Kim D.S.,Cutaneous Biology Research Institute |
Shin D.,Cutaneous Biology Research Institute |
Jee H.,Cutaneous Biology Research Institute |
Kim T.-G.,Cutaneous Biology Research Institute |
And 5 more authors.
Journal of Dermatology | Year: 2015
Circulating inflammatory cytokines and markers are increased in patients with psoriasis. Recent studies have shown that a higher red blood cell distribution width (RDW) is associated with disease activity in various disorders. Our objective was to investigate whether RDW is increased in psoriasis patients, and to evaluate its possible association with disease severity. We conducted a retrospective study of psoriasis patients seen in a university hospital in South Korea. Information about demographics, hematological parameters and disease severity were collected. Statistical analysis was performed using Student's t-test, multivariable logistic regression, Fisher's exact test and Spearman's rank correlation coefficient analysis as appropriate. A total of 261 psoriasis patients and 102 healthy controls were included in our study. The mean RDW value was significantly increased in psoriasis patients compared with healthy control (P = 0.037). Compared with mild psoriasis patients (Psoriasis Area and Severity Index [PASI], <7), moderate to severe patients (PASI, ≥7) showed significantly higher RDW values (P = 0.044). However, RDW did not show significant correlation with PASI (P = 0.358). When patients were divided into two groups according to their RDW value (<14.6% and ≥14.6%), the mean value of PASI was not significantly different (P = 0.219). Patients with psoriasis showed increased RDW values compared with healthy controls. It was also higher in the moderate and severe disease group than the mild group. Though this is only a pilot study, it is possible that RDW value can reflect the inflammatory status of psoriasis patients. © 2015 Japanese Dermatological Association. Source
Scripnic V.,Social Republic |
Zemtsovsky E.,Saint Petersburg State Pediatric Medical Academy |
Saulea A.,Social Republic |
Sontea V.,Technical University Gheorghe Asachi |
And 3 more authors.
2011 E-Health and Bioengineering Conference, EHB 2011 | Year: 2011
In this article are discussed questions of some rare (small) arrhythmias classification and their physiological value from the point of view of synergetic and reliability of the health in extreme conditions. © 2011 GR T Popa University. Source
People infected with the hepatitis C virus may have an increased risk of developing Parkinson’s disease, according to a new study out of Taiwan. Hepatitis C is a liver infection caused by a virus. Between 130 million and 150 million people worldwide have chronic hepatitis C infection, according to the World Health Organization. The study, published Dec. 23 in Neurology, was conducted retrospectively using the National Health Insurance Research Database in Taiwan. Study author, Cynthia Hsin-Hsi Tsai, M.D., from the National Taiwan University Hospital in Taiwan, told Bioscience Technology that the research has provided the idea of an association of hepatitis C virus (HCV) and Parkinson’s disease (PD) from an epidemiological perspective. “Our study discovered a 2.5-fold risk of PD in patients with HCV infection than controls (no hepatitis B virus, no HCV),” she said. “After adjustment for age, sex, and multiple comorbidities, there was still a 1.3-fold risk of PD in patients having HCV infection.” Hsin-Hsi Tsai noted that there are many factors for risk of developing Parkinson’s, and this study shows that a hepatitis C infection can be one of those risk factors. “The positive association between HCV infection and PD implicates the importance of diagnosing PD or subclinical PD in HCV patients for high endemic HCV areas, such as Taiwan,” she told Bioscience Technology. “More detailed neurological tests and functional images might help us detect early PD in anti-HCV(+) patients.” The study included 199,868 people without hepatitis, and 49,967 people with hepatitis. Those with hepatitis were split into three groups, depending on what form of the virus they had. Twenty-one percent were infected with hepatitis C, 71 percent had hepatitis B and 8 percent had both viruses. The most common cause of the virus in Taiwan during the time of the study was blood transfusions. After being followed for an average of 12 years, 270 of the participants with hepatitis developed Parkinson’s, including 120 people with hepatitis C. Of participants who did not have hepatitis, 1,060 developed the disease. After controlling for a number of factors, researchers found that participants with hepatitis C were almost 30 percent more likely to develop Parkinson’s than those who did not have the virus. There was no increased risk for people with hepatitis B or both viruses than those who did not have hepatitis. Hsin-Hsi Tsai stressed that the findings show a positive association but do not necessarily mean causality. Limitations of the study include disease coding done through ICD-9-CM codes, instead of clinical assessment, laboratory data or neuroimaging study, for identifying PD and viral hepatitis profiles. Hsin-Hsi Tsai also said that evidence derived from a retrospective cohort study is typically lower in statistical quality because of inherent bias. “At the population and epidemiology level, HCV infection and PD are strongly associated,” Hsin-Hsi Tsia said. Up next, the researchers will investigate this association clinically, to see if there is any evidence of dopaminergic neuronal damage in patients with HCV infection.
Risk of bleeding and arterial thromboembolism in patients with non-valvular atrial fibrillation either maintained on a vitamin K antagonist or switched to a non-vitamin K-antagonist oral anticoagulant: A retrospective, matched-cohort study
Bouillon K.,French National Agency for Medicines and Health Products Safety |
Bertrand M.,French National Agency for Medicines and Health Products Safety |
Maura G.,National Health Insurance |
Blotiere P.-O.,National Health Insurance |
And 2 more authors.
The Lancet Haematology | Year: 2015
BACKGROUND: Patients with non-valvular atrial fibrillation who are receiving or have been previously exposed to a vitamin K antagonist could be switched to a non-vitamin K-antagonist oral anticoagulant (NOAC) but little information is available about the risk of bleeding and arterial thromboembolism after such a switch. We aimed to compare the risk of bleeding between individuals who switched and those who remained on a vitamin K antagonist (non-switchers) in real-world conditions. METHODS: We did a matched-cohort study with information from French health-care databases. We extracted data for adults (aged ≥18 years) with non-valvular atrial fibrillation who received their first prescription for a vitamin K antagonist (fluindione, warfarin, or acenocoumarol) between Jan 1, 2011, and Nov 30, 2012, and who were either switched to a NOAC (dabigatran or rivaroxaban) or maintained on the vitamin K antagonist. Each switcher was matched with up to two non-switchers on the basis of eight variables, including sex, age, and international normalised ratio number. The primary endpoint was incidence of bleeding (intracranial haemorrhage, gastrointestinal haemorrhage, or other) in switchers versus non-switchers, and switchers stratified by type of NOAC versus non-switchers, noted from databases of hospital admissions. Each patient was followed up to 1 year; the study closed on Oct 1, 2013. FINDINGS: Of 17 410 participants, 6705 switched to a NOAC (switchers) and 10 705 remained on vitamin K-antagonist therapy (non-switchers). Median age of participants was 75 years (IQR 67-82), 8339 (48%) were women, and the median duration of vitamin K-antagonist exposure before a switch was 8·1 months (IQR 3·9-14·0). After a median follow-up of 10·0 months (IQR 9·8-10·0), we noted no difference between groups for bleeding events (99 [1%] in switchers vs 193 [2%] in non-switchers, p=0·54). In adjusted multivariate analyses, the risk of bleeding in switchers was not different from that in non-switchers (hazard ratio [HR] 0·87; 95% CI 0·67-1·13, p=0·30). Additionally, no differences were noted when the risk of bleeding was compared between switchers from a vitamin K antagonist to dabigatran (HR 0·78, 95% CI 0·54-1·09, p=0·15), switchers from a vitamin K antagonist to rivaroxaban (HR 1·04, 95% CI 0·68-1·58, p=0·86), and non-switchers. INTERPRETATION: In this matched-cohort study, our findings suggest that patients with non-valvular atrial fibrillation who switch their oral anticoagulant treatment from a vitamin K antagonist to a non-vitamin K antagonist are not at increased risk of bleeding. Future studies with longer follow-up might be needed. FUNDING: None. © 2015 Elsevier Ltd. All rights reserved. Source
Roussel R.,French Institute of Health and Medical Research |
Roussel R.,University Paris Diderot |
Chaignot C.,National Health Insurance |
Weill A.,National Health Insurance |
And 9 more authors.
PLoS ONE | Year: 2015
Background and Aim According to guidelines, diabetic patients with high cardiovascular risk should receive a statin. Despite this consensus, fibrate monotherapy is commonly used in this population. We assessed the frequency and clinical consequences of the use of fibrates for primary prevention in patients with diabetes and high cardiovascular risk. Design Retrospective cohort study based on nationwide data from the medical and administrative databases of French national health insurance systems (07/01/08-12/31/09) with a followup of up to 30 months. Methods Lipid-lowering drug-naive diabetic patients initiating fibrate or statin monotherapy were identified. Patients at high cardiovascular risk were then selected: patients with a diagnosis of diabetes and hypertension, and >50 (men) or 60 (women), but with no history of cardiovascular events. The composite endpoint comprised myocardial infarction, stroke, amputation, or death. Results Of the 31,652 patients enrolled, 4,058 (12.8%) received a fibrate. Age-and gender-adjusted annual event rates were 2.42% (fibrates) and 2.21%(statins). The proportionality assumption required for the Cox model was not met for the fibrate/statin variable. A multivariate model including all predictors was therefore calculated by dividing data into two time periods, allowing Hazard Ratios to be calculated before (HR<540) and after 540 days (HR>540) of follow-up. Multivariate analyses showed that fibrates were associated with an increased risk for the endpoint after 540 days: HR<540 = 0.95 (95% CI: 0.78-1.16) and HR>540 = 1.73 (1.28-2.32). Copyright: © 2015 Roussel et al. Source