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  • 1
    ISSN: 1432-1173
    Keywords: Schlüsselwörter Venenthrombose ; Resistenz gegen aktiviertes Protein C ; Mutation des Faktor V-Gens ; Chronisch venöse Ulzera ; Key words Venous thrombosis ; Activated protein C resistance ; Factor V gene mutation ; Chronic venous leg ulcers
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Deep venous thromboses, in particular when recurrent, can be associated with chronic venous leg ulcers. Such complications are often seen in dermatology departments and frequently represent a therapeutic problem. Resistance to activated protein C (APCR) has recently been identified as the most frequent coagulation defect associated with an increased risk of venous thrombosis. In most cases, APCR is caused by a point mutation in the factor V gene which results in an impaired inactivation of activated factor V (Va). As a consequence of this, an important anticoagulant mechanism in the physiological balance of the hemostatic system is abolished. This autosomal dominantly inherited genetic defects affects about 5% of the general population. In this article we draw attention to the existence of this recently identified, genetically determined risk factor for venous thrombosis, describe recent diagnostic developments and discuss therapeutic options.
    Notes: Zusammenfassung Tiefe Venenthrombosen können insbesondere bei rezidivierendem Auftreten zur Manifestation chronisch venöser Unterschenkelulzera beitragen. Derartige Komplikationen werden regelmäßig in dermatologischen Kliniken gesehen und stellen nicht selten ein therapeutisches Problem dar. Vor kurzem konnte die erbliche Resistenz gegen aktiviertes Protein C (APCR) als häufigster Gerinnungsdefekt identifiziert werden, der mit einem erhöhten Thromboserisiko assoziiert ist. In den meisten Fällen wird diese Resistenz durch eine Punktmutation im Gen für den Gerinnungsfaktor V verursacht, die eine gestörte Inaktivierung des aktivierten Faktor V (Va) zur Folge hat. Dadurch wird ein wichtiger antikoagulatorischer Mechanismus für das physiologische Gleichgewicht im Hämostasesystem aufgehoben. Von diesem genetischen Defekt sind etwa 5% der Allgemeinbevölkerung betroffen. Mit diesem Beitrag möchten wir auf diesen erst vor kurzem aufgeklärten genetisch determinierten Risikofaktor venöser Thrombosen aufmerksam machen, der autosomal-dominant vererbt wird. Es werden neuere diagnostische Entwicklungen beschrieben und therapeutische Konsequenzen erörtert.
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  • 2
    ISSN: 1432-1440
    Keywords: Acute myelofibrosis ; Megakaryoblastic leukemia ; Platelet peroxidase ; Cytogenetics ; β-Thromboglobulin ; Flow cytometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In a 45-year-old woman with severe normochromic anemia (Hb 2.8 g%) an extensive myelofibrosis and infiltration of the bone marrow with small blasts was observed histologically. Cytochemical examination of the blasts showed a negative peroxidase and a strongly positive alpha-NE reaction. PAS reaction was slightly granular positive in the cytoplasmic protuberances of the blasts and in the platelets. Marker analysis yielded no evidence of lymphatic origin of the blasts. In flow-cytometric studies of 230,000 cells a homogeneous 2c blast population could be identified. Cytogenetic analysis revealed an abnormal pseudo-diploid karyotype characterized by 2 acrocentric marker chromosomes caused by a translocation of chromosomes 8 and 14, as usually seen in Burkitt type lymphoma. Finally the reaction product of platelet-specific peroxidase could be demonstrated in the perinuclear cisternae of the endoplasmic reticulum by electron microscopy. Highly elevated β-thromboglobulin and platelet factor 4 plasma levels were also measured. Following an ineffective treatment with daunoblastine and ARA-C, the patient died of pseudomonas aeruginosa septicemia after having received high-dose ARA-C treatment.
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  • 3
    ISSN: 1432-1440
    Keywords: Splenectomy ; Platelet defects ; Myeloproliferative disorders ; Hodgkin's disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Functional and morphometric platelet abnormalities may be influenced by splenectomy and thus contribute to postoperative thrombohaemorrhagic complications, especially in patients with splenomegaly and/or platelet defects. We investigated platelet function, platelet secretion, and platelet morphometry before and one week after splenectomy in seven patients with normal platelet production and normal spleen size (Hodgkin's disease) and five patients with splenomegaly and platelet abnormalities (4 with myeloproliferative disorders and 1 with chronic myelomonocytic leukemia). Severe postoperative thrombohaemorrhagic complications occurred only in patients with myeloproliferative disorders, although platelet count and mean platelet volume increased in almost all patients after splenectomy. Four patients with myeloproliferative disorders had impaired platelet aggregation before splenectomy that improved in only one patient after surgery. Platelet buoyant density in this patient group was decreased before splenectomy and normalised thereafter. Concomitantly, intraplatelet concentrations ofα-granular proteins increased. Before splenectomy, there was a positive correlation between platelet density and platelet volume in patients with Hodgkin's disease (r=0.59,p〈0.001), but not in patients with myeloproliferative disorders. There was no correlation between platelet density and platelet volume after splenectomy in either patient group. In conclusion, morphometric platelet abnormalities were found in all patients after splenectomy. In patients with myeloproliferative/myelodysplastic disorders, decreased platelet buoyant density normalised and intraplatelet concentrations ofα-granule proteins were elevated after splenectomy. However, platelet function defects in this patient group were not corrected and may have been a major cause of thrombohaemorrhagic complications in the postoperative period.
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  • 4
    ISSN: 1432-1440
    Keywords: Thrombotic microangiopathy ; Pathogenesis of disseminated platelet thrombi ; Diagnosis and differential diagnosis ; new forms of therapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Thrombotic thrombocytopenic purpura (TTP) is an uncommon disorder which usually occurs in young adults. It is characterized by a pentad of clinical findings: fever, neurological abnormalities, renal dysfunction, microangiopathic hemolytic anemia and thrombocytopenia. The histological hallmark is the presence of platelet thrombi occluding the microcirculation of multiple organs. The etiology and pathogenesis of disseminated platelet aggregation are uncertain and obviously not uniform in individual patients. Experimental findings suggest that microthrombi may result from intravascular platelet activation or form secondarily at sites of vessel wall damage. The differential diagnosis of TTP includes the hemolytic uremic syndrome in which the microangiopathic changes are exclusively found in the kidneys. When untreated, TTP invariably runs a progressive and fatal course. In recent years, prognosis has been improved by new forms of therapy such as plasmapheresis or infusions of fresh frozen plasma which may lead to recovery in about 80% of patients.
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  • 5
    ISSN: 1432-1440
    Keywords: Acute leukemias ; Granulocytopenia ; Fungal infections ; Amphotericin B ; Renal failure ; Sodium chloride loading
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An open, prospective study was performed to evaluate the clinical usefulness of sodium chloride loading for prevention of amphotericin-B-induced nephrotoxicity in 37 patients requiring 44 courses of amphotericin B treatment. The median duration of the treatment course was 22 days (range, 9–136 days), and mean cumulative dose per patient was 1117 mg (range, 231–7831 mg). During amphotericin B treatment, all patients received 50 to 100 ml of 10% sodium chloride (85 to 171 mmol NaCl) via an intravenous line for prevention of amphotericin-B-induced nephrotoxicity evaluated by serum creatinine levels. Using this regimen, none of the patients developed significant nephrotoxicity (increase in serum creatinine of more than twice baseline level, or serum creatinine level ≥2.0 mg/dl, respectively) despite the co-administration of other potentially nephrotoxic drugs. It was not necessary to discontinue treatment with amphotericin B in any of the patients. There were no side effects due to sodium chloride loading. Our results demonstrate that sodium chloride loading is useful for the prevention of amphotericin-B-induced nephrotoxicity.
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  • 6
    ISSN: 1432-1440
    Keywords: Liver cirrhosis ; Thrombocytopenia ; DIC
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Besides decreased platelet production and an increased platelet sequestration in the spleen chronic DIC is thought to cause thrombocytopenia in chronic liver diseases. To investigate if this mechanism could play a role in patients with severe, but stable hepatic cirrhosis, we studied 32 pts. Twenty-eight of them had portal hypertension, 22 had bleeding episodes from oesophageal varices. To evaluate platelet activity, thrombin generation and fibrinolytic activity in vivo, plasma and platelet levels ofβ-thromboglobulin (β-TG) and platelet factor 4 (PF4) as well as fibrinopeptide A (FPA) and the fibrinogen degradation product FCB-3, generated by the action of plasmin, were determined radioimmunologically. Plasma levels and platelet content of serotonin (5-HT) were measured fluorometrically. The mean platelet count/µl was reduced in pts. (109.000±67.000) compared to a control group (n=25, 264,000±52,000,p〈0.001). Factor VII (45±20%), prothrombin time (63±16%) AT-III activity (65±19%) and AT-III concentration (67±23%) were decreased in the pts'. group (p〈0.01). In contrast, plasma levels ofβ-TG (17±7 ng/ml) and of PF4 (4±2 ng/ml) as well as platelet content (µg/109 platelets) ofβ-TG (59±18), PF4 (21±6) and 5-HT (400±210) were found to be in the normal range. Neither mean FPA plasma concentration (3±2 ng/ml) nor mean FCB-3 scrum level (11±5 pmol/ml) differed significantly from controls. Our results demonstrate that pts. with thrombocytopenia and stable hepatic cirrhosis do not have evidence of chronic DIC, primary fibrinolysis or increased platelet activity in vivo. However, our results are compatible with increased platelet sequestration in the spleen and/or decreased platelet survival due to faster extravascular platelet clearance, or decreased platelet production within the bone marrow.
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  • 7
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 65 (1987), S. 143-143 
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
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  • 9
    ISSN: 1432-0428
    Keywords: Haemostasis ; hyperinsulinaemia ; platelet function
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The role of variations in plasma insulin concentrations as a factor possibly involved in abnormalities of haemostatic functions, and (or) the development of arterial disease, has been the subject of controversy. This study examines the “in vivo” effect of hyperinsulinaemia on haemostatic parameters in seven healthy men. Two studies were carried out in random order: (a) Hyperinsulinaemia study. Human insulin was infused by a calibrated infusion pump (0.7 mU kg−1 min−1, for 8 h) during a euglycaemic glucose clamp, and (b) Control study 0.15 mmol/l NaCl solution was infused over 8 h. Plasma epinephrine and norepinephrine concentrations remained constant throughout the studies. Mean insulin levels during the hyperinsulinaemia study were 46.2±1.6 μU/ml, i.e. approximately eightfold higher than those at baseline, whereas plasma glucose levels remained constant at 4.9±0.1 mmol/l. During the control study, mean insulinaemia was 5.0±0.9 μU/ml, and plasma glucose 5.2±0.1 mmol/l. No statistically significant changes were observed during, or after insulin or 0.15 mmol/l NaCl infusions with regard to platelet parameters, blood coagulation, and coagulation inhibitors. These data suggest that abnormalities of the haemostatic function described during insulin-induced hypoglycaemia or in hyperinsulinaemic patients are not due to a direct action of insulin.
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  • 10
    ISSN: 1432-0584
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
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