OBJECTIVE: This study was to explore the association between having a usual source of care and adherence to medicines in patient with chronic diseases. METHODS: The 2012 Korea Health Panel was used as a data source. We analyzed 4,418 respondents that were diagnosed with chronic diseases and utilized health care services. Non-adherence to medication, a dependent variable, was defined as "not taking the medicines that were prescribed for treating chronic disease" or "not following the direction for medication". Whether having a usual source of care or not was used as a key independent variable, which was defined as having a regular site or a regular doctor for medical test, treatment, and consultation. Sex, age, education level, marital status, income, the type of health insurance, the number of chronic disease and CCI (Charlson Comorbidity Index) were included as covariates in the analysis. We conducted a multivariate logistic regression. RESULTS: Totally, 30 percent of respondents reported to experience nonadherence to medication. Having a usual source of care was significantly associated with lower non-adherence to medication regardless its type, which is a regular doctor (OR=0.61, 95% CI=0.53-0.70) or a regular site (OR=0.67, 95% CI=0.58-0.78). Furthermore, having a usual source of care was associated with both of medication persistence (OR=0.66, 95% CI=0.54-0.81) and compliance (OR=0.65, 95% CI=0.56-0.76). CONCLUSION: Our results showed the possibility that usual source of care is able to conduct a positive role in improving adherence to medication with better management of chronic disease.
Chronic Disease* ; Comorbidity ; Compliance ; Delivery of Health Care ; Education ; Humans ; Information Storage and Retrieval ; Insurance, Health ; Korea ; Logistic Models ; Marital Status ; Medication Adherence ; Surveys and Questionnaires

BACKGROUND: Dual antiplatelet therapy (aspirin and clopidogrel) is used to prevent adverse cardiac events in patients undergoing percutaneous coronary intervention (PCI). Some patients do not respond adequately to clopidogrel. Beta-thromboglobulin (beta-TG) and platelet factor 4 (PF-4) can act as markers to detect platelet activation. We investigated the relationship between clopidogrel response and the dynamics of beta-TG and PF4 concentrations. METHODS: This study included 36 myocardial infarction (MI) patients, who underwent PCI and was indicated for dual antiplatelet therapy. Platelet reactivity, using the VerifyNow P2Y12 assay, was measured on the 3rd day of PCI. At the time of admission, and on the 3rd and 10th day of PCI, the plasma beta-TG and PF4 concentrations were quantified. RESULTS: Ten patients (27.8%) were clopidogrel non-responders displaying >208 P2Y12 reaction units. At the time of admission, levels of beta-TG in patients were elevated than that in the healthy controls (P<0.001). A similar trend was observed on the 3rd and 10th day of PCI (P<0.001). The beta-TG levels on the 10th day were reduced than those at the time of admission and on the 3rd day of PCI. PF4 levels were not different between patients and controls, and were not significantly reduced after PCI. Higher beta-TG levels were observed in clopidogrel non-responders on the 10th day, but not significant. CONCLUSIONS: Clopidogrel therapy in MI reduce beta-TG concentration, but the beta-TG and PF4 levels before and after therapy are not associated with the response to clopidogrel. Platelet-derived markers may not be suitable for distinguishing clopidogrel non-responders.
beta-Thromboglobulin ; Blood Platelets* ; Humans ; Infarction* ; Myocardial Infarction ; Percutaneous Coronary Intervention ; Plasma ; Platelet Activation* ; Platelet Factor 4

Although atopic dermatitis (AD) is characterized by cytokine production predominantly mediated by T helper (Th) 2 cells, AD pathogenesis also involves innate immune and Th1 cells. To optimize the cytokine milieu required for accurate reproduction of AD-related gene expression profile in vitro, we evaluated the expression pattern of CCL22, CCL17, IL5, IL13, IL33, IL25, TSLP, FLG, and LOR in human lesional AD skin and cytokine-stimulated HaCaT cells. An increase in Th2 mediators (IL5, IL13, CCL22, CCL17, IL25, IL33, and TSLP) and a decrease in genes related to cornified cell envelope (filaggrin and loricrin) were observed in human AD lesions. Innate (tumor necrosis factor-α) and/or Th1/Th2 adaptive cytokines (interferon-γ/IL-4) were required for inducing these inflammatory changes in HaCaT cells, implying that a complex network of innate, Th1, and Th2 cytokines drives AD-like changes. Therefore, stimulation with various combinations of cytokines, beyond Th2 polarization, is necessary when HaCaT cell line is used to study genetic changes implicated in AD pathogenesis.
Cell Line* ; Cytokines ; Dermatitis, Atopic ; Gene Expression* ; Humans ; In Vitro Techniques ; Interleukin-13 ; Interleukin-33 ; Interleukin-5 ; Keratinocytes* ; Necrosis ; Reproduction ; Skin ; Th1 Cells ; Transcriptome