Abstract: In end-stage renal disease, particularly when treated with haemodialysis, the function of platelets,coagulation and fibrinolytic systems can be disturbed; those patients may show both thrombotic complications and bleeding abnormalities. Thus, it is essential to investigate haemostatic alterations in patients on hemodialysis so that adequate regime for anticoagulant therapy could be implemented. Haemostatic changes in patients on hemodialysis may result from alterations in vessel wall integrity and platelet function, and reduced blood flow in the native arteriovenous fistula. We study the haemostatic abnormalities associated with thrombosis in long term hemodialytic patients to determine whether coagulation and fibrinolysis are enhanced or not in 42 uremia patients on chronic regular hemodialysis treatment (20 of them had history of thrombotic events "group I" and the remaining 22 patients showed no history of thrombosis" group II") and 20 apparently health control group. Plasma levels of some blood coagulation fibrinolysis parameters were measured including platelet count, prothrombin time/concentration (PT/PC), activated partial thromboplastin time (aPTT), thrombin time (TT), fibrinogen and D-Dimer, platelet aggregation (induced by adenosine diphosphate, collagen, Ristocetin, and Arachedonic acid), and the levels of natural anticoagulant protein C, protein S and antithrombin-III (AT-III). The mean platelet count was normal in all studied groups, while higher mean value of platelet count was observed among patients in group I than group II. Prolonged PT/sec., aPTT/sec and TT in patients groups were observed; those differences were statistically highly significant in comparison with healthy controls (p 0.001). The mean plasma fibrinogen (g/l) concentration was normal in all groups although levels above normal limits were noted in group I, fibrinogen level was significantly higher (p 0.05) in group I patients than in normal controls. The mean value of D-dimer (ng/ml) was significantly higher in group I than group II and in comparison with control group (p 0.001). We did not find differences between group I patients and control group as regard platelet aggregation induced with all agents, while there were statistically significant difference were observed between group II and control except for collagen. In contrast, the level of natural anticoagulants (protein C, protein S and AT III) were significantly reduced in patients groups than control and they were statistically significant, and the levels were lower in group I than group II. In conclusion, our results showed that the long term haemodialysis procedure affects the haemostatic process and may contribute to a thrombotic tendency. Careful weighing of risks and benefits of pharmacological prevention of thrombosis in patients on hemodialysis is crucial and this area certainly warrants further investigation

Abstract: In end-stage renal disease, particularly when treated with haemodialysis, the function of platelets,coagulation and fibrinolytic systems can be disturbed; those patients may show both thrombotic complications and bleeding abnormalities. Thus, it is essential to investigate haemostatic alterations in patients on hemodialysis so that adequate regime for anticoagulant therapy could be implemented. Haemostatic changes in patients on hemodialysis may result from alterations in vessel wall integrity and platelet function, and reduced blood flow in the native arteriovenous fistula. We study the haemostatic abnormalities associated with thrombosis in long term hemodialytic patients to determine whether coagulation and fibrinolysis are enhanced or not in 42 uremia patients on chronic regular hemodialysis treatment (20 of them had history of thrombotic events "group I" and the remaining 22 patients showed no history of thrombosis" group II") and 20 apparently health control group. Plasma levels of some blood coagulation fibrinolysis parameters were measured including platelet count, prothrombin time/concentration (PT/PC), activated partial thromboplastin time (aPTT), thrombin time (TT), fibrinogen and D-Dimer, platelet aggregation (induced by adenosine diphosphate, collagen, Ristocetin, and Arachedonic acid), and the levels of natural anticoagulant protein C, protein S and antithrombin-III (AT-III). The mean platelet count was normal in all studied groups, while higher mean value of platelet count was observed among patients in group I than group II. Prolonged PT/sec., aPTT/sec and TT in patients groups were observed; those differences were statistically highly significant in comparison with healthy controls (p 0.001). The mean plasma fibrinogen (g/l) concentration was normal in all groups although levels above normal limits were noted in group I, fibrinogen level was significantly higher (p 0.05) in group I patients than in normal controls. The mean value of D-dimer (ng/ml) was significantly higher in group I than group II and in comparison with control group (p 0.001). We did not find differences between group I patients and control group as regard platelet aggregation induced with all agents, while there were statistically significant difference were observed between group II and control except for collagen. In contrast, the level of natural anticoagulants (protein C, protein S and AT III) were significantly reduced in patients groups than control and they were statistically significant, and the levels were lower in group I than group II. In conclusion, our results showed that the long term haemodialysis procedure affects the haemostatic process and may contribute to a thrombotic tendency. Careful weighing of risks and benefits of pharmacological prevention of thrombosis in patients on hemodialysis is crucial and this area certainly warrants further investigation

Abstract: In end-stage renal disease, particularly when treated with haemodialysis, the function of platelets,coagulation and fibrinolytic systems can be disturbed; those patients may show both thrombotic complications and bleeding abnormalities. Thus, it is essential to investigate haemostatic alterations in patients on hemodialysis so that adequate regime for anticoagulant therapy could be implemented. Haemostatic changes in patients on hemodialysis may result from alterations in vessel wall integrity and platelet function, and reduced blood flow in the native arteriovenous fistula. We study the haemostatic abnormalities associated with thrombosis in long term hemodialytic patients to determine whether coagulation and fibrinolysis are enhanced or not in 42 uremia patients on chronic regular hemodialysis treatment (20 of them had history of thrombotic events "group I" and the remaining 22 patients showed no history of thrombosis" group II") and 20 apparently health control group. Plasma levels of some blood coagulation fibrinolysis parameters were measured including platelet count, prothrombin time/concentration (PT/PC), activated partial thromboplastin time (aPTT), thrombin time (TT), fibrinogen and D-Dimer, platelet aggregation (induced by adenosine diphosphate, collagen, Ristocetin, and Arachedonic acid), and the levels of natural anticoagulant protein C, protein S and antithrombin-III (AT-III). The mean platelet count was normal in all studied groups, while higher mean value of platelet count was observed among patients in group I than group II. Prolonged PT/sec., aPTT/sec and TT in patients groups were observed; those differences were statistically highly significant in comparison with healthy controls (p 0.001). The mean plasma fibrinogen (g/l) concentration was normal in all groups although levels above normal limits were noted in group I, fibrinogen level was significantly higher (p 0.05) in group I patients than in normal controls. The mean value of D-dimer (ng/ml) was significantly higher in group I than group II and in comparison with control group (p 0.001). We did not find differences between group I patients and control group as regard platelet aggregation induced with all agents, while there were statistically significant difference were observed between group II and control except for collagen. In contrast, the level of natural anticoagulants (protein C, protein S and AT III) were significantly reduced in patients groups than control and they were statistically significant, and the levels were lower in group I than group II. In conclusion, our results showed that the long term haemodialysis procedure affects the haemostatic process and may contribute to a thrombotic tendency. Careful weighing of risks and benefits of pharmacological prevention of thrombosis in patients on hemodialysis is crucial and this area certainly warrants further investigation

Abstract: In end-stage renal disease, particularly when treated with haemodialysis, the function of platelets,coagulation and fibrinolytic systems can be disturbed; those patients may show both thrombotic complications and bleeding abnormalities. Thus, it is essential to investigate haemostatic alterations in patients on hemodialysis so that adequate regime for anticoagulant therapy could be implemented. Haemostatic changes in patients on hemodialysis may result from alterations in vessel wall integrity and platelet function, and reduced blood flow in the native arteriovenous fistula. We study the haemostatic abnormalities associated with thrombosis in long term hemodialytic patients to determine whether coagulation and fibrinolysis are enhanced or not in 42 uremia patients on chronic regular hemodialysis treatment (20 of them had history of thrombotic events "group I" and the remaining 22 patients showed no history of thrombosis" group II") and 20 apparently health control group. Plasma levels of some blood coagulation fibrinolysis parameters were measured including platelet count, prothrombin time/concentration (PT/PC), activated partial thromboplastin time (aPTT), thrombin time (TT), fibrinogen and D-Dimer, platelet aggregation (induced by adenosine diphosphate, collagen, Ristocetin, and Arachedonic acid), and the levels of natural anticoagulant protein C, protein S and antithrombin-III (AT-III). The mean platelet count was normal in all studied groups, while higher mean value of platelet count was observed among patients in group I than group II. Prolonged PT/sec., aPTT/sec and TT in patients groups were observed; those differences were statistically highly significant in comparison with healthy controls (p 0.001). The mean plasma fibrinogen (g/l) concentration was normal in all groups although levels above normal limits were noted in group I, fibrinogen level was significantly higher (p 0.05) in group I patients than in normal controls. The mean value of D-dimer (ng/ml) was significantly higher in group I than group II and in comparison with control group (p 0.001). We did not find differences between group I patients and control group as regard platelet aggregation induced with all agents, while there were statistically significant difference were observed between group II and control except for collagen. In contrast, the level of natural anticoagulants (protein C, protein S and AT III) were significantly reduced in patients groups than control and they were statistically significant, and the levels were lower in group I than group II. In conclusion, our results showed that the long term haemodialysis procedure affects the haemostatic process and may contribute to a thrombotic tendency. Careful weighing of risks and benefits of pharmacological prevention of thrombosis in patients on hemodialysis is crucial and this area certainly warrants further investigation

Objective: Many patients with transfusional iron overload are at risk for progressive organ dysfunction and early death. Poor compliance with iron chelators is believed to be a major contributing factor. The aim of this study is to evaluate the efficacy of deferasirox in comparison with deferoxamine for the treatment of transfusional iron overload in patients with β-thalassemia major. Patients and Methods: The prospective study was designed to evaluate once-daily deferasirox for 48 weeks in forty patients ≥2 years with β-thalassaemia major with iron overload who were previously either had no chelating agent or chelated with deferoxamine. Most patients began treatment with deferasirox 10 mg⁄ kg ⁄ day and may be increased to 30 mg/kg /day. Serum ferritin level was assessed before and after beginning of deferasirox (Exjade) treatment at 3 months interval for 48 weeks. Results: Adverse events most commonly associated with deferasirox were mild, including transient nausea, vomiting, diarrhea, abdominal pain and skin rash. The mean serum ferritin level had significantly decreased in all β-thalassaemia major patients with iron overload treated with deferasirox compared to those on deferoxamine. Conclusion Administration of Exjade therapy as an oral drug is considered to be preferable and effective than the parenteral iron chelating therapy due to the poor patient compliance and poor practical regimen of parenteral infusions.

Objective: Many patients with transfusional iron overload are at risk for progressive organ dysfunction and early death. Poor compliance with iron chelators is believed to be a major contributing factor. The aim of this study is to evaluate the efficacy of deferasirox in comparison with deferoxamine for the treatment of transfusional iron overload in patients with β-thalassemia major. Patients and Methods: The prospective study was designed to evaluate once-daily deferasirox for 48 weeks in forty patients ≥2 years with β-thalassaemia major with iron overload who were previously either had no chelating agent or chelated with deferoxamine. Most patients began treatment with deferasirox 10 mg⁄ kg ⁄ day and may be increased to 30 mg/kg /day. Serum ferritin level was assessed before and after beginning of deferasirox (Exjade) treatment at 3 months interval for 48 weeks. Results: Adverse events most commonly associated with deferasirox were mild, including transient nausea, vomiting, diarrhea, abdominal pain and skin rash. The mean serum ferritin level had significantly decreased in all β-thalassaemia major patients with iron overload treated with deferasirox compared to those on deferoxamine. Conclusion Administration of Exjade therapy as an oral drug is considered to be preferable and effective than the parenteral iron chelating therapy due to the poor patient compliance and poor practical regimen of parenteral infusions.

Treatment of steroid refractory autoimmune hemolytic anemia (AIHA) is challenging especially with no evidence based consensus guide lines and limited resources. The aim of this study was to evaluate the efficacy of pulse cyclophosphamide therapy in patients with severe refractory warm AIHA. The prospective study was designed to evaluate the efficacy of pulse cyclophosphamide—1 g/month for four consecutive months—in 17 patients (10 males and 7 females) with severe refractory warm AIHA [13 primary AIHA and 4 (females) secondary to SLE], all studied patients failed to respond to high dose of steroid therapy ± azathioprine ± intravenous immunoglobulin ± oral cyclophosphamide. Mean hemoglobin level, reticulocytic count and direct antiglobulin test were assessed before and after cyclophosphamide treatment every month. After the 4th cycle of cyclophosphamide (82 %, 14 patients) achieved partial response while the remaining (17 %, 3 patients) showed no response, while after 6 months follow up 47 % (8 patients) show complete response, while 53 % (9 patients) showed partial response. The mean hemoglobin levels were significantly increased after the 1st, 2nd, 3rd and 4th months of pulse cyclophosphamide therapy when compared to before treatment (P0.01, P0.001, P0.001 and P0.001) respectively, and the mean reticulocyte (%) were significantly decreased after the 2nd, 3rd and 4th months (P0.05, P0.01 and P0.001) respectively. We conclude that pulse cyclophosphamide therapy is well tolerated and induces good response in patients with severe refractory warm AIHA.

Treatment of steroid refractory autoimmune hemolytic anemia (AIHA) is challenging especially with no evidence based consensus guide lines and limited resources. The aim of this study was to evaluate the efficacy of pulse cyclophosphamide therapy in patients with severe refractory warm AIHA. The prospective study was designed to evaluate the efficacy of pulse cyclophosphamide—1 g/month for four consecutive months—in 17 patients (10 males and 7 females) with severe refractory warm AIHA [13 primary AIHA and 4 (females) secondary to SLE], all studied patients failed to respond to high dose of steroid therapy ± azathioprine ± intravenous immunoglobulin ± oral cyclophosphamide. Mean hemoglobin level, reticulocytic count and direct antiglobulin test were assessed before and after cyclophosphamide treatment every month. After the 4th cycle of cyclophosphamide (82 %, 14 patients) achieved partial response while the remaining (17 %, 3 patients) showed no response, while after 6 months follow up 47 % (8 patients) show complete response, while 53 % (9 patients) showed partial response. The mean hemoglobin levels were significantly increased after the 1st, 2nd, 3rd and 4th months of pulse cyclophosphamide therapy when compared to before treatment (P0.01, P0.001, P0.001 and P0.001) respectively, and the mean reticulocyte (%) were significantly decreased after the 2nd, 3rd and 4th months (P0.05, P0.01 and P0.001) respectively. We conclude that pulse cyclophosphamide therapy is well tolerated and induces good response in patients with severe refractory warm AIHA.