Different reticulocyte volume in diabetes mellitus patients with and without hypercholesterolemia and/or hypertriglyceridemia.

Red cells and reticulocytes from patients with diabetes mellitus (DM) were analysed using laser and computer technology of H*3 hematology analyzer. Four groups of diabetes mellitus patients: diabetes with normolipemia (DM) (n = 12) and DM patients with excess triglyceride (DM-T) (n = 7) or cholesterol (DM-C) (n = 21) or both (DM-TC) (n = 21) were studied. Mean corpuscular volume of mature red cells (Mean +/- SD = 93.6 +/- 5.5 fl) and reticulocyte (119.1 +/- 12.3 fl) of patients with DM-T was not significantly increased from normal (red cell, 90.0 +/- 3.5 fl; reticulocyte, 115.2 +/- 7.3 fl). Plasma triglyceride levels had no significant correlation with red cell MCV, reticulocyte MCV and %Hb A1c. This suggests that high triglyceride levels in DM are not dose-dependent in producing increased MCV of red cells and reticulocytes. Comparing between DM-T and DM-C, red cells and reticulocytes from DM-C patients had significantly decreased MCV (red cell, 85.5 +/- 6.1 fL; reticulocyte, 103.8 +/- 7.4 fL). Plasma cholesterol levels were inversely correlated with MCV of red cells (r = -0.377, p = 0.003) and also MCV of reticulocytes (r = -0.418, p = 0.001). In addition, cholesterol levels showed considerable correlation with Hb A1c (r = 0.572, p = 0.004). The red cell volume change in DM-C patients may be partly due to the shift in balance of cholesterol exchange between red cell membranes and serum lipoproteins.

Reticulocyte analysis in iron deficiency anemia and hemolytic anemia.

Reticulocyte analysis was studied in 28 anemic patients, 15 with iron deficiency anemia (IDA), and 13 with hemolytic anemia including 9 glucose 6 phosphate dehydrogenase deficiency (G6PD def.), and 4 with G6PD def. combined with HbE trait or alpha thalassemia trait (alpha thal trait). The reticulocyte analysis among these patients showed the increased number of reticulocyte percentage with low degree of maturation in both IDA and G6PD def. patients. The significantly decreased reticulocyte hemoglobin content (CHr) was found in IDA (CHr = 21.74 +/- 4.61 pg in IDA vs 28.41 +/- 1.34 pg in normal; p-value = < 0.0001), whereas, increased CHr was found in G6PD def. patients. In addition, the G6PD def. patients also showed a significant increase in mean corpuscular reticulocyte volume (MCVr) when compared to normal (MCVr = 132.0 +/- 8.39 fl. in G6PD def. vs 110.39 +/- 5.09 in normal; p-value = < 0.0001). However, a significant decrease in MCVr was found in IDA patients (MCVr = 95.89 +/- 8.57 fl.; p-value = < 0.0001 vs normal). From this study, we can suggest that the reticulocyte hemoglobin content (CHr) and mean corpuscular reticulocyte volume (MCVr) are the important defects in patients with iron deficiency anemia.

Reticulocyte analysis in systemic lupus erythematosus and chronic renal failure using flow cytometry.

The number and maturation of circulating reticulocytes were measured in patients with systemic lupus erythematosus (SLE) and chronic renal failure (CRF) using an automated hematological analyzer (Technicon H*3 RTX) for their erythropoietic activities. Both SLE and CRF patients had increased reticulocyte numbers with a low degree of maturation. The SLE patients had no changes in mean reticulocyte corpuscular volume (MCVr) as compared to normal subjects (110.20 +/- 15.43 fl. in SLE and 110.39 +/- 5.09 fl. in normal), whereas CRF patients had significantly increased mean corpuscular reticulocyte volume (MCVr = 120.99 +/- 8.09 fl., p-value = 0.0019 as compared with normal). Three cases of SLE with nephrotic syndrome (NS) had high degree of MCVr (113.4, 125.0 and 133.1 fl., respectively). The renal involvement in SLE patients and CRF patients may associate with increased reticulocyte corpuscular volume.

Red cell parameters in alpha-thalassemia with and without beta-thalassemia trait or hemoglobin E trait.

Eighty-five patients who attended at Ramathibodi Hospital during November 1994 to June 1996 were investigated for thalassemia genotype, hemoglobin (Hb) typing and blood cell parameters. All patients were screened primarily for complete blood count using the Technicon H*3 automated hematology analyzer and Hb typing using the automated HPLC. Their genotypes were evaluated by in vitro gene amplification using primers for detection of common alpha-thalassemic genes found in the Thai population. We found 45 cases out of 85 were alpha-thalassemia trait with A2A typing, 10 were normal, 7 were alpha-thalassemia trait complicated by beta-thalassemia trait or HbE trait, 18 were HbH disease or HbH with Hb Constant Spring (HbH/CS), and 5 were AE Bart's disease. The alpha-thalassemia 1 trait had heterogeneity in red cell population as shown by increased red cell distribution width (RDW), the increased percent microcytic red cell (%Micro) and decreased mean cell volume (MCV). Red cell parameters in alpha-thalassemia 2 trait and HbCS trait were not significantly different from normal. The cases with coinheritance of alpha-thalassemia trait with beta-thalassemia trait or with HbE trait showed variation in their red cell parameters: one case showed less abnormal red cell parameters than those of uncomplicated alpha-thalassemia but the other two cases showed unimproved values. The homozygous alpha-thalassemia 2 showed similar red cell parameters to the alpha-thalassemia 1 trait. In conclusion, we can screen the alpha-thalassemia 1 trait and homozygous alpha-thalassemia 2 by using the simple red cell parameters such as the MCV and RDW; however, they must be confirmed for alpha-thalassemic genes. Unfortunately, red cell parameters of alpha-thalassemia 2 trait or HbCS trait were not different from those of normal subjects.