Investigation of neutrophil lymphocyte ratio and blood glucose regulation in patients with type 2 diabetes mellitus
Objective Leukocytosis is thought to be directly associated with the pathogenesis of atherosclerosis and metabolic syndrome. Increased white blood cell (WBC) count is related to cardiovascular disease in patients with type 2 diabetes mellitus; raised neutrophil lymphocyte ratio (NLR) is associated w...
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Published in | Journal of international medical research Vol. 42; no. 2; pp. 581 - 588 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
London, England
SAGE Publications
01.04.2014
Sage Publications |
Subjects | |
Online Access | Get full text |
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Summary: | Objective
Leukocytosis is thought to be directly associated with the pathogenesis of atherosclerosis and metabolic syndrome. Increased white blood cell (WBC) count is related to cardiovascular disease in patients with type 2 diabetes mellitus; raised neutrophil lymphocyte ratio (NLR) is associated with metabolic syndrome. There is little information, however, concerning a correlation between glycosylated haemoglobin (HbA1c) and NLR. The aim of the present study was to investigate the relationship between NLR and blood glucose regulation.
Methods
This retrospective study was conducted in patients with type 2 diabetes mellitus, divided into two groups according to HbA1c levels: group 1, HbA1c levels ≤ 7%; group 2, HbA1c levels > 7%. Venous WBC, neutrophil and lymphocyte counts were determined.
Results
Of 71 patients included, fasting serum glucose, neutrophil and WBC counts were significantly higher in group 2 compared with group 1. NLR had a positive correlation with HbA1c.
Conclusion
There may be a significant relationship between NLR and blood glucose regulation. The authors propose that increased NLR may be associated with elevated HbA1c in patients with type 2 diabetes mellitus. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0300-0605 1473-2300 |
DOI: | 10.1177/0300060513516944 |