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P Giesen

Publications and source records attributed to P Giesen.

4 recordsLinked to original sources
PubMed2006

Patients either contacting a general practice cooperative or accident and emergency department out of hours: a comparison.

INTRODUCTION: Lack of collaboration between general practice (GP) cooperatives and accident and emergency (A&E) departments and many self referrals may lead to inefficient out-of-hours care. METHODS: We retrospectively analysed the records of all patients contacting the GP cooperative and all patients self referring to the A&E department out of hours in a region in the Netherlands. RESULTS: 258 patients contacted the GP cooperative and 43 self referred to the A&E department per 1000 patients per year. A wide range of problems were seen in the GP cooperative, mainly related to infections (26.2%). The A&E department had a smaller range of problems, mainly related to trauma (66.1%). Relatively few urgent problems were seen in the GP cooperative (4.6%) or for self referrals in the A&E department (6.1%). Women, children, the elderly, and rural patients chose the GP cooperative significantly more often, as did men and patients with less urgent complaints, infections, and heart and airway problems. DISCUSSION: The contact frequency of self referrals to the A&E department is much lower than that at the GP cooperative. Care is complementary: the A&E department focuses on trauma while the GP cooperative deals with a wide range of problems. The self referrals concern mostly minor, non-urgent problems and can generally be treated by the general practitioner, by a nurse, or by advice over the telephone, particularly in the case of optimal collaboration in an integrated care facility of GP cooperatives and A&E departments with one access point to medical care for all patients.

Adolescent↗
PubMed1997

Tissue factor in the pathogenesis of atherosclerosis.

TF antigen and activity are found in abundance in human atherosclerotic plaques, particularly in the lipid-rich core. TF is also readily induced in the arterial wall by balloon injury and accumulates in the resulting neointima. In chronic atherosclerosis, the macrophage is likely to be the major source of TF within the plaque. TF accumulates as an early event associated with the migration of monocytes to the vessel wall in response to chemoattractants, such as MCP-1, and their differentiation into macrophages. As SMC become activated in the developing plaque, they provide a second source of TF. Macrophages and SMC accumulate lipid and become foam cells, ultimately degenerating into a necrotic core rich in TF. Spontaneous plaque rupture or acute interventions expose active TF in the core to circulating blood, triggering thrombosis. In acute arterial injury, SMC appear to be the chief source of TF. In normal vessels, the induction of TF in the medial SMC is not sufficient to generate fibrin, presumably because the TF is not readily accessible on the luminal surface. In contrast, endothelial denudation of previously injured arteries may expose intimal TF to circulating blood, resulting in rapid fibrin deposition. In advanced human atherosclerosis, it is likely that even in areas that do not contain "unstable" or "stable" plaques, the vessel wall is not normal and more closely resembles that of a previously injured artery possessing an active intima. Interventions, such as balloon angioplasty, coronary atherectomy, or stent placement may expose intimal TF, leading to fibrin deposition. As the initiator of coagulation, TF is a potential target for inhibiting the thrombotic complications of atherosclerosis. TFPI (reviewed in 52) is currently under clinical investigation as an anticoagulant and its effects on intimal hyperplasia in animal models are being studied. Direct factor Xa inhibitors, such as tick anticoagulant peptide (TAP) and leech anticoagulant peptide (ATS), are also under investigation (53-54). Finally, the recent crystallization of TF (55) and the TF:VIIa (56) should provide important new insights into the design of molecules for directly inhibiting TF.

Animals↗
PubMedDate not supplied

The calibrated automated thrombogram (CAT): a universal routine test for hyper- and hypocoagulability.

By using a "slow" fluorogenic thrombin substrate and continuous comparison to a simultaneously run calibrator, thrombin generation can be monitored automatically, on line, in clotting PPP or PRP at a throughput of up to 100 samples per hour. The resulting "Thrombogram" in PPP measures hypocoagulability (haemophilias, oral anticoagulants, heparins (-likes), direct inhibitors) and hypercoagulabilities (AT deficiency, prothrombin hyperexpression, prot. C and S deficiency, factor V Leiden, oral contraceptives). In PRP it is diminished in thrombopathies, in von Willebrand disease, by antibodies blocking GPIIb-IIIa or GPIb, or by antiplatelet drugs like aspirin and clopidogrel. Lupus anticoagulant both retards and increases thrombin generation. The thrombogram thus appears to be a broad function test of the haemostatic-thrombotic mechanism of the blood.

Blood Coagulation Disorders↗