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Aspirin
Kinds of Aspirin Terms modified by Aspirin Selected AbstractsPossible Interaction Between Aspirin and ACE Inhibitors: Update on Unresolved ControversyCONGESTIVE HEART FAILURE, Issue 6 2000Israel M. Barbash BmedSc The widespread use of aspirin and angiotensin converting enzyme (ACE) inhibitors in patients with coronary artery disease contributes significantly to the reduction in morbidity and mortality from this common health problem. These agents are widely and concomitantly used, and they share mechanisms that may interact in negative or positive pathways. Data derived from in vitro preparations, animal studies, human studies, and case-control studies are inconsistent. No study has established firm evidence regarding the safety or adverse effect of aspirin on patients who are on ACE inhibitors. The efficacy and safety of aspirin in combination with ACE inhibitors has been questioned and debated. If a negative interaction does exist, it will affect daily practice in treating patients with coronary artery disease and heart failure. This article reviews the available data regarding the safety of combined aspirin and ACE-inhibitor treatment among patients with ischemic heart disease, to assess the possible interaction between the two drugs and to discuss thesignificance and implications of the data. [source] Aspirin reduces anticardiolipin antibodies in patients with coronary artery diseaseEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 12 2006I. Ikonomidis Abstract Background, Anticardiolipin antibodies (aCL) have been found to be elevated in patients with coronary artery disease (CAD) and have been associated with an adverse outcome owing to their prothrombotic activity. The aim of this study was to investigate the effect of aspirin treatment on aCL levels in patients with chronic CAD. Materials and methods, Forty patients with chronic CAD scheduled for elective coronary artery bypass graft surgery (CABG) and 40 healthy controls participated in the study. Patients were treated with 300 mg of aspirin once daily (o.d.) for the first 12 days and placebo for the following 12 days before CABG in a double-blind, cross-over trial. Immunoglobulin (Ig) G-, IgM-, IgA-aCL and C-reactive protein (CRP) levels were measured in the controls and at the end of each treatment period in the patients with CAD. Results, The IgA- and IgG-aCL levels were greater in patients with CAD than in the controls. Compared with the placebo, IgA, IgG subtypes and CRP levels were reduced after aspirin treatment (P = 0·001, P = 0·02, P = 0·04, respectively). The percentage reduction of IgA- and IgG-aCL was related to the percentage reduction of CRP after aspirin (P < 0·05). Conclusion, Aspirin treatment with 300 mg o.d. reduced the serum levels of IgA and IgG subtypes in patients with chronic CAD in parallel to a reduction in CRP. These findings offer an additional pathophysiological mechanism of the beneficial effects of aspirin in patients with chronic CAD. [source] ADP-induced platelet aggregation in acute ischemic stroke patients on aspirin therapyEUROPEAN JOURNAL OF NEUROLOGY, Issue 12 2008J.-K. Cha Background and purpose:, Aspirin is an important therapeutic regimen to prevent the recurrent ischemic events or death after acute ischemic stroke. In this study, we evaluated the relationship between the extent of adenosine diphosphate (ADP) -induced platelet aggregation and outcome in acute ischemic stroke patients on aspirin therapy. Methods:, We selected 107 acute ischemic stroke patients who had been prescribed aspirin and evaluated platelet function test by using optic platelet aggregometer test after 5 days of taking it and investigated the prognosis 90 days after ischemic events. Kaplan,Meyer curve was used for survival analysis. Results:, After stratification of the subjected patients by tertiles of ADP-induced platelet aggregation, the events rates were 7.4%, 9.3% and 30.8% (P = 0.023). In multiple logistic regression analysis, old age over 70 years (OR, 13.7; 95% CI, 2.14,88.07; P = 0.001) and the increased ADP-induced platelet aggregation had independent significance to the risk of primary end-points after acute ischemic stroke (OR, 1.1; 95% CI 1.01 to 1.20; P = 0.026). Conclusions:, This study showed that the increased ADP-induced platelet aggregation under using aspirin is associated with poor outcome after acute ischemic stroke. [source] Acetaminophen, Aspirin, and Caffeine Versus Sumatriptan Succinate in the Early Treatment of Migraine: Results From the ASSET Trial,A CommentHEADACHE, Issue 4 2007Frederick J. Derosier DO No abstract is available for this article. [source] Acetaminophen, Aspirin, and Caffeine Versus Sumatriptan Succinate in the Early Treatment of Migraine: Results From the ASSET trial,A response to Drs. Derosier and KoriHEADACHE, Issue 4 2007Jerome Goldstein MD No abstract is available for this article. [source] Effects of Aspirin on the Development of Helicobacter pylori -Induced Gastric Inflammation and Heterotopic Proliferative Glands in Mongolian GerbilsHELICOBACTER, Issue 1 2008Guo Qing Li Abstract Background: Helicobacter pylori infection is a major cause of gastritis and gastric carcinoma. Aspirin has anti-inflammatory and antineoplastic activity. The aim of the present study was to determine the effects of aspirin on H. pylori -induced gastritis and the development of heterotopic proliferative glands. Methods: H. pylori strain SS1 was inoculated into the stomachs of Mongolian gerbils. Two weeks after inoculation, the animals were fed with the powder diets containing 0 p.p.m. (n = 10), 150 p.p.m. (n = 10), or 500 p.p.m. (n = 10) aspirin. Mongolian gerbils were killed after 36 weeks of infection. Uninfected Mongolian gerbils (n = 10) were used as controls. Histologic changes, epithelial cell proliferation and apoptosis, and prostaglandin E2 (PGE2) levels of gastric tissue were determined. Results: H. pylori infection induced gastric inflammation. Administration of aspirin did not change H. pylori -induced gastritis, but alleviated H. pylori -induced hyperplasia and the development of heterotopic proliferative glands. Administration of aspirin accelerated H. pylori -associated apoptosis but decreased H. pylori -associated cell proliferation. In addition, the increased gastric PGE2 levels due to H. pylori infection were suppressed by treatment with aspirin, especially at the dose of 500 p.p.m. Conclusions: Aspirin alleviates H. pylori -induced hyperplasia and the development of heterotopic proliferative glands. Moreover, aspirin increases H. pylori -induced apoptosis. We demonstrated the antineoplastic activities of aspirin in H. pylori -related gastric carcinogenesis. [source] Aspirin: not currently for primary prevention in diabetesINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 6 2009G. Jackson No abstract is available for this article. [source] Prevention of secondary stroke and transient ischaemic attack with antiplatelet therapy: the role of the primary care physician roleINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 10 2007H. S. Kirshner Summary Background:, Stroke risk is heightened among patients who have had a primary stroke or transient ischaemic attack (TIA). The primary care physician is in the best position to monitor these patients for stroke recurrence. Because stroke recurrence can occur shortly after the primary event, guidelines recommend initiating antiplatelet therapy as soon as possible. Aspirin, with or without extended-release dipyridamole (ER-DP), and clopidogrel are options for such patients. Low-dose aspirin (75,150 mg/day) has the same efficacy as higher doses but with less gastrointestinal bleeding. Clopidogrel remains an option for prevention of secondary events and may benefit patients with symptomatic atherothrombosis, but its combined use with aspirin can harm patients with multiple risk factors and no history of symptomatic cerebrovascular, cardiovascular or peripheral vascular disease. Results:, Low dose aspirin is effective in secondary stroke prevention. Trials assessing aspirin plus ER-DP have shown that the combination is more effective than aspirin monotherapy in preventing stroke, with efficacy increasing among higher risk patients, notably those with prior stroke/TIA. Clopidogrel does not appear to have as much advantage over aspirin in secondary stroke prevention as aspirin plus ER-DP. Smoking cessation and cholesterol, blood glucose and blood pressure control are also important concerns in preventing recurrent stroke. In choosing pharmacological therapy, the physician must consider the individual patient's risk factors and tolerance, as well as other issues, such as use of aspirin among patients with ulcers. Conclusion:, Antiplatelet therapy is effective in secondary stroke prevention. Low dose aspirin can be used first-line, but aspirin plus ER-DP improves efficacy. Clopidogrel is another option in secondary stroke prevention, especially for aspirin-intolerant patients, but it appears to have less advantage over aspirin than aspirin plus ER-DP, and its combined use with aspirin has only marginally better efficacy and increased bleeding risk. [source] The genetics of aspirin resistanceINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 5 2007Timothy Goodman Summary Aspirin is widely used for the prophylaxis of cardiovascular events in patients with cardiovascular risk factors or established atherosclerotic disease. However, despite aspirin treatment, a substantial number of patients experience recurrent events. Such ,aspirin resistance' is generally defined as failure of aspirin to produce an expected biological response, for example inhibition of platelet aggregation or of thromboxane A2 synthesis. Whilst its aetiology is multifactorial, genetic factors are also likely to play their part. Here we review the evidence for and against such a genetic contribution, as well as the data suggesting the involvement of specific genes. [source] Antithrombotic therapy for congestive heart failureINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 1 2006I. Chung Summary Patients with congestive heart failure (CHF) are at increased risk of thromboembolic events. However, there is much debate and uncertainty over the use of antithrombotic therapy in these patients. The evidence for oral anticoagulation is limited, although large randomised trial data are forthcoming. Aspirin may be detrimental for heart failure due to a possible interaction with angiotensin-converting enzyme inhibitors, leading to increased hospitalisations from decompensated heart failure. The objective of this review article is to summarise the available evidence regarding the risk of stroke and thromboembolic events in CHF patients, as well as the effectiveness and risks of antithrombotic therapy in these patients. [source] Regular or "Super-Aspirins"?JOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 4 2001A Review of Thienopyridines or Aspirin to Prevent Stroke PURPOSE: To review the evidence for the effectiveness and safety of the thienopyridines (ticlopidine and clopidogrel) compared with aspirin for the prevention of vascular events among patients at high risk of vascular disease. BACKGROUND: Atherosclerosis and resultant cardiovascular disease are important causes of morbidity and mortality in older people. In particular, atherosclerosis of the cerebral arteries can lead to transient ischemic attacks (TIAs) and stroke. Stroke ranks as the third-leading cause of death in the United States and in 1997 was responsible for over 150,000 fatalities.1 In addition to the mortality associated with this disease, stroke is also a leading source of long-term disability in survivors. Nearly 4.5 million stroke survivors are alive today,1 highlighting the fact that primary, but also secondary, prevention are extremely important for minimizing the complications of this illness. DATA SOURCES: Specialized trial registers of the Cochrane Stroke Group and the Antithrombotic Trialist's Collaboration, MEDLINE, and Embase were searched. Additional unpublished information and data were sought from Sanofi, the pharmaceutical company that developed and manufactures ticlopidine and clopidogrel, as well as the principal investigators of the Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events (CAPRIE) trial,7 the largest of the trials identified. STUDY SELECTION CRITERIA: All unconfounded randomized trials comparing either ticlopidine or clopidogrel with aspirin among patients at high risk of vascular disease (those with symptoms of ischemia of the cerebral, coronary, or peripheral circulations) who were followed for at least 1 month for the recurrence of vascular events were included. DATA EXTRACTION: Data were extracted from four completed randomized trials completed in the past 20 years, which included 22,656 patients.7,10 Two authors independently extracted the data from these trials for the following information: the types of patients enrolled; the entry and exclusion criteria; the randomization method; the number of patients originally allocated to the treatment and control groups; the method and duration of follow-up; the number of patients in each group lost to follow-up; information on compliance with the treatment allocated; the definitions of outcome events; the number of outcome events in each treatment group; and any method used for blinding patients, treating clinicians, and outcome assessors to treatment allocation. MAIN RESULTS: Four completed trials involving a total of 22,656 patients were identified. Aspirin was compared with ticlopidine in three trials (3,471 patients)8,10 and with clopidogrel in one trial (19,185 patients).7 A recent TIA or ischemic stroke was the qualifying event in 9,840 patients, a recent myocardial infarction in 6,302 patients, and symptomatic peripheral arterial disease in 6,514 patients. The average age of the patients was approximately 63, with approximately two-thirds of the patients being male and white. The duration of follow-up ranged from 12 to 40 months. CONCLUSIONS: This systematic review demonstrates that, compared with aspirin, thienopyridines are only modestly more effective in preventing serious vascular events in high-risk patients. For patients who are intolerant of, or allergic to aspirin, the available safety and efficacy data suggest that clopidogrel is an appropriate, but more-expensive, alternative antiplatelet drug. It appears safer than ticlopidine and as safe as aspirin but it should not replace aspirin as the first-choice antiplatelet agent for all patients. Further studies are necessary to determine which, if any, particular types of patients would benefit most and least from clopidogrel instead of aspirin. [source] Inhibitory effects of aspirin and indometacin on the growth of Helicobacter pylori in vitroJOURNAL OF DIGESTIVE DISEASES, Issue 4 2002Wei Hong WANG OBJECTIVE: The interactions between non-steroidal anti-inflammatory drugs and Helicobacter pylori have not been sufficiently documented to date. The aim of this study was to investigate the possible effects of aspirin and indometacin on the growth of H. pylori and to determine the effects of aspirin on the susceptibility of H. pylori to some antimicrobials. METHODS: Kinetic studies were performed by inoculating strains of H. pylori in brucella broth with different concentrations of aspirin and indometacin. Growth of bacteria in the broth was assessed spectrophotometrically and by viable colony counts after incubation for 24 and 48 h. Bacterial morphology was determined by Gram stain under light microscopy. The minimal inhibitory concentration (MIC) of aspirin and indometacin was determined by the standard agar dilution method. The MIC of amoxicillin, clarithromycin and metronidazole was measured in the presence and absence of aspirin by the E -test method. RESULTS: Kinetic studies revealed that aspirin and indometacin inhibited the growth of H. pylori in a dose-dependent manner. The bactericidal activity of these agents was expressed by cell lysis. Aspirin at 400 µg/mL produced an almost 2-log decrease in the number of CFU/mL at 48 h. Similar inhibitory effects were obtained when 100 µg/mL indometacin was tested. The MIC at which 90% of H. pylori was inhibited was 512 µg/mL and 128 µg/mL for aspirin and indometacin, respectively. Increased susceptibility of H. pylori to amoxicillin, clarithromycin and metronidazole was found in the presence of aspirin. CONCLUSIONS: Aspirin and indometacin could significantly inhibit the growth of H. pylori when incubated in brucella broth in vitro. A subinhibitory concentration of aspirin enhanced the susceptibility of H. pylori to some antimicrobial agents. [source] Crushed Clopidogrel Administered via Nasogastric Tube Has Faster and Greater Absorption than Oral Whole TabletsJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 4 2009M. UROOJ ZAFAR M.B.B.S. Objectives: To compare the absorption of 300 mg clopidogrel administered crushed via nasogastric (NG) tube versus whole tablets taken orally in healthy volunteers. Background: Earlier antiplatelet therapy has proven benefits in treatment of myocardial infarction and in patients undergoing PCI. Aspirin can be delivered early in crushed form via NG tube after CABG surgery to prevent graft occlusion. If clopidogrel given crushed via NG tube provides faster absorption, it could allow earlier clopidogrel loading. Methods: Nine healthy human subjects (34.7 ± 11.1 years, 5 males) were given 300 mg clopidogrel in crushed form via NG tube with 30 mL water after 8 hours of fasting. Plasma levels of the primary circulating inactive clopidogrel metabolite SR26334 were measured after 20 minutes, 40 minutes, 1, 2, 4, 8, 12, and 24 hours of dosing. Following ,2 week washout, same subjects swallowed 300 mg clopidogrel (four 75 mg tablets) after an 8-hour fasting and SR26334 levels were measured at the same time points. Results: Plasma SR26334 concentrations peaked earlier after crushed delivery than after oral intake (44 vs. 70 minutes, P = 0.023) and the median peak was 80% higher (13,083 vs. 7,255 ng/mL, respectively, P = 0.021). At 40 minutes, area under the curve was almost twofold greater with NG administration than oral administration (geometric means ratio = 0.5299, 95% CI = 0.28,0.99, P = 0.048), but was similar over the 24-hour period with both administration methods (geometric means ratio = 1.05, 95% CI = 0.84,1.32, P = 0.646). Conclusions: A 300 mg loading dose of crushed clopidogrel administered via NG tube provides faster and greater bioavailability than an equal dose taken orally as whole tablets. The clinical benefits of this strategy need to be investigated. [source] Transatrial Access to the Normal Pericardial Space For Local Cardiac Therapy: Preclinical Safety Testing with Aspirin and Pulmonary Artery HypertensionJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 5 2001TODD C. PULERWITZ M.D. The reliability, rapidity, and safety of nonsurgical, transatrial pericardial access for local cardiac therapy have been demonstrated in healthy animals. Since many patients take aspirin or have increased right-sided pressures, we evaluated the procedure's safety under these conditions. Transatrial pericardial access was performed in anesthetized pigs following aspirin administration (162 mg po, n = 6) or during experimental pulmonary artery hypertension (n = 4 different animals) and required only 3 minutes following guide catheter positioning. Platelet aggregability testing with arachidonic acid confirmed aspirin effectiveness. Mean pericardial fluid hematocrit was 0.1 ± 0.1% after 2 days of aspirin therapy and 1.9 ± 1.1% at sacrifice 24 hours later (NS). Mean pericardial fluid hematocrit was 1.0 ± 0.5% after 45 minutes of pulmonary artery hypertension and 4.3 ± 0.8% at sacrifice 30 minutes later (NS). Histologic analysis in both groups revealed a small thrombus and localized inflammation at the site of puncture. Neither aspirin use nor pulmonary artery hypertension causes significant bleeding into the pericardial space following transatrial access and thus does not preclude this route for local cardiac drug delivery. [source] Mechanisms of non-steroid anti-inflammatory drugs action on ASICs expressed in hippocampal interneuronsJOURNAL OF NEUROCHEMISTRY, Issue 1 2008Natalia A. Dorofeeva Abstract The inhibitory action of non-steroid anti-inflammatory drugs was investigated on acid-sensing ionic channels (ASIC) in isolated hippocampal interneurons and on recombinant ASICs expressed in Chinese hamster ovary (CHO) cells. Diclofenac and ibuprofen inhibited proton-induced currents in hippocampal interneurons (IC50 were 622 ± 34 ,M and 3.42 ± 0.50 mM, respectively). This non-competitive effect was fast and fully reversible for both drugs. Aspirin and salicylic acid at 500 ,M were ineffective. Diclofenac and ibuprofen decreased the amplitude of proton-evoked currents and slowed the rates of current decay with a good correlation between these effects. Simultaneous application of acid solution and diclofenac was required for its inhibitory effect. Unlike amiloride, the action of diclofenac was voltage-independent and no competition between two drugs was found. Analysis of the action of diclofenac and ibuprofen on activation and desensitization of ASICs showed that diclofenac but not ibuprofen shifted the steady-state desensitization curve to more alkaline pH values. The reason for this shift was slowing down the recovery from desensitization of ASICs. Thus, diclofenac may serve as a neuroprotective agent during pathological conditions associated with acidification. [source] Efficacy of different doses of aspirin in decreasing blood levels of inflammatory markers in patients with cardiovascular metabolic syndromeJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 11 2009Dr Xiu-ren Gao Abstract Objectives Inflammation and platelet aggregation and activation are key processes in the initiation of a cardiovascular event. Patients with metabolic syndrome have a high risk of cardiovascular events. This study determined whether small and medium doses of aspirin have anti-inflammation and antiplatelet aggregation effects in patients with metabolic syndrome. Methods One hundred and twenty-one consecutive patients with metabolic syndrome were randomized into three groups, receiving 100 mg/day of aspirin, 300 mg/day of aspirin or a placebo, respectively, for 2 weeks. The blood levels of thromboxane B2 (TXB2), a stable product of the platelet aggregation mediator TXA2, 6-keto-prostaglandin F1-, (6-keto-PGF1-,), a stable product of the endogenous cyclooxygenase metabolite prostaglandin I2, and inflammatory mediators including high-sensitivity C-reactive protein (hs-CRP), tumour necrosis factor-, (TNF-,) and interleukin-6 (IL-6), were determined by ELISA and radioimmunoassay. Key findings The blood levels of hs-CRP, TNF-,, IL-6 and TXB2 were significantly decreased after 2 weeks of treatment with 300 mg/day of aspirin. Patients who received 100 mg/day of aspirin had decreased blood levels of hs-CRP and TXB2. The blood level of IL-6 in the 300 mg/day aspirin group was significantly lower than that in the other two groups after 2 weeks of therapy. Aspirin at either dose did not affect the blood level of 6-keto-PGF1-,. Conclusions Aspirin at all doses suppresses the blood levels of inflammatory markers and the platelet aggregation mediator TXA2 in Chinese patients with metabolic syndrome. Since the suppression induced by 300 mg/day of aspirin was greater than that induced by 100 mg/day of aspirin, these data suggest that 300 mg/day of aspirin may be beneficial in decreasing the risk of cardiovascular events in Chinese patients with metabolic syndrome. [source] Systematic review: Helicobacter pylori and the risk of upper gastrointestinal bleeding risk in patients taking aspirinALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 7 2010E. H. Fletcher Aliment Pharmacol Ther 2010; 32: 831,839 Summary Background, Aspirin is widely used to modify the risk of recurrent vascular events. It is, however, associated with increased upper gastrointestinal bleeding risk. The influence of Helicobacter pylori on this risk is uncertain. Aim, To determine the influence of H. pylori on upper gastrointestinal bleeding risk in patients taking aspirin. Methods, MEDLINE and EMBASE databases were searched. All studies providing data regarding H. pylori infection in adults taking aspirin and presenting with upper gastrointestinal bleeding were included. Results, A total of 13 studies that included 1 case,control, 10 cohort studies and 2 randomized-controlled trials (RCTs) were analysed. The case,control study (n = 245) determined H. pylori to be a significant independent risk factor for upper gastrointestinal bleeding. The cohort studies were heterogeneous, varying in inclusion criteria, doses and duration of aspirin used, mode of H. pylori testing and causative GI pathology considered. Comprising 5465 patients, H. pylori infection was tested for in 163 (0.03%) aspirin users with upper gastrointestinal bleeding. The RCTs yielded no significant results. Conclusions, The current data are not sufficient to allow meta-analyses. The widely held belief that H. pylori is a risk factor for upper gastrointestinal bleeding in regular aspirin users is not supported by the very limited evidence available. [source] Aspirin, 110 years laterJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 2009C. PATRONO Summary., Although conceived at the end of the 19th century as a synthetic analgesic agent with improved gastric tolerability vs. naturally occurring salicylates, acetylsalicylic acid (marketed as aspirin in 1899) turned out to be an ideal antiplatelet agent about 90 years later, following the understanding of its mechanism of action, the development of a mechanism-based biomarker for dose-finding studies, and the initiation of a series of appropriately sized, randomized clinical trials to test its efficacy and safety at low doses given once daily. At the turn of its 110th anniversary, aspirin continues to attract heated debates on a number of issues including (i) the optimal dose to maximize efficacy and minimize toxicity; (ii) the possibility that some patients may be ,resistant' to its antiplatelet effects; and (iii) the balance of benefits and risks in primary vs. secondary prevention. [source] Aspirin in the prevention and treatment of venous thromboembolism: a rebuttalJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 1 2007L. MAILLARDET [source] Aspirin in the prevention and treatment of venous thromboembolism: reply to a rebuttalJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 1 2007M. M. C. HOVENS [source] Aspirin inhibits endothelial cell activation induced by antiphospholipid antibodiesJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 7 2004S. Dunoyer-Geindre Summary., Background : Antiphospholipid antibodies (APLA) have been shown to activate endothelial cells (EC) in vitro, as documented by an increased expression of tissue factor as well as leukocyte adhesion molecules such as intercellular adhesion molecule-1, vascular cell adhesion molecule (VCAM)-1 and E-selectin. Currently, treatment of patients with the antiphospholipid syndrome includes aspirin, particularly for women with recurrent fetal loss. Objective : The present study was undertaken to investigate whether aspirin interferes with EC activation induced by APLA in vitro. Methods : IgG from 14 patients with APLA, and suffering from thrombotic complications and/or pregnancy morbidity, and control IgG were tested for their ability to modify the expression of VCAM-1 in human umbilical vein endothelial cells. VCAM-1 antigen was measured by flow cytometry and its mRNA by quantitative reverse transcriptase-polymerase chain reaction. Results : Incubation of EC with IgG from most of the patients led to a higher VCAM-1 expression compared with incubation with control IgG. The effect of aspirin was studied for the eight IgG samples that induced a more than 50% increase in VCAM-1. Aspirin (10 mm) treatment of the cells significantly reduced the VCAM-1 response to these APLA. Conclusions : Our results indicate that besides its antiplatelet properties, aspirin exerts a protective effect towards APLA at the EC level by decreasing leukocyte adhesion molecule expression at the cell surface. [source] Aspirin and salicylate inhibit colon cancer medium- and VEGF-induced endothelial tube formation: correlation with suppression of cyclooxygenase-2 expressionJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 10 2003M. I. Shtivelband Summary., To determine whether aspirin and salicylate suppress colon cancer cell-mediated angiogenesis, we evaluated the effects of aspirin and sodium salicylate on endothelial tube formation on Matrigel. Aspirin and sodium salicylate concentration-dependently inhibited human endothelial cell (EC) tube formation induced by conditioned medium collected from DLD-1, HT-29 or HCT-116 colon cancer cells. Aspirin and sodium salicylate at pharmacological concentrations were equally effective in blocking tube formation. Neutralizing antivascular endothelial growth factor (VEGF) antibodies blocked colon cancer medium-induced tube formation. VEGF receptor 2 but not receptor 1 antibodies inhibited tube formation to a similar extent as anti-VEGF antibodies. These results indicate that VEGF interaction with VEGF receptor 2 is the primary mechanism underlying colon cancer-induced angiogenesis. Aspirin or sodium salicylate inhibited VEGF-induced tube formation in a concentration-dependent manner comparable to that of inhibition of colon cancer medium-induced endothelial tube formation. It has been shown that cyclooxygenase-2 (COX-2) is pivotal in cancer angiogenesis. We found that colon cancer medium-induced COX-2 protein expression in EC and aspirin or sodium salicylate suppressed the cancer-induced COX-2 protein levels at concentrations correlated with those that suppressed endothelial tube formation. Furthermore, aspirin and sodium salicylate inhibited COX-2 expression stimulated by VEGF. These findings indicate that aspirin and other salicylate drugs at pharmacological concentrations inhibit colon cancer-induced angiogenesis which is correlated with COX-2 suppression. [source] Low-dose aspirin reduces the gene expression of gastrokine-1 in the antral mucosa of healthy subjectsALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 6 2008G. MARTIN Summary Background, Gastrokine 1 (GKN1), one of the most abundant transcripts in normal stomach, is down-regulated by Helicobacter pylori infection. Aspirin (ASA), which is often used for secondary prevention of cardiovascular events, can damage gastric-duodenal mucosa within 1 or 2 h of ingestion. Aim, To study the gastric mucosal expression of GKN1 during acute low-dose ASA consumption. Methods, Ten H. pylori -negative human volunteers took 100 mg ASA per day for 1 week, and underwent multiple upper GI endoscopies. GKN1 expression was analysed in antral and corpus mucosa by quantitative reverse-transcriptase polymerase chain reaction, western blot and immunohistochemistry (IHC). Gastric mucosal damage was detected endoscopically and histologically. Results, Gastrokine 1 was similarly expressed in both antral and corpus mucosa. The use of low-dose ASA led to a significant decrease (3.07 a.u. vs. 0.23 a.u., P < 0.001) in antrum at day 7, while GKN1 transcript levels in corpus mucosa were slightly elevated (twofold, P < 0.005). Western blot and IHC confirmed these changes at the protein level. Furthermore, IHC revealed a vesicular staining pattern in the cytoplasm for GKN1 that was confirmed by transfected human gastric adenocarcinoma cell line expressing GKN1. Conclusion, Our data demonstrated that low-dose ASA downregulates GKN1 expression specifically in antral mucosa. [source] Interactions between Helicobacter pylori and other risk factors for peptic ulcer bleedingALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 3 2002W. A. Stack To investigate the role of Helicobacter pylori, expressing the virulence marker CAGA (cytotoxin associated gene product A) in ulcer complications and its interaction with nonsteroidal anti-inflammatory drugs (NSAIDs) and other risk factors. Design: Case control study using conditional logistic regression analysis. Setting: University and City Hospitals, Nottingham. Subjects: 203 consecutive patients with ulcer bleeding and 203 age- and sex-matched controls. Results: Ulcer bleeding was more likely with positive H. pylori serology (odds ratio = 3.3, 95% CI: 1.7,6.6 for CagA positive, but only OR = 1.6, 95% CI: 0.7,3.7 for CagA negative serology), current smoking (OR 2.2, 95% CI: 1.04,4.7), aspirin , 300 mg daily (OR 7.7, 95% CI: 2.8,20.6), all other nonsteroidal anti-inflammatory drugs (NSAIDs: OR 10.6, 95% CI: 3.1,35.7 for , 1 defined daily dose lower and OR 22.6, 95% CI: 6.2,82.0 for higher doses) and past ulcer history (OR 5.6, 95% CI: 2.3,14.1). Aspirin , 300 mg daily was used by 25.1% of patients vs. 7.4% of controls. Smoking only enhanced risk in the presence of H. pylori, with a synergistic interaction (interaction odds ratio = 4.9, 2.4,9.9, P=0.002). Conversely, risks with non-aspirin NSAIDs were reduced in the presence of H. pylori, particularly if CagA-positive (interaction odds ratio=0.21, 0.05,0.9, P=0.03). Conclusions: CagA positive H. pylori infection is associated with an increased risk of ulcer bleeding. The risk from non-aspirin NSAIDs is even higher, but is less in H. pylori infected people. Low-dose aspirin is now commonly associated with ulcer bleeding. [source] Uncoupling of intestinal mitochondrial oxidative phosphorylation and inhibition of cyclooxygenase are required for the development of NSAID-enteropathy in the ratALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 5 2000Somasundaram Background: The pathogenesis of NSAID-induced gastrointestinal damage is believed to involve a nonprostaglandin dependent effect as well as prostaglandin dependent effects. One suggestion is that the nonprostaglandin mechanism involves uncoupling of mitochondrial oxidative phosphorylation. Aims: To assess the role of uncoupling of mitochondrial oxidative phosphorylation in the pathogenesis of small intestinal damage in the rat. Methods: We compared key pathophysiologic events in the small bowel following (i) dinitrophenol, an uncoupling agent (ii) parenteral aspirin, to inhibit cyclooxygenase without causing a ,topical' effect and (iii) the two together, using (iv) indomethacin as a positive control. Results: Dinitrophenol altered intestinal mitochondrial morphology, increased intestinal permeability and caused inflammation without affecting gastric permeability or intestinal prostanoid levels. Parenteral aspirin decreased mucosal prostanoids without affecting intestinal mitochondria in vivo, gastric or intestinal permeability. Aspirin caused no inflammation or ulcers. When dinitrophenol and aspirin were given together the changes in intestinal mitochondrial morphology, permeability, inflammation and prostanoid levels and the macro- and microscopic appearances of intestinal ulcers were similar to indomethacin. Conclusions: These studies allow dissociation of the contribution and consequences of uncoupling of mitochondrial oxidative phosphorylation and cyclooxygenase inhibition in the pathophysiology of NSAID enteropathy. While uncoupling of enterocyte mitochondrial oxidative phosphorylation leads to increased intestinal permeability and low grade inflammation, concurrent decreases in mucosal prostanoids appear to be important in the development of ulcers. [source] EAACI/GA2LEN guideline: aspirin provocation tests for diagnosis of aspirin hypersensitivityALLERGY, Issue 10 2007E. Ni, ankowska-Mogilnicka Abstract:, Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most common causes of adverse drug reactions. Majority of them are of the hypersensitivity type. The two frequent clinical presentations of aspirin hypersensitivity are: aspirin-induced bronchial asthma/rhinosinusitis (AIA/R) and aspirin-induced urticaria/angioedema (AIU). The decisive diagnosis is based on provocation tests with aspirin, as the in vitro test does not hold diagnostic value as yet. Detailed protocols of oral, bronchial and nasal aspirin provocation tests are presented. Indications, contraindications for the tests, the rules of drug withdrawal and equipment are reviewed. Patient supervision and interpretations of the tests are proposed. [source] Laboratory evaluation of aspirin responsiveness,AMERICAN JOURNAL OF HEMATOLOGY, Issue 5 2010Kristi J. Smock Aspirin is the most commonly used antiplatelet medication. Laboratory monitoring of aspirin response has recently become a topic of interest due to potential impacts on patient management and clinical outcomes. This article summarizes available laboratory testing of aspirin response with focus on technical issues, limitations, and current opinion on the utility of routine patient testing. Am. J. Hematol., 2010. © 2010 Wiley-Liss, Inc. [source] Aspirin increases mortality in diabetic patients without cardiovascular disease: a Swedish record linkage study,PHARMACOEPIDEMIOLOGY AND DRUG SAFETY, Issue 12 2009Lennart Welin MD Abstract Purpose Aspirin is effective in secondary prevention of cardiovascular disease. The results are less convincing when aspirin is used for primary prevention even in high-risk patients (i.e., patients with diabetes). We therefore analyzed the effect of aspirin on mortality and serious bleeding in diabetic patients with and without cardiovascular disease. Methods We performed a record linkage study of the patient registry of the Västra Götaland region in south-western Sweden, the Swedish mortality register and the Swedish register of dispensed drugs. All diabetic patients (n,=,58,465) from 1 July 2005 to 30 June 2006 were followed up with respect to bleeding until 31 October 2006, and mortality until 31 December 2006. Results When 19 confounding factors (diseases and interventions) were assessed, aspirin significantly increased mortality in diabetic patients without cardiovascular disease from 17% (95% confidence interval; 95%CI, 1,36) at age 50 years to 29% (16,43) at age 85 years. In contrast aspirin tended to decrease mortality among elderly diabetic patients with cardiovascular disease. Theoretical calculations indicated that aspirin caused 107 excess deaths among diabetic patients without cardiovascular disease and prevented 164 deaths among diabetic patients with cardiovascular disease. Aspirin also increased the risk of serious bleeding by 46% (95%CI, 22,75) in diabetic patients without cardiovascular disease but decreased the risk among those with cardiovascular disease. Conclusion Aspirin use in diabetes patients without cardiovascular disease remains controversial and current guidelines should be revised until results from ongoing large randomized controlled trials become available. Copyright © 2009 John Wiley & Sons, Ltd. [source] Inhibition of cyclooxygenase (COX) enzymes by compounds from Daucus carota L. SeedsPHYTOTHERAPY RESEARCH, Issue 8 2003kali A. Momin Abstract Cyclooxygenase (COX) enzymes inhibitory assay directed investigation of Daucus carota seed extracts resulted in the isolation and characterization of compounds, 2,4,5-trimethoxybenzaldehyde (1), oleic acid (2), trans -asarone (3) and geraniol (4). Compounds 1,4 showed 3.32, 45.32, 46.15, and 3.15% of prostaglandin H endoperoxide synthase-I (COX-I) inhibitory activity and 52.69, 68.41, 64.39 and 0% prostaglandin H endoperoxide synthase-II (COX-II) inhibitory activity, respectively at 100 mg mL,1. Compound 1 showed selectivity towards COX-II enzyme inhibition at 100 µg mL,1. The COX-II/COX-I ratio for compound 1 was 17.68 at 100 µg mL,1 compared to solvent control. Ibuprofen, Naproxen, Aspirin, Celebrex and Vioxx at concentrations of 2.06, 2.52, 180, 1.67 and 1.67 µg mL,1, respectively, gave COX-II/COX-I ratios of 1.13, 0.92, 0.24, 16 and 75, respectively. The inhibition of COX-II enzymes by compounds 1 at 100 µg mL,1 was signi,cant when compared to Aspirin, Ibuprofen, Naproxen and Celebrex at concentrations studied. Copyright © 2003 John Wiley & Sons, Ltd. [source] Attitudes to prescription of antiplatelet drugs by diabetes health workersPRACTICAL DIABETES INTERNATIONAL (INCORPORATING CARDIABETES), Issue 8 2007A Woodward RN, MPhill Diabetes Specialist Nurse Abstract The aim of this survey was to explore the attitudes to antiplatelet drug use amongst a group of UK diabetes specialist medical and nursing personnel. A postal questionnaire survey was circulated to all consultant diabetologists, specialist registrars in diabetes and diabetes specialist nurses working in the Mersey Deanery area. Seventy-eight questionnaires were sent out, 63 (81%) returned. The perceived use of antiplatelet therapy was significantly higher for type 2 diabetes compared with type 1 diabetes, especially in the absence of complications or cardiovascular risk factors (52% vs 21%, p = 0.0004). Responses were more variable for type 1 diabetes: more nurses than doctors advised antiplatelet drugs in the absence of risk factors (46% vs 5%, p = 0.0002) and in the presence of smoking (79% vs 51%, p = 0.034). Aspirin was first-line choice of antiplatelet drug; clopidogrel was generally used for gastric intolerance and aspirin allergy. We conclude that the combination of limited evidence base and imprecise guidelines is not favouring proper usage of antiplatelet drugs and that more evidence-based didactic guidelines are required. Copyright © 2007 John Wiley & Sons. [source] | |||||||||||||||||||||||||||||||||||||||||||||||||