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PubMed1991

Effect of the somatostatin analogue octreotide acetate on hemostasis in humans.

Octreotide acetate is a somatostatin analogue that has been shown to ameliorate the side effects of excessive secretion of hormone from benign and malignant tumors. The ability of this drug to inhibit the growth of malignant cells and to control gastrointestinal hemorrhage will prompt additional clinical trials. Because some of these patients may have thrombocytopenia, platelet dysfunction, or a coagulopathy, we studied tests of platelet function and blood coagulation in 15 patients before and after 14 days of therapy with octreotide acetate at a dosage of 500 micrograms three times daily. We found no substantial change in the results of these tests, and no patient experienced bleeding or thrombosis. These results suggest that octreotide acetate does not adversely affect platelet function or the coagulation system in humans.

Adenoma, Islet Cell↗
PubMed1997

Pharmacodynamic models to evaluate antithrombotics in clinical pharmacology.

The need to prevent thromboembolic events effectively and safely has stimulated an intense search for novel antithrombotics. Parameters derived from in vitro tests with patients' blood are essential for therapeutic monitoring of anticoagulants. Clinical pharmacologic evaluation of novel antithrombotic therapies based on such parameters can easily fail, however, by neglecting pivotal pathophysiologic determinants of thrombus formation. When vascular injury occurs, blood cells, plasma proteins, and the vessel wall intimately cooperate for an adequate local repair. Much remains to be learned about the local and transient interaction of these components. In most tests of platelet function and coagulation proteins, blood samples from treated individuals are stimulated in vitro to assess inhibitory effects. Limitations of such a test strategy for dose-finding studies with antithrombotics may be overcome by measuring activation markers specifically generated on the surface of blood cells or in plasma at the site of thrombosis in patients.

Animals↗
PubMed1983

In vivo platelet activation with in vitro hyperaggregability to arachidonic acid in renal allograft recipients.

Renal allograft recipients were investigated to determine the extent and possible nature of in vivo platelet activation. In 92 allografted patients stable for more than 4 months' duration, intraplatelet serotonin in circulating platelets was depleted significantly. In a further 16 patients studied serially for 12 to 16 weeks following transplantation, intraplatelet serotonin fell abruptly within 4 days from transplantation to very low levels, and remained thus for 10 weeks, rising toward normal at about 12 weeks. Although some patients showed abrupt falls in intraplatelet serotonin coincident with acute rejection episodes, there was no difference in intraplatelet serotonin in seven patients whose grafts functioned well immediately and remained stable, and seven in whom repeated rejection led to graft loss within 3 months. Thus, these tests of platelet function do not permit diagnosis of rejection or prediction of graft outcome. Plasma platelet factor 4 (PF4) concentrations, in contrast, were normal in most patients during the first 6 weeks after grafting, then rose and remained abnormal up to 13 years following the allograft in the long-term stable graft recipients. This discrepancy suggests a different mode of platelet activation in the first few weeks after grafting from subsequent months. Despite universal depletion of intraplatelet amines and alpha-granule contents only four out of 14 early allograft recipients had an abnormal bleeding time, and platelet aggregation thresholds with adenosine-5'-diphosphate and collagen were not different from controls. However, thresholds for platelet aggregation with arachidonic acid were reduced significantly (P less than 0.01) and thromboxane B2 generation was increased in vitro. There was no correlation between depletion of intraplatelet serotonin and circulating platelet-agglutinating material, but nine of 17 biopsy specimens from rejecting allografts taken during the first 3 months showed extensive glomerular localization of platelet membrane antigens and PF4.

Adenosine Diphosphate↗
PubMedDate not supplied

Comparison of different assays for von Willebrand factor in hemodialysis patients.

Von Willebrand factor (vWF) abnormalities are involved in the hemostatic disturbances of uremia. Studies of vWF in both anemic and recombinant erythropoietin (EPO)-treated maintenance hemodialysis (HD) patients have given inconsistent results that could be partially dependent on the methodology. Therefore, the reciprocal relationships between four different vWF assays were studied in HD patients in relation to EPO therapy. Plasma vWF activity measured by ELISA using monoclonal antibodies against platelet glycoprotein (GP) Ibalpha (vWF:Act), plasma vWF antigen concentration by ELISA employing polyclonal antihuman vWF antibodies (vWF:Ag), and functional vWF activity by ristocetin-induced platelet aggregation (RIPA) in both platelet-rich plasma (PRP) and whole blood were studied in 70 HD patients. In the whole group, no correlations between these assays were found. In the non-EPO patients (n = 32), vWF:Act was correlated with vWF:Ag (r = 0.504, p = 0.003) but not with vWF activity by RIPA in PRP. In the EPO-treated patients (n = 38), vWF:Act was higher than in the untreated ones (p = 0.001), and vWF:Ag was related to the whole-blood RIPA (r = 0.386, p = 0.016). In conclusion, the platelet GP Ibalpha-binding epitope of the vWF molecule assessed by vWF:Act ELISA is intact in HD patients. However, this assay does not reflect the functional vWF activity as measured by RIPA in PRP. In EPO-treated patients, the GP Ibalpha-binding domains of vWF are more available but the plasmatic vWF monomers are neither more numerous by vWF:Ag ELISA nor more hemostatically active by RIPA PRP. The whole blood RIPA test has some potential for the quantification of vWF monomers in EPO-treated HD patients.

Clinical Chemistry Tests↗
PubMed1995

Laboratory evaluation of platelet dysfunction.

Platelet dysfunction, especially acquired forms, is a common cause of hemorrhage, especially when associated with trauma or surgery. Although the hereditary platelet function defects are generally rare, hereditary storage pool disease is common enough to be suspected in an individual, usually a child, with characteristic historical and clinical findings. The acquired platelet function defects, especially those resulting from drugs, are very common and should promptly be suspected in patients with easy and spontaneous bruising, mild-to-moderate mucosal membrane hemorrhage, or unexplained bleeding associated with trauma or surgery. The template bleeding time is generally useful as a screening test of platelet function, but a normal template bleeding time, in the face of a suggestive history, suggestive clinical findings, or in the patient frankly bleeding, is not reliable, and platelet aggregation or lumi-aggregation should be done in applicable clinical situations. Prolongation of the template bleeding time is an unreliable predictor of clinical bleeding propensity. The mainstay of therapy for all of these defects, if bleeding is important, is the liberal infusion of suitable numbers of platelet concentrates. The acquired platelet function defects should also be managed by attempts to treat or control the underlying disease, if possible, and offending drugs or potentially offending drugs should immediately be stopped.

Blood Platelet Disorders↗
PubMed1993

Changes in the blood endotoxin concentration after digestive surgery.

Blood endotoxin concentrations measured in 57 patients with digestive disorders pre- and postoperatively, were found to peak one day after surgery, then gradually return to the preoperative level. The plasma endotoxin concentration was not significantly different in patients with and without liver cirrhosis before surgery, but was significantly higher in the cirrhosis group one day after surgery. The preoperative endotoxin concentration did not correlate with the white blood count (WBC), platelet count, or routine biochemical liver function tests, however, a significant negative correlation was observed between the plasma endotoxin and fibronectin concentrations. The ability of plasma to inactivate endotoxin was quantified by serial measurements of the endotoxin concentration following the addition of a known quantity to each patient's plasma. The plasma from normal subjects quickly inactivated endotoxin, but inactivation was decreased in the plasma from patients with liver failure.

Digestive System Diseases↗
PubMed1989

Abnormal bleeding.

Animals with disorders of hemostasis are often presented as emergency patients and, as such, offer a challenge to the attending clinician. This article reviews the basic physiology of hemostasis and laboratory tests used for diagnosis. Guidelines for the evaluation and treatment of patients with bleeding disorders are provided.

Animals↗
PubMed2004

Does hemodilution enhance coagulability?

UNLABELLED: Recent publications reported enhanced coagulability in hemodilution determined by TEG. In contrast, earlier reports have shown prolongation of in-vivo bleeding time in anemia. In order to take a closer look at this discrepancy undiluted and diluted anticoagulated blood samples (20 % with saline solution, hydroxyl-ethyl starch 6 % (HES), autologous platelet poor plasma (PPP)) were investigated by TEG (n = 10), ball (n = 10), and hook coagulometer (n = 15) as well as tests simulating primary hemostasis ex vivo (Platelet Function Analyzer PFA-100, n = 10). RESULTS: Dilution with plasma changed TEG parameters in a way, when started by recalcification of the blood sample, which is characteristic of enhanced coagulability (r decreased in all and k in 8 of 10 samples, maximal amplitude increased in 9 out of 10). With HES, changes in TEG parameters mainly indicated reduced coagulability (k increased in 7 out of 10, MA decreased in 10 out of 10). When the coagulation was additionally activated by PTT reagent (InTEG) the TEG parameters also mainly showed hypocoagulation with the three dilution solutions. Coagulation times with ball and hook coagulometers were significantly prolonged by dilution especially with saline (+ 25 % and + 17 %, p < 0.001). Dilution always significantly (often abnormally) prolonged closure time in PFA-100 (saline + 41 +/- 18 %, PPP + 37 +/- 20 %, HES + 69 +/- 24 %) demonstrating disturbance of primary hemostasis, particularly with HES. CONCLUSIONS: From the results obtained it can be concluded that the changes in the classical TEG (without addition of PTT-reagent), suggesting an enhanced coagulability, may be caused methodically as they are also found with autologous PPP. On the other hand, a disturbance of the primary hemostasis in hemodilution has to be taken into account from the results seen with the PFA-100 and a number of published data.

Blood Coagulation↗
PubMed1986

[Prolonged bleeding time in severe anemia].

The frequency and importance of prolonged bleeding time were studied in patients affected by a severe anemia (haemoglobin less than 8 g/dl). A Simplate bleeding time test was performed in 25 patients suffering from various haematological disorders, with a platelet count greater than 100,000/cu mm and a normal or increased factor VIII complex. Patients with acute leukaemia, myeloproliferative disorders or chronic renal impairment were excluded from the study. Bleeding time was prolonged in 12 patients; their mean haematocrit was not different from that of the 13 other patients whose bleeding time was in the normal range. Bleeding time was less prolonged than in patients with chronic renal insufficiency in spite of a lower mean haematocrit (previous study). Fifteen patients were investigated a second time after partial or full correction of the haematocrit; in all but one, the bleeding time was reduced and/or normalized. This study suggests that severe anaemia may be an additional hemorrhagic risk factor in patients with another cause of bleeding.

Anemia↗
PubMed1986

An automatic pneumatically driven autotransfusion system: a hematologic evaluation in dogs.

An automatic, pneumatically driven autotransfusion system (ATS) was developed because ATSs driven by roller pumps are complicated to set up and require an experienced operator. In this ATS blood is aspirated into a cardiotomy reservoir by means of a constant vacuum applied on that reservoir. Damage to blood cells is reduced by an electronic device that regulates an automatic tubing clamp in the suction line to prevent suction of air along with blood (controlled suction). The blood is reinfused by a diaphragm pump driven by alternating vacuum and compressed air. The frequency of this pump is regulated by a level sensor in the cardiotomy reservoir to maintain a constant preset level. When we tested this automatic ATS in dogs, platelet function and platelet numbers substantially recovered after a dip during an autotransfusion period of 1 hour. Advantages of this ATS are that it causes only minor blood damage, it does not require a specially trained operator, and it is ready to use in every operating room. The diaphragm pump can be made disposable and integrated in the bottom of a cardiotomy reservoir.

Animals↗
PubMed1992

The in vivo effect in humans of pyridoxal-5'-phosphate on platelet function and blood coagulation.

Vitamin B6 has an antithrombotic effect. This, based on the results of in vitro studies, has been attributed to an antiplatelet effect. We assessed the in vivo effect of vitamin B6 by measuring the effect of long-term administration of vitamin B6 on platelet function and blood coagulation. Vitamin B6 (pyridoxine hydrochloride), 100mg twice daily p.o. for fifteen days, was administered to 10 healthy volunteers. The bleeding time was measured before the first dose and 15 days after. A baseline value, the acute effect, chronic effect, and the acute-on-chronic effect of vitamin B6 was estimated by measuring platelet function. The following tests were performed: platelet aggregation induced by collagen, ADP and epinephrine; thromboxane A2 (TxA2)-production and prostacyclin inhibition of ADP-induced aggregation. The effects on the coagulation system were monitored by measuring: the prothrombin time, activated partial thromboplastin time and levels of coagulation factor. Vitamin B6 significantly prolonged the bleeding time from 4.1 +/- 1.1 minutes to 6.8 +/- 1.0 minutes (p = 0.0063). Aggregation of platelets with collagen was slightly but not significantly inhibited. Platelet aggregation induced with the agonists ADP or epinephrine was significantly inhibited by vitamin B6, and the platelets tended to aggregate at a slightly decreased rate. The mean TxA2-production was slightly, but not significantly, decreased. Vitamin B6 had no effect on the sensitivity of platelets to prostacyclin, or on the coagulation system. Our results indicate that the antithrombotic effects of vitamin B6 is limited to inhibition of platelet function; there was no measurable influence on coagulation. The results of this in vivo study are however such that clinical trials are warranted to further assess the efficacy of vitamin B6 as an antiplatelet drug.

Blood Coagulation↗