Objective: Mood instability (MI) is a clinically significant trait associated with psychiatric disorders. However, there are no concise measurements to evaluate MI. The initial Mood Instability Questionnaire-Trait (MIQ-T) was developed to fill this gap. The current study aimed to create a short form of MIQ-T (MIQ-T-SF) that measures MI with high validity and reliability in the Korean general population. Methods: Of the 59 items in the MIQ-T, 17 items were chosen for the MIQ-T-SF following the factor analysis process. In total, 540 participants completed the MIQ-T-SF. Cronbach’s alpha and McDonald’s omega were used to evaluate reliability. Exploratory factor analysis (EFA) and confirmatory factor analysis (CFA) were used to determine construct validity. Concurrent validity was confirmed via comparisons with Personality Assessment Inventory-Borderline Features Scale. Measurement invariance across gender and age groups was confirmed before analyzing differences in scores using Kruskal-Wallis test. Results: The MIQ-T-SF displayed expected correlations and high internal consistency (α=0.71–0.90, Ωt=0.72–0.92). Using EFA and CFA, a five-factor structure was confirmed. Measurement invariance was supported, and gender differences were observed. Conclusion The MIQ-T-SF is an accurate and reliable method to detect MI in the Korean general population. The study’s results offer new perspectives for future studies on MI.

Objective: Mood disorder and borderline personality pathology (BPP) are frequently comorbid and relate to childhood trauma. We investigated the relationship between childhood trauma and BPP features in mood disorder patients versus controls. Methods: A total of 488 mood disorder patients, particularly major depressive disorder (MDD), bipolar I disorder (BD I), and bipolar II disorder (BD II), and 734 controls were included. We examined between-group BPP-related differences and correlated between BPP and childhood trauma using the Childhood Trauma Questionnaire-Short Form (CTQ) and the Personality Assessment Inventory–Borderline Features Scale. Results: BD II patients showed significantly higher BPP. Emotional abuse and neglect were prominently associated with BPP, while affective instability and negative relationships exhibited a stronger association with childhood trauma. We also found a positive relationship between childhood trauma and BPP in MDD, BD I, and BD II patients. Conclusion The findings of the present study imply that BPP features are more likely to be found in patients with BD II than BD I or MDD. Mood disorder patients with severe childhood trauma may have higher BPP features. Thus, further study of the relationship between childhood trauma and BPP features could improve the therapeutic approaches and help understand patients with mood disorders.

OBJECTIVES: This study aimed to investigate the medication adherence rate and related factors in chronic schizophrenia. METHODS: A total of 65 (34 male and 31 female) outpatients with schizophrenia and with less than 5 years schizophrenia treatment were randomly selected to participate in the study survey. Medication adherence rate was evaluated by counting remaining tablets. The Korean version of Drug Attitude Inventory-10 (KDAI-10) was used to determine the subjective adherence rate. Adherence was defined as a patient taking more than 80% of their total prescribed medication. Positive KDAI-10 scores indicate good adherence. RESULTS: The rate of good adherence was 87.7%. Our analysis showed that an older age (r=0.323, p=0.009), longer duration of illness (r=0.296, p=0.017), employment (F=4.41, p=0.016), remaining married (F=5.26, p=0.008), and being supported by family members, especially spouse or siblings (F=3.02, p=0.025) were significantly associated with good adherence. Presence of symptoms such as delusion (p=0.033) and hallucination (p=0.032) were related to poor adherence. CONCLUSION: The results indicate that future study should investigate patient characteristics associated with medication adherence and analyze the clinician/patient alliance and its affect on adherence. The results also show that further studies might be useful in developing and validating measures of adherence, as well as in designing and evaluating interventions to improve adherent behaviors.
Delusions ; Employment ; Hallucinations ; Humans ; Male ; Medication Adherence* ; Outpatients* ; Schizophrenia* ; Siblings ; Spouses ; Tablets

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

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*

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