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Biomedical subjects

E Malan

Publications and source records attributed to E Malan.

At least 19 recordsLinked to original sources

Platelet antibody levels do not correlate with response to therapy in idiopathic thrombocytopenic purpura.

Platelet bound antibody was measured at presentation in 67 patients with idiopathic thrombocytopenic purpura by means of a quantitative antiglobulin consumption technique. The amounts of antibody present on the platelets of patients who failed steroid therapy were similar to those present on the platelets of patients who achieved a remission of their illness. It was also not possible on the basis of these data to identify those patients whose illness would remit after splenectomy. It is concluded that the pretreatment platelet antibody level does not assist in predicting the responses to treatment.

Adult

Complement (C3) binding to platelets in autoimmune thrombocytopenia.

In view of conflicting reports on the occurrence of complement binding to platelets in idiopathic autoimmune thrombocytopenic purpura (AITP) we performed measurements of platelet bound C3 in patients with AITP who had elevated levels of platelet bound IgG. Using a quantitative antiglobulin consumption technique 38 out of 42 patients were found to have fixed abnormally large amounts of C3 to their platelets, and a significant positive correlation between the amounts of platelet bound IgG and C3 was shown to exist. In additional experiments antibody eluates were prepared from AITP platelets and were shown to cause the fixation of C3 to normal donor platelets in vitro. Taken together these findings strongly suggest that the C3 binding in AITP is specifically related to the disease process.

Autoantibodies

Platelet-bound IgG measurements in idiopathic thrombocytopenic purpura.

A quantitative antiglobulin consumption technique has been used to measure antiplatelet antibody (platelet-bound IgG) in 25 patients with idiopathic thrombocytopenic purpura (ITP). The assay confirmed the presumptive clinical diagnosis in all patients. Additional observations however, have demonstrated that if thrombocytopenic patients have platelet counts greater than 75 x 10(9)l, false-negative results may be obtained. Antiplatelet antibody levels closely mirrored the clinical progress of patients receiving therapy, but the level of antibody at the time of diagnosis was not of value in predicting the response to corticosteroid treatment. In a proportion of patients receiving corticosteroids, platelet counts returned to normal before antibody levels, implying a reduction in the sequestration of antibody-sensitized platelets within the reticulo-endothelial system. Because this response was observed in proportionately more patients in whom drug therapy was successful than others, this steroid effect may in some patients be an important factor in determining the successful outcome of medical treatment. Four out of 10 patients in clinical remission had evidence of disease activity based on platelet antibody and platelet survival measurements. The pattern of results obtained demonstrates that disease activity may go unrecognized in some patients unless both measurements are performed.

Adolescent

Effects of the sulphonylurea drugs gliclazide and glibenclamide on blood glucose control and platelet function.

Platelet aggregation and adhesion are commonly increased in diabetes mellitus. These abnormalities may in part be responsible for the increased incidence of vascular disease in diabetics. We have investigated the effects of diet, diet plus glibenclamide, and diet plus gliclazide on plasma glucose control and platelet function in 10 newly diagnosed maturity-onset diabetics who had not previously been treated. Before treatment, the mean postprandial plasma glucose value was 13,4 +/- 0,8 mmol/l, which fell insignificantly on dietary treatment, to 12,2 +/- 1,0 mmol/l (P greater than 0,05). Both glibenclamide and gliclazide, when added to the diet, significantly lowered mean plasma glucose values to 9,3 +/- 0,8 mmol/l and 7,8 +/- 0,8 mmol/l respectively (P less than 0,05). Platelet aggregation in response to 1 mumol adenosine diphosphate (ADP) was increased in the diet period, whereas aggregation in response to 10 mumol and 100 mumol was normal. This suggests an increased sensitivity of the platelets to ADP in diabetic patients. The addition of both glibenclamide and gliclazide reduced the magnitude of the response to within the normal range. Platelet aggregation in response to 10 mumol adrenaline and 750 micrograms/ml collagen was significantly reduced by glibenclamide (P less than 0,05). We conclude that sulphonylurea therapy appears to reduce the increased platelet aggregation which occurs in diabetics. This may play a role in the prevention of vascular disease.

Adult