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  • Author: Ligia Coroș x
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Simona Cernea, Adina Huţanu, Ligia Coroş and Minodora Dobreanu

Abstract

Objectives: The primary aim of this study was to assess residual beta cell function at diagnosis of type 2 diabetes and identify accessible laboratory markers that best estimate it. The secondary objective was to evaluate the change in beta cell function 6 months after starting different therapeutical regimens. Materials and methods: Forty seven subjects were included in the study and each performed a 75-g oral glucose tolerance test (OGTT) at baseline and after 6 months. Metabolic and immunologic parameters were determined from fasting samples. According to the degree of metabolic decompensation, specific therapy was started: metformin, metformin plus gliclazide or insulin therapy (with/out metformin). Early and total beta cell function was evaluated by the disposition index (DI) calculated for 30 minutes and 120 minutes, respectively. Results: At diagnosis, fasting blood glucose (BG) and HbA1c varied largely (129-521 mg/dl and 5.5-14%, respectively). The DI30 and DI120 decreased with more severe glycemic decompensation. For both DI30 and DI120 significant negative correlations were found for glycemic markers (HbA1c, 2-hour BG and maximal BG amplitude) and positive correlation for 2- hour C peptide (p<0.0001 for all). HbA1c value of 7% discriminated an important decrease of DI30 and DI120. Insulin and combined therapy significantly improved DI120 at 6 months (p: 0.0062 and 0.01, respectively), while DI30 was improved only with insulin therapy (p: 0.0326). Conclusions: Beta cell function at onset correlated with HbA1c, 2-hour BG and C peptide during OGTT. Thus OGTT and HbA1c are pivotal for evaluation of beta cell function. Insulin therapy improved early and total insulin secretion at 6 months.

Open access

Nicoleta Dora Pop, Anca Bacârea, Ligia Coroș, Grigore Aloiziu Dogaru, Ioan Hosu, Vladimir Bacârea and Attila Nagy

Abstract

In this study, different aspects of anemia in chronic kidney disease have been observed, starting from the fact that the severity of anemia is associated with the degree of kidney dysfunction, the main cause being the erythropoietin deficiency, which is synthesized mostly by the kidneys. 58 persons were included in this study, 19 patients with non-dialysis-dependent chronic kidney disease, 18 patients with chronic kidney disease who received kidney transplantation and 21 apparently healthy persons. We evaluated the serum level of erythropoietin, serum creatinine, proteinuria, the glomerular filtration rate, the erythrocyte parameters and the correlations between them. The prevalence of anemia in patients with chronic kidney disease was of 51.35%. The hemoglobin concentration in patients with kidney transplantation (12.4 ± 2.7 g/dL) and in non-dialysis-dependent patients (11.7 ± 1.4 g/dL) is significantly different compared to the apparently healthy persons (14.6 ± 0.8 g/dL) (p<0.05). In the case of the non-dialysis-dependent patients who were not treated with erythropoiesis- stimulating agents we found positive associations between the glomerular filtration rate and the number of erythocytes (r = 0.71), hemoglobin (r = 0.65) and hematocrit (r = 0.73), as well as negative associations between creatinine and the number of erythrocytes (r = -0.72), hemoglobin (r = -0.86) and hematocrit (r = -0.88). In patients with kidney transplantation and anemia we observed positive correlations between erythropoietin and the number of erythrocytes (r = 0.69), between the glomerular filtration rate and the number of erythrocytes (r = 0.78) and erythropoietin (r = 0.97), as well as negative correlations between proteinuria and the number of erythrocytes (r= -0.89), hemoglobin (r= -0.72), hematocrit (r = -0.72), and erythropoietin (r = -0.67), and between creatinine and the number of erythrocytes (r = -0.75) and erythropoietin (r = -0.86).