Only few studies have shown the efficacy and safety of glucose-control strategies using the quadruple drug combination. Therefore, the aim of the present study was to investigate the usefulness of the quadruple combination therapy with oral hypoglycemic agents (OHAs) in patients with uncontrolled type 2 diabetes mellitus (T2DM).

Only few studies have shown the efficacy and safety of glucose-control strategies using the quadruple drug combination. Therefore, the aim of the present study was to investigate the usefulness of the quadruple combination therapy with oral hypoglycemic agents (OHAs) in patients with uncontrolled type 2 diabetes mellitus (T2DM).

Background: Only few studies have shown the efficacy and safety of glucose-control strategies using the quadruple drug combination. Therefore, the aim of the present study was to investigate the usefulness of the quadruple combination therapy with oral hypoglycemic agents (OHAs) in patients with uncontrolled type 2 diabetes mellitus (T2DM). Methods: From March 2014 to December 2018, data of patients with T2DM, who were treated with quadruple hypoglycemic medications for over 12 months in 11 hospitals in South Korea, were reviewed retrospectively. We compared glycosylated hemoglobin (HbA1c) levels before and 12 months after quadruple treatment with OHAs. The safety, maintenance rate, and therapeutic patterns after failure of the quadruple therapy were also evaluated. Results: In total, 357 patients were enrolled for quadruple OHA therapy, and the baseline HbA1c level was 9.0%±1.3% (74.9± 14.1 mmol/mol). After 12 months, 270 patients (75.6%) adhered to the quadruple therapy and HbA1c was significantly reduced from 8.9%±1.2% to 7.8%±1.3% (mean change, –1.1%±1.2%; P<0.001). The number of patients with HbA1c <7% increased significantly from 5 to 68 (P<0.005). In addition, lipid profiles and liver enzyme levels were also improved whereas no changes in body weight. There was no significant safety issue in patients treated with quadruple OHA therapy. Conclusion This study shows the therapeutic efficacy of the quadruple OHA regimen T2DM and demonstrates that it can be an option for the management of T2DM patients who cannot use insulin or reject injectable therapy.

Background: Hodgkin's lymphoma (HL) constitutes 10%–20% of all malignant lymphomas and has a high cure rate (5-year survival, around 90%). Recently, interest has increased concerning preventing secondary complications (secondary cancer, endocrine disorders) in long-term survivors. We aimed to study the epidemiologic features and therapeutic outcomes of HL in children, adolescents, and young adults in Korea. Methods: We performed a multicenter, retrospective study of 224 patients aged < 25 years diagnosed with HL at 22 participating institutes in Korea from January 2007 to August 2016. Results: A higher percentage of males was diagnosed at a younger age. Nodular sclerosis histopathological HL subtype was most common, followed by mixed cellularity subtype.Eighty-one (36.2%), 101 (45.1%), and 42 (18.8%) patients were classified into low, intermediate, and high-risk groups, respectively. Doxorubicin, bleomycin, vinblastine, dacarbazine was the most common protocol (n = 102, 45.5%). Event-free survival rate was 86.0% ± 2.4%, while five-year overall survival (OS) rate was 96.1% ± 1.4%: 98.7% ± 1.3%, 97.7% ± 1.6%, and 86.5% ± 5.6% in the low, intermediate, and high-risk groups, respectively (P = 0.021). Five-year OS was worse in patients with B-symptoms, stage IV disease, highrisk, splenic involvement, extra-nodal lymphoma, and elevated lactate dehydrogenase level.In multivariate analysis, B-symptoms and extra-nodal involvement were prognostic factors for poor OS. Late complications of endocrine disorders and secondary malignancy were observed in 17 and 6 patients, respectively. Conclusion This is the first study on the epidemiology and treatment outcomes of HL in children, adolescents, and young adults in Korea. Future prospective studies are indicated to develop therapies that minimize treatment toxicity while maximizing cure rates in children, adolescents, and young adults with HL.

PURPOSE: The purpose of this study was to analyze opinions about the action plan for implementation of clinical performance exam as part of the national nursing licensing examination and presents the expected effects of the performance exam and aspects to consider regarding its implementation. METHODS: This study used a mixed-methods design. Quantitative data were collected by a questionnaire survey, while qualitative data were collected by focus group interviews with experts. The survey targeted 200 nursing professors and clinical nurses with more than 5 years of work experience, and the focus group interviews were conducted with 28 of professors, clinical instructors, and nurses at hospitals. RESULTS: First, nursing professors and clinical specialists agreed that the current written tests have limitations in evaluating examinees' ability, and that the introduction of a clinical performance exam will yield positive results. Clinical performance exam is necessary to evaluate and improve nurses' work ability, which means that the implementation of a performance exam is advisable if its credibility and validity can be verified. Second, most respondents chose direct performance exams using simulators or standardized patients as the most suitable format of the test. CONCLUSION: In conclusion, the current national nursing licensing exam is somewhat limited in its ability to identify competent nurses. Thus, the time has come for us to seriously consider the introduction of a performance exam. The prerequisites for successfully implementing clinical performance exam as part of the national nursing licensing exam are a professional training process and forming a consortium to standardize practical training.
Focus Groups ; Humans ; Korea* ; Licensure* ; Licensure, Nursing ; Nursing* ; Specialization ; Surveys and Questionnaires

PURPOSE: It has been reported that daily recombinant human growth hormone (GH) treatment showed beneficial effects on growth in prepubertal children with idiopathic short stature (ISS). The present study aimed to validate the GH (Eutropin(R)) effect on growth promotion and safety after short-term GH treatment. MATERIALS AND METHODS: This study was an open-label, multicenter, interventional study conducted at nine university hospitals in Korea between 2008 and 2009. Thirty six prepubertal children with ISS were enrolled in this study to receive 6-month GH treatment. Yearly growth rate, height standard deviation score (SDS), and adverse events were investigated during treatment. RESULTS: After 26 weeks of GH treatment, the height velocity significantly increased by 6.36+/-3.36 cm/year (p<0.001). The lower end of one-sided 95% confidence interval was 5.22 cm/year, far greater than the predefined effect size. The gain in height SDS at week 26 was 0.57+/-0.27 (p<0.0001). Bone age significantly increased after GH treatment, however, bone maturation rate (bone age for chronological age) showed limited advancement. This 26-week GH treatment was effective in increasing serum levels of insulin-like growth factor (IGF)-I and IGF binding protein (IGFBP)-3 from baseline (p<0.0001). Eutropin was well tolerated and there were no withdrawals due to adverse events. No clinically significant changes in laboratory values were observed. CONCLUSION: This 6-month daily GH treatment in children with ISS demonstrated increased height velocity, improved height SDS, and increased IGF-I and IGFBP-3 levels with a favorable safety profile.
Child ; Female ; Growth Disorders/blood/*drug therapy ; Growth Hormone/*therapeutic use ; Humans ; Insulin-Like Growth Factor Binding Protein 3/blood ; Insulin-Like Growth Factor I/metabolism ; Male ; Treatment Outcome

Heparin, a widely used anticoagulant, is currently the anticoagulant of choice in long-term hemodialysis (HD). Heparin-induced thrombocytopenia (HIT) is one of the most serious side effects of heparin which can cause arterial or venous thromboembolism associated with substantial morbidity and mortality. We experienced two patients who had thrombocytopenia and vascular access occlusion during the induction period of HD with the use of unfractionated heparin. Thrombocytopenia was improved after discontinuation of heparin. HIT was confirmed with anti-heparin/platelet factor 4 antibody test. HD was conducted and arteriovenous fistula was created successfully after switch of heparin to argatroban (Novastan(R)) or nafamostat mesilate (Futhan(R)). Nephrologist should rule out HIT first when thrombocytopenia and thromboembolic complications occur after use of heparin, especially during the induction period of HD. For suspicious patients, immediate cessation of heparin and switch to alternative anticoagulant is very important to avoid serious complications.
Arteriovenous Fistula ; Heparin ; Humans ; Mesylates ; Mortality ; Renal Dialysis* ; Thrombocytopenia* ; Venous Thromboembolism

Pulmonary hypertension (PH) is characterized by structural and functional changes in the lung including proliferation of vascular smooth muscle cells (VSMCs) and excessive collagen synthesis. Although connective tissue growth factor (CTGF) is known to promote cell proliferation, migration, adhesion, and extracellular matrix production in various tissues, studies on the role of CTGF in pulmonary hypertension have been limited. Here, we examined CTGF expression in the lung tissues of male Sprague Dawley rats treated with monocrotaline (MCT, 60 microgram/kg), a pneumotoxic agent known to induce PH in animals. Establishment of PH was verified by the significantly increased right ventricular systolic pressure and right ventricle/left ventricle weight ratio in the MCT-treated rats. Histological examination of the lung revealed profound muscular hypertrophy in the media of pulmonary artery and arterioles in MCT-treated group. Lung parenchyma, vein, and bronchiole did not appear to be affected. RT-PCR analysis of the lung tissue at 5 weeks indicated significantly increased expression of CTGF in the MCT-treated group. In situ hybridization studies also confirmed abundant CTGF mRNA expression in VSMCs of the arteries and arterioles, clustered pneumocytes, and infiltrated macrophages. Interestingly, CTGF mRNA was not detected in VSMCs of vein or bronchiole. In saline-injected control, basal expression of CTGF was seen in bronchial epithelial cells, alveolar lining cells, and endothelial cells. Taken together, our results suggest that CTGF upregulation in arterial VSMC of the lung might be important in the pathogenesis of pulmonary hypertension. Antagonizing the role of CTGF could thus be one of the potential approaches for the treatment of PH.
Animals ; Blood Pressure/drug effects ; Bronchi/cytology/drug effects/metabolism ; Endothelial Cells/cytology/drug effects/metabolism ; Epithelial Cells/cytology/drug effects/metabolism ; Hypertension, Pulmonary/chemically induced/*metabolism ; Immediate-Early Proteins/genetics/*metabolism ; Intercellular Signaling Peptides and Proteins/genetics/*metabolism ; Lung/cytology/drug effects/*metabolism ; Male ; Monocrotaline/*toxicity ; Pulmonary Alveoli/cytology/drug effects/metabolism ; Pulmonary Artery/cytology/drug effects/metabolism ; Rats ; Rats, Sprague-Dawley ; Research Support, Non-U.S. Gov't ; Reverse Transcriptase Polymerase Chain Reaction ; Up-Regulation

The effect of aldosterone on connective tissue growth factor (CTGF) was examined in rat embryonic ventricular myocytes. Upon aldosterone treatment, CTGF expression was significantly increased in a dose and time-dependent manner. To explore the molecular mechanism for this upregulation, we examined the role of mineralocorticoid receptor. Pre-treatment of an antagonist (spironolactone) at 5-fold excess of aldosterone blocked the CTGF induction by aldosterone, suggesting that the upregulation was mediated by mineralocorticoid receptor. Aldosterone treatment resulted in activation of ERK1/2, p38 MAPK, and JNK pathways with a more transient pat-tern in p38 MAPK. Blocking studies using pre-treatment of the inhibitor of each path-way revealed that p38 MAPK cascade may be important for aldosterone-mediated CTGF upregulation as evidenced by the blocking of CTGF induction by SB203580 (p38 MAPK inhibitor), but not by PD098059 (ERK1/2 inhibitor) and JNK inhibitor I. Interestingly, JNK inhibitor I and PD098059 decreased the basal level of CTGF expression. On the other hand, pre-treatment of spironolactone abrogated the p38 MAPK activation, indicating that mineralocorticoid receptor mechanism is linked to p38 MAPK pathway. Taken together, our findings suggest that aldosterone induces CTGF expression via both p38 MAPK cascade and mineralocorticoid receptor and that cross-talk exists between the two pathways.
Aldosterone/*pharmacology ; Animals ; Cells, Cultured ; Dose-Response Relationship, Drug ; Gene Expression Regulation/drug effects/physiology ; Heart Ventricles/drug effects/embryology/metabolism ; Immediate-Early Proteins/*metabolism ; Intercellular Signaling Peptides and Proteins/*metabolism ; Myocytes, Cardiac/*drug effects/*metabolism ; Rats ; Receptors, Mineralocorticoid/*metabolism ; Research Support, Non-U.S. Gov't ; Signal Transduction/drug effects/physiology ; Spironolactone/pharmacology ; Up-Regulation/drug effects/physiology ; p38 Mitogen-Activated Protein Kinases/*metabolism