engaged mainly in the oil and gas industry. Rivers state has a population of about 5.1 million people.

Patients

Ninety type 2 diabetic patients attending the outpatient clinic for follow-up were assessed. Patients without acute complications were recruited consecutively.

Study design

The study is a cross-sectional descriptive study.

Exclusion criteria

  1. Patients with severe hyperglycemia ± ketonuria.
  2. Patients who had not been on a stable oral anti-diabetic drug regimen for at least two months.
  3. Newly-diagnosed patients at less than six months of diagnosis.


Procedure

On each day of the study, the patients were asked to come to the clinic between 8 a.m and 9 a.m, and had been asked to fast from the previous night for eight to ten hours. Each patient had to fill a structured questionnaire, to obtain the demographic data of age, gender, time since diagnosis, and type of diabetic treatment. Clinical assessments of weight and height were made using the standard scales. Body mass index was calculated with the formula weight (kg) / Height 2 (m). Overweight was defined as BMI of 25 - 29.9 kg / m 2 , while obesity was defined as BMI ≥ 30 k / m 2 . Blood pressure was then measured with a mercury sphygmomanometer on the right arm, and the average of two readings, taken five minutes apart, was recorded for each participant. Hypertension was said to be present in those with systolic blood pressure ≥ 140 mmHg and / or diastolic blood pressure ≥ 90 mmHg or use of anti-hypertensive medication. A fasting venous sample was then collected for the measurement of fasting plasma glucose. A drop of the blood sample was then extracted using the blood key of the in2it machine for the assessment of glycated hemoglobin. This was then put into the cartridges and the HbA1c was assessed immediately after calibration of the machine, according to the manufacturer's instructions. The in2it machine measured Hba1c using the boronate affinity method and it was Diabetes Control and Complications Trial (DCCT) calibrated. The rest of the sample was placed in fluoride oxalate bottles and immediately sent to the laboratory, where it was centrifuged and the plasma separated to measure the plasma glucose, using the glucose oxidase method. Each patient was then served the appropriate doses of their drugs and after 30 minutes each was asked to consume a test meal that had been prepared by the hospital dietitian. The meal was measured to provide 500 kcal of energy and contained 50 g of glucose. The meal was made up of 53% carbohydrate, 17% protein, and 30% lipids. Each patient was asked to finish the meal in fifteen minutes.

Two hours from the onset of the meal another venous blood sample was collected for the measurement of PPG and analyzed in the laboratory in the same manner as the FPG analysis. An FPG of 7.2 mmol / L, PPG 10.0 mmol / L, and HbA1c < 7% were considered satisfactory according to the ADA guidelines. The patients were considered to have isolated postprandial hyperglycemia if they had FPG < 7.2 mmol / L and PPG > 10.0 mmol / L.

Statistical analysis

This was done with the SPSS version 15 package. The mean ages, duration of diabetes, systolic blood pressure, diastolic blood pressures, and BMI were calculated. The Pearsons correlation coefficient was used to assess the linear correlations between FPG and PPG, PPG and HbA1c, Age and PPG, and duration of diabetes and PPG. A P value of < 0.05 was considered to be significant. Other continuous variables were compared with the student's t-test, while categorical variables were assessed with the Chi-square test.


   Results Top


The clinical characteristics of the study population are as shown in [Table 1]. Oral drugs were the most frequently prescribed anti-diabetic agents and were used either singly or in combination in 71.1% of the patients. Only six patients (6.7%) were on diet and lifestyle measures alone, while 20 were on insulin treatment, either alone or in combination with metformin. Even as the mean fasting plasma glucose in the study population was 7.5 ± 3.3 mmol / L,- the mean two hour postprandial glucose (PPG) of the study population was 11.0 ± 4.0 mmol / L and the mean HBA1c for the study population was 9.0 ± 2.5%.
Table 1: Clinical characteristics of the study population

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The proportion of patients with satisfactory glycemic control in the various modalities is as shown in [Table 2].
Table 2: Proportion of patients with satisfactory glycemic control in various parameters

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There was a significant correlation between PPG and HbA1c (P = 0.000). Isolated postprandial hyperglycemia was seen in 24.4% of the population. The major characteristics of the patients with isolated postprandial hyperglycemia are as listed in [Table 3]. In this sub-set of patients, the highest mean PPG was recorded in patients on oral drugs and the least in those on insulin, although the difference was not statistically significant (P = 0.31). Their mean HBA1c was 7.9%.
Table 3: Characteristics of patients with isolated postprandial hyperglycemia

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There was a significant negative correlation between age and PPG. (r = - 0.296, P = 0.005). There was a positive correlation between postprandial glucose and duration of diabetes after adjusting for fasting plasma glucose, (r = 0.24, P = 0.02). There was a negative correlation between body mass index and PPG, but it was not statistically significant. (r = - 0.197, P = 0.066). The difference in the mean postprandial glucose was not statistically significant across the BMI groups, however, those who had a normal BMI tended to have higher postprandial glucose than those who were obese or underweight (11.9 mmol / L vs. 10.5 mmol / L, P = 0.103). Comparison of mean PPG among those on oral drugs or diet and those on insulin showed that the difference in their mean PPG was statistically significant. Those on insulin had the highest mean PPG (f = 4.8, P = 0.010). When the patients were further subdivided, those on metformin alone had a lower mean PPG than those on a combination of metformin and sulfonylurea and those on sulfonylurea alone. The difference in means was, however, not statistically significant (P = 0.18, P = 0.15, respectively).


   Discussion Top


Recent studies have shown that postprandial hyperglycemia is detrimental, as it is an independent risk factor for cardiovascular disease. [3] Our study set out to estimate the prevalence and correlates of postprandial hyperglycemia in patients with type 2 diabetes and also to identify patients with isolated postprandial hyperglycemia, who are presumed to have optimal glycemic control.

The prevalence of postprandial hyperglycemia (75.6%) was high in the study population. It could be argued that the high prevalence of postprandial hyperglycemia in the patients was a reflection of the high fasting glucose levels in them. This was because there was a significant positive correlation between FPG and PPG. [11] There was also a positive correlation between postprandial glucose and HbA1c. This significant correlation has been reported in other studies. [7],[11] Hence it can be seen that the three parameters of glycemic control are closely related.

The high prevalence of postprandial hyperglycemia noted in this study was similarly reported in studies by Bonora [7] and Erlinger, [12] although patients in these studies had lower fasting plasma glucose levels. Isolated postprandial hyperglycemia was defined in this study as elevated PPG in patients with normal FPG levels. The prevalence of isolated postprandial hyperglycemia was 24.4%. This was similar to the prevalence reported in the study by Bonora, [7] who reported isolated postprandial hyperglycemia in 38% of the patients.

These patients with isolated postprandial hyperglycemia are at risk of cardiovascular disease as studies have described elevated PPG levels as independent cardiovascular risk factors. Hence, it is important to identify this sub-set of patients who apparently have good metabolic control, but are at risk of cardiovascular disease. The characteristics of these patients are summarized in [Table 2], to see if there are any simple clinical characteristics that can identify them. It has been noted that these patients were older, had a longer duration of diabetes, and tended to be overweight. This is similar to the findings by Bonora et al. [7] The mean HbA1c of these patients was 7.9%, suggesting that they had a fairly good glycemic control. This suggests that in these patients, the major determinant of their glycated hemoglobin level is their PPG levels, hence, at near-normal HbA1c levels postprandial glucose becomes the key determinant of HbA1c and this is in agreement with other studies. [13],[14] Monnier et al. demonstrated that PPG becomes a major contributor to overall glycemic control at an HbA1c level of 8.4%. [13] It is therefore likely that further reductions in glycated hemoglobin levels in this group of patients will be more easily achieved with drugs that specifically target postprandial glucose.

In this study, PPG was found to be significantly associated with age, duration of diabetes, and fasting plasma glucose. Younger patients had higher postprandial glucose levels and there was a negative correlation between age and postprandial glucose. However, in the overall patient population, the younger patients also had a significantly higher FPG (P = 0.000). In contrast, the patients with isolated postprandial hyperglycemia were older; therefore, after excluding those with high fasting glucose, older age appeared to be significantly associated with elevated postprandial glucose.

Postprandial glucose also showed a significant positive correlation with the duration of diabetes and patients with isolated postprandial hyperglycemia had a longer duration of diabetes. This suggested that the longer the duration of diabetes, the more likely it was that a patient would have elevated postprandial glucose, possibly also due to a declining beta cell function. This relationship between PPG and the duration of diabetes was also observed in the study by Bonora. [7]

In our study, patients who were not obese or overweight had higher PPG levels than obese patients. This, however, did not reach statistical significance. This was in sharp contrast to our finding in patients with isolated postprandial hyperglycemia, who tended to be overweight. Hence, obesity may not be a significant determinant of PPG levels in our patients. Bonora et al. [7] reported that the absence of obesity was significantly associated with elevated PPG.

The highest mean PPG was recorded in patients who were managed with insulin. This was, however, as expected, because they also had the highest mean fasting blood glucose and mean HbA1c than those on other modalities of treatment, hence, they had a poorer glycemic control. Also, the type of insulin known to be beneficial in reducing PPG, that is, rapid-acting insulin, such as aspart or rapid acting / isophane mixture such as Novolog mix or Humalog mix were not being used by the patients in this study. [15] In a similar study by Singh et al. in South Africa, [15] they evaluated the effects of three types of basal insulin on PPG, and reported that basal insulin was ineffective in controlling postprandial hyperglycemia, and recommended the use of a combination of rapid-acting / newer long-acting analogs such as glargine.

Patients on metformin alone had lower postprandial glucose levels than those on sulfonylureas, although this difference was not statistically significant. This was similar to the findings by Bonora et al., [7] who noted that treatment with sulfonylureas was associated with higher PPG levels. In that study, however, patients on insulin were excluded.

Limitations

The study was limited by its cross-sectional nature. Blood glucose measurements were done only once. This may not reflect the daily variations normally seen in patients.

Recommendations

  1. There is a need for improved diabetic control overall through patient education and self-monitoring of blood glucose.
  2. There is a need for increased awareness and monitoring of postprandial blood glucose in patients.
  3. Patients with isolated postprandial hyperglycemia should be identified and treated.
  4. In developing countries where glycated hemoglobin may not be routinely tested in patients, monitoring PPG levels in addition to FPG should be advocated and may be an excellent way to prevent complications of diabetes.



   Conclusion Top


In this study elevated postprandial glucose levels were found to occur in patients with normal or near-normal HbA1c levels. In these patients, who were near the HbA1c target, postprandial glucose became the significant contributor for poor glycemic control and drugs specifically targeting postprandial glucose were more likely to help them achieve their target HbA1c levels, hence, reducing the incidence of long-term diabetic complications. Older age, longer duration of diabetes, and the absence of obesity could predict postprandial hyperglycenia and could be used to identify patients, who might need more extensive investigation and monitoring of their PPG levels. The use of FPG and HbA1c alone, for monitoring may be insufficient to prevent long-term complications of diabetes, especially cardiovascular complications.

 
   References Top

1.American Diabetes Association. Tests of glycemia in diabetes. Diabetes Care 2002;25 Suppl 1:S97-9.  Back to cited text no. 1
    
2.American Diabetes Association. Post-prandial Glucose-Consensus Statement. Diabetes Care 2001;24:775-8.  Back to cited text no. 2
    
3.Bonora E, Muggeo M. Postprandial glucose as a risk factor for cardiovascular disease in Type II diabetes: The epidemiological evidence. Diabetologia 2001;44:2107-14.  Back to cited text no. 3
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4.Shaw JE, Hodge AM, de Couten M, Chitson P, Zimmet PZ. Isolated Post-challenge Hyperglycemia confirmed as a risk factor for mortality. Diabetologia 1999;42:1050-4.  Back to cited text no. 4
    
5.Kawano H, Motoyama T, Hirashima O, Hirai N, Miyao Y, Sakamoto T, et al. Hyperglycemia rapidly suppresses flow-mediated endothelium-dependent vasodilation of brachial artery. J Am Coll Cardiol 1999;34:146-54.  Back to cited text no. 5
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6.Temelkova-Kurktschiev TS, Koehler C, Henkel E, Leonhardt W, Fuecker K, Hanefeld M. Plasma glucose and glycemic spikes are more strongly associated with atherosclerosis than fasting glucose or HbA1c level. Diabetes Care 2000;23:1830-4.  Back to cited text no. 6
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7.Bonora E, Corrao G, Bagnardi V, Ceriello A, Comaschi M, Montanari P, et al. Prevalence and correlates of post-prandial hyperglycemia in a large sample of patients with type 2 diabetes mellitus. Diabetologia 2000;49:846-54.  Back to cited text no. 7
    
8.Ceriello A, Colagiuri S. Guideline for the management of post-meal blood glucose (IDF). Diabetes Voice 2007;52:9-11.  Back to cited text no. 8
    
9.European Diabetes Policy Group. A desktop guide to Type 2 diabetes mellitus. Diabet Med 1999;16:716-30.  Back to cited text no. 9
    
10.Lebovitz HE, Austin MM, Blonde L, Davidson JA, Del Prato S, Gavin JR 3rd, et al.; ACE / AACE Diabetes Recommendations Implementation Writing Committee.ACE / AACE consensus conference on the implementation of outpatient management of diabetes mellitus: Consensus conference recommendations. Endocr Pract 2006;12:6-12.  Back to cited text no. 10
[PUBMED]    
11.Carroll M, Izard A, Riboni K, Burge MR, Schade DS. Fasting hyperglycemia predicts the magnitude of postprandial hyperglycemia. Diabetes Care 2002;25:1247-8.  Back to cited text no. 11
    
12.Erlinger PT, Brancati FL. Postchallenge Hyperglycemia in a National Sample of U.S. adults with Type 2 diabetes. Diabetes Care 2001;24:1734-8.  Back to cited text no. 12
    
13.Monnier L, Lainski H, Collette C. Contributions of fasting and postprandial plasma glucose increments to the overall diurnal hyperglycemia of Type 2 diabetic patients. Variations with increasing levels of HbA1c. Diabetes Care 2003;26:881-5.  Back to cited text no. 13
    
14.Soonthornpun S, Rattarasarn C, Leelawattana R, Setasuban W. Postprandial plasma glucose: A good index of glycemic control in type 2 diabetic patients having near-normal fasting glucose levels. Diabetes Res Clin Pract 1999;46:23-7.  Back to cited text no. 14
[PUBMED]  [FULLTEXT]  
15.Singh N, Rambiritch V, Mayet L. An evaluation of postprandial glucose excursions in type 2 diabetic mellitus subjects on Monotard® HM (ge) versus Humulin N® or Humulin L® insulin, each in combination with metformin. South African Fam Pract 2007: 49 ; 14a - 14d.  Back to cited text no. 15
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3]



 

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