Masafumi Koga1, Hiroshi Saito2, Soji Kasayama3. 1. Department of Internal Medicine, Kawanishi City Hospital, Hyogo, Japan. Electronic address: m-koga@kawanishi-city-hospital.com. 2. Department of Internal Medicine, Kinki Central Hospital, Hyogo, Japan. 3. Department of Medicine, Nissay Hospital, Osaka, Japan.
Abstract
OBJECTIVES: When diabetes treatment is started, added, or changed (intensification of treatment) in patients with poor glycemic control, GA (glycated albumin) decreases within a few weeks, while HbA1c increases in some patients, resulting in a discrepancy between changes in GA and HbA1c. In the present study, we investigated the pathophysiology of such discrepancies. DESIGN AND METHODS: Four diabetic patients with poor glycemic control in whom GA showed a decrease while HbA1c showed an increase at a few weeks after intensification of treatment, resulting in a discrepancy between the time course of HbA1c and that of GA, were studied. RESULTS: In all patients HbA1c increased during the course before intensification of treatment; GA measured in two patients before the intensification of treatment also increased. After the intensification of treatment, GA decreased in all patients. On the other hand, HbA1c increased even after the intensification of treatment, but it decreased later in these patients. CONCLUSIONS: In patients in whom HbA1c increased in spite of a decrease in GA after the intensification of diabetes treatment, glycemic control got worsened before the intensification of treatment. In such patients, therapeutic effect may be misinterpreted if glycemic control is evaluated by HbA1c, and thus it is preferable to evaluate glycemic control by fasting plasma glucose, GA and fructosamine in such situations.
OBJECTIVES: When diabetes treatment is started, added, or changed (intensification of treatment) in patients with poor glycemic control, GA (glycated albumin) decreases within a few weeks, while HbA1c increases in some patients, resulting in a discrepancy between changes in GA and HbA1c. In the present study, we investigated the pathophysiology of such discrepancies. DESIGN AND METHODS: Four diabeticpatients with poor glycemic control in whom GA showed a decrease while HbA1c showed an increase at a few weeks after intensification of treatment, resulting in a discrepancy between the time course of HbA1c and that of GA, were studied. RESULTS: In all patients HbA1c increased during the course before intensification of treatment; GA measured in two patients before the intensification of treatment also increased. After the intensification of treatment, GA decreased in all patients. On the other hand, HbA1c increased even after the intensification of treatment, but it decreased later in these patients. CONCLUSIONS: In patients in whom HbA1c increased in spite of a decrease in GA after the intensification of diabetes treatment, glycemic control got worsened before the intensification of treatment. In such patients, therapeutic effect may be misinterpreted if glycemic control is evaluated by HbA1c, and thus it is preferable to evaluate glycemic control by fasting plasma glucose, GA and fructosamine in such situations.