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PubMedDate not supplied

FR128998 ameliorates liver injury in extended liver resection with ischemia in dogs.

BACKGROUND/AIMS: Platelet-activating factor is one of the most potent phospholipid mediators associated with inflammatory conditions such as ischemia and reperfusion injury. FR128998 (FR) is a novel platelet-activating factor receptor antagonist. In this study, we evaluated the effect of FR during an extended liver resection with ischemia in a canine model. METHODOLOGY: Animals were divided into two groups: the control group (n = 8), and the FR-treated group (n = 7) in which FR was administered via the portal vein. While the right portal pedicle was clamped for 60 min, the left portal branch remained patent to avoid splanchnic congestion. Following reperfusion, 75% of the liver (including the right central, quadrate, left central, left lateral, and papillary lobes) was resected. Hepatic venous blood was collected to measure GPT, GOT, and LDH levels. Hepatic tissue blood flow was measured by a laser Doppler flow meter. The liver specimen was harvested for histological study. RESULTS: GPT, GOT, and LDH levels after reperfusion were significantly (P < 0.05) lower in the FR-treated group than in the control group. Hepatic tissue blood flow was maintained significantly (P < 0.05) higher in the FR-treated group than in the control group. Histologically, accumulation of polymorphonuclear neutrophils significantly (P < 0.05) decreased in the FR-treated group compared with the control group. The 2-day survival rate was statistically (P < 0.05) better in the FR-treated group than in the control group. CONCLUSIONS: FR128998 provides a protective effect for liver parenchyma and sinusoidal endothelial cells during extended liver resection with ischemia.

Alanine Transaminase↗
PubMed1987

[HELLP syndrome: a life-threatening form of pre-eclampsia].

A rather unusual but dramatic form of EPH gestosis or pregnancy-induced hypertension is presented via the case of a 30-year old second gravida in the 30th week of pregnancy. This is a case of pre-eclampsia combined with haemolysis, elevated liver function tests and low platelet counts. Diagnostic features, pattern and pathophysiology are discussed with regard to international literature.

Adult↗
PubMed1981

Comparative effects of aspirin and acetaminophen on hemostasis.

The influences of aspirin and of acetaminophen on hemostasis were studied in normal healthy volunteers and in patients with either severe hemophilia A or hemophilia B. Acetaminophen did not alter the template bleeding time or the results of tests of platelet function in either group. Aspirin did prolong the template bleeding time and impaired platelet aggregation; these changes were most pronounced in patients with either form of hemophilia, and some (7/19) required plasma component therapy. Neither drug influenced the coagulation proteins or the fibrinolytic mechanism, as measured. The influences of a single dose (ranging from 975 to 1,950 mg) of acetaminophen and of a single dose (ranging from 325 to 2,925 mg) of aspirin were similar to those observed in persons receiving multiple doses. Acetaminophen is preferred in patients in whom a hemostatic influence is undesirable. However, either aspirin or acetaminophen can be used in normal healthy subjects.

Acetaminophen↗
PubMed2004

Absence of interaction between atorvastatin or other statins and clopidogrel: results from the interaction study.

BACKGROUND: Some, but not all, post hoc analyses have suggested that the antiplatelet effects of clopidogrel are inhibited by atorvastatin. We sought to address this issue prospectively by performing serial measurements of 19 platelet characteristics using conventional aggregometry, rapid analyzers, and flow cytometry. METHODS: The Interaction of Atorvastatin and Clopidogrel Study (Interaction Study) was designed for patients undergoing coronary stenting. All patients (n = 75) received 325 mg of aspirin daily for at least 1 week and 300 mg of clopidogrel immediately prior to stent implantation. They had been taking atorvastatin (n = 25), any other statin (n = 25), or no statin (n = 25) for at least 30 days prior to stenting. The main outcome measure was comparison of platelet biomarkers 4 and 24 hours after clopidogrel administration between study groups. RESULTS: At baseline, patients from both statin groups exhibited diminished platelet aggregation and reduced platelet expression of G-protein-coupled protease-activated thrombin receptor (PAR)-1. There were no significant differences in measured platelet characteristics among the study groups 4 and 24 hours after clopidogrel intake, with the exception of a lower collagen-induced aggregation at 24 hours and a constantly diminished expression of PAR-1 in patients treated with any statin. CONCLUSIONS: Statins in general, and atorvastatin in particular, do not affect the ability of clopidogrel to inhibit platelet function in patients undergoing coronary stenting. These prospective data also suggest that statins may inhibit platelets directly via yet unknown mechanism(s) possibly related to the regulation of the PAR-1 thrombin receptors.

Aged↗
PubMed2006

Sex differences in platelet reactivity and response to low-dose aspirin therapy.

CONTEXT: Recent randomized trials suggest that women may not accrue the same cardioprotective benefits as men do from low-dose aspirin therapy used in primary prevention. Failure of aspirin to suppress platelet aggregation in women is one hypothesized mechanism. OBJECTIVE: To examine differential platelet reactivity to low-dose aspirin therapy by sex. DESIGN, SETTING, AND PARTICIPANTS: A clinical trial of aspirin at 81 mg/d for 14 days was conducted in 571 men and 711 women. Baseline and post-aspirin therapy measures included platelet aggregation to arachidonic acid, adenosine diphosphate, epinephrine, and platelet function analyzer closure time. MAIN OUTCOME MEASURE: Sex differences in cyclooxygenase 1 (COX-1) direct and indirect platelet activation pathways before and after administration of aspirin. RESULTS: In 10 of the 12 platelet agonist exposures, women's platelets were significantly more reactive at baseline. However, after aspirin therapy, the percent aggregation to arachidonic acid (the direct COX-1 pathway) decreased more in women than in men (P<.001) and demonstrated near total suppression of residual platelet reactivity in both men and women. In COX-1 indirect pathways, women experienced the same or more platelet inhibition than men in 8 of the 9 assays yet retained modestly greater platelet reactivity after aspirin therapy. In multivariable analysis, female sex significantly predicted aggregation to 2 muM and 10 muM of adenosine diphosphate (P = .02 and <.001, respectively) and collagen at 5 mug/mL (P<.001) independent of risk factors, age, race, menopausal status, and hormone therapy. CONCLUSIONS: Women experienced the same or greater decreases in platelet reactivity after aspirin therapy, retaining modestly more platelet reactivity compared with men. However, most women achieved total suppression of aggregation in the direct COX-1 pathway, the putative mechanism for aspirin's cardioprotection.

Adenosine Diphosphate↗
PubMed2003

Rapid platelet inhibition after a single capsule of Aggrenox: challenging a conventional full-dose aspirin antiplatelet advantage?

Aggrenox is a novel combination of 25 mg of aspirin with 200 mg of sustained release dipyridamole. In a recent large trial (ESPS-2), Aggrenox was twice as effective for secondary stroke prevention as either aspirin or dipyridamole alone, suggesting superior platelet inhibition for combination therapy. We sought to compare the time course of platelet inhibition with Aggrenox compared with escalating doses of non-enteric coated aspirin. Data from 10 healthy volunteers were analyzed. Fasting subjects sequentially ingested aspirin in the following order: 325 mg, 81 mg, 25 mg, and then one pill of Aggrenox after a 3-week interval for aspirin washout. Platelet function was assessed at baseline, 15, 30, 60, and 120 min post-medication with 5 microM epinephrine and 5 microM ADP using conventional aggregometry. Aspirin provided significant (P < 0.01) reduction of platelet aggregation at 15 min post 325 mg, 30 min post 81 mg, and unexpectedly within 60 min after taking 25 mg of aspirin. A single pill of Aggrenox also inhibited platelet aggregation within 1 hr after administration. Aspirin inhibits platelets remarkably fast. Both Aggrenox and a matching dose of aspirin (25 mg) exhibit significant antiplatelet properties within 60 min after ingestion. These findings could be relevant for the optimal balance between the reduction of vascular events via sufficient and rapid platelet inhibition and low risk of bleeding complications associated with the Aggrenox therapy.

Adenosine Diphosphate↗
PubMed2003

Simple, rapid, and automated method for detection of hyperaggregability of platelets using a hematology analyzer.

Estimation of hyperaggregability of platelets is important for diagnosis and prevention of vascular events. We have developed and evaluated a simple and rapid method for detection of a hyperaggregable state of platelets by using an Abbott CELL-DYN(R) 4000 hematology analyzer. Citrated blood samples were collected from 62 patients with chronic cerebral infarction (CCI), of whom 19 patients were treated with ticlopidine, and from 9 healthy subjects. Platelet clumps were detected in the scatter plots for white blood cell populations with the hematology analyzer. Platelet clumps were positive in 20 of 43 (46.5%) CCI patients who were not treated with anti-platelet agents but not at all in 9 healthy subjects and in 19 CCI patients treated with ticlopidine. The detection of platelet clumps in citrated blood by the hematology analyzer was proved useful in detecting a platelet hyperaggregability in CCI patients. This method is simple, rapid, and automated and thus should be suitable for routine clinical use for monitoring indications and the efficacy of anti-platelet drugs.

Aged↗
PubMed2006

Use of whole blood platelet lumi-aggregometry to optimize anti-platelet therapy in patients with chronic myeloproliferative disorders.

Twenty-seven patients with chronic myeloproliferative disorders and in vitro evidence of platelet hyperactivity on whole blood platelet lumi-aggregometry were commenced on anti-platelet therapy comprising aspirin, clopidogrel, and/or odorless garlic and the studies were repeated to assess the efficacy of the therapeutic agent(s). Only 8 patients showed clear evidence of anti-platelet effect while receiving the standard low-dose (100 mg/day) aspirin therapy. Thirteen patients required a higher dosage of aspirin and/or an additional anti-platelet agent to achieve therapeutic adequacy. Lumi-aggregometry also proved useful to optimize therapy in the 6 patients who received clopidogrel or odorless garlic because of aspirin intolerance.

Aspirin↗
PubMed1987

Correction of the bleeding time in treated patients with severe von Willebrand disease is not solely dependent on the normal multimeric structure of plasma von Willebrand factor.

Even though it is generally held that cryoprecipitate and fraction I-O correct the prolonged bleeding time (BT) in patients with von Willebrand disease (VWD), perusal of reported data indicates that the correction is usually short-lasting and often partial. We decided to do a controlled study of the relationship between the multimeric structure of von Willebrand factor (VWF) and the BT in five patients with severe (type III) VWD after infusion of three plasma concentrates ("wet" cryoprecipitate, lyophilized cryoprecipitate, and fraction I-O) given in random order. The dosage of concentrates was tailored from in vitro measurements to achieve post-infusion levels of ristocetin cofactor above the lower normal limit (50 U/dL) for at least 3 hours. The postinfusion BT became transiently normal in only two of five patients treated with wet cryoprecipitate, whereas it remained prolonged in all five patients treated with lyophilized cryoprecipitate or fraction I-O. For all the concentrates, the proportion of large VWF multimers calculated by scanning the electrophoretic gels were the same as those for normal standard plasmas. An intact multimeric structure was recovered in postinfusion plasmas of patients treated with wet cryoprecipitate, whereas there was a postinfusion loss of large multimers after lyophilized cryoprecipitate and fraction I-O. These findings indicate that the attainment of a normal BT is the exception rather than the rule after the infusion of three plasma fractions used in the treatment of severe VWD, and that an intact multimeric structure in concentrates and postinfusion plasmas is necessary but not sufficient to sustain a normal BT.

Bleeding Time↗
PubMed1989

Subcutaneous desmopressin (DDAVP) shortens the bleeding time in uremia.

The intravenous infusion of 1-deamino-8-D-arginine vasopressin (DDAVP) is used as a nontransfusional form of treatment in patients with congenital and acquired bleeding disorders, including patients with uremia associated with prolonged bleeding times. Since uremic patients experience minor bleeding episodes that might be self-managed at home (particularly epistaxis, gingival bleeding, and menorrhagia), we carried out a double-blind, placebo-controlled crossover study in nine uremics to evaluate whether the prolonged bleeding times could be shortened by subcutaneous injections of DDAVP. One hour after administration, the bleeding time was significantly shortened (P less than .01) and became normal in seven of nine patients. After 4 hr, the bleeding time was still shorter than baseline (P less than .01), but in only three patients was it still normal. There was no significant bleeding time change after placebo. When the same patients were treated with the same dose of DDAVP infused intravenously, the bleeding times were not significantly different from those measured after subcutaneous administration. Hence, subcutaneous DDAVP is an alternative method for short-term shortening of the bleeding time in uremia, at least as effective as intravenous DDAVP but with the possibility of self-administration by the patients at home.

Adult↗
PubMed1989

Platelet glass bead retention is useful in monitoring response to 1-deamino-8-D-arginine-vasopressin (d-DAVP).

Seven patients with a suspected mild bleeding disorder had consistently abnormal glass bead platelet retention. This was the only coagulation abnormality detected in six of these patients; the seventh individual showed evidence of mild von Willebrand disease. Nevertheless, platelets from the six that were studied behaved in a similar fashion in the two-stage platelet retention assay of McPherson and Zucker. This indicated that their platelets were defective in maintaining repetitive platelet-platelet interaction in the second phase of this assay but functioned normally in the first phase. Their one-stage platelet retention defects consistently normalized following the infusion of 1-deamino-8-D-arginine-vasopressin (d-DAVP). The duration of response was variable and easily defined by monitoring this parameter. These findings suggest platelet retention analysis may be useful in identifying mild bleeding disorder patients, who may benefit from d-DAVP.

Adult↗
PubMed1991

Benign familial thrombocytosis.

A 13-year-old girl was found to have a platelet count in excess of 4 million/microliters while being evaluated for a minor bleeding episode. Her father and two sisters also had thrombocytosis. All four affected patients were asymptomatic and had no clinical or laboratory evidence of a myeloproliferative disorder other than an elevated platelet count. This represents the second reported instance of benign familial thrombocytosis.

Adolescent↗
PubMed2004

Prolonged bleeding time and lupus anticoagulant: a second paradox in the antiphospholipid syndrome.

OBJECTIVE: Systemic lupus erythematosus and antiphospholipid syndrome (APS) often appear concomitantly. Lupus nephritis and antiphospholipid antibody-related ischemic nephropathy cannot be distinguished clinically, although their etiology and treatment differ greatly. Examination of a renal biopsy sample is therefore essential in order to provide the correct treatment. We have observed that patients with lupus anticoagulant (LAC), a serologic marker for APS, often have a prolonged bleeding time, which is a contraindication for performing a percutaneous renal biopsy. We undertook this study to evaluate systematically the bleeding time in 27 consecutive patients. METHODS: The bleeding time was measured in 27 patients who were persistently positive for LAC and who were not exposed to aspirin or nonsteroidal antiinflammatory drugs. Platelet function and von Willebrand factor (vWF) parameters were subsequently assessed in patients with a prolonged bleeding time. RESULTS: Twenty-one of 27 patients (78%) had a prolonged bleeding time despite a normal platelet count in the majority of patients (81%). Platelet functioning and vWF parameters in these 21 patients were normal, except for those in 1 patient with a mild storage pool disease. CONCLUSION: With this study, we introduce yet another paradox in the phenomenon of APS. Although a prolonged bleeding time is generally accepted to be a sign of defective primary hemostasis, LAC is associated with thrombosis. Further studies are needed to elucidate the mechanism behind this disturbance of primary hemostasis.

Adult↗
PubMed2001

The platelet function dose-response to abciximab during percutaneous coronary revascularization is variable.

The platelet function dose-response to incremental abciximab (Reopro, Eli Lilly/Centocor, Indianapolis, IN) bolus dosing during percutaneous coronary intervention (PCI) was evaluated in 85 patients using a point-of-service platelet function assay. Patients received incremental bolus doses of abciximab at 10- to 20-min intervals; platelet function was measured at 10-min intervals during dosing. The percentage of patients achieving > or = 80% inhibition of platelet function after 50%, 75%, and 100% of a standard abciximab bolus was 40%, 87%, and 95%, respectively. There were no significant associations between the platelet function dose-response to abciximab and age, weight, platelet count, hematocrit, heparin dose, peak activated clotting time, thienopyridine use prior to PCI, gender, cigarette smoking, diabetes mellitus, or clinical syndrome. This study demonstrated significant interpatient variability in platelet function dose-response to abciximab with a substantial proportion (87%) of patients achieving high-level platelet function inhibition with less than the standard abciximab bolus dose.

Abciximab↗
PubMed1984

The effect of radiographic contrast agents on bleeding time and platelet aggregation.

The purpose of this study was to determine whether the use of relatively small amounts of radiographic contrast agents may impair hemostasis. Before and after injection of contrast agents, we measured the template bleeding time, platelet count in whole blood and platelet-rich plasma, platelet aggregation induced by epinephrine and adenosine diphosphate (ADP), and percent disaggregation of ADP-induced platelet aggregates in platelet-rich plasma of 18 patients. Ten patients received 50-100 ml of sodium iothalamate (66.8%) for intravenous urography and 8 patients received 125-200 ml of a combination of meglumine diatrizoate (66%) and sodium diatrizoate (10%) for coronary angiography and left ventriculography. Neither group demonstrated a statistically significant mean difference (p greater than 0.05) for any parameter measured before and after administration of the contrast agents. However, 2 patients who received diatrizoate had lengthening of their bleeding times to greater than twice the baseline value without any change in in vitro platelet aggregation. Physicians should be aware of this potential cause of bleeding which could be of particular danger to patients undergoing cardiopulmonary bypass with its inherent hemostatic defects.

Bleeding Time↗
PubMed1989

Thromboxane synthase activity and platelet function after furegrelate administration in man.

Furegrelate sodium (U-63,557A), a pyridine-derivative thromboxane synthase inhibitor, was administered orally in single doses of 200 to 1600 mg to normal male subjects. Furegrelate produced a dose-related inhibition of thromboxane synthesis for 8-12 hours when measured either ex vivo from platelet-rich plasma (PRP) or in vivo from urine. In general, the extent of thromboxane synthesis inhibition was greater in PRP than in urine. Furegrelate significantly inhibited platelet aggregation, but the effect was variable and measurements of thromboxane synthase did not predict the impact on platelet aggregation. Bleeding times and coagulation parameters were not altered significantly. Furegrelate was well absorbed orally with Tmax = 1 hr and t1/2 = 3.5 to 5 hrs. There was no marked metabolism; elimination was primarily by renal excretion of parent compound. Thus, furegrelate is an effective inhibitor of thromboxane synthase in man with a relatively long biologic and circulating half-life.

Adolescent↗