ABSTRACT
The aim of the present study was to investigate the prevalence of fear of hypoglycemia, in association with severe hypoglycemia and social factors, in insulin-treated patients with type 2 diabetes mellitus. A questionnaire survey on hypoglycemia and patient-physician communication was carried out in 355 patients with insulin-treated type 2 diabetes mellitus patients at 16 hospitals and clinics. A fear of hypoglycemia was reported by 27.7% of patients. A stepwise logistic regression analysis found that severe hypoglycemia during the past 1 year was a significant determinant of fear of hypoglycemia (odds ratio 2.16, 95% confidence interval 1.06-4.41; P = 0.034), and age (odds ratio 1.02, 95% confidence interval 1.00-1.05, P = 0.038) and living alone (odds ratio 1.93, 95% confidence interval 1.00-3.73, P < 0.05) were significantly higher in patients with fear of hypoglycemia than in those without it.
ABSTRACT
AIM: Glucagon is recommended to treat severe hypoglycemia in nonhospital environments, when a patient with type 1 diabetes mellitus (T1DM) is unconscious and unable to eat or drink. However, the actual possession rate of glucagon in Japan has not been investigated. SUBJECTS AND METHODS: We recruited 208 T1DM patients older than 15 years of age. The patients were treated at 16 hospitals and clinics in different regions of Japan. Answers were obtained using a self-administered questionnaire about the possession, the experience of usage, and the preference to possess glucagon after reading what is glucagon and when it is used. A stepwise logistic regression analysis was performed to assess the influence of various factors on the possession of glucagon. RESULTS: The possession rate of glucagon was 15.9%, and the rate of those who had experience of using glucagon to treat severe hypoglycemia was 6.0%. The rate of preference to possess glucagon at home after reading the description of glucagon was 39.0%. The possession of glucagon was significantly associated with results of the Glucagon Knowledge Test (odds ratio=24.1; 95% confidence interval, 3.2-183.3; P=0.002) and the history of severe hypoglycemia within 1 year (odds ratio=4.8; 95% confidence interval, 2.0-12.0; P=0.001). CONCLUSIONS: Glucagon as a measure to treat severe hypoglycemia was underutilized among T1DM patients in Japan.
Subject(s)
Diabetes Mellitus, Type 1/drug therapy , Gastrointestinal Agents/therapeutic use , Glucagon/therapeutic use , Hypoglycemia/drug therapy , Adult , Aged , Confidence Intervals , Diabetes Complications/drug therapy , Diabetes Complications/epidemiology , Diabetes Mellitus, Type 1/epidemiology , Drug Utilization/statistics & numerical data , Female , Health Knowledge, Attitudes, Practice , Humans , Hypoglycemia/epidemiology , Japan/epidemiology , Logistic Models , Male , Middle Aged , Odds Ratio , Surveys and QuestionnairesSubject(s)
Diabetes Mellitus, Type 1/therapy , Exercise Therapy , Blood Glucose , Diabetes Mellitus, Type 1/blood , Diabetes Mellitus, Type 1/diet therapy , Diet, Diabetic , Dietary Carbohydrates/administration & dosage , Dietary Fiber/administration & dosage , Exercise Therapy/adverse effects , Glycemic Index , Humans , Hypoglycemia/etiology , Hypoglycemia/prevention & control , Insulin/administration & dosageABSTRACT
BACKGROUND/AIMS: We investigated basal levels of serum and urinary lipocalin-type prostaglandin D synthase/beta-trace (L-PGDS) in type-2 diabetic patients and explored whether glycemic control affects L-PGDS status in another 55 diabetic inpatients with normoalbuminuria. METHODS: Fifty-five type-2 diabetic outpatients (HbA1c, 9.14 +/- 0.20%; creatinine (Cr), 85.1 +/- 2.4 micromol/l), and 55 age-matched healthy control subjects were recruited. Serum and urinary levels of L-PGDS were determined with respect to the stage of diabetic nephropathy. The L-PGDS was localized by immunohistochemistry. RESULTS: The urinary L-PGDS index increased in diabetic patients, compared with the controls (234.8 +/- 27.4 vs. 73.8 +/- 7.8 microg/mmol Cr, p < 0.001). Even in normoalbuminuric patients as well as in microalbuminuric patients, urinary L-PGDS indexes were higher than the controls (166.0 +/- 21.1, p < 0.0001 and 338.6 +/- 62.5 microg/mmol Cr, p < 0.0001, respectively), although the serum L-PGDS level was equal to that in the control subjects. Multiple regression analysis revealed that the urinary L-PGDS index was predicted solely by glucose levels and type-IV collagen index, whereas the serum L-PGDS was determined mainly by age and serum Cr. Glycemic control reduced the urinary L-PGDS index towards the normal range in diabetic patients with normoalbuminuria (172.3 +/- 6.6 vs. 118.1 +/- 2.6 (SE) microg/mmol Cr, p < 0.0001). Immunohistochemistry showed that L-PGDS was uniquely present in the renal tubules in diabetes while in nondiabetics, L-PGDS occurred solely in the peritubular interstitium, not in the tubular cells. CONCLUSION: Inadequate glycemic control is responsible for urinary L-PGDS excretion in the diabetic patients. Urinary L-PGDS is useful to predict subclinical renal injury associated with type-2 diabetes.
