PubMed Health⌕ Search

Biomedical subjects

R E Scharf

Publications and source records attributed to R E Scharf.

67 records · Page 4Linked to original sources
PubMed1985

[Thrombotic thrombocytopenic purpura].

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.

Blood Coagulation Factors↗
PubMed1984

[Differential therapy of thrombotic-thrombopenic purpura. Administration of fresh plasma versus plasma separation].

In a 29-year-old man with primary thrombotic-thrombocytopenic purpura a significantly increased plasma concentration of platelet-specific proteins was demonstrated as an expression of increased intravascular platelet activation and destruction during the acute phase of the disease. There was also abnormally elevated IgG loading of platelets. During administration of fresh plasma alone (total of six litres over one week) the clinical state deteriorated further into coma and failure of spontaneous ventilation. The marked thrombocytopenia and microangiopathic haemolytic anaemia remained unchanged. Only after repeated plasmapheresis was it possible to break through the acute disease process. Remission (restoration of vital functions, normalization of platelet count and haemolysis signs) was achieved after five courses of plasmapheresis with a total exchange volume of 20 litres. At least in this case, the therapeutic success of plasmapheresis argues for an immunological-toxic genesis of thrombotic-thrombocytopenic purpura.

Acute Kidney Injury↗
PubMed1984

Thrombin pretreatment of human platelets impairs thromboxane A2 synthesis from endogenous precursors in the presence of normal cyclooxygenase activity.

Exposure of horse platelets to thrombin has been reported to cause nearly complete inactivation of cyclooxygenase within 30 sec. This contrasts with the observation that human platelets, depleted of their granule constituents by stimulation with thrombin, still aggregate in response to arachidonic acid, a reaction presumably mediated by thromboxane A2 (TxA2) formation. Because of this conflicting evidence, TxA2 formation was measured by radioimmunoassay in washed human platelets depleted of their alpha- and dense-storage granule constituents by prior stimulation with thrombin. These platelets aggregated in response to adenosine diphosphate (ADP), collagen, arachidonic acid, and thrombin, and formed TxA2. However, collagen- and thrombin-induced TxA2 formation by these platelets was reduced in comparison to control platelets that had not been depleted of their storage granule constituents by prior thrombin stimulation. In contrast, arachidonic acid-induced TxA2 formation was not significantly different in thrombin-depleted and control platelets. These results demonstrate that thrombin can induce degranulation of platelets without concomitant inactivation of cyclooxygenase.

Arachidonic Acid↗
PubMed1984

[Thrombocyte activity in dilatative cardiomyopathy and latent cardiomyopathy compared to coronary heart disease].

In a comparative study on the pathomechanism of myocardial hypoxia we determined a parameter each of platelet activity and thrombin activity in 46 patients with angina pectoris, i.e., 15 patients with dilatative cardiomyopathy (DCM), 15 patients with latent cardiomyopathy (LCM) and 16 patients with coronary heart disease (CHD) compared to 15 normal subjects (N). beta-thromboglobulin (beta TG) and fibrinopeptide A (FPA) were measured both at rest (I) and after symptom-limited maximal exercise (II) in plasma. In N, beta TG was not increased in any case, neither at rest nor on exertion (I: 20.5 +/- 6.1 ng/ml, II: 22.4 +/- 6.7 ng/ml). Patients with LCM did not differ significantly from N (I: 20.9 +/- 6.1 ng/ml, II: 22.7 +/- 7.9 ng/ml). beta TG values of some patients with DCM and CHD were increased at rest and especially under exercise (DCM I: 27.9 +/- 9.6 ng/ml, vs. N p less than 0.025; II: 49.9 +/- 45.5 ng/ml, vs. N p less than 0.01; CHD I: 25.2 +/- 7.7 ng/ml, vs. N p less than 0.05; II: 38.6 +/- 34.3 ng/ml, vs. N p less than 0.01). Patients with DCM developing significant angina under exercise showed a higher beta TG under these exercise conditions than those with mild or no angina (p less than 0.01). In patients with coronary heart disease, this correlation was not to be found. With regard to FPA the four investigated groups differed in an analogous way, as they did with regard to beta TG; but only a weak correlation within both values was shown.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Platelets↗
PubMed1982

[Mitral valve prolapse and platelet activity in young patients with cerebral ischaemia (author's transl)].

In 47 patients under 45 years of age (average age 35.4 years) with more or less localised cerebral ischaemia without evidence of arteriosclerosis echocardiography showed mitral valve prolapse in 13 cases. This was slightly more frequent than in an age and sex-matched control group. The difference was not statistically significant. In three quarters of the patients (n = 35) a significantly raised beta-thromboglobulin level was found indicating increased platelet activity. No definite conclusions can be drawn as to the cause of cerebral ischaemia which is probably due to embolism. However, treatment with platelet aggregation inhibitors should be considered.

Adult↗
PubMedDate not supplied

Cerebral ischemia in young patients: it is associated with mitral valve prolapse and abnormal platelet activity in vivo?

The etiology of cerebrovascular disease (CDV) in young patients is difficult to establish if the common causes of a focal neurological deficit are excluded by appropriate investigations. Since in some observations prolapse of the mitral-valve (MVP), alterations of platelet function, or both have been linked with cerebral ischemic events, we studied the in vivo platelet release reaction and the incidence of MVP in 47 patients (12 males, 35 females) under 45 years of age with TIA or stroke of unknown cause and in an age- and sex-matched control group. The mean plasma beta-thromboglobulin (beta-TG) level of the patients (mean = 54.9 +/- 31.4 ng/ml) was significantly higher than that of the controls (mean = 20.6 /- 6.9 ng/ml, p less than 0.001). MVP was demonstrated in 13 of 47 patients in contrast to 4 of the controls (p less than 0.01). However, the beta-T levels of patients with MVP (n = 13, 52.9 +/- 25.5 ng/ml) did not differ from those of patients without MVP (n = 34, 55.7 +/- 33.7 ng/ml) significantly (p less than 0.4). Our results confirm that the incidence of MVP is higher in young patients with cerebral ischemia of unknown cause than in asymptomatic controls. The significantly elevated plasma beta-TG concentrations in the patient's group indicate an increased platelet activity in vivo. Since there was no significant difference between beta-TG levels of patients with and without MVP, the mitral-valve abnormality can not be the cause for the altered platelet activity.

Blood Platelets↗