Immunoglobulin E in renal failure

In this work serum IgE level was found significantly higher in patients with chronic renal failure [32 patients] in comparison to normal control subjects [10 subjects].The highest level was in patients under conservative treatment followed by patients under haemodialysis then patients under dialysis.We did not find any correlation between age, sex, blood urea or serum creatinine on one hand and serum IgE level on the other hand. IgE level was found positively related to the duration of peritoneal dialysis.The explaination for this may be due to possible alteration in T-cell regulation of immunoglobulin synthesis. Active molecules have been described to regulate the function of T-cells controlling IgE production. If these molecules are proved later to be in the range of middle molecules, it would explain our findings. This needs more investigations and work to reach to the truth

Some hemostatic variables in diabetes mellitus

The pathogenesis of diabetic vascular disease remains obscure and elusive to all methods of investigations. Recent evidences suggest involvement of the haemostatic system in the initiation and/or the propagation of vascular lesions. Our study included sixty diabetic patients [21 males and 39 females] and 23 normal controls. Diabetics were divided according to their response to insulin and the presence or absence of vascular complications. At III, plasma fibrinogen level and euglobulin lysis time were estimated. Significant high levels of AT III were found in IDD patients and complicated diabetics. Significant high levels of plasma fibrinogen were found in all diabetic subgroups with insignificant difference between complicated and uncomplicated cases. Similarly significantly prolonged lysis time was found in all cases with insignificant difference between complicated and uncomplicated diabetics. Our data showed evidence of hypercoagulable state, as shown by raised fibrinogen levels and decreased fibrinolytic activity, accompanying the diabetic state from the start regardless of the onset of vascular complications. This may support the suggestion that haemostatic abnormalities could have a possible initivative role in the pathogenesis of diabetic vascular disease