Exploration of hematological and immunological changes associated with the severity of type 2 diabetes mellitus in Japan
Abstract It has been postulated that immune modulation and activation play an important role in the pathogenesis of type 2 diabetes mellitus (T2DM), but evidence for this has not yet been well documented. We explored the changes in peripheral immunocompetent cells in relationship to the severity of T2DM in 142 patients, and 34 healthy individuals in Japan. A severity index with 0–12 grades was derived based on the HbA1c level and the number of complications. By multiple regression analysis, the severity index was positively associated with neutrophil counts and negatively associated with platelet and CD19+ lymphocyte counts. However, we did not observe any significant changes in other lymphocyte subsets such as CD4+, CD8+, and CD56+. These results suggest that poor diabetic control may be marked by changes in some blood cell types.
Available from: Caroline E Brett
- "Some limited data on the relationship between neutrophils and platelets are available from 34 healthy controls, mostly men, who participated in a study of the effects of type 2 diabetes on leukocyte and platelet counts . Neutrophils, lymphocytes and monocyte counts were all lower in healthy controls than people with diabetes, this being more marked for neutrophils and monocytes than for lymphocytes. "
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ABSTRACT: Reference ranges are available for different blood cell counts. These ranges treat each cell type independently and do not consider possible correlations between cell types.
Participants were identified from the Community Health Index as survivors of the 1947 Scottish Mental Survey, all born in 1936, who were resident in Lothian (potential n = 3,810) and invited to participate in the study. Those who consented were invited to attend a Clinical Research Facility where, amongst other assessments, blood was taken for full blood count. First we described cell count data and bivariate correlations. Next we performed principal components analysis to identify common factors. Finally we performed confirmatory factor analysis to evaluate suitable models explaining relationships between cell counts in men and women.
We examined blood cell counts in 1027 community-resident people with mean age 69.5 (range 67.6-71.3) years. We determined normal ranges for each cell type using Q-Q plots which showed that these ranges were significantly different between men and women for all cell types except basophils. We identified three principal components explaining around 60% of total variance of cell counts. Varimax rotation indicated that these could be considered as erythropoietic, leukopoietic and thrombopoietic factors. We showed that these factors were distinct for men and women by confirmatory factor analysis: in men neutrophil count was part of a 'thrombopoietic' trait whereas for women it was part of a 'leukopoietic' trait.
First, normal ranges for haematological indices should be sex-specific; at present this only pertains to those associated with erythrocytes. Second, differences between individuals across a range of blood cell counts can be explained to a considerable extent by three major components, but these components are not the same in men and women.
Available from: Alexander D Roshal
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Cardiovascular complications are the leading cause of mortality in type 2 diabetes (T2DM), in which onset and progression of atherosclerosis is linked to chronic inflammation. Activation status of innate immune cells (granulocytes [Gc], monocytes [Mc]), as reflected by increased CD11b, CD66b, and other surface markers, increases their endothelial and cytokines/chemokines release. Whereas this inflammatory activation seems inversely related to poor glycemic control, the effect of acute spontaneous hyperglycemia on innate immune cell activation remains unclear.
Expression of key markers (CD11b, CD14, CD16, CD62L, and CD66b) was therefore determined by flow cytometry on whole blood of healthy subjects and patients with T2DM with spontaneous fasting euglycemia or hyperglycemia both at baseline and after 30, 90, and 240 minutes of incubation at room temperature.
Hyperglycemic patients with T2DM had significantly higher Gc and Mc CD11b and Gc CD66b surface mean fluorescence intensity compared with the euglycemic patients with T2DM whose values were similar to those of the healthy controls. CD16 expression in CD14+CD16+ Mc was elevated in all patients with T2DM, regardless of glycemic levels.
Our data suggest that whereas the presence of diabetes per se may have a proinflammatory effect, hyperglycemia seems to further acutely exacerbate innate cell inflammatory status and their consequent endothelial adhesion and vascular damage potential.
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