Background/Aims: Distinguishing gastric ectopic pancreas (GEP) from malignant tumors is relatively difficult. This study evaluated the endosonography findings of pathologically proven GEP. Methods: Thirty-one patients diagnosed with GEP based on a histopathological analysis from January 2004 to July 2018 were enrolled in this study. All patients underwent EUS and an endoscopic resection. Results: Seventeen patients were female, and the median age was 41.1 years (range, 14-74). The lesions were localized most commonly in the antrum. The mean size of the GEP was 10.6 mm (range, 7-15). Superficial type lesions, lesions with heterogeneous echogenicity, mixed pattern lesions, and lesions with indistinct borders were commonly observed on EUS. Calcification, anechoic duct-like structures, and thickening of the muscularis propria were observed in some patients. Endoscopic mucosal resection (41.9%) and endoscopic submucosal dissection (58.1%) were performed. The mean procedure time was 22.5 minutes. Complete resection was achieved for 71% of patients. No statistically significant results between the endosonography findings and complete resection rates were obtained. The mean follow-up esophagogastroduodenoscopy duration was 4.5 months. None of the patients presented with residual lesions on subsequent endoscopy. Conclusions EUS can help identify the features of GEP. Careful observations of the EUS findings can avoid unnecessary removal of GEP.

BACKGROUND: Little is known about the relative contribution of long-term glycemic variability to the risk of macrovascular complications in type 2 diabetes. This study was conducted to evaluate the effect of A1C variability on the progression of carotid artery intima-media thickness (IMT) in type 2 diabetic patients. METHODS: Among type 2 diabetic patients who visited Hallym University Sacred Heart Hospital from March 2007 to September 2009, 120 patients who had carotid artery IMT measured annually and A1C checked every three months for at least one year were analyzed. Individual A1C variability was defined as the standard deviation (SD) of five A1C levels taken every three months for approximately one year. Change in IMT was defined as an increase in IMT on follow-up measurement. The association between the SD of A1C and changes in IMT was evaluated. RESULTS: With greater A1C variability, there was a greater increase in the mean IMT (r = 0.350, P < 0.001) of the carotid artery. After adjusting for confounding factors that may influence IMT, A1C variability was significantly associated with the progression of IMT (r = 0.222, P = 0.034). However, the SD of A1C was not a significant independent risk factor for the progression of IMT in multiple regression analysis (beta = 0.158, P = 0.093). CONCLUSION: Higher A1C variability is associated with IMT progression in type 2 diabetic patients; however, it is not an independent predictor of IMT progression. Overall glycemic control is the most important factor in the progression of IMT.
Atherosclerosis ; Carotid Arteries ; Carotid Artery Diseases ; Diabetes Mellitus, Type 2 ; Follow-Up Studies ; Heart ; Humans ; Risk Factors

BACKGROUND AND OBJECTIVES: It is well known that the higher the blood pressure, the greater the chance of cardiovascular disease, but the factors that are responsible for this association remain largely unknown. We sought to determine whether blood pressure, in a dose-dependent way, is associated with systemic inflammation, which is a known risk factor for cardiovascular events. SUBJECTS AND METHODS: We analyzed the data from 5,626 participants, aged 40-65 years, of the Third National Health and Nutrition Examination Survey (NHANES III). We quantified the blood pressure by dividing the participants into the normal, pre-, stage 1 and stage 2 hypertension groups based on the Joint National Committee 7 (JNC) classification. We used multiple linear and logistic regression models to determine the relationship between blood pressure and the levels of inflammatory markers. RESULTS: After adjustments were made for various co-morbidities, participants with stage 2 systolic hypertension had higher circulating leukocyte levels [840/microliter (95% confidence interval [CI], 374 to 939/microliter)] and fibrinogen levels [24.5 mg/dL (95% CI, 8.9 to 31.9 mg/dL)] than those participants with normal blood pressure. They also showed higher circulating C-reactive protein levels (C-reactive protein>10.0 mg/L: p for trend=0.001). There was a dose-dependent increase for the circulating levels of the risk factors across the different levels of systolic blood pressure, but not for diastolic blood pressure. CONCLUSION: These findings demonstrate that an elevated systolic blood pressure is an independent risk factor for systemic inflammation and this may explain why systolic hypertension is a risk factor for atherosclerosis and cardiovascular events.
Atherosclerosis ; Blood Pressure ; C-Reactive Protein ; Cardiovascular Diseases ; Classification* ; Fibrinogen ; Hypertension* ; Inflammation ; Joints ; Leukocytes ; Logistic Models ; Nutrition Surveys ; Risk Factors*

BACKGROUND: Coronary artery disease (CAD) has recently become one of the major causes of mortality and morbidity in Korea. However, not much epidemiologic and demographic data has yet been reported. The purpose of this study was to investigate the clinical features as well as the prognostic factors of patients with CAD. METHODS: We prospectively enrolled 1,665 consecutive patients with CAD who had been admitted to the Catholic University Hospitals from December 1999 to April 2003. RESULTS: Acute myocardial infarction (AMI) was the most common cause of admission (n=715, 42.9%). Dyslipidemia, hypertension and smoking were the most common risk factors. More than 70% of the patients who underwent percutaneous coronary intervention (PCI) received stent implantation. A total of 965 (612 males) patients were followed at least for 6 months (the mean follow-up duration was 23.8+/-12.2 months). The incidence rates of major adverse cardiac events (MACE: cardiac death, acute myocardial infarction, target vessel revascularization) and cardiac death were 15.1% (n=146) and 2.2% (n=21), respectively. There was no difference in overall survival between the patients treated with medical therapy and those treated with PCI. By Cox regression analysis, the independent prognostic factors for MACE were PCI (95% CI: 1.75-4.85; p<0.01) and multivessel disease (95% CI: 1.03-2.04; p<0.05), and the independent prognostic factors for cardiac death were medical therapy (95% CI: 1.08-14.41; p<0.05) and old age (95% CI: 1.13-16.13; p<0.05). CONCLUSIONS: There was no difference in overall survival between the patients treated with medical therapy and those treated with PCI. However, PCI was superior to medical therapy for preventing death of the patients with acute coronary syndrome.
Acute Coronary Syndrome ; Coronary Artery Disease* ; Coronary Disease ; Coronary Vessels* ; Death ; Dyslipidemias ; Follow-Up Studies ; Heart* ; Hospitals, University ; Humans ; Hypertension ; Incidence ; Korea ; Mortality ; Myocardial Infarction ; Percutaneous Coronary Intervention ; Prognosis ; Prospective Studies ; Risk Factors ; Smoke ; Smoking ; Stents

BACKGROUND AND OBJECTIVES: Passive smoking increases the risk of cardiovascular disease, but the factors responsible for this association remain largely unknown. We sought to determine whether passive smoke exposure is associated with systemic inflammation in a dose-dependent fashion, which is a known risk factor for cardiovascular events. SUBJECTS AND METHODS: We analyzed the data of self-reported non-smokers, > or =40 years of age, who were from the Third National Health and Nutrition Examination Survey (n=6,595). We quantified the passive nicotine exposure by dividing the non-smokers into quartiles, as based on the serum cotinine values. We used multiple linear and logistic regression models to determine the independent relationship between serum cotinine and the levels of C-reactive protein, fibrinogen and leukocytes, and the platelet expression. RESULTS: After adjustments were done for age, gender, body mass index and race, the participants in the highest serum cotinine quartile (quartile 4) had circulating platelet, fibrinogen and homocysteine levels that were 6,893/microliter higher (95% confidence interval [CI]: 1,886 to 11,900/microliter, p=0.007), 8.74 mg/dL (95% CI: 2.63 to 14.84 mg/dL, p=0.005) and 0.90 micromol/L (95% CI: 0.36 to 1.43 (micromol/L, p=0.001), respectively, than in those in the lowest quartile of serum cotinine (quartile 1). There was a dose-dependent increase in the circulating fibrinogen, homocysteine and platelet levels across the quartiles of cotinine. CONCLUSION: These findings indicate that even among nonsmokers, elevated serum cotinine is an independent risk factor for systemic inflammation. This suggests that passive smoke exposure promotes systemic inflammatory response in a dose-dependent fashion. These observations may explain why passive smoking is a risk factor for atherosclerosis and cardiovascular events.
Atherosclerosis ; Blood Platelets ; Body Mass Index ; C-Reactive Protein ; Cardiovascular Diseases ; Continental Population Groups ; Cotinine ; Epidemiology ; Fibrinogen ; Homocysteine ; Humans ; Inflammation* ; Leukocytes ; Logistic Models ; Nicotine ; Nutrition Surveys ; Observational Study* ; Risk Factors ; Smoke* ; Tobacco Smoke Pollution

BACKGROUND AND OBJECTIVES: Chlamydia pneumoniae (CP) has been linked with atherosclerosis. While several studies have shown that CP contributes to the acceleration of atherosclerotic lesions, any studies on the initiation of atherosclerosis are sparse. The present study investigated whether CP infection could initiate atherosclerotic lesions in rats that are known to be resistant to atherosclerosis; further, we investigated if these lesions do form, then how does the CP participate in this and develop of atherosclerosis in these rats. MATERIALS AND METHODS: Thirty 11-week-old Otsuka Long-Evans Tokushima Fatty (OLETF) rats, thirty type 2 diabetic rats and thirty age-matched Long-Evans Tokushima Fatty (LETO) rats that were maintained on a high-cholesterol diet were either mock-inoculated or inoculated intranasally 3 times at 11, 13 and 15 weeks of age. The serum levels of the lipid profiles, plasminogen activator inhibitor-1 (PAI-1), monocyte chemoattractant protein-1 (MCP-1) and C-reactive protein (CRP) were measured by performing ELISA at 24 weeks and 40 weeks of age. The atherosclerotic lesion areas were analyzed, and immunohistochemical staining using chlamydia genus-specific monoclonal antibody and PDGF-B was performed in the ascending aorta at 40 weeks of age. RESULTS: Immunohistochemical staining with using specific monoclonal antibody demonstrated CP infection in the vessel walls. The serum PAI-1 level of the OLETF rats was higher than that of the LETO rats (p<0.05) regardless of the state of the CP infection, but there were no differences in the serum MCP-1 and CRP levels between the OLETF rats and the LETO rats. While no atherosclerotic lesion was observed in the mock-infected LETO rats, early-to-advanced atherosclerotic lesions were found in the other rat groups. CP-infected OLETF rats showed more advanced atherosclerotic lesions and greater mean lesion areas than the other rat groups (LT-N, 0 mm2; LETO-CP, 3.29+/-1.23 mm2; OT-N, 4.91+/-2.11 mm2; OT-CP, 9.20+/-4.62 mm2)(p<0.05). The characteristics of the atherosclerotic lesions in the rats were intimal thickening that was mainly composed of smooth muscle cells. The atherosclerotic lesion area positively correlated with the presence and the extent of PDGF-B staining in the aortic wall (p<0.01). CONCLUSION: Chronic infection of CP in the vessel walls initiated the development of atherosclerosis in the LETO rats and it accelerated the atherosclerosis in the OLETF rats. CP-induced smooth muscle proliferation and the resultant intimal thickening may be mediated by PDGF-B in these atherosclerotic lesions.
Acceleration ; Animals ; Aorta ; Atherosclerosis* ; C-Reactive Protein ; Chemokine CCL2 ; Chlamydia* ; Chlamydophila pneumoniae* ; Diet ; Enzyme-Linked Immunosorbent Assay ; Muscle, Smooth ; Myocytes, Smooth Muscle ; Plasminogen Activator Inhibitor 1 ; Plasminogen Activators ; Rats* ; Rats, Inbred OLETF

BACKGROUND AND OBJECTIVES: This study was designed to investigate whether the serum concentration of the carboxy-terminal propeptide of procollagen type I PIP, a marker of myocardial fibrosis, was related to the change of the ventricular filling dynamics in patients with early type 2 diabetes mellitus (DM). SUBJECTS AND METHODS: Echocardiography was performed in 28 patients with type 2 DM and 32 age-matched healthy controls, ranging from 31-69 years of age, with normal left ventricular (LV) systolic function and ECG at rest. Subjects with diabetic complications, including microalbuminuria, nephropathy (Cr>1.3 mg/dL), severe obesity (BMI> or =30 kg/m2), LV hypertrophy (LV septal thickness and/or posterior wall thickness 12 mm on M-mode) and hypertension, were excluded. The serum concentrations of PIP and Transforming growth factor TGF-beta1 were measured by enzyme immunoassay methods. RESULTS: The type 2 DM group had lower mitral (Type 2 DM vs. Control: 0.88+/-0.28 vs. 1.17+/-0.34, p<0.01) and tricuspid E/A ratios (1.15+/-0.25 vs. 1.30+/-0.25, p=0.01) than the control group. The level of serum PIP was higher (p<0.05) in patients with type 2 DM than in the control group (131.1+/-45.6 vs. 109.3+/-32.5). The difference in the duration between transmitral forward (A) and pulmonary venous retrograde (Ar) waves (A-Ar) was considered an estimate of a passive diastolic function. A-Ar was inversely related with the serum PIP level in type 2 diabetes (r=-0.43, p=0.03). CONCLUSION: These results show a relationship between the LV diastolic function and the serum concentration of PIP in early type 2 DM. These findings suggest that the determination of the serum level of PIP is a useful method for the screening and early diagnosis of myocardial fibrosis associated with DM.
Collagen Type I ; Diabetes Complications ; Diabetes Mellitus ; Diabetes Mellitus, Type 2* ; Diastole ; Early Diagnosis ; Echocardiography ; Electrocardiography ; Fibrosis* ; Humans ; Hypertension ; Hypertrophy ; Immunoenzyme Techniques ; Mass Screening ; Obesity, Morbid ; Procollagen ; Transforming Growth Factor beta1 ; Transforming Growth Factors

BACKGROUND AND OBJECTIVES: Receptor for advanced glycosylation end product (RAGE) plays an important role in the development of myocardial fibrosis in diabetics. Activation of peroxisome proliferator activated receptor (PPAR)-gamma agonist, rosiglitazone, reduces the RAGE expression. We investigated whether rosiglitazone could prevent left ventricle (LV) diastolic dysfunction and attenuate the myocardial fibrosis in a type 2 diabetic rat model. MATERIALS AND METHODS: Otsuka Long-Evans Tokushima Fatty (OLETF) rats were treated with rosiglitazone (20 mg/kg/d) for 20 weeks. At the age of 20 and 40 weeks, all rats underwent intraperitoneal glucose tolerance tests, hemodynamic studies and Doppler echocardiography. At the age of 40 weeks, the hearts were examined by performing histopathological and immunohistochemical analyses. RESULTS: At the age of 40 weeks, rosiglitazone significant improved the parameters of the LV diastolic function such as the E/A ratio (treated vs. untreated: 1.7+/-0.1 vs. 1.5+/-0.1, p<0.05), the deceleration time and the isovolumic relaxation time in the OLETF rats, and this was correlated histologically to the reduced LV collagen volume fraction in the rosiglitazonetreated OLETF rats (3.2+/-1.3% vs. 5.7+/-2.0%, respectively, p<0.001). Rosiglitazone also significantly reduced the percentage of staining of the LV CTGF (7.4+/-2.5% vs. 15.4+/-4.7%, respectively, p<0.001) and RAGE (1.1+/-0.4% vs. 2.0+/-0.8%, respectively, p<0.001), as compared with the untreated OLETF rats. CONCLUSION: These results suggest that rosiglitazone could prevent LV diastolic dysfunction and attenuate myocardial fibrosis in type 2 diabetic rats by its inhibition of the RAGE and CTGF expression. PPAR-gamma agonist may provide a potential therapeutic approach for diabetic heart disease.
Animals ; Collagen ; Deceleration ; Echocardiography, Doppler ; Fibrosis* ; Glucose Tolerance Test ; Glycosylation ; Heart ; Heart Diseases ; Heart Ventricles ; Hemodynamics ; Intercellular Signaling Peptides and Proteins ; Models, Animal* ; Peroxisomes ; Rage ; Rats* ; Rats, Inbred OLETF ; Relaxation

BACKGROUND: Radioiodine treatment is effective for the removal of remnant thyroid tissues after thyroidectomy in patients with differentiated thyroid carcinoma. To induce the elevation of serum TSH level which facilitates the uptake of radioiodine into remnants, a 4 to 6 week interval between thyroidectomy and radioiodine administration has been established. During the period of preparation, most patients have experienced overt symptoms of hypothyroidism which have led to the development of alternative strategies. Some reports have suggested that the interval could be reduced to about 3 weeks with less symptoms. We reevaluated the adequate time needed for the elevation of serum TSH level above 30microU/mL after thyroidectomy. METHODS: Forty five patients who had undergone total thyroidectomy for differentiated thyroid carcinoma were investigated. Serum TSH and free T4 levels were measured one or more times within 3 weeks after operation(total 97 blood samples). Eighty nine blood samples were obtained within 15 days. RESULTS: In 41 patients (91.1%) serum TSH levels increased to 30 microU/mL until 15 days after operation. Until postoperative 21 days, serum TSH levels in all the other patients reached 30microU/mL. In linear equation, the daily increment of serum TSH levels was 2.62microU/mL for the first 8 days after operation and 5.34micorU/mL for the next 7 days. The half-life of serum free T4 levels showed marked individual variations. CONCLUSION: Measurement of serum TSH level at about 15 days after total thyroidectomy for differentiated thyroid carcinoma may be useful in determining the time of radioiodine administration.
Half-Life ; Humans ; Hypothyroidism ; Thyroid Gland* ; Thyroid Neoplasms* ; Thyroidectomy ; Thyrotropin

Human chorionic gonadotropin(HCG) is a member of the glycoproteins family synthesized by the placenta, which consists of 2 noncovalently joined subunits(alpha(alpha) and beta(beta)). The alpha- and beta-subunits have a structural homology with the alpha- and beta-subunits of TSH and LH. The thyrotropic action of HCG results from its structural similarity to TSH, so beta-HCG can bind to the TSH receptor in the thyroid gland. A high level of HCG accompanied by an increased thyroid hormone level, can be observed in gestational trophoblastic disease (GTD), such as a hydatidiform mole or a choriocarcinoma, but the clinical symptoms of hyperthyroidism are rarely observed. We experienced a case of Hashimoto's thyroiditis, where the patient was diagnosed with T3-thyrotoxicosis, which had initially been induced by excess beta-HCG due to an H-mole; after evacuation of the H-mole, the condition was diagnosed as hypothyroidism. It has been speculated that a patient with Hashimoto's thyroiditis could have hyperthyroidism, induced by beta-HCG, due to an H-mole
Choriocarcinoma ; Chorion ; Female ; Gestational Trophoblastic Disease ; Glycoproteins ; Humans ; Hydatidiform Mole* ; Hyperthyroidism ; Hypothyroidism ; Placenta ; Pregnancy ; Receptors, Thyrotropin ; Thyroid Gland* ; Thyroiditis*