Search

Ischaemic heart disease, sudden cardiac death and arrhythmias, heart failure, stroke and peripheral arterial disease make up >50% of the causes of death in advanced chronic kidney disease (CKD). Calcification of the vascular tree and heart valves is partially related to these complications and has received growing attention in the literature. However, the main focus of research has been on the pathophysiology and consequences of vascular calcification, with less attention being paid to valvular calcification (VC) and its impact on the survival of CKD patients. Although VC has long been seen as an age-related degenerative disorder with minimal functional impact, several studies proved that it carries an increased risk of death and clinical consequences different from those of vascular calcification. In dialysis patients, the annual incidence of aortic valve calcification is nearly 3.3% and the reported prevalence of aortic and mitral VC varies between 25% and 59%. Moreover, calcification of both valves occurs 10–20 years earlier in CKD patients compared with the general population. Therefore, the purpose of this review is to summarize the current knowledge on the pathophysiology and relevance of VC in CKD patients, and to highlight specific clinical consequences and potential therapeutic implications. © The Author(s) 2019. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.

Background As an alternative to vitamin K antagonist and low-dose aspirin ( 2). Conclusion Non vitamin K oral anticoagulants are associated with a higher risk on all-cause mortality, particularly in men and in patients with higher stroke risk., International Journal of Clinical Pharmacy, 41 (6), ISSN:2210-7703, ISSN:0928-1231, ISSN:2210-7711

Introduction and objectives: To assess the effectiveness of direct oral anticoagulants vs vitamin K antagonists in real-life patients with atrial fibrillation. Methods: A systematic review was performed according to Cochrane methodological standards. The results were reported according to the PRISMA statement. The ROBINS-I tool was used to assess risk of bias. Results: A total of 27 different studies publishing data in 30 publications were included. In the studies with a follow-up up to 1 year, apixaban (HR, 0.93; 95%CI, 0.71-1.20) and dabigatran (HR, 0.95; 95%CI, 0.80-1.13) did not significantly reduce the risk of ischemic stroke vs warfarin, whereas rivaroxaban significantly reduced this risk (HR, 0.83; 95%CI, 0.73-0.94). Apixaban (HR, 0.66; 95%CI, 0.55-0.80) and dabigatran (HR, 0.83; 95%CI, 0.70-0.97) significantly reduced the major bleeding risk vs warfarin, but not rivaroxaban (HR, 1.02; 95%CI, 0.95-1.10), although with a high statistical heterogeneity among studies. Apixaban (HR, 0.56; 95%CI, 0.42-0.73), dabigatran (HR, 0.45; 95%CI, 0.39-0.51), and rivaroxaban (HR, 0.66; 95%CI, 0.49-0.88) significantly reduced the risk of intracranial bleeding vs warfarin. Reduced doses of direct oral anticoagulants were associated with a slightly better safety profile, but with a marked reduction in stroke prevention effectiveness. Conclusions: Data from this meta-analysis suggest that, vs warfarin, the stroke prevention effectiveness and bleeding risk of direct oral anticoagulants may differ in real-life patients with atrial fibrillation. Full English text available from: www.revespcardiol.org/en © 2018 Sociedad Española de Cardiología

Aims: The efficacy and safety of oral anticoagulation (OAC) using the vitamin K antagonists (VKA) are closely associated with the quality of anticoagulation, reflected by time in therapeutic range (TTR). The SAMe-TT2R2 is a risk score developed to predict the quality of anticoagulation control among VKA users. To analyse the quality of anticoagulation and its clinical determinants based on different methods in a prospective cohort of atrial fibrillation patients on VKA treatment participating in the multicentre Spanish observational registry FANTASIIA. Methods and results: Estimated TTR was calculated from Rosendaal, direct method, international normalized ratio variability, and NICE criteria. Time in therapeutic range values were compared for those patients with a SAMe-TT2R2 score 0-2 and >2. One thousand four hundred and seventy patients were analysed (56.4% male, mean age 74.1 ± 9.5 years). Mean TTR was 61.5 ± 25.1 with Rosendaal and 64.7 ± 24.2 with direct method. There was a high correlation between both methods (q = 0.805). The prevalence of poor anticoagulation control was 55%. Diabetes mellitus [odds ratio (OR) 1.38; P = 0.008], peripheral artery disease (PAD, OR 1.62; P = 0.048), and HAS-BLED (OR 1.13; P = 0.022) were independently associated with TTR < 70%. SAMe-TT2R2 score 0-2 had a higher mean TTR than patients with SAMe-TT2R2 >2 (P = 0.044), with a specificity of > 90% for predicting TTR < 70%. Patients with TTR < 70% had higher risk of events (21.7 vs. 16.8%; P = 0.021). Conclusion: In a multicentre prospective registry, 55% of AF patients had poor anticoagulation control with diabetes mellitus, PAD, and HAS-BLED being independently associated with TTR < 70%. A high SAMe-TT2R2 scores had a high specificity for predicting a TTR < 70% as an indicator of poor quality anticoagulation. © 2017 The Author(s).

The Irish National Consent Policy (NCP)¹ proposes that the legal requirement for consent extends to all forms of interventions, investigations and treatment, carried out on or behalf of the Health Service Executive (HSE). This study employs a quantitative descriptive approach to investigate the practices for obtaining consent for an identified group of routine neonatal procedures in neonatal facilities throughout Ireland. The BAPM (British Association of Perinatal Medicine)² guidelines were identified as ‘gold standard’ for the purposes of this study. The results indicated a lack of consistency between participating units pertaining to the modes of consent utilised and notable variances from ‘gold standard’ guidelines. Unanimity was evident for 3 procedures only (administering BCG, 6-in-1, and donor breast milk to infant). Significant findings related to EEG with video recordings, MRI/CT and gastro intestinal imaging, screening of an infant with suspected substance abuse or retinopathy of prematurity screening (ROP), administration of Vitamin K, and the carrying out of a lumbar puncture.

Objective:To perform a systematic review and meta-analysis of studies reporting recurrent intracranial hemorrhage (ICH) and ischemic stroke (IS) in ICH survivors with atrial fibrillation (AF) during long-term follow-up.Methods:A comprehensive literature search including MEDLINE, EMBASE, Cochrane library, clinical trials registry was performed following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement. We considered studies capturing outcome events (ICH recurrence and IS) for ≥3 months and treatment exposure to vitamin K antagonists (VKAs), antiplatelet agents (APAs), or no antithrombotic medication (no-ATM). Corresponding authors provided aggregate data for IS and ICH recurrence rate between 6 weeks after the event and 1 year of follow-up for each treatment exposure. Meta-analyses of pooled rate ratios (RRs) were conducted with the inverse variance method.Results:Seventeen articles met inclusion criteria. Seven observational studies enrolling 2,452 patients were included in the meta-analysis. Pooled RR estimates for IS were lower for VKAs compared to APAs (RR = 0.45, 95% confidence interval [CI] 0.27–0.74, p = 0.002) and no-ATM (RR = 0.47, 95% CI 0.29–0.77, p = 0.002). Pooled RR estimates for ICH recurrence were not significantly increased across treatment groups (VKA vs APA: RR = 1.34, 95% CI 0.79–2.30, p = 0.28; VKA vs no-ATM: RR = 0.93, 95% CI 0.45–1.90, p = 0.84).Conclusions:In observational studies, anticoagulation with VKA is associated with a lower rate of IS than APA or no-ATM without increasing ICH recurrence significantly. A randomized controlled trial is needed to determine the net clinical benefit of anticoagulation in ICH survivors with AF.

Management strategies for patients with atrial fibrillation (AF) in association with valvular heart disease (VHD) have been less informed by randomized trials, which have largely focused on 'non-valvular AF' patients. Thromboembolic risk also varies according to valve lesion and may also be associated with CHA 2 DS 2 -VASc score risk factor components, rather than only the valve disease being causal. Given the need to provide expert recommendations for professionals participating in the care of patients presenting with AF and associated VHD, a task force was convened by the European Heart Rhythm Association (EHRA) and European Society of Cardiology (ESC) Working Group (WG) on Thrombosis, with representation from the ESC WG on Valvular Heart Disease, Heart Rhythm Society (HRS), Asia Pacific Heart Rhythm Society (APHRS), South African Heart (SA Heart) Association and Sociedad Latinoamericana de Estimulación Cardíaca y Electrofisiología (SOLEACE) with the remit to comprehensively review the published evidence, and to produce a consensus document on the management of patients with AF and associated VHD, with up-to-date consensus statements for clinical practice for different forms of VHD, based on the principles of evidence-based medicine. This is an executive summary of a consensus document which proposes that the term 'valvular AF' is outdated and given that any definition ultimately relates to the evaluated practical use of oral anticoagulation (OAC) type, we propose a functional EHRA (Evaluated Heartvalves, Rheumatic or Artificial) categorization in relation to the type of OAC use in patients with AF, as follows: (1) EHRA (Evaluated Heartvalves, Rheumatic or Artificial) type 1 VHD, which refers to AF patients with 'VHD needing therapy with a vitamin K antagonist (VKA)' and (2) EHRA (Evaluated Heartvalves, Rheumatic or Artificial) type 2 VHD, which refers to AF patients with 'VHD needing therapy with a VKA or a non-VKA oral anticoagulant also taking into consideration CHA 2 DS 2 -VASc score risk factor components. © 2017 Schattauer.

Background: Imitating the design of a randomized controlled trial in an observational study is one of the recent methodological approaches that has been developed to improve the usefulness of observational studies in assessing drug effectiveness (efficacy of drugs in routine clinical care); however, the usefulness of this approach has not been investigated from non-inferiority perspective. Objectives: To imitate the design of the ROCKET AF (Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Embolism Trial in Atrial Fibrillation) non-inferiority trial in an observational study. Methods: A retrospective cohort study was conducted using the British Clinical Practice Research Datalink (CPRD). Applying the eligibility criteria of the trial, patients who were diagnosed with non-valvular AF and were prescribed either rivaroxaban or warfarin (incident users) from October 2008 were included and followed to the end of the study period (December 2017). Non-inferiority of rivaroxaban to warfarin in the prevention of the composite endpoint of stroke or systemic embolism was assessed using a non-inferiority margin of hazard ratio (HR) 1.46 (the margin that was used in the triak). Cox-proportional hazards regression was used to estimate the study outcomes adjusting for time-fixed and time-varying confounders. Results: We included 25,473 incident users of rivaroxaban (n = 4,008) or warfarin (n = 21,465). Similar to the trial, non-inferiority in the primary outcome was demonstrated: HR1.04 (95% confidence interval [CI] 0.84 to 1.30) in the intention-to-treat population and in another two analysis populations. The target population of the trial is mostly treated in the real-world settings (i.e. the proportion of patients who did not meet the exclusion criteria was small), thus affecting the precision of analysis in the latter. Finally, the event rate of the primary outcome in warfarin group was lower compared with that in the trial and this may affect the applicability of the trial's non-inferiority margin in our study. Conclusions: imitating the design of a non-inferiority trial in observational study led to consistent results with that of the trial in similar patient population, however, an adjustment for the trial's non-inferiority margin is needed to take into account the variation in the effect of the active comparator in observational settings.

Central venous catheters (CVCs) are used extensively in cancer patients for the administration of therapy and phlebotomy. An important complication of CVCs is the development of catheter-related thrombosis (CRT), which becomes symptomatic in approximately 5% of the patients. Several factors, such as insertion location and position of the catheter tip, increase the risk of CRT. Prevention of CRT with systemic anticoagulant prophylaxis has largely been ineffective. In addition, the optimal diagnostic strategy and anticoagulant treatment are unclear due to the lack of well-designed studies. The most recent American College of Chest Physicians guidelines recommend (color) Doppler ultrasound more than venography as the initial diagnostic test in patients with suspected arm thrombosis. Only if the ultrasound is negative and clinical suspicion is high is further testing with D-dimer, serial ultrasound, or venography advocated. In case of CRT, removal of the catheter is not necessary if it is functional and needed for chemotherapy. Anticoagulant treatment of CRT consists of treatment with low-molecular-weight heparin (LMWH) followed by vitamin K antagonists for at least 3 months. Whether long-term treatment with LMWH is more effective than vitamin K antagonists in cancer patients with CRT is unknown, but LMWH may be advocated following the recommendations in lower limb thrombosis and cancer. In addition, the effect of new anticoagulants in CRT has not been studied.

Central venous catheters (CVCs) are used extensively in cancer patients for the administration of therapy and phlebotomy. An important complication of CVCs is the development of catheter-related thrombosis (CRT), which becomes symptomatic in approximately 5% of the patients. Several factors, such as insertion location and position of the catheter tip, increase the risk of CRT. Prevention of CRT with systemic anticoagulant prophylaxis has largely been ineffective. In addition, the optimal diagnostic strategy and anticoagulant treatment are unclear due to the lack of well-designed studies. The most recent American College of Chest Physicians guidelines recommend (color) Doppler ultrasound more than venography as the initial diagnostic test in patients with suspected arm thrombosis. Only if the ultrasound is negative and clinical suspicion is high is further testing with D-dimer, serial ultrasound, or venography advocated. In case of CRT, removal of the catheter is not necessary if it is functional and needed for chemotherapy. Anticoagulant treatment of CRT consists of treatment with low-molecular-weight heparin (LMWH) followed by vitamin K antagonists for at least 3 months. Whether long-term treatment with LMWH is more effective than vitamin K antagonists in cancer patients with CRT is unknown, but LMWH may be advocated following the recommendations in lower limb thrombosis and cancer. In addition, the effect of new anticoagulants in CRT has not been studied.

Anticoagulants are effective agents in reducing the risk of thromboembolism but the most important adverse effect of these agents is the occurrence of bleeding. Bleeding complications may occur spontaneously but the risk of bleeding is particularly increased in case of trauma or around invasive procedures. If patients being treated with anticoagulants need to undergo an invasive intervention, physicians need to consider whether to interrupt the use of this medication or to allow its use to be continued. Suspending the use of anticoagulants increases the risk of thrombosis, whereas continued use may cause bleeding complications. To shorten the period in which anticoagulant treatment is interrupted, bridging strategies have been advocated. No evidence-based scientific research has been carried out regarding best practice for the perioperative use of anticoagulants. The periprocedural anticoagulation policy in patients should be individualised based on the risk of a thromboembolic complication (which can be estimated with available scoring systems) offset against the bleeding risk associated with the intervention. © Van Zuiden Communications B.V. All rights reserved.

The most important adverse effect of antithrombotic treatment is the occurrence of bleeding. in case of serious or even life-threatening bleeding in a patient who uses anticoagulant agents or when patient on anticoagulants needs to undergo an urgent invasive procedure, anticoagulant treatment can be reversed by various specific strategies. heparin and heparin derivatives can be counteracted by protamine sulphate, whereas the anticoagulant effect of vitamin K antagonists may be neutralised by administration of vitamin K or prothrombin complex concentrates. the antihaemostatic effect of aspirin and other antiplatelet strategies can be corrected by the administration of platelet concentrate and/or desmopressin, if needed. recently, a new generation of anticoagulants with a greater specificity towards activated coagulation factors has been introduced and most of these agents are currently being evaluated in clinical studies, showing promising results. the new-generation anticoagulants include specific inhibitors of factor iia or factor Xa (including pentasaccharides) and antiplatelet agents belonging to the class of thienopyridine derivatives. a limitation of the new class of anti-iia and anti-Xa agents may be the lack of an appropriate strategy to reverse the effect if a bleeding event occurs, although in some cases the administration of recombinant factor VIIa may be an option. © Van Zuiden Communications B.V. All rights reserved.

Glanzmann Thrombasthenia (GT) is a genetic platelet dysfunction and a life threatening disease. Although it is a rare disease, it is the most common genetic platelet disorder. Symptoms and signs are mucosal and dermal petechia, recurring epistaxis and gastrointestinal (GI) bleeding and menorrhagia. Findings may be mild to life threatening in severity (1). Ankaferd Blood Stopper (ABS) is a topical hemostatic agent of herbal origin which has recently become available for clinical use (2). It has been approved by the Turkish Republic Health Ministry for local use in bleeding due to superficial skin and dental disease. In the literature, there is a vast number of case reports regarding the application of ABS in gastrointestinal bleeding after surgical and dental procedures, both clinically and experimentally (3,4). In this case presentation, a patient with GT is reported in whom 3 months of gastrointestinal bleeding refractory to all medical therapies was controlled within a short time of using oral ABS.

It is increasingly acknowledged that mineral and bone disorders (MBDs) contribute to the excessively high cardiovascular (CV) disease morbidity and mortality observed in patients with chronic kidney disease (CKD). There is ongoing debate as to whether screening for CV calcification, one of the hallmarks of CKD-MBD, should be implemented in clinical practice in patients with CKD. Issues to be considered in this controversy relate to prevalence, severity, relevance, and last but not least, modifiability and reversibility of vascular and valvular calcifications in the setting of CKD. The recent expansion of the armamentarium to treat CKD-MBD (calcium-free phosphate binders and calcimimetics) creates new opportunities. Mounting experimental and clinical evidence indicates that progression of CV calcification may indeed be attenuated. Whether this will translate into better outcomes remains to be proven. We acknowledge that hard outcome data so far are limited and, overall, yielded inconclusive results. Nevertheless, in an era in which personalized medicine has gained much popularity, we consider it reasonable, awaiting the results of additional studies, to screen for CV calcification in selected individuals. This policy may help to stratify CV risk and to guide therapy. We speculate that such an approach will ultimately improve outcomes and reduce health costs. © © The Author 2015. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.

Background: Upper gastrointestinal bleeding is one of the most frequent causes of morbidity and mortality in the course of liver cirrhosis. Several treatments are used for upper gastrointestinal bleeding in people with liver diseases. One of them is vitamin K administration, but it is not known whether it benefits or harms people with acute or chronic liver disease and upper gastrointestinal bleeding. This is an update of this Cochrane review. Objectives: To assess the beneficial and harmful effects of vitamin K for people with acute or chronic liver disease and upper gastrointestinal bleeding. Search methods: We searched The Cochrane Hepato-Biliary Controlled Trials Register (February 2015), the Cochrane Central Register of Controlled Trials (CENTRAL) (Issue 2 of 12, 2015), MEDLINE (Ovid SP) (1946 to February 2015), EMBASE (Ovid SP) (1974 to February 2015), Science Citation Index EXPANDED (1900 to February 2015), and LILACS (1982 to 25 February 2015). We sought additional randomised trials from two registries of clinical trials: the World Health Organization Clinical Trials Search Portal and the metaRegister of Controlled Trials. We looked through the reference lists of the retrieved publications and review articles. Selection criteria: Randomised clinical trials irrespective of blinding, language, or publication status for assessment of benefits and harms. We considered observational studies for assessment of harms only. Data collection and analysis: We aimed to summarise data from randomised clinical trials using Standard Cochrane methodology and assess them according to the GRADE approach. Main results: We found no randomised trials on vitamin K for upper gastrointestinal bleeding in people with liver diseases assessing benefits and harms of the intervention. We identified no quasi-randomised studies, historically controlled studies, or observational studies assessing harms. Authors' conclusions: This updated review found no randomised clinical trials of vitamin K for upper gastrointestinal bleeding in people with liver diseases. The benefits and harms of vitamin K need to be tested in randomised clinical trials. Until randomised clinical trials are conducted to assess the trade-offbetween benefits and harms, we cannot recommend or refute the use of vitamin K for upper gastrointestinal bleeding in people with liver diseases. © 2015 The Cochrane Collaboration.

WOS: 000372137700022 Oral anticoagulant therapy with warfarin is commonly used to prevent thromboembolic events in, high risk patients. A spontaneous intramural intestinal hematoma is a rare complication of the anticoagulant therapy. Small intestinal obstruction, which is developed due to intramural hematoma, is an even more rarely encountered state. Early diagnosis is very important since it responses to the treatment very well without requiring operation on the most patients. In our unstable case, although there is no risk factor, INR was reduced quickly by using prothrombin complex concentrate (Factor II/VII/IX); this raised the possibility of patient's treatment without complication.

Objective-The beneficial effect of dietary fish oil, rich in omega-3 polyunsaturated fatty acids (PUFAs), on cardiovascular disease is multifactorial and may partly rely on their anticoagulant action. We studied how fish oil intake influenced thrombin generation in plasma and which factors were involved herein. Methods and Results-Twenty-five healthy males with borderline overweight received 3.0 g omega-3 PUFAs daily for 4 weeks. Fish oil intake reduced plasma triglycerides and lowered platelet integrin activation, as well as plasma levels of fibrinogen and factor V, but had no effect on vitamin K-dependent coagulation factors. Before fish oil intake, thrombin generation (reflecting the coagulant potential) considerably varied between plasmas from individual subjects, which were partly explained by variation in prothrombin, antithrombin, fibrinogen, and factor V levels. Fish oil intake reduced thrombin generation in the presence and absence of platelets. This reduction correlated with the fish oil effect on fibrinogen and factor V levels. Interestingly, the lowering effect of fish oil on thrombin generation and fibrinogen clustered around subjects with high fibrinogen carrying a structural fibrinogen α-chain polymorphism. Conclusions-Dietary omega-3 PUFAs provoke a hypocoagulant, vitamin K-independent effect in humans, the degree of which may depend on fibrinogen level. Chemicals / CAS: antithrombin, 9000-94-6; blood clotting factor 5, 9001-24-5, 9013-23-4; cholesterol, 57-88-5; fibrinogen, 9001-32-5; fish oil, 8016-13-5; protein C, 60202-16-6; prothrombin, 9001-26-7; thrombin, 9002-04-4; vitamin K group, 12001-79-5; Cholesterol, LDL; Factor V, 9001-24-5; Fatty Acids, Omega-3; Fibrinogen, 9001-32-5; Fish Oils; Peptide Fragments; Thrombin, 3.4.21.5; Triglycerides; thrombin receptor peptide (42-47)

Recent reports of several bone-derived substances, some of which have hormonal properties, have shed new light on the bone-cardiovascular axis. Deranged concentrations of humoral factors are not only epidemiologically connected to cardiovascular morbidity and mortality, but can also be causally implicated, especially in chronic kidney disease. FGF23 rises exponentially with advancing chronic kidney disease, seems to reach maladaptive concentrations, and then induces left ventricular hypertrophy, and is possibly implicated in the process of vessel calcification. Sclerostin and DKK1, both secreted mainly by osteocytes, are important Wnt inhibitors and as such can interfere with systems for biological signalling that operate in the vessel wall. Osteocalcin, produced by osteoblasts or released from mineralised bone, interferes with insulin concentrations and sensitivity, and its metabolism is disturbed in kidney disease. These bone-derived humoral factors might place the bone at the centre of cardiovascular disease associated with chronic kidney disease. Most importantly, factors that dictate the regulation of these substances in bone and subsequent secretion into the circulation have not been researched, and could provide entirely new avenues for therapeutic intervention. © 2014 Elsevier Ltd.

Anticoagulants are effective agents in reducing the risk of thromboembolism but the most important adverse effect of these agents is the occurrence of bleeding. Bleeding complications may occur spontaneously but the risk of bleeding is particularly increased in case of trauma or around invasive procedures. If patients being treated with anticoagulants need to undergo an invasive intervention, physicians need to consider whether to interrupt the use of this medication or to allow its use to be continued. Suspending the use of anticoagulants increases the risk of thrombosis, whereas continued use may cause bleeding complications. To shorten the period in which anticoagulant treatment is interrupted, bridging strategies have been advocated. No evidence-based scientific research has been carried out regarding best practice for the perioperative use of anticoagulants. The periprocedural anticoagulation policy in patients should be individualised based on the risk of a thromboembolic complication (which can be estimated with available scoring systems) offset against the bleeding risk associated with the intervention. © Van Zuiden Communications B.V. All rights reserved.

The most important adverse effect of antithrombotic treatment is the occurrence of bleeding. in case of serious or even life-threatening bleeding in a patient who uses anticoagulant agents or when patient on anticoagulants needs to undergo an urgent invasive procedure, anticoagulant treatment can be reversed by various specific strategies. heparin and heparin derivatives can be counteracted by protamine sulphate, whereas the anticoagulant effect of vitamin K antagonists may be neutralised by administration of vitamin K or prothrombin complex concentrates. the antihaemostatic effect of aspirin and other antiplatelet strategies can be corrected by the administration of platelet concentrate and/or desmopressin, if needed. recently, a new generation of anticoagulants with a greater specificity towards activated coagulation factors has been introduced and most of these agents are currently being evaluated in clinical studies, showing promising results. the new-generation anticoagulants include specific inhibitors of factor iia or factor Xa (including pentasaccharides) and antiplatelet agents belonging to the class of thienopyridine derivatives. a limitation of the new class of anti-iia and anti-Xa agents may be the lack of an appropriate strategy to reverse the effect if a bleeding event occurs, although in some cases the administration of recombinant factor VIIa may be an option. © Van Zuiden Communications B.V. All rights reserved.

A case of mushroom poisoning by false morel, Gyromitra esculenta (Pers.) Fr. (Ascomycetes), in Denizli, Turkey, is reported and documented. A short description of the taxon, case of poisoning, and taxonomic discussions of G. esculenta is presented. © 2009 by Begell House, Inc.

Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-27T11:23:37Z No. of bitstreams: 0 Made available in DSpace on 2014-05-27T11:23:37Z (GMT). No. of bitstreams: 0 Previous issue date: 2008-08-01 Serviço de Cirurgia Cardiovascular Hosp. Das Clinicas da Universidade Estadual Paulista Julio de Mesquita Filho (HC-Unesp - Botucatu) Departamento de Cirurgia e Ortopedia Faculdade de Medicina de Botucatu Universidade Estadual Paulista Júlio de Mesquita Filho (Unesp - Botucatu) Serviço de Cirurgia Cardiovascular Hosp. Das Clinicas da Universidade Estadual Paulista Julio de Mesquita Filho (HC-Unesp - Botucatu) Departamento de Cirurgia e Ortopedia Faculdade de Medicina de Botucatu Universidade Estadual Paulista Júlio de Mesquita Filho (Unesp - Botucatu)

Objective-The beneficial effect of dietary fish oil, rich in omega-3 polyunsaturated fatty acids (PUFAs), on cardiovascular disease is multifactorial and may partly rely on their anticoagulant action. We studied how fish oil intake influenced thrombin generation in plasma and which factors were involved herein. Methods and Results-Twenty-five healthy males with borderline overweight received 3.0 g omega-3 PUFAs daily for 4 weeks. Fish oil intake reduced plasma triglycerides and lowered platelet integrin activation, as well as plasma levels of fibrinogen and factor V, but had no effect on vitamin K-dependent coagulation factors. Before fish oil intake, thrombin generation (reflecting the coagulant potential) considerably varied between plasmas from individual subjects, which were partly explained by variation in prothrombin, antithrombin, fibrinogen, and factor V levels. Fish oil intake reduced thrombin generation in the presence and absence of platelets. This reduction correlated with the fish oil effect on fibrinogen and factor V levels. Interestingly, the lowering effect of fish oil on thrombin generation and fibrinogen clustered around subjects with high fibrinogen carrying a structural fibrinogen α-chain polymorphism. Conclusions-Dietary omega-3 PUFAs provoke a hypocoagulant, vitamin K-independent effect in humans, the degree of which may depend on fibrinogen level. Chemicals / CAS: antithrombin, 9000-94-6; blood clotting factor 5, 9001-24-5, 9013-23-4; cholesterol, 57-88-5; fibrinogen, 9001-32-5; fish oil, 8016-13-5; protein C, 60202-16-6; prothrombin, 9001-26-7; thrombin, 9002-04-4; vitamin K group, 12001-79-5; Cholesterol, LDL; Factor V, 9001-24-5; Fatty Acids, Omega-3; Fibrinogen, 9001-32-5; Fish Oils; Peptide Fragments; Thrombin, 3.4.21.5; Triglycerides; thrombin receptor peptide (42-47)

Plant sterols and their saturated derivatives, known as stanols, reduce serum cholesterol when consumed in amounts of approximately 2 g per day. Stanol fatty acid esters have been developed as a highly fat-soluble form that may lower cholesterol more effectively than stanols. Stanol esters occur naturally in human diets, but at levels far below those known to lower cholesterol. The present study was conducted to assess the safety of stanol esters upon subchronic ingestion at levels comparable to or exceeding those recommended for lowering cholesterol. Two stanol fatty acid ester preparations, wood-derived stanol esters and vegetable oil-derived stanol esters, were fed to groups of 20 male and 20 female Wistar rats for 13 weeks, at dietary concentrations of 0, 0.2, 1, and 5% total stanols (equivalent to 0, 0.34, 1.68, and 8.39% wood-derived stanol esters and 0, 0.36, 1.78, and 8.91% vegetable oil-derived stanol esters). Both preparations were well tolerated as evidenced by the absence of clinical changes or major abnormalities in growth, food and water consumption, ophthalmoscopic findings, routine hematological and clinical chemistry values, renal concentrating ability, composition of the urine, appearance of the feces, estrus cycle length, organ weights, gross necropsy findings, and histopathological findings. Plasma cholesterol and phospholipids were slightly decreased in males fed the stanol esters. In both sexes, plasma levels of plant sterols were decreased whereas those of stanols tended to increase. Fecal excretion of sterols, including cholesterol, and stanols was markedly increased in the stanol ester groups. Compared to controls, male rats fed stanol esters showed somewhat lower liver weights and more pronounced glycogen depletion. These hepatic changes were considered to reflect an altered nutritional condition and not a pathological condition. Plasma levels of vitamin E, vitamin K1, and, to a lesser extent, vitamin D were decreased in males and females fed the high-dose diets. Hepatic levels of vitamins E and D showed similar changes (vitamin K1 in the liver was not determined). For both preparations, the mid-dose level (1% total stanols in the diet) was a no-observed-adverse-effect level. This dietary level provided approximately 0.5 g total stanols/kg body wt/day.

Plant sterols and their saturated derivatives, known as stanols, reduce serum cholesterol when consumed in amounts of approximately 2 g per day. Stanol fatty acid esters have been developed as a highly fat-soluble form that may lower cholesterol more effectively than stanols. Stanol esters occur naturally in human diets, but at levels far below those known to lower cholesterol. The present study was conducted to assess the safety of stanol esters upon subchronic ingestion at levels comparable to or exceeding those recommended for lowering cholesterol. Two stanol fatty acid ester preparations, wood-derived stanol esters and vegetable oil-derived stanol esters, were fed to groups of 20 male and 20 female Wistar rats for 13 weeks, at dietary concentrations of 0, 0.2, 1, and 5% total stanols (equivalent to 0, 0.34, 1.68, and 8.39% wood-derived stanol esters and 0, 0.36, 1.78, and 8.91% vegetable oil-derived stanol esters). Both preparations were well tolerated as evidenced by the absence of clinical changes or major abnormalities in growth, food and water consumption, ophthalmoscopic findings, routine hematological and clinical chemistry values, renal concentrating ability, composition of the urine, appearance of the feces, estrus cycle length, organ weights, gross necropsy findings, and histopathological findings. Plasma cholesterol and phospholipids were slightly decreased in males fed the stanol esters. In both sexes, plasma levels of plant sterols were decreased whereas those of stanols tended to increase. Fecal excretion of sterols, including cholesterol, and stanols was markedly increased in the stanol ester groups. Compared to controls, male rats fed stanol esters showed somewhat lower liver weights and more pronounced glycogen depletion. These hepatic changes were considered to reflect an altered nutritional condition and not a pathological condition. Plasma levels of vitamin E, vitamin K1, and, to a lesser extent, vitamin D were decreased in males and females fed the high-dose diets. Hepatic levels of vitamins E and D showed similar changes (vitamin K1 in the liver was not determined). For both preparations, the mid-dose level (1% total stanols in the diet) was a no-observed-adverse-effect level. This dietary level provided approximately 0.5 g total stanols/kg body wt/day.