Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 20 de 58
Filter
1.
Article in English | WPRIM | ID: wpr-924947

ABSTRACT

Background@#High-density lipoprotein cholesterol (HDL-C) plays an important role in the reverse cholesterol transport pathway and prevents atherosclerosis-mediated disease. It has also been suggested that HDL-C may be a protective factor against cancer. However, an inverse correlation between HDL-C and cancer has not been established, and few studies have explored thyroid cancer. @*Methods@#The study participants received health checkups provided by the Korean National Health Insurance Service from 2009 to 2013 and were followed until 2019. Considering the variability of serum HDL-C level, low HDL-C level was analyzed by grouping based on four consecutive health checkups. The data analysis was performed using univariate and multivariate Cox proportional hazard regression models. @*Results@#A total of 3,134,278 total study participants, thyroid cancer occurred in 16,129. In the crude model, the hazard ratios for the association between repeatedly measured low HDL-C levels and thyroid cancer were 1.243, 1.404, 1.486, and 1.680 (P for trend <0.01), respectively, which were significant even after adjusting for age, sex, lifestyle factors, and metabolic diseases. The subgroup analysis revealed that low HDL-C levels likely had a greater impact on the group of patients with central obesity (P for interaction= 0.062), high blood pressure (P for interaction=0.057), impaired fasting glucose (P for interaction=0.051), and hyperlipidemia (P for interaction=0.126). @*Conclusion@#Repeatedly measured low HDL-C levels can be considered a risk factor for cancer as well as vascular disease. Low HDL-C levels were associated with the risk of thyroid cancer, and this correlation was stronger in a metabolically unhealthy population.

2.
Article in English | WPRIM | ID: wpr-898205

ABSTRACT

Background@#Prospective comparative studies on the effects of various antidiabetic agents on bone metabolism are limited. This study aimed to assess changes in bone mass and biochemical bone markers in postmenopausal patients with type 2 diabetes mellitus (T2DM). @*Methods@#This prospective, multicenter, open-label, comparative trial included 264 patients with T2DM. Patients who had received a metformin, or sulfonylurea/metformin combination (Group 1); a thiazolidinedione combination (Group 2); a dipeptidyl peptidase-4 inhibitor (gemigliptin) combination (Group 3); or an sodium-glucose cotransporter 2 inhibitor (empagliflozin) combination (Group 4) were prospectively treated for 12 months; bone mineral density (BMD) and bone turnover marker (BTM) changes were evaluated. @*Results@#The femoral neck BMD percentage changes were −0.79%±2.86% (Group 1), −2.50%±3.08% (Group 2), −1.05%±2.74% (Group 3), and −1.24%±2.91% (Group 4) (P<0.05). The total hip BMD percentage changes were −0.57%±1.79% (Group 1), −1.74%±1.48% (Group 2), −0.75%±1.87% (Group 3), and −1.27%±1.72% (Group 4) (P<0.05). Mean serum BTM (C-terminal type 1 collagen telopeptide and procollagen type 1 amino-terminal propeptide) levels measured during the study period did not change over time or differ between groups. @*Conclusion@#Significant bone loss in the femoral neck and total hip was associated with thiazolidinedione combination regimens. However, bone loss was not significantly associated with combination regimens including gemigliptin or empagliflozin. Caution should be exercised during treatment with antidiabetic medications that adversely affect the bone in patients with diabetes at a high risk of bone loss.

3.
Article in English | WPRIM | ID: wpr-890501

ABSTRACT

Background@#Prospective comparative studies on the effects of various antidiabetic agents on bone metabolism are limited. This study aimed to assess changes in bone mass and biochemical bone markers in postmenopausal patients with type 2 diabetes mellitus (T2DM). @*Methods@#This prospective, multicenter, open-label, comparative trial included 264 patients with T2DM. Patients who had received a metformin, or sulfonylurea/metformin combination (Group 1); a thiazolidinedione combination (Group 2); a dipeptidyl peptidase-4 inhibitor (gemigliptin) combination (Group 3); or an sodium-glucose cotransporter 2 inhibitor (empagliflozin) combination (Group 4) were prospectively treated for 12 months; bone mineral density (BMD) and bone turnover marker (BTM) changes were evaluated. @*Results@#The femoral neck BMD percentage changes were −0.79%±2.86% (Group 1), −2.50%±3.08% (Group 2), −1.05%±2.74% (Group 3), and −1.24%±2.91% (Group 4) (P<0.05). The total hip BMD percentage changes were −0.57%±1.79% (Group 1), −1.74%±1.48% (Group 2), −0.75%±1.87% (Group 3), and −1.27%±1.72% (Group 4) (P<0.05). Mean serum BTM (C-terminal type 1 collagen telopeptide and procollagen type 1 amino-terminal propeptide) levels measured during the study period did not change over time or differ between groups. @*Conclusion@#Significant bone loss in the femoral neck and total hip was associated with thiazolidinedione combination regimens. However, bone loss was not significantly associated with combination regimens including gemigliptin or empagliflozin. Caution should be exercised during treatment with antidiabetic medications that adversely affect the bone in patients with diabetes at a high risk of bone loss.

4.
Article | WPRIM | ID: wpr-832395

ABSTRACT

Background@#Discordances between glycated hemoglobin (HbA1c) levels and glycemic control are common in clinical practice. We aimed to investigate the consistency of the glycation gap with the hemoglobin glycation index (HGI). @*Methods@#From 2016 to 2019, 36 patients with type 2 diabetes were enrolled. HbA1c, glycated albumin (GA), and fasting blood glucose levels were simultaneously measured and 72-hour continuous glucose monitoring (CGM) was performed on the same day. Repeated tests were performed at baseline and 1 month later, without changing patients’ diabetes management. The HGI was calculated as the difference between the measured HbA1c and the predicted HbA1c that was derived from CGM. The glycation gap was calculated as the difference between the measured and GA-based predicted HbA1c levels. @*Results@#Strong correlations were found between the mean blood glucose (MBG)-based HGI and the prebreakfast glucose-based HGI (r=0.867, P<0.001) and between the glycation gap and the MBG-based HGI (r=0.810, P<0.001). A close correlation was found between the MBG-based HGI at baseline and that after 1 month (r=0.729, P<0.001), with a y-intercept of 0 and a positive slope. @*Conclusion@#The HGI and glycation gap were highly reproducible, and the magnitudes of repeated determinations were closely correlated. Patients with similar mean glucose levels may have significantly different HbA1c levels.

5.
Article | WPRIM | ID: wpr-832394

ABSTRACT

Background@#Endothelial-to-mesenchymal transition (EndMT) contributes to inflammatory conditions inducing conversion of endothelial cells (ECs) into activated fibroblasts, promoting fibrotic diseases. Pro-inflammatory cytokine is the most potent inducer of EndMT. We investigated inhibition of interleukin-1β (IL-1β)-induced EndMT by gemigliptin, a dipeptidyl peptidase-IV inhibitor. @*Methods@#We exposed human umbilical vein endothelial cells (HUVECs) to 10 ng/mL IL-1β/20 μM gemigliptin and analyzed the expression of endothelial, smooth muscle, mesenchymal, and osteoblastic markers, bone morphogenetic protein (BMP), Smad, and non-Smad signaling pathway proteins. @*Results@#Morphological changes showed gemigliptin blocked IL-1β-induced EndMT, upregulated EC markers, and downregulated smooth muscle and mesenchymal markers. IL-1β activation of HUVECs is initiated by the BMP/Smad and non-smad BMP signaling pathways. Gemigliptin inhibited IL-1β induction of BMP2 and 7, activin receptor type IA, BMP receptor type IA, and BMP receptor type II. Reversal of IL-1β-mediated inhibition of BMP-induced Smad1/5/8, Smad2, and Smad3 phosphorylation by gemigliptin suggests involvement of the Smad pathway in gemigliptin action. In the non-Smad BMP pathway, gemigliptin treatment significantly increased the deactivation of extracellular regulated protein kinase (ERK), p38, and JNK by IL-1β. Gemigliptin treatment suppressed BMP-2-induced expression of key osteoblastic markers including osterix, runt-related transcription factor 2, and hepcidin during IL-1β-induced EndMT. @*Conclusion@#We demonstrated a novel protective mechanism of gemigliptin against fibrosis by suppressing IL-1β-induced EndMT.

6.
Article in English | WPRIM | ID: wpr-898036

ABSTRACT

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.

7.
Article in English | WPRIM | ID: wpr-890332

ABSTRACT

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.

8.
Article in English | WPRIM | ID: wpr-763694

ABSTRACT

BACKGROUND: The natural course of thyroid cancer nodules and benign nodules is different. This study was to compare the changes in size between thyroid cancer nodules and thyroid benign nodules. The risk factors associated with the changes of thyroid cancer nodules were assessed. METHODS: This study contains retrospective observational and prospective analysis. A total of 113 patients with 120 nodules were recruited in the cancer group, and 116 patients with 119 nodules were enrolled in the benign group. Thyroid ultrasonography was performed at least two times at more than 1-year interval. RESULTS: The mean follow-up durations were 29.5±18.8 months (cancer group) and 31.9±15.8 months (benign group) (P=0.32). The maximum diameter change in length was 0.36±0.97 mm/year in the cancer group and –0.04±0.77 mm/year in the benign group (P<0.01). The volume was significantly increased in the cancer group compared with the benign group (0.06±0.18 mL/year vs. 0.004±0.05 mL/year, respectively, P<0.01; 26.9%±57.9%/year vs. 1.7%±26.0%/year, P<0.01). Initial maximum diameter (β=0.02, P<0.01) and initial volume (β=0.13, P<0.01) were significantly associated with volume change (mL)/year. Initial maximum standardized uptake value did not predict the nodule growth. CONCLUSION: It is suggested that thyroid cancer nodules progress rapidly compared with benign nodules. Initial size and volume of nodule were independent risk factors for cancer nodule growth.


Subject(s)
Biopsy, Fine-Needle , Follow-Up Studies , Humans , Prospective Studies , Retrospective Studies , Risk Factors , Thyroid Gland , Thyroid Neoplasms , Thyroid Nodule , Tumor Burden , Ultrasonography
9.
Article in English | WPRIM | ID: wpr-717359

ABSTRACT

BACKGROUND: Whether pancreatic steatosis has a local or systemic effect, like ectopic fat of other major organs, remains unknown. Data on the influence of pancreatic steatosis on microvascular complication are rare. Therefore, we investigated the relationship between pancreatic steatosis and diabetic retinopathy (DR) in patients with type 2 diabetes mellitus (T2DM). METHODS: The attenuation of three pancreatic regions (head, body, and tail) and the spleen (S) in 186 patients with T2DM was measured using non-enhanced computed tomography imaging. We used three parameters for the assessment of pancreatic steatosis (‘P’ mean: mean attenuation of three pancreatic regions; P–S: difference between ‘P’ mean and ‘S’; P/S: the ‘P’ mean to ‘S’ ratio). The presence of DR was assessed by an expert ophthalmologist using dilated fundoscopy. RESULTS: The average P mean was 29.02 Hounsfield units (HU), P–S was −18.20 HU, and P/S was 0.61. The three pancreatic steatosis parameters were significantly associated with the prevalence of DR in non-obese T2DM patients. In the non-obese group, the odds ratios of P mean, P–S, and P/S for the prevalence of DR, after adjustment for age, sex, and glycosylated hemoglobin level, were 2.449 (P=0.07), 2.639 (P=0.04), and 2.043 (P=0.02), respectively. CONCLUSION: In this study, pancreatic steatosis was significantly associated with DR in non-obese patients with T2DM. Further studies are necessary to clarify the causal relationship between pancreatic steatosis and the development of DR.


Subject(s)
Diabetes Mellitus, Type 2 , Diabetic Retinopathy , Fats , Glycated Hemoglobin A , Humans , Odds Ratio , Pancreas , Prevalence , Spleen
10.
Article in English | WPRIM | ID: wpr-227305

ABSTRACT

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)
Cardiovascular Diseases , Cohort Studies , Coronary Artery Disease , Diabetes Mellitus, Type 2 , Follow-Up Studies , Humans , Hypertension , Insulin , Lipoprotein(a) , Peptidyl-Dipeptidase A , Proportional Hazards Models , Prospective Studies , Risk Factors , Stroke
11.
Article in English | WPRIM | ID: wpr-728538

ABSTRACT

Here, we investigated whether hyperglycemia and/or free fatty acids (palmitate, PAL) aff ect the expression level of bone morphogenic protein 4 (BMP4), a proatherogenic marker, in endothelial cells and the potential role of BMP4 in diabetic vascular complications. To measure BMP4 expression, human umbilical vein endothelial cells (HUVECs) were exposed to high glucose concentrations and/or PAL for 24 or 72 h, and the effects of these treatments on the expression levels of adhesion molecules and reactive oxygen species (ROS) were examined. BMP4 loss-of-function status was achieved via transfection of a BMP4-specific siRNA. High glucose levels increased BMP4 expression in HUVECs in a dose-dependent manner. PAL potentiated such expression. The levels of adhesion molecules and ROS production increased upon treatment with high glucose and/or PAL, but this eff ect was negated when BMP4 was knocked down via siRNA. Signaling of BMP4, a proinflammatory and pro-atherogenic cytokine marker, was increased by hyperglycemia and PAL. BMP4 induced the expression of infl ammatory adhesion molecules and ROS production. Our work suggests that BMP4 plays a role in atherogenesis induced by high glucose levels and/or PAL.


Subject(s)
Atherosclerosis , Diabetes Mellitus , Diabetic Angiopathies , Endothelial Cells , Fatty Acids, Nonesterified , Glucose , Human Umbilical Vein Endothelial Cells , Humans , Hyperglycemia , Reactive Oxygen Species , RNA, Small Interfering , Transfection
12.
Article in Korean | WPRIM | ID: wpr-726753

ABSTRACT

Diabetic muscle infarction (DMI) is a rare condition that usually occurs in diabetic patients who have longstanding microvascular complication. The typical presentation is a painful swelling with abrupt onset in the lower limbs, particularly involving hyper-intense signals in T2-weighted magnetic resonance imaging (MRI) images. The treatment consists of bed rest, analgesics, and physical therapy. The authors encountered a case of DMI with bilateral tender swelling on the anteromedial aspect of the thighs. DMI is less likely to develop in patients with good glycemic control. Recently, however, a few cases demonstrated that DMI can also develop in patients with good glucose control. However, diffuse and extensive infarction of muscle, such as in our case, is rare. It is important to consider differential diagnoses in order to avoid misdiagnosis and non-essential treatment such as overuse of antibiotics or steroid treatment. In this case, we diagnosed the patient using MRI, muscle biopsy, and electromyography and successful treatment involved bed rest and analgesics. We herein report a case of 76-year-old man with very extensive and diffuse DMI in spite of well-controlled type 2 diabetes.


Subject(s)
Aged , Analgesics , Anti-Bacterial Agents , Bed Rest , Biopsy , Diabetes Complications , Diabetes Mellitus , Diagnosis, Differential , Diagnostic Errors , Electromyography , Glucose , Humans , Infarction , Lower Extremity , Magnetic Resonance Imaging , Thigh
13.
Article in English | WPRIM | ID: wpr-145679

ABSTRACT

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)
Cardiovascular Diseases , Diabetes Mellitus, Type 2 , Diabetic Nephropathies , Follow-Up Studies , Glycated Hemoglobin A , Humans , Hypertension , Hypoglycemia , Insulin , Mortality
14.
Article in English | WPRIM | ID: wpr-111910

ABSTRACT

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)
Albuminuria , Cohort Studies , Diabetes Mellitus, Type 2 , Diabetic Retinopathy , Diagnosis , Follow-Up Studies , Glycated Hemoglobin A , Humans , Incidence , Korea , Mass Screening , Prospective Studies , Retinaldehyde , Risk Factors , Weights and Measures
15.
Article in English | WPRIM | ID: wpr-121892

ABSTRACT

OBJECTIVE: This study investigated the association between small-dense low-density lipoprotein (sdLDL) and diabetic nephropathy (DN) in type 2 diabetic patients. METHODS: A total of 172 type 2 diabetic patients (95 men and 77 women) who had not taken lipid-lowering agents were enrolled in this study. Measured LDL cholesterol fractionates into seven parts (LDL1 through 7) according to the size and the extent of charge. Using this system, we analyzed mean LDL particle size and the proportion of sdLDL (the percent of LDL3 through 7 over whole LDL). DN was defined as the albumin-to-creatinine ratio (ACR) ≥30 mg/g after excluding other causes of proteinuria. RESULTS: The mean LDL cholesterol, LDL cholesterol size, proportion of sdLDL and ACR did not differ significantly between males and females. The presence of DN was negatively correlated with mean LDL size (r=-0.33, p value=0.02) and positively correlated with the proportion of sdLDL (r=0.34, p value=0.01) in females but not in males. After adjusting for other confounding factors related to DN, mean LDL size and proportion of sdLDL remained independent risk factors for DN in females [for mean LDL size, Odds ratio (OR)=0.86, 95% Confidence interval (CI)=0.77-0.96, p=0.01; for proportion of sdLDL, OR=1.07, 95% CI: 1.10-1.12, p=0.01], but not in males. CONCLUSION: sdLDL is closely related to DN in female type 2 diabetic patients. Further studies are necessary to clarify the association of sdLDL and DN with gender.


Subject(s)
Cholesterol, LDL , Diabetes Mellitus, Type 2 , Diabetic Nephropathies , Female , Humans , Lipoproteins , Male , Odds Ratio , Particle Size , Proteinuria , Risk Factors
16.
Article in English | WPRIM | ID: wpr-154201

ABSTRACT

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)
Diabetes Mellitus, Type 2 , Electrocardiography , Emergency Service, Hospital , Female , Heart , Humans , Hypoglycemia , Incidence , Male
17.
Article in English | WPRIM | ID: wpr-154200

ABSTRACT

BACKGROUND: Some patients with type 2 diabetes mellitus (T2DM) do not develop diabetic kidney disease (DKD) despite the presence of advanced diabetic retinopathy (DR). We aimed to investigate the presence of DKD and its risk factors in patients with T2DM and advanced DR. METHODS: We conducted a cross-sectional study in 317 patients with T2DM and advanced DR. The phenotypes of DKD were divided into three groups according to the urine albumin/creatinine ratio (uACR, mg/g) and estimated glomerular filtration rate (eGFR, mL/min/1.73 m²): no DKD (uACR <30 and eGFR ≥60), non-severe DKD (uACR ≥30 or eGFR <60), and severe DKD (uACR ≥30 and eGFR <60). Mean systolic and diastolic blood pressure, mean glycosylated hemoglobin (HbA1c) level, and HbA1c variability (standard deviation [SD] of serial HbA1c values or HbA1c-SD) were calculated for the preceding 2 years. RESULTS: The prevalence of no DKD, non-severe DKD, and severe DKD was 37.2% (n=118), 37.0% (n=117), and 25.8% (n=82), respectively. HbA1c-SD and the triglyceride/high density lipoprotein cholesterol (TG/HDL-C) ratio correlated positively with uACR and negatively with eGFR. Multiple linear regression analyses showed that the HbA1c-SD and TG/HDL-C ratio were significantly related with eGFR. Multiple logistic regression analyses after adjusting for several risk factors showed that HbA1c-SD and the TG/HDL-C ratio were significant risk factors for severe DKD. CONCLUSION: The prevalence of DKD was about 60% in patients with T2DM and advanced DR. HbA1c variability and TG/HDL-C ratio may affect the development and progression of DKD in these patients.


Subject(s)
Blood Pressure , Cholesterol , Cholesterol, HDL , Cross-Sectional Studies , Diabetes Mellitus, Type 2 , Diabetic Nephropathies , Diabetic Retinopathy , Glomerular Filtration Rate , Glycated Hemoglobin A , Humans , Linear Models , Lipoproteins , Logistic Models , Phenotype , Prevalence , Risk Factors , Triglycerides
18.
Article in English | WPRIM | ID: wpr-149423

ABSTRACT

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)
Cardiovascular Diseases , Cohort Studies , Diabetes Complications , Diabetes Mellitus, Type 2 , Education , Emergency Service, Hospital , Follow-Up Studies , Hospitalization , Humans , Hypertension , Hypoglycemia , Insulin , Prospective Studies , Renal Insufficiency, Chronic , Risk Factors
19.
Journal of Korean Diabetes ; : 116-123, 2014.
Article in Korean | WPRIM | ID: wpr-726975

ABSTRACT

BACKGROUND: Gestational diabetes mellitus (GDM) is a hyperglycemic condition caused by increased insulin resistance and impaired insulin secretion during pregnancy. It is known to be temporary, but it can cause perinatal complications in the mother and baby. Additionally, it may progress to type 2 diabetes mellitus (T2DM). In the present study, we evaluated the risk factors for complications and progression to T2DM in patients with GDM. METHODS: The study included 130 pregnant women who were diagnosed with GDM at gestational weeks 24-28 in 2011. Body mass index and the levels of glucose, total cholesterol, lipoproteins, and coagulation factors (von Willebrand factor and plasminogen activator inhibitor-1) were assessed in all patients. RESULTS: The level of high-density lipoprotein (HDL) was significantly lower and the triglyceride/HDL ratio and coagulation factor levels were significantly higher in the group of patients with perinatal complications compared to those in the group of patients without complications. After delivery, the level of HDL was lower and the value of homeostasis model assessment of insulin resistance (HOMA-IR) was higher in women with impaired glucose metabolism compared to those in women with normal glucose metabolism. In logistic regression analysis, perinatal complications were independently associated with HDL and PAI-1 levels (OR = 0.929 and 1.101, respectively). CONCLUSION: The findings of our study show that the levels of HDL and coagulation factors are notable risk factors of perinatal complications. Additionally, we showed that lower HDL level may influence the progression to T2DM. Large-scale population studies are needed to verify our findings.


Subject(s)
Blood Coagulation Factors , Body Mass Index , Cholesterol , Diabetes Mellitus , Diabetes Mellitus, Type 2 , Diabetes, Gestational , Female , Glucose , Homeostasis , Humans , Insulin , Insulin Resistance , Lipoproteins , Lipoproteins, HDL , Logistic Models , Metabolism , Mothers , Plasminogen Activator Inhibitor 1 , Plasminogen Activators , Postpartum Period , Pregnancy , Pregnant Women , Risk Factors , von Willebrand Factor
20.
Article in English | WPRIM | ID: wpr-70749

ABSTRACT

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 , Area Under Curve , Diabetes Mellitus, Type 2/complications , Female , Folic Acid/blood , Humans , Hypoglycemic Agents/adverse effects , Immunoassay , Male , Metformin/adverse effects , Middle Aged , Odds Ratio , Patients , Prevalence , ROC Curve , Time Factors , Vitamin B 12/blood , Vitamin B 12 Deficiency/diagnosis
SELECTION OF CITATIONS
SEARCH DETAIL