AIMS: In type 1 diabetic patients, some have glycemic instability while others glycemic stability. We have developed criteria for evaluating glycemic instability and investigated the factors responsible. METHODS: Glycemic instability in 52 type 1 diabetic patients was assessed by the mean amplitude of glycemic excursions (MAGE) and M-value, and clinical characteristics of good, fair and poor control groups were compared. RESULTS: The median MAGE and M-value was 6.6mmol/L and 18.7, respectively. Then MAGE >or=6.6mmol/L and M-value >or=18.7 was defined as poor control. In the 32 patients without detectable C-peptide levels, 18 patients (56%) showed poor control. The frequency of ketosis or ketoacidosis at onset of diabetes was dramatically higher in the poor control group not only in the patients as a whole but also in those without detectable C-peptide levels. CONCLUSIONS: A decreased level of C-peptide is a significant factor in glycemic instability. However, some patients have glycemic stability though beta-cell function is completely depleted. The presence of ketosis or ketoacidosis at onset of diabetes may be a factor in later glycemic instability, suggesting the importance of examining patients in detail at onset of diabetes for careful follow-up to prevent progression of acute and chronic complications of diabetes.
AIMS: In type 1 diabeticpatients, some have glycemic instability while others glycemic stability. We have developed criteria for evaluating glycemic instability and investigated the factors responsible. METHODS: Glycemic instability in 52 type 1 diabeticpatients was assessed by the mean amplitude of glycemic excursions (MAGE) and M-value, and clinical characteristics of good, fair and poor control groups were compared. RESULTS: The median MAGE and M-value was 6.6mmol/L and 18.7, respectively. Then MAGE >or=6.6mmol/L and M-value >or=18.7 was defined as poor control. In the 32 patients without detectable C-peptide levels, 18 patients (56%) showed poor control. The frequency of ketosis or ketoacidosis at onset of diabetes was dramatically higher in the poor control group not only in the patients as a whole but also in those without detectable C-peptide levels. CONCLUSIONS: A decreased level of C-peptide is a significant factor in glycemic instability. However, some patients have glycemic stability though beta-cell function is completely depleted. The presence of ketosis or ketoacidosis at onset of diabetes may be a factor in later glycemic instability, suggesting the importance of examining patients in detail at onset of diabetes for careful follow-up to prevent progression of acute and chronic complications of diabetes.