| 1. |
- Andrén, Lennart, 1946, et al.
(författare)
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Stress and platelet activation.
- 1983
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Ingår i: Acta haematologica. - 0001-5792. ; 70:5, s. 302-6
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Tidskriftsartikel (refereegranskat)abstract
- Severe stress, with increased secretion of adrenaline, is likely to cause platelet activation. The aim of the present study was to investigate if moderate stress, which usually is not accompanied by adrenaline secretion, could induce activation of platelets, as measured by changes in the plasma concentrations of platelet factor 4 (PF-4). Noise stimulation (100 dBA for 10 min) caused a significant increase in the diastolic (10%, p less than 0.01) and mean arterial pressures (4%, p less than 0.01) of 10 healthy male volunteers. The plasma levels of PF-4 and the venous platelet concentrations were, however, unaffected during noise exposure. The results therefore suggest that stress not accompanied by adrenal medullary activation, does not induce platelet activation.
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| 2. |
- Kutti, Jack, et al.
(författare)
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Plasma concentrations of platelet-specific proteins in young female acute myocardial infarction survivors and their age-matched female controls.
- 1983
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Ingår i: European heart journal. - 0195-668X. ; 4:5, s. 300-5
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Tidskriftsartikel (refereegranskat)abstract
- The steady state plasma concentrations of the two platelet-specific proteins beta-thromboglobulin (BTG) and platelet factor 4 (PF4) were determined in two groups of females: 36 acute myocardial infarction (AMI) survivors, and 38 age-matched control subjects. For the AMI patients the mean BTG and PF4 values were 57 +/- 4 and 14.1 +/- 1.7 ng/ml, respectively. These two means significantly exceeded the corresponding means for the controls, 40 +/- 2 and 10.3 +/- 0.6 ng/ml, respectively. Similar results have recently been reported by other workers who investigated patients with coronary artery disease; however, in no previous study were the values for BTG and PF4 related to those obtained for control subjects matched with respect to sex and age. The present results therefore further support the concept that increased platelet activation and secretion is taking place in steady state patients who previously have sustained an AMI.
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| 3. |
- Kutti, Jack, et al.
(författare)
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Plasma levels of platelet factor 4 in patients admitted to a coronary care unit.
- 1981
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Ingår i: Scandinavian journal of haematology. - 0036-553X. ; 26:3, s. 235-40
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Tidskriftsartikel (refereegranskat)abstract
- Blood was obtained from 63 consecutive patients within 24 h period after the admission to a coronary care unit for the determination of plasma platelet factor 4 (PF-4) concentration. 28 of the subjects proved to have an acute myocardial infarction (MI), 24 had evidence of ischaemic heart disease (IHD) but no MI, and the remaining 11 patients had no signs of IHD. 40 healthy subjects served as controls. The mean PF-4 value in the MI group was 10.5 +/- 0.8 ng/ml. The corresponding values for patients with and without IHD were 8.7 +/- 0.6 and 8.3 +/- 0.6 ng/ml, respectively. The control mean (5.4 +/- 0.3 ng/ml) was significantly lower (P less than 0.001) than the means for all 3 groups of patients studied. The difference between the group of MI patients and patients with IHD as well as patients without IHD was only of borderline significance (0.10 greater than P greater than 0.05).
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| 4. |
- Kutti, Jack, et al.
(författare)
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Plasma platelet factor 4: a potentially useful predictor of ischaemic heart disease?
- 1983
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Ingår i: Folia haematologica (Leipzig, Germany : 1928). - 0323-4347. ; 110:6, s. 868-73
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Tidskriftsartikel (refereegranskat)abstract
- The aim was to investigate whether plasma platelet factor 4 (PF-4) in suspected acute myocardial infarction (AMI) patients could serve as a prognostic tool and identify patients at risk for future death from AMI or ischaemic heart disease (IHD). Therefore, upon admission to our coronary care unit plasma PF-4 was measured on 109 consecutive patients. 53 of them proved to have AMI, and 50 IHD but no AMI; the remaining 6 had no evidence of IHD. 24 patients died in hospital or during the follow-up period which was an average of 16.7 +/- 2.4 months. The decreased were subgrouped into those dying of AMI (n = 16), and those dying of IHD but with no AMI (n = 8). No deaths from other causes were recorded. As compared with survivors there was a tendency towards higher PF-4 values among those who died of AMI. However, patients who during follow-up suffered death from IHD proved to have significantly (p less than 0.05) higher PF-4 levels than survivors.
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| 5. |
- Kutti, Jack, et al.
(författare)
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Successful treatment of refractory autoimmune haemolytic anaemia by plasmapheresis.
- 1984
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Ingår i: Scandinavian journal of haematology. - 0036-553X. ; 32:2, s. 149-52
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Tidskriftsartikel (refereegranskat)abstract
- A 16-year-old female was admitted because of rapidly progressive fatigue, severe anaemia and icterus. The S-bilirubin was 190 mumol/l, COHb 7.3% and high amounts of free Hb in plasma were present. The Coombs' direct test was strongly positive with anti-IgG but negative with anti-IgM and anti-C3. Conventional therapy with very high doses of hydrocortisone i.v., cyclophosphamide, azathioprine, and transfusions of washed packed red cells proved ineffective. During 5 consecutive days she also received i.v. infusions of gamma-globulin (25 g each day). Nevertheless, her condition deteriorated and 3 plasma exchanges were carried out with impressive clinical and laboratory effects. After the 3rd plasma exchange, the patient did not require further transfusions of packed red cells. Therapy with corticosteroids could be rapidly reduced and she was discharged after 5 weeks with a normal blood picture. Since then she has remained in excellent health.
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| 6. |
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| 7. |
- Wadenvik, Hans, 1955, et al.
(författare)
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Plasma concentrations of platelet factor 4 in acute myocardial infarction.
- 1981
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Ingår i: Scandinavian journal of haematology. - 0036-553X. ; 26:5, s. 359-63
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Tidskriftsartikel (refereegranskat)abstract
- The aim was to investigate whether in the acute stage of myocardial infarction (MI) platelet activation, as measured by plasma platelet factor 4 (PF-4), excluding that in ischaemic heart disease (IHD) is taking place. Over a period of 4 d the plasma levels of PF-4 were determined on 44 consecutive patients admitted to a coronary care unit with suspected MI. 21 of them had a definite acute MI (group 1), and 13 had evidence of IHD but no MI (group 2). In the remaining 10 subjects there was no evidence of either MI or IHD. On the first day the mean plasma PF-4 concentrations in group 1 and 2 patients were 11,8 +/- 1.1 and 15.0 +/- 2.3 ng/ml, respectively; the difference between means was not statistically significant. A peak mean PF-4 for group 1 patients (17.5 +/- 4.6 ng/ml) was recorded on the second day of study. The corresponding value for group 2 patients was lower, but not significantly so. In the latter subjects no peak PF-4 was recorded. During the last 2 d of study the plasma PF-4 concentrations tended to decrease, but the means for the 2 groups did not differ statistically. Thus, at no point in time was there a significant difference between the PF-4 values for MI and IHD patients present.
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