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Background/Aims@#Although people with diabetes have been shown to have higher mortality than people without diabetes, there is a lack of data on the association between fasting plasma glucose (FPG) levels and cause-specific mortality rates in the general population. @*Methods@#A total of 326,547 Korean adults over 20 years of age, who had received a health checkup between 2006 and 2008 were selected from the Korean National Health Insurance Service sample cohort dataset and followed until 2015. We estimated hazard ratios (HRs) of all-cause mortality and cause-specific mortality relative to various range of FPG levels. All causes of death were classified according to International Classification of Diseases (ICD)-10 codes. @*Results@#During follow-up (mean, 8.5 years), a total of 13,536 deaths (mortality rate 4.89/1,000 person-year) occurred; 4,916 deaths from cancer, 2,133 from cardiovascular disease, 762 from infectious disease, 199 from renal disease, and 5,526 from other causes. The overall mortality rate increased with an increase in FPG category (HR, 1.78; 95% confidence interval, 1.65 to 1.92; in the ≥ 160 mg/dL). In addition, a J-shaped associations was found between FPG levels and all-cause mortality after adjustment for age, sex, smoking, drinking, physical activity, body mass index, diabetes mellitus medication, hypertension, and dyslipidemia. In particular, the risk of cancer-mortality with high FPG levels was increased for men but not women. @*Conclusions@#The risk of all-cause and cause-specific mortality showed the tendency to increase when the FPG level was outside of the normal range, indicating a J-shaped relationship, in both men and women.
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Background/Aims@#Although people with diabetes have been shown to have higher mortality than people without diabetes, there is a lack of data on the association between fasting plasma glucose (FPG) levels and cause-specific mortality rates in the general population. @*Methods@#A total of 326,547 Korean adults over 20 years of age, who had received a health checkup between 2006 and 2008 were selected from the Korean National Health Insurance Service sample cohort dataset and followed until 2015. We estimated hazard ratios (HRs) of all-cause mortality and cause-specific mortality relative to various range of FPG levels. All causes of death were classified according to International Classification of Diseases (ICD)-10 codes. @*Results@#During follow-up (mean, 8.5 years), a total of 13,536 deaths (mortality rate 4.89/1,000 person-year) occurred; 4,916 deaths from cancer, 2,133 from cardiovascular disease, 762 from infectious disease, 199 from renal disease, and 5,526 from other causes. The overall mortality rate increased with an increase in FPG category (HR, 1.78; 95% confidence interval, 1.65 to 1.92; in the ≥ 160 mg/dL). In addition, a J-shaped associations was found between FPG levels and all-cause mortality after adjustment for age, sex, smoking, drinking, physical activity, body mass index, diabetes mellitus medication, hypertension, and dyslipidemia. In particular, the risk of cancer-mortality with high FPG levels was increased for men but not women. @*Conclusions@#The risk of all-cause and cause-specific mortality showed the tendency to increase when the FPG level was outside of the normal range, indicating a J-shaped relationship, in both men and women.
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Background/Aims@#We examined the concordance rate among fasting plasma glucose (FPG), 2-hour post-challenge glucose (2hr PG), and hemoglobin A1c (HbA1c) in the diagnosis of diabetes in a population with a high-risk for type 2 diabetes mellitus (T2DM) in Korea. @*Methods@#Among the participants from the Korean Diabetes Prevention Study, individuals with FPG ≥ 100 mg/dL, body mass index (BMI) ≥ 23.0 kg/m2, and no previous history of T2DM were consecutively enrolled after a 75 g glucose tolerance test. We analyzed the differences in the clinical characteristics in subjects with stage 1 (FPG, 100 to 109 mg/dL) and stage 2 (FPG, 110 to 125 mg/dL) impaired fasting glucose (IFG). @*Results@#Of 1,637 participants, 27.2% had T2DM and 59.3% had IFG and/or impaired glucose tolerance (IGT). The mean age was 55.0 ± 8.1 years and the mean BMI was 26.3 ± 2.7 kg/m2. Based on FPG criteria, 515 (31.4%) and 352 (21.5%) subjects were classified as having stage 1 and stage 2 IFG, respectively. The 19.0% of stage 1 and 43.5% of stage 2 subjects showed 2hr PG levels in the diabetic range. Even for those in the normal FPG range, 63 (9.5%) participants showed a 2hr PG level of ≥ 200 mg/dL. Of 446 subjects with newly-diagnosed diabetes, 340 (76.2%) showed FPG levels < 126 mg/dL. @*Conclusions@#The oral glucose tolerance test should be actively considered for Korean adults who are overweight or obese with the IFG range (FPG, 100 to 125 mg/ dL) to allow for early detection of diabetes and prompt intervention.
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BackgroundHypoxia can occur in pancreatic islets in type 2 diabetes mellitus. Pancreatic stellate cells (PSCs) are activated during hypoxia. Here we aimed to investigate whether PSCs within the islet are also activated in hypoxia, causing β-cell injury.MethodsIslet and primary PSCs were isolated from Sprague Dawley rats, and cultured in normoxia (21% O2) or hypoxia (1% O2). The expression of α-smooth muscle actin (α-SMA), as measured by immunostaining and Western blotting, was used as a marker of PSC activation. Conditioned media (hypoxia-CM) were obtained from PSCs cultured in hypoxia.ResultsIslets and PSCs cultured in hypoxia exhibited higher expressions of α-SMA than did those cultured in normoxia. Hypoxia increased the production of reactive oxygen species. The addition of N-acetyl-L-cysteine, an antioxidant, attenuated the hypoxia-induced PSC activation in islets and PSCs. Islets cultured in hypoxia-CM showed a decrease in cell viability and an increase in apoptosis.ConclusionPSCs within the islet are activated in hypoxia through oxidative stress and promote islet cell death, suggesting that hypoxia-induced PSC activation may contribute to β-cell loss in type 2 diabetes mellitus.
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BackgroundHypoxia can occur in pancreatic islets in type 2 diabetes mellitus. Pancreatic stellate cells (PSCs) are activated during hypoxia. Here we aimed to investigate whether PSCs within the islet are also activated in hypoxia, causing β-cell injury.MethodsIslet and primary PSCs were isolated from Sprague Dawley rats, and cultured in normoxia (21% O2) or hypoxia (1% O2). The expression of α-smooth muscle actin (α-SMA), as measured by immunostaining and Western blotting, was used as a marker of PSC activation. Conditioned media (hypoxia-CM) were obtained from PSCs cultured in hypoxia.ResultsIslets and PSCs cultured in hypoxia exhibited higher expressions of α-SMA than did those cultured in normoxia. Hypoxia increased the production of reactive oxygen species. The addition of N-acetyl-L-cysteine, an antioxidant, attenuated the hypoxia-induced PSC activation in islets and PSCs. Islets cultured in hypoxia-CM showed a decrease in cell viability and an increase in apoptosis.ConclusionPSCs within the islet are activated in hypoxia through oxidative stress and promote islet cell death, suggesting that hypoxia-induced PSC activation may contribute to β-cell loss in type 2 diabetes mellitus.
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BACKGROUND: We evaluated the efficacy and safety of acarbose add-on therapy in Korean patients with type 2 diabetes mellitus (T2DM) who are inadequately controlled with metformin and sitagliptin. METHODS: A total of 165 subjects were randomized to metformin and sitagliptin (Met+Sita, n=65), metformin, sitagliptin, and acarbose (Met+Sita+Acarb, n=66) and sitagliptin and acarbose (Sita+Acarb, exploratory assessment, n=34) therapy in five institutions in Korea. After 16 weeks of acarbose add-on or metformin-switch therapy, a triple combination therapy was maintained from week 16 to 24. RESULTS: The add-on of acarbose (Met+Sita+Acarb group) demonstrated a 0.44%±0.08% (P<0.001 vs. baseline) decrease in glycosylated hemoglobin (HbA1c) at week 16, while changes in HbA1c were insignificant in the Met+Sita group (−0.09%±0.10%, P=0.113). After 8 weeks of triple combination therapy, HbA1c levels were comparable between Met+Sita and Met+Sita+Acarb group (7.66%±0.13% vs. 7.47%±0.12%, P=0.321). Acarbose add-on therapy demonstrated suppressed glucagon secretion (area under the curve of glucagon, 4,726.17±415.80 ng·min/L vs. 3,314.38±191.63 ng·min/L, P=0.004) in the absence of excess insulin secretion during the meal tolerance tests at week 16 versus baseline. The incidence of adverse or serious adverse events was similar between two groups. CONCLUSION: In conclusion, a 16-week acarbose add-on therapy to metformin and sitagliptin, effectively lowered HbA1c without significant adverse events. Acarbose might be a good choice as a third-line therapy in addition to metformin and sitagliptin in Korean subjects with T2DM who have predominant postprandial hyperglycemia and a high carbohydrate intake.
Subject(s)
Humans , Acarbose , Diabetes Mellitus, Type 2 , Drug Therapy, Combination , Glucagon , Glycated Hemoglobin , Hyperglycemia , Incidence , Insulin , Korea , Meals , Metformin , Sitagliptin PhosphateABSTRACT
BACKGROUND/AIMS: As the prevalence of diabetes mellitus and its complications increase rapidly, diabetic foot ulcers (DFUs), which are a major diabetic complication, are expected to increase. For prevention and effective treatment, it is important to understand the clinical course of DFUs. The aim of this study was to investigate the natural course and predictors of amputation in patients with DFUs who required hospitalization. METHODS: A total of 209 patients with type 2 diabetes, aged 30 to 85 years, who visited emergency department or needed hospitalization due to DFUs were consecutively enrolled from May 2012 to January 2016, by retrospective medical record review. The main outcome was lower extremity amputation (LEA). RESULTS: Among 192 patients who completed follow-up, 113 patients (58.9%) required LEAs. Compared to patients without amputation, baseline levels of white blood cell counts and C-reactive protein were higher in patients with amputation. In addition, bone and joint involvement was more frequently observed in patients with amputation. Multivariable regression analysis revealed that combined infection (odds ratio [OR], 11.39; 95% confidence interval [CI], 2.55 to 50.93; p = 0.001) and bone or joint involvement (OR, 3.74; 95% CI, 1.10 to 12.70; p = 0.035) were significantly associated with an increased risk of LEA. CONCLUSIONS: The depth of the wound and combined infection of DFU, rather than the extent of the wound, were significant prognostic factors of LEAs in patients with type 2 diabetes.
Subject(s)
Humans , Amputation, Surgical , C-Reactive Protein , Diabetes Complications , Diabetes Mellitus , Diabetic Foot , Emergency Service, Hospital , Follow-Up Studies , Hospitalization , Joints , Leukocyte Count , Lower Extremity , Medical Records , Prevalence , Prognosis , Retrospective Studies , Ulcer , Wounds and InjuriesABSTRACT
BACKGROUND/AIMS: Oxidative stress plays an important role in the pathogenesis and progression of diabetic complications and antagonists of renin-angiotensin system and amlodipine have been reported previously to reduce oxidative stress. In this study, we compared the changes in oxidative stress markers after valsartan and amlodipine treatment in type 2 diabetic patients with hypertension and compared the changes in metabolic parameters. METHODS: Type 2 diabetic subjects with hypertension 30 to 80 years of age who were not taking antihypertensive drugs were randomized into either valsartan (n = 33) or amlodipine (n = 35) groups and treated for 24 weeks. We measured serum nitrotyrosine levels as an oxidative stress marker. Metabolic parameters including serum glucose, insulin, lipid profile, and urine albumin and creatinine were also measured. RESULTS: After 24 weeks of valsartan or amlodipine treatment, systolic and diastolic blood pressure decreased, with no significant difference between the groups. Both groups showed a decrease in serum nitrotyrosine (7.74 ± 7.30 nmol/L vs. 3.95 ± 4.07 nmol/L in the valsartan group and 8.37 ± 8.75 nmol/L vs. 2.68 ± 2.23 nmol/L in the amlodipine group) with no significant difference between the groups. Other parameters including glucose, lipid profile, albumin-to-creatinine ratio, and homeostasis model assessment of insulin resistance showed no significant differences before and after treatment in either group. CONCLUSIONS: Valsartan and amlodipine reduced the oxidative stress marker in type 2 diabetic patients with hypertension.
Subject(s)
Humans , Amlodipine , Antihypertensive Agents , Blood Glucose , Blood Pressure , Creatinine , Diabetes Complications , Diabetes Mellitus, Type 2 , Glucose , Homeostasis , Hypertension , Insulin , Insulin Resistance , Oxidative Stress , Renin-Angiotensin System , ValsartanABSTRACT
BACKGROUND/AIMS: Oxidative stress plays an important role in the pathogenesis and progression of diabetic complications and antagonists of renin-angiotensin system and amlodipine have been reported previously to reduce oxidative stress. In this study, we compared the changes in oxidative stress markers after valsartan and amlodipine treatment in type 2 diabetic patients with hypertension and compared the changes in metabolic parameters. METHODS: Type 2 diabetic subjects with hypertension 30 to 80 years of age who were not taking antihypertensive drugs were randomized into either valsartan (n = 33) or amlodipine (n = 35) groups and treated for 24 weeks. We measured serum nitrotyrosine levels as an oxidative stress marker. Metabolic parameters including serum glucose, insulin, lipid profile, and urine albumin and creatinine were also measured. RESULTS: After 24 weeks of valsartan or amlodipine treatment, systolic and diastolic blood pressure decreased, with no significant difference between the groups. Both groups showed a decrease in serum nitrotyrosine (7.74 ± 7.30 nmol/L vs. 3.95 ± 4.07 nmol/L in the valsartan group and 8.37 ± 8.75 nmol/L vs. 2.68 ± 2.23 nmol/L in the amlodipine group) with no significant difference between the groups. Other parameters including glucose, lipid profile, albumin-to-creatinine ratio, and homeostasis model assessment of insulin resistance showed no significant differences before and after treatment in either group. CONCLUSIONS: Valsartan and amlodipine reduced the oxidative stress marker in type 2 diabetic patients with hypertension.
Subject(s)
Humans , Amlodipine , Antihypertensive Agents , Blood Glucose , Blood Pressure , Creatinine , Diabetes Complications , Diabetes Mellitus, Type 2 , Glucose , Homeostasis , Hypertension , Insulin , Insulin Resistance , Oxidative Stress , Renin-Angiotensin System , ValsartanABSTRACT
BACKGROUND/AIMS: Elevated lipoprotein(a) (Lp[a]) level is known to be a risk factor for cardiovascular disease (CVD). However, the data that has been reported on the association between the Lp(a) level and CVD in type 2 diabetes has been limited and incoherent. The aim of this study was to investigate the relationship between the Lp(a) concentration and new onset CVD in type 2 diabetes. METHODS: From March 2003 to December 2004, patients with type 2 diabetes without a prior history of CVD were consecutively enrolled. CVD was defined as the occurrence of coronary artery disease or ischemic stroke. Cox proportional hazards models were used to identify the associations between the Lp(a) and CVD after adjusting for confounding variables. RESULTS: Of the 1,183 patients who were enrolled, 833 participants were evaluated with a median follow-up time of 11.1 years. A total of 202 participants were diagnosed with CVD (24.2%). The median Lp(a) level for 1st and 4th quartile group was 5.4 (3.5 to 7.1) and 55.7 mg/dL (43.1 to 75.3). Compared with patients without CVD, those with CVD were older, had a longer duration of diabetes and hypertension, and used more insulin and angiotensin converting enzyme inhibitors/angiotensin receptor blockers at baseline. A Cox hazard regression analysis revealed that the development of CVD was significantly associated with serum Lp(a) level (hazard ratio, 1.92; 95% confidence interval [CI], 1.26 to 2.92; p < 0.001, comparing the 4th vs. 1st quartile of Lp[a]). CONCLUSIONS: Elevated Lp(a) level was an independent predictable risk factor for CVD in type 2 diabetes. Other cardiovascular risk factors should be treated more intensively in type 2 diabetic patients with high Lp(a) levels.
Subject(s)
Humans , Cardiovascular Diseases , Cohort Studies , Coronary Artery Disease , Diabetes Mellitus, Type 2 , Follow-Up Studies , Hypertension , Insulin , Lipoprotein(a) , Peptidyl-Dipeptidase A , Proportional Hazards Models , Prospective Studies , Risk Factors , StrokeABSTRACT
BACKGROUND: We investigated the association between severe hypoglycemia (SH) and the risk of cardiovascular (CV) or all-cause mortality in patients with type 2 diabetes. METHODS: The study included 1,260 patients aged 25 to 75 years with type 2 diabetes from the Vincent Type 2 Diabetes Resgistry (VDR), who consecutively enrolled (n=1,260) from January 2000 to December 2010 and were followed up until May 2015 with a median follow-up time of 10.4 years. Primary outcomes were death from any cause or CV death. We investigated the association between the CV or all-cause mortality and various covariates using Cox proportional hazards regression analysis. RESULTS: Among the 906 participants (71.9%) who completed follow-up, 85 patients (9.4%) had at least one episode of SH, and 86 patients (9.5%) died (9.1 per 1,000 patient-years). Patients who had died were older, had a longer duration of diabetes and hypertension, received more insulin, and had more diabetic microvascular complications at baseline, as compared with surviving patients. The experience of SH was significantly associated with an increased risk of all-cause mortality (hazard ratio [HR], 2.64; 95% confidence interval [CI], 1.39 to 5.02; P=0.003) and CV mortality (HR, 6.34; 95% CI, 2.02 to 19.87; P=0.002) after adjusting for sex, age, diabetic duration, hypertension, mean glycosylated hemoglobin levels, diabetic nephropathy, lipid profiles, and insulin use. CONCLUSION: We found a strong association between SH and increased risk of all-cause and CV mortality in patients with type 2 diabetes.
Subject(s)
Humans , Cardiovascular Diseases , Diabetes Mellitus, Type 2 , Diabetic Nephropathies , Follow-Up Studies , Glycated Hemoglobin , Hypertension , Hypoglycemia , Insulin , MortalityABSTRACT
BACKGROUND: There were a limited number of studies about β-cell function after insulin initiation in patients exposed to long durations of sulfonylurea treatment. In this study, we aimed to evaluate the recovery of β-cell function and the efficacy of concurrent sulfonylurea use after the start of long-acting insulin. METHODS: In this randomized controlled study, patients with type 2 diabetes mellitus (T2DM), receiving sulfonylurea for at least 2 years with glycosylated hemoglobin (HbA1c) >7%, were randomly assigned to two groups: sulfonylurea maintenance (SM) and sulfonylurea reduction (SR). Following a 75-g oral glucose tolerance test (OGTT), we administered long-acting basal insulin to the two groups. After a 6-month follow-up, we repeated the OGTT. RESULTS: Among 69 enrolled patients, 57 completed the study and were analyzed: 31 in the SM and 26 in the SR group. At baseline, there was no significant difference except for the longer duration of diabetes and lower triglycerides in the SR group. After 6 months, the HbA1c was similarly reduced in both groups, but there was little difference in the insulin dose. In addition, insulin secretion during OGTT was significantly increased by 20% to 30% in both groups. A significant weight gain was observed in the SM group only. The insulinogenic index was more significantly improved in the SR group. CONCLUSION: Long-acting basal insulin replacement could improve the glycemic status and restore β-cell function in the T2DM patients undergoing sulfonylurea-based treatment, irrespective of the sulfonylurea dose reduction. The dose reduction of the concurrent sulfonylurea might be beneficial with regard to weight grain.
Subject(s)
Humans , Diabetes Mellitus, Type 2 , Follow-Up Studies , Glucose Tolerance Test , Glycated Hemoglobin , Insulin , Insulin, Long-Acting , Triglycerides , Weight GainABSTRACT
BACKGROUND: We investigated an association between baseline heart rate-corrected QT (QTc) interval before severe hypoglycemia (SH) and prolongation of QTc interval during SH in patients with type 2 diabetes mellitus (T2DM). METHODS: Between January 2004 and June 2014, 208 patients with T2DM, who visited the emergency department because of SH and underwent standard 12-lead electrocardiography within the 6-month period before SH were consecutively enrolled. The QTc interval was analyzed during the incidence of SH, and 6 months before and after SH. QTc intervals of 450 ms or longer in men and 460 ms or longer in women were considered abnormally prolonged. RESULTS: The mean age and diabetes duration were 68.1±12.1 and 14.1±10.1 years, respectively. The mean QTc intervals at baseline and SH episodes were 433±33 and 460±33 ms, respectively (P<0.001). One hundred and fourteen patients (54.8%) had a prolonged QTc interval during SH. There was a significant decrease in the prolonged QTc interval within 6 months after SH (QTc interval prolongation during SH vs. after recovery, 54.8% vs. 33.8%, P<0.001). The prolonged QTc interval was significantly associated with baseline QTc interval prolongation (odds ratio, 2.92; 95% confidence interval, 1.22 to 6.96; P=0.016) after adjusting for multiple confounders. CONCLUSION: A prolonged QTc interval at baseline was significantly associated with prolongation of the QTc interval during SH in patients with T2DM, suggesting the necessity of QTc interval monitoring and attention to those with a prolonged QTc interval to prevent SH.
Subject(s)
Female , Humans , Male , Diabetes Mellitus, Type 2 , Electrocardiography , Emergency Service, Hospital , Heart , Hypoglycemia , IncidenceABSTRACT
BACKGROUND: We investigated clinical course and risk factors for diabetic retinopathy (DR) in patients with type 2 diabetes mellitus (T2DM). METHODS: A total of 759 patients with T2DM without DR were included from January 2001 to December 2004. Retinopathy evaluation was performed at least annually by ophthalmologists. The severity of the DR was classified into five categories according to the International Clinical Diabetic Retinopathy Severity Scales. RESULTS: Of the 759 patients, 523 patients (68.9%) completed the follow-up evaluation. During the follow-up period, 235 patients (44.9%) developed DR, and 32 patients (13.6%) progressed to severe nonproliferative DR (NPDR) or proliferative DR (PDR). The mean duration of diabetes at the first diagnosis of mild NPDR, moderate NPDR, and severe NPDR or PDR were 14.8, 16.7, and 17.3 years, respectively. After adjusting multiple confounding factors, the significant risk factors for the incidence of DR risk in patients with T2DM were old age, longer duration of diabetes, higher mean glycosylated hemoglobin (HbA1c), and albuminuria. Even in the patients who had been diagnosed with diabetes for longer than 10 years at baseline, a decrease in HbA1c led to a significant reduction in the risk of developing DR (hazard ratio, 0.73 per 1% HbA1c decrement; 95% confidence interval, 0.58 to 0.91; P=0.005). CONCLUSION: This prospective cohort study demonstrates that glycemic control, diabetes duration, age, and albuminuria are important risk factors for the development of DR. More aggressive retinal screening for T2DM patients diagnosed with DR should be required in order to not miss rapid progression of DR.
Subject(s)
Humans , Albuminuria , Cohort Studies , Diabetes Mellitus, Type 2 , Diabetic Retinopathy , Diagnosis , Follow-Up Studies , Glycated Hemoglobin , Incidence , Korea , Mass Screening , Prospective Studies , Retinaldehyde , Risk Factors , Weights and MeasuresABSTRACT
BACKGROUND: We investigated whether an intensive individualized reinforcement education program could influence the prevention of hypoglycemic events in patients with type 2 diabetes. METHODS: From March 2013 to September 2013, patients aged 35 to 75 years with type 2 diabetes who had not previously participated in diabetes education, and treated with insulin or a sulfonylurea-containing regimen were included in the study. After structured group education, the patients assigned to the intensive individualized education group (IT) were requested to visit for reinforcement. All subjects in the IT were encouraged to self-manage dose adjustments. Participants in both groups (control group [CG, group education only; n=22] and IT [n=24]) attended follow-up visits at 2, 8, 12, and 24 weeks. At each visit, all patients were asked whether they had experienced hypoglycemia. RESULTS: The total study population consisted of 20 men (43.5%; mean age and diabetic duration of 55.9+/-11.0 and 5.1+/-7.3 years, respectively). At 24 weeks, there were no significant differences in hemoglobin A1c values between the CG and IT. The total number of hypoglycemic events per patient was 5.26+/-6.5 in the CG and 2.58+/-2.3 times in the IT (P=0.004). Adherence to lifestyle modification including frequency of exercise, self-monitoring of blood glucose, or dietary habit was not significantly different between the groups. However, adherence to hypoglycemia management, especially the dose adjustment of medication, was significantly higher in the IT compared with the CG. CONCLUSION: Compared with the structured group education, additional IT resulted in additional benefits in terms of avoidance of hypoglycemia and treating hypoglycemia in patients with type 2 diabetes.
Subject(s)
Humans , Male , Blood Glucose , Diabetes Mellitus, Type 2 , Education , Follow-Up Studies , Feeding Behavior , Hypoglycemia , Insulin , Life StyleABSTRACT
BACKGROUND: To investigate whether a history of prior cardiovascular disease (CVD) is associated with severe hypoglycemia (SH) in patients with type 2 diabetes. METHODS: We conducted a prospective cohort study from January 2001 to December 2012 with a median follow-up time of 9.5 years (5,814 person-years). Patients aged 25 to 75 years with type 2 diabetes and without chronic kidney disease were enrolled (n=894), and 624 patients completed follow-up. SH was defined as hypoglycemic episodes requiring hospitalization or medical care in an emergency department. We used the Cox proportional hazards regression analysis to test associations between SH episodes and potential explanatory variables. RESULTS: Among the 624 participants who completed follow-up, 60 patients (9.6%) had previous CVD. Compared to patients without CVD, patients with previous CVD were older, had a longer duration of diabetes and hypertension, received more insulin, and had more diabetic microvascular complications at baseline. During follow-up, 62 patients (9.9%) experienced at least one SH episode (incidence of 1.33 per 100 patient-years). The development of SH was associated with a history of CVD (hazard ratio, 1.99; 95% confidence interval, 1.07 to 3.72; P=0.031) after adjusting for sex, age, diabetic duration, hypertension, hemoglobin A1c levels, diabetic complications, cardiovascular autonomic neuropathy, and insulin use. CONCLUSION: A history of CVD was an independent risk factor for the development of SH in patients with type 2 diabetes mellitus. For patients with CVD, modulation of glycemic targets and diabetic education for the prevention of hypoglycemia should be implemented.
Subject(s)
Humans , Cardiovascular Diseases , Cohort Studies , Diabetes Complications , Diabetes Mellitus, Type 2 , Education , Emergency Service, Hospital , Follow-Up Studies , Hospitalization , Hypertension , Hypoglycemia , Insulin , Prospective Studies , Renal Insufficiency, Chronic , Risk FactorsABSTRACT
We evaluated the prevalence of vitamin B12 deficiency and associated factors in type 2 diabetes patients using metformin. A total of 799 type 2 diabetes patients using metformin was enrolled. Vitamin B12 and folate levels were quantified by chemiluminescent enzyme immunoassay. Vitamin B12 deficiency was defined as vitamin B12 4 ng/mL). The prevalence of vitamin B12 deficiency in metformin-treated type 2 diabetes patients was 9.5% (n = 76), and the mean vitamin B12 level was 662.5 +/- 246.7 pg/mL. Vitamin B12 deficient patients had longer duration of metformin use (P or = 2,000 mg were 2.52 (95% CI, 1.27-4.99, P = 0.008) and 3.80 (95% CI, 1.82-7.92, P or = 10 yr were 4.65 (95% CI, 2.36-9.16, P 1,000 mg) and longer durations (> or = 4 yr) of treatment.
Subject(s)
Aged , Female , Humans , Male , Middle Aged , Area Under Curve , Diabetes Mellitus, Type 2/complications , Folic Acid/blood , Hypoglycemic Agents/adverse effects , Immunoassay , Metformin/adverse effects , Odds Ratio , Patients , Prevalence , ROC Curve , Time Factors , Vitamin B 12/blood , Vitamin B 12 Deficiency/diagnosisABSTRACT
BACKGROUND: This study investigated the rate of relapse of dyslipidemia and the factors which could predict relapse following a short-term statin discontinuation after achieving a target low density lipoprotein cholesterol (LDL-C) level in type 2 diabetic patients without cardiovascular disease (CVD). METHODS: Ninety-nine subjects on rosuvastatin treatment and whose LDL-C level was lower than 100 mg/dL were randomly assigned to discontinue or maintain statin treatment at a 2:1 ratio. The subjects were followed-up after 10 weeks. A relapse of dyslipidemia was defined as a reascent of LDL-C level to greater than 100 mg/dL. RESULTS: The statin discontinuation group had a significant rate of relapse compared to the maintenance group (79% vs. 3%, respectively). Pretreatment and baseline lipid levels, their ratios, and hemoglobin A1c level were significantly different between the relapse and nonrelapse groups. The pretreatment and baseline lipid profiles and their ratios were independently associated with relapse. The pretreatment LDL-C level was the most useful parameter for predicting a relapse, with a cutoff of 123 mg/dL. During the follow-up period, no CVD event was noted. CONCLUSION: The relapse rate of dyslipidemia was high when statins were discontinued in type 2 diabetic patients without CVD. Statin discontinuation should be considered carefully based on the pretreatment lipid profiles of patients.
Subject(s)
Humans , Cardiovascular Diseases , Cholesterol, LDL , Diabetes Mellitus, Type 2 , Dyslipidemias , Follow-Up Studies , Hydroxymethylglutaryl-CoA Reductase Inhibitors , Recurrence , Rosuvastatin CalciumABSTRACT
BACKGROUND: We investigated the relationship between endothelial dysfunction and diabetic retinopathy (DR) in patients with type 2 diabetes. METHODS: We used a cross-sectional design to examine 167 patients with type 2 diabetes mellitus. All patients underwent biochemical and ophthalmological examination. We assessed endothelial dysfunction by a flow-mediated vasodilation method of the brachial artery. Changes in vasodilation (flow-mediated vasodilatation, %FMD) were expressed as percent change over baseline values. RESULTS: The mean+/-standard deviation of patient age was 54.1+/-8.6 years. The %FMD was significantly lower in patients with DR than without DR. The prevalence of retinopathy decreased across increasing tertiles of %FMD. After adjusting for patients' age, sex, diabetes duration, use of insulin, use of antihypertensive, antiplatelet, and lipid lowering medications, systolic blood pressure, fasting plasma glucose, 2-hour plasma glucose, glycated hemoglobin, and urinary albumin excretion, participants with a reduced %FMD were more likely to have DR (odds ratio, 11.819; 95% confidence interval, 2.201 to 63.461; P=0.004, comparing the lowest and highest tertiles of %FMD). CONCLUSION: Endothelial dysfunction was associated with DR, which was most apparent when the endothelial dysfunction was severe. Our study provides insights into the possible mechanism of the influence of endothelial dysfunction on the development of DR.