|Year : 2015 | Volume
| Issue : 4 | Page : 230-233
Clinical study of abnormal glucose metabolism screening for acute ischemic cerebral apoplexy in patients
Wen-Zhen He, Xian-Guang Chen, Wen-Jie Chen, Xiao-Ling Xu
Shantou Medical College, Shantou 515000, Guangdong Province, China
|Date of Web Publication||23-Nov-2015|
Shantou Medical College, Shantou - 515 000, Guangdong Province
Source of Support: None, Conflict of Interest: None
Ischemic stroke refers to a focal neurological deficit attributable to the conditions created by the occlusion of an intracranial artery. We investigated how screening for abnormal glucose metabolism in acute ischemic cerebral apoplexy inpatients might be used to develop a more reasonable treatment plan and improve the prognosis of patients with acute ischemic stroke. A total of 686 patients with acute ischemic stroke, hospitalized from January 2007 to December 2010 in the neurological department of the first affiliated hospital in China Shantou Medical College, was examined in this study. We recorded each patient's sex, age, smoking history, height, weight, blood pressure, waist circumference, random blood glucose, and fasting blood glucose, also noting if the patient had a record of having high blood sugar. In addition, we conducted a 75 g oral glucose tolerance test (OGTT) for undiagnosed diabetes patients in order to determine the status of glucose metabolism. We find that there were 368 (66.1%) cases of hospitalized cerebral vascular disease patients with abnormal glucose metabolism of which 185 (33.2%) cases are diabetes, and 183 cases (32.9%) are with impaired glucose regulation, and 189 cases (33.9%) are with normal glucose tolerance. Totally, 130 cases had been diagnosed as diabetes before their admission, accounting for 23.3% of all patients. Totally, 427 patients are without diabetes history, however, 29 diabetes cases (accounting for 15.7% of all diabetic patients) were found after a non-OGTT. We concluded that patients with acute ischemic stroke are often associated with abnormal glucose metabolism, and so OGTT screening tests will help doctors to recognize acute ischemic stroke patients.
Keywords: Blood glucose, diabetes, epidemiology, glucose tolerance test, ischemic stroke
|How to cite this article:|
He WZ, Chen XG, Chen WJ, Xu XL. Clinical study of abnormal glucose metabolism screening for acute ischemic cerebral apoplexy in patients. SRM J Res Dent Sci 2015;6:230-3
|How to cite this URL:|
He WZ, Chen XG, Chen WJ, Xu XL. Clinical study of abnormal glucose metabolism screening for acute ischemic cerebral apoplexy in patients. SRM J Res Dent Sci [serial online] 2015 [cited 2022 May 24];6:230-3. Available from: https://www.srmjrds.in/text.asp?2015/6/4/230/170249
| Introduction|| |
Ischemic stroke refers to a focal neurological deficit attributable to the conditions created by the occlusion of an intracranial artery. A period of several hours or days elapses before the arterial occlusion produces an infarct,  a lesion defined as an area of coagulation necrosis of presumed ischemic origin that in most cases develops as a result of an arterial occlusion.  Areas of coagulation necrosis, in the brain but not in other organs, are typically replaced by a fluid-filled cavity several weeks or months after the original arterial occlusion. Under special circumstances - if the ischemia is of either short or moderate severity - arterial occlusions may induce brain lesions different from an infarct or area of pannecrosis. Because in such instances, the necrosis affects only a limited number of cells, and the long-term effect is not cavitation, the name "incomplete brain infarct" has been suggested for such lesions. 
Ischemic strokes comprise about 80% of all strokes and are caused by thrombotic or embolic occlusion of a major cerebral artery (most often the middle cerebral artery) or its branches. Researchers may address specific questions about pathologic events occurring after ischemic stroke as well as explore ways to develop novel stroke therapies in an experimental stroke model. An ischemic cascade resulting from blood flow reduction in a brain territory will trigger a series of multistep pathophysiologic events.
Cerebrovascular disease is one of the hazards to human health and is one of the most common diseases, having a high disability rate, high mortality, and high recurrence rate. Diabetes is a risk factor of cerebrovascular disease, and blood glucose level has an important influence on the prognosis of acute ischemic stroke.  However, the current epidemic status as it relates to glucose metabolism abnormalities in patients with acute ischemic stroke has not been sampled in a large survey. Therefore, we measured aspects of glucose metabolism in all hospitalized patients with acute cerebrovascular disease in order to:
- Investigate abnormal glucose metabolism in the acute ischemic cerebral apoplexy inpatient patients;
- Develop a more reasonable treatment plan and
- Improve the prognosis of patients with acute ischemic stroke.
| Materials and methods|| |
A total of 686 patients with acute ischemic stroke, hospitalized from January 2007 to December 2010 in the neurological department of the first affiliated hospital in China Shantou Medical College, was selected for this study. The average age of male patients was 67 10.9 (n = 308), and the average age of female patients was 66.9 10.9 (n = 278). All the patients or their legal guardians signed a written informed consent for this study.
The criteria for acute ischemic stroke diagnosis are as follows:
- Acute onset;
- Focal neurological deficits;
- Symptoms and signs lasting several hours or more; and
- Has a positioning infarction focus after brain computed tomography (CT) or magnetic resonance imaging (MRI). Diseases with cerebral hemorrhage detected after brain CT or MRI are not considered acute ischemic strokes.
However, patients could be unintentional as acute ischemic stroke diagnosis with the following criteria:
- Patients with elevated blood sugar after using of corticosteroids or nonsteroidal anti-inflammatory drugs;
- Patients in critical condition, the general condition of the patient is not stable or they are unwilling to sign the informed consent;
- Patients with chronic autoimmune disease or with connective tissue disease; and
- Acute ischemic stroke patients caused by atrial fibrillation or heart valve disease.
Illness history collection and physical examination
We recorded patients' sex, age, past hypertension history, brain stroke history, diabetes history, and smoking history. We also recorded patients' height, weight, blood pressure and waist circumference (WC) after their admission, in which blood pressure and WC were measured in a fasting quiet state. WC is taken from the crest midpoint of the lower rib margin to the iliac. All data accuracy was set at 0.1 cm.
Blood sugar detection
We measured the blood glucose of the patients one time after their admission, and we measured the fasting blood glucose (FPG) for the diabetes patients on the second morning. In additional to FPG measurement, we also measured the 2 h blood postprandial glucose (2 hPG). We carried out standard 75 g oral glucose tolerance test (75 g oral glucose tolerance test [OGTT]) for patients without diabetes history in a stable condition after 1-week of their illness onset.
Subjects should be fasting overnight over 10 h, and 75 g OGTT was carried out between 7:00 and 9:00 o'clock next morning. OGTT only detects FPG and two points of 2 h blood sugar 2 hPG after the glucose loaded, OGTT test was only carried out one time. Sugar glucose was measured with hexokinase methods, the coefficient of variation (CV) is set <2.5% for samples within one group, and CV is set <3.5% for samples among different groups.
Classifications of glucose metabolism status
Normal glucose tolerance (NGT) (NGT, FPG ≤6.1 mmol/L and 2 hPG <7.8 mmol/L); impaired glucose regulation (IGR) includes simple impaired fasting glucose (I-IFG, 6.1 mmol/L = FPG <7.0 mmol/L and 2 hPG <7.8 mmol/L), impaired glucose tolerance (simple I-IGT, FPG <6.1 mmol/L and the 7.8 mmol/L = 2 hPG <11.1 mmol/L), the amount of damaged composite sugar tolerance (IGT + IFG, mmol/L = 6.1 FPG <7.0 mmol/L and 7.8 mmol/L = 2 hPG <11.1 mmol/L); diabetes include simple fasting hyperglycemia (IFH, FPG = 7 mmol/L, and 2 hPG <11.1 mmol/L), isolated postprandial hyperglycemia (IPH, FPG <7.0 mmol/L and the 2 hPG = 11.1 mmol/L), composite hyperglycemia (CH, FPG is more than or equal to 7 mmol/L, and 2 hPG = 11.1 mmol/L). The I-IGT, I-IFG, IGT + IFG are collectively referred to as IGR.
Data were analyzed with Excel 2000 and SPSS 13.0. x s was used to represent distribution characteristics of continuous variables. Wilcoxon (Mann-Whitney) rank was applied to compare and test two mean numbers. The significant test is done with Chi-square for discrete variables.
| Results|| |
There were 368 (66.1%) cases of hospitalized cerebral vascular disease patients with abnormal glucose metabolism of which 185 (33.2%) cases are diabetes and 183 cases (32.9%) are with IGR, and 189 cases (33.9%) are with NGT. A total of 130 cases had been diagnosed as diabetes before their admission, accounting for 23.3% of all patients. Totally, 427 patients are without diabetes history, however, 29 diabetes cases (accounting for 15.7% of all diabetic patients) were found after a non-OGTT.
Twenty-six diabetes cases (accounting for 14.1% of all diabetic patients) were found after a OGTT, 183 cases are found with IGR, four (accounting for 0.7%) cases are with I-IFG, 163 (29.3%) subjects are with I-IGT, and 16 (2.9%) cases are with IFG + IGT in the 183 cases. About 64.7% (238/368) patients with abnormal glucose metabolism (including diabetes mellitus and IGR) are undiagnosed before their admission.
We missed 89.1% (163/183, i.e., patients with I-IGT) patients with IGR. At the same time, 26 cases (14.1%) are missed in the 185 diabetes mellitus patients, 51.4% patients with abnormal glucose metabolism are missed if we don't conduct OGTT test and only conduct simple FPG test for them.
| Discussion|| |
Diabetes is a high-risk factor for cerebral vascular disease, the risk of diabetic patients with cerebrovascular disease is two to four times higher than nondiabetes patients.  Blood glucose level plays an important influence on the prognosis after the acute cerebrovascular disease occurrence, the prognosis of patients with high blood sugar is worse than those with normal blood glucose, especially the prognosis of combined diabetes patients is generally more worse than that those of pure cerebral vascular disease.
Glucose metabolism status of acute cerebral vascular disease is an important indicator to predict the prognosis, ,, acute cerebral vascular disease has become an important cause for diabetic patients death, diabetes increase the possibility of stroke patients mortality, which is an independent risk for cerebral apoplexy patients death. , If hyperglycemia was found in cerebral vascular disease patients at an early stage and make corresponding treatments, the harm of high blood sugar would be reduced, therefore, it is necessary to strengthen monitoring blood glucose for cerebral vascular disease patients.
Recent clinical studies  found a higher abnormal sugar metabolism morbidity in cerebral vascular disease patients. Abnormal sugar metabolism was undiagnosed ubiquitously in cerebrovascular disease patients who were without diabetes mellitus history. One second abnormal glucose metabolism patients would be missed.  In order to survey metabolic abnormalities patients with acute cerebral vascular disease, Matz et al.  selected 286 stroke patients for blood glucose monitoring, their results showed two-thirds acute cerebral vascular disease patients had an abnormal glucose metabolism, and this situation was often unknown. Our results showed 66.1% acute cerebral vascular disease patients had an abnormal glucose metabolism. Totally, 55 complicated diabetes patients were undiagnosed before admission, which accounts for 29.8% of all diabetic patients, and 64.7% abnormal glucose metabolism patients are undiagnosed before admission. Besides, we found that 14.1% impaired diabetic patients and 89.1% glucose regulation patients would be missed if not conducting OGTT test and only checking simple FBG. Besides, 51.4% abnormal glucose metabolism patients would be missed, which was consistent with the report of Hu and Yang.  At present, high blood glucose in cerebral vascular disease patients has not been attracted enough attention, only few cerebrovascular disease patients check FPG, postprandial blood glucose level or OGTT. Abnormal glucose metabolism would be undiagnosed if only checking their FPG. Apparently, cerebrovascular disease patients need further blood sugar detection. We suggest stroke patients without diabetes history should conduct an oral glucose tolerance screening.
Previous study  indicated poststroke hyperglycemia is caused by stress, which did not mean glucose metabolism disorder in these patients. Glucose tolerance damage was detected in early stage of the stroke patients who were not diagnosed as stroke patients with diabetes mellitus in the 106 acute brain stroke patients without diabetes history.  This damage last 3 months in two-thirds patients, and the prognosis of high blood sugar was bad during the acute period. Prompt blood glucose disorder after stroke is not a simple stress phenomenon; however, abnormal glucose metabolism existed in patients themselves before acute cerebrovascular diseases prevalence. At present, the risk of diabetic patients with cerebral vascular diseases had arose much attention; however, people often ignored their harms on vascular at the earlier stage of diabetes including IFG and impaired glucose, which made the risk of cerebrovascular disease increased. Besides, patients with cerebral vascular disease faced the threat of abnormal glucose metabolism. Atherosclerosis would occur before diabetes for diabetes patients, , it has obvious atherosclerosis at IGT stage, the degree was similar to diabetes, and IGT was a risk factor for early atherosclerosis. ,,
| References|| |
Garcia JH, Yoshida Y, Chen H, Li Y, Zhang ZG, Lian J, et al.
Progression from ischemic injury to infarct following middle cerebral artery occlusion in the rat. Am J Pathol 1993;142:623-35.
DIMD (Dorland′s Illustrated Medical Dictionary). 28 th
ed. Philadelphia, Pa: WB Saunders Co.; 1994. p. 837.
Lassen NA. Incomplete cerebral infarction - Focal incomplete ischemic tissue necrosis not leading to emollision. Stroke 1982;13:522-3.
Bai CL. Effect of blood glucose level on the prognosis of acute cerebral infarction. J Clin Med Pract 2005;14:739-40.
CAN (China Association of Neurosurgery). Diagnostic criteria for various cerebrovascular disease. Chin J Neurol 1996;29:379-80.
Qiu M, Liu R. Clinical analysis of diabetes mellitus complicated with acute cerebrovascular disease. Chin Mod Med 2006;8:3-5.
Tuomilehto J, Rastenyte D, Jousilahti P, Sarti C, Vartiainen E. Diabetes mellitus as a risk factor for death from stroke. Prospective study of the middle-aged Finnish population. Stroke 1996;27:210-5.
Ivey FM, Ryan AS, Hafer-Macko CE, Garrity BM, Sorkin JD, Goldberg AP, et al.
High prevalence of abnormal glucose metabolism and poor sensitivity of fasting plasma glucose in the chronic phase of stroke. Cerebrovasc Dis 2006;22:368-71.
Matz K, Keresztes K, Tatschl C, Nowotny M, Dachenhausen A, Brainin M, et al.
Disorders of glucose metabolism in acute stroke patients: an underrecognized problem. Diabetes Care 2006;29:792-7.
Hu DY, Yang JG. Focus on glucose metabolism in patients with coronary heart disease. Abnorm Dep Intern Med Mag 2006;45:793-5.
Vancheri F, Curcio M, Burgio A, Salvaggio S, Gruttadauria G, Lunetta MC, et al.
Impaired glucose metabolism in patients with acute stroke and no previous diagnosis of diabetes mellitus. QJM 2005;98:871-8.
Jin W, Pan C, Lu J. Impaired glucose tolerance and atherosclerosis. J Endocrinol Metab 2004;20:136-9.
Zhang Y, Zhan W, Jie H. The relationship between impaired glucose tolerance of carotid artery intima-media thickness and metabolic parameters. Chin J Diabetes Mellitus 2005;13:23-6.
Stegmayr B, Asplund K. Diabetes as a risk factor for stroke. A population perspective. Diabetologia 1995;38:1061-8.