Abstract Objectives: To evaluate the role of prophylactic magnesium sulfate administration in preventing postoperative atrial fibrillation (POAF), attenuating the inflammatory response and promoting myocardial protection after isolated cardiac valve replacement surgery in adult patients with rheumatic heart disease. Design: Prospective randomized, double-blind placebo-controlled trial. Methods: Sixty-four adult patients undergoing isolated cardiac valve replacement surgery were divided into two equal groups (32 patients in each). Patients in magnesium group (group M) received 2.5 gm of magnesium sulfate (dissolved in 100 mL of isotonic saline and infused over 2 h), twelve h preoperatively, within the first hour of ICU arrival, and on the 2nd and 3rd postoperative days (group M). Patients in the control group (group C) received a placebo of isotonic saline at the same time periods. Results: Prophylactic magnesium sulfate significantly decreased the incidence of POAF compared to the placebo group (P=0.005). White blood cell (WBC) count showed no significant difference between the two groups. C-reactive protein (CRP) level showed significant reduction during the 3rd, 4th, and 5th postoperative days in group M compared to group C (P=0.001, 0.001 & 0.012 respectively). Serum level of interleukin-6 (IL-6) showed a significant reduction on the 5th postoperative day in group M compared to group C (P=0.001). Both groups showed no significant differences in serum levels of troponin I during the study. Conclusion: Prophylactic use of magnesium sulfate in patients with rheumatic heart disease undergoing isolated cardiac valve replacement surgery can decrease the incidence of POAF. It may play a role in attenuating the inflammatory process associated with the use of cardiopulmonary bypass (CPB)

Abstract Objectives: To evaluate the role of prophylactic magnesium sulfate administration in preventing postoperative atrial fibrillation (POAF), attenuating the inflammatory response and promoting myocardial protection after isolated cardiac valve replacement surgery in adult patients with rheumatic heart disease. Design: Prospective randomized, double-blind placebo-controlled trial. Methods: Sixty-four adult patients undergoing isolated cardiac valve replacement surgery were divided into two equal groups (32 patients in each). Patients in magnesium group (group M) received 2.5 gm of magnesium sulfate (dissolved in 100 mL of isotonic saline and infused over 2 h), twelve h preoperatively, within the first hour of ICU arrival, and on the 2nd and 3rd postoperative days (group M). Patients in the control group (group C) received a placebo of isotonic saline at the same time periods. Results: Prophylactic magnesium sulfate significantly decreased the incidence of POAF compared to the placebo group (P=0.005). White blood cell (WBC) count showed no significant difference between the two groups. C-reactive protein (CRP) level showed significant reduction during the 3rd, 4th, and 5th postoperative days in group M compared to group C (P=0.001, 0.001 & 0.012 respectively). Serum level of interleukin-6 (IL-6) showed a significant reduction on the 5th postoperative day in group M compared to group C (P=0.001). Both groups showed no significant differences in serum levels of troponin I during the study. Conclusion: Prophylactic use of magnesium sulfate in patients with rheumatic heart disease undergoing isolated cardiac valve replacement surgery can decrease the incidence of POAF. It may play a role in attenuating the inflammatory process associated with the use of cardiopulmonary bypass (CPB)

Abstract Objectives: To evaluate the role of prophylactic magnesium sulfate administration in preventing postoperative atrial fibrillation (POAF), attenuating the inflammatory response and promoting myocardial protection after isolated cardiac valve replacement surgery in adult patients with rheumatic heart disease. Design: Prospective randomized, double-blind placebo-controlled trial. Methods: Sixty-four adult patients undergoing isolated cardiac valve replacement surgery were divided into two equal groups (32 patients in each). Patients in magnesium group (group M) received 2.5 gm of magnesium sulfate (dissolved in 100 mL of isotonic saline and infused over 2 h), twelve h preoperatively, within the first hour of ICU arrival, and on the 2nd and 3rd postoperative days (group M). Patients in the control group (group C) received a placebo of isotonic saline at the same time periods. Results: Prophylactic magnesium sulfate significantly decreased the incidence of POAF compared to the placebo group (P=0.005). White blood cell (WBC) count showed no significant difference between the two groups. C-reactive protein (CRP) level showed significant reduction during the 3rd, 4th, and 5th postoperative days in group M compared to group C (P=0.001, 0.001 & 0.012 respectively). Serum level of interleukin-6 (IL-6) showed a significant reduction on the 5th postoperative day in group M compared to group C (P=0.001). Both groups showed no significant differences in serum levels of troponin I during the study. Conclusion: Prophylactic use of magnesium sulfate in patients with rheumatic heart disease undergoing isolated cardiac valve replacement surgery can decrease the incidence of POAF. It may play a role in attenuating the inflammatory process associated with the use of cardiopulmonary bypass (CPB)

Background Primary immune thrombocytopenia (ITP) is a common hematological disorder of unknown etiology. DNA methylation is a major epigenetic modification of the DNA. It has a golden role in gene expression. It is mediated by DNA methyltransferases (DNMTs). The promoter of DNMT3B gene contains some single-nucleotide polymorphisms (SNPs) including that at position −149 (C/T), which was suggested to be implicated in the genetic susceptibility to ITP. The DNMT3A −448 G/A SNP in the gene promoter was found to have a protective effect against systemic lupus erythematosus. Aim The aim of the study was to investigate the association between DNMT3A −448 G/A SNP (rs1550117) and DNMT3B −149C/T SNP (rs2424913), and the risk for primary ITP and to evaluate the association between these SNPs and patients’ response to therapy. Participants and methods This prospective case–control study was conducted on 60 primary ITP patients and 30 healthy age-matched and sex-matched controls. Genotype analysis of DNMT3A −448 G/A and DNMT3B −149C/T was done using PCR-restriction fragment length polymorphism. Results The frequency of the DNMT3A −448 G/A SNP variant A-allele was significantly decreased in primary ITP patients compared with controls (odds ratio=0.829, 95% CI=0.097–0.964). DNMT3B −149C/T SNP variant T-allele was significantly higher in ITP patients with almost doublefold increase in the risk of ITP in comparison to controls (odds ratio=1.731, 95%CI=1.121–2.582). Conclusion The DNMT3A −448 SNP variant A-allele might has a protective effect against ITP. Also, the DNMT3B −149 SNP variant T-allele could be considered as a molecular risk factor for ITP.

Background Primary immune thrombocytopenia (ITP) is a common hematological disorder of unknown etiology. DNA methylation is a major epigenetic modification of the DNA. It has a golden role in gene expression. It is mediated by DNA methyltransferases (DNMTs). The promoter of DNMT3B gene contains some single-nucleotide polymorphisms (SNPs) including that at position −149 (C/T), which was suggested to be implicated in the genetic susceptibility to ITP. The DNMT3A −448 G/A SNP in the gene promoter was found to have a protective effect against systemic lupus erythematosus. Aim The aim of the study was to investigate the association between DNMT3A −448 G/A SNP (rs1550117) and DNMT3B −149C/T SNP (rs2424913), and the risk for primary ITP and to evaluate the association between these SNPs and patients’ response to therapy. Participants and methods This prospective case–control study was conducted on 60 primary ITP patients and 30 healthy age-matched and sex-matched controls. Genotype analysis of DNMT3A −448 G/A and DNMT3B −149C/T was done using PCR-restriction fragment length polymorphism. Results The frequency of the DNMT3A −448 G/A SNP variant A-allele was significantly decreased in primary ITP patients compared with controls (odds ratio=0.829, 95% CI=0.097–0.964). DNMT3B −149C/T SNP variant T-allele was significantly higher in ITP patients with almost doublefold increase in the risk of ITP in comparison to controls (odds ratio=1.731, 95%CI=1.121–2.582). Conclusion The DNMT3A −448 SNP variant A-allele might has a protective effect against ITP. Also, the DNMT3B −149 SNP variant T-allele could be considered as a molecular risk factor for ITP.

Background Primary immune thrombocytopenia (ITP) is a common hematological disorder of unknown etiology. DNA methylation is a major epigenetic modification of the DNA. It has a golden role in gene expression. It is mediated by DNA methyltransferases (DNMTs). The promoter of DNMT3B gene contains some single-nucleotide polymorphisms (SNPs) including that at position −149 (C/T), which was suggested to be implicated in the genetic susceptibility to ITP. The DNMT3A −448 G/A SNP in the gene promoter was found to have a protective effect against systemic lupus erythematosus. Aim The aim of the study was to investigate the association between DNMT3A −448 G/A SNP (rs1550117) and DNMT3B −149C/T SNP (rs2424913), and the risk for primary ITP and to evaluate the association between these SNPs and patients’ response to therapy. Participants and methods This prospective case–control study was conducted on 60 primary ITP patients and 30 healthy age-matched and sex-matched controls. Genotype analysis of DNMT3A −448 G/A and DNMT3B −149C/T was done using PCR-restriction fragment length polymorphism. Results The frequency of the DNMT3A −448 G/A SNP variant A-allele was significantly decreased in primary ITP patients compared with controls (odds ratio=0.829, 95% CI=0.097–0.964). DNMT3B −149C/T SNP variant T-allele was significantly higher in ITP patients with almost doublefold increase in the risk of ITP in comparison to controls (odds ratio=1.731, 95%CI=1.121–2.582). Conclusion The DNMT3A −448 SNP variant A-allele might has a protective effect against ITP. Also, the DNMT3B −149 SNP variant T-allele could be considered as a molecular risk factor for ITP.

Background Primary immune thrombocytopenia (ITP) is a common hematological disorder of unknown etiology. DNA methylation is a major epigenetic modification of the DNA. It has a golden role in gene expression. It is mediated by DNA methyltransferases (DNMTs). The promoter of DNMT3B gene contains some single-nucleotide polymorphisms (SNPs) including that at position −149 (C/T), which was suggested to be implicated in the genetic susceptibility to ITP. The DNMT3A −448 G/A SNP in the gene promoter was found to have a protective effect against systemic lupus erythematosus. Aim The aim of the study was to investigate the association between DNMT3A −448 G/A SNP (rs1550117) and DNMT3B −149C/T SNP (rs2424913), and the risk for primary ITP and to evaluate the association between these SNPs and patients’ response to therapy. Participants and methods This prospective case–control study was conducted on 60 primary ITP patients and 30 healthy age-matched and sex-matched controls. Genotype analysis of DNMT3A −448 G/A and DNMT3B −149C/T was done using PCR-restriction fragment length polymorphism. Results The frequency of the DNMT3A −448 G/A SNP variant A-allele was significantly decreased in primary ITP patients compared with controls (odds ratio=0.829, 95% CI=0.097–0.964). DNMT3B −149C/T SNP variant T-allele was significantly higher in ITP patients with almost doublefold increase in the risk of ITP in comparison to controls (odds ratio=1.731, 95%CI=1.121–2.582). Conclusion The DNMT3A −448 SNP variant A-allele might has a protective effect against ITP. Also, the DNMT3B −149 SNP variant T-allele could be considered as a molecular risk factor for ITP.

The inherited qualitative platelet disorders (IPFD) are important causes of bleeding, and there is considerable heterogeneity in their features. This heterogeneity poses diagnostic challenges because the specialized testing needed to evaluate platelet disorders is often restricted to tertiary referral centers, and there are no simple tests that adequately detect or sub-categorize all forms of congenital platelet disorders. The aim of this study was to assess inherited qualitative platelet disorders in Upper Egypt. This study was carried out at the Clinical Pathology Department at Assiut University Hospitals in the period from January 2015 to December 2015. Platelet function defects could be detected by Light Transmission Aggregometry (LTA) in the presence of normal screening tests of haemostasis after exclusion of acquired platelet function disorders in the presence of normal liver and kidney function. The diagnosis was considered as primary diagnosis of IPFD in 88 patients out of 404 patients (21.7%) presented with bleeding tendency to the Haemostasis laboratory, Clinical Pathology Department at Assiut University Hospitals. The age of IPFD patients ranged from 1 month up to 60 years, forty six (52.3%) of them were less than 10 years, female patients represented 55.7% (49/88). Positive family history for qualitative platelet disorders was present only in 5 (5.7%) patients. The IPFDs detected in the studied patients were enzyme deficiency (cyclooxygenase or thromboxane synthetase deficiency) which was found in 39 cases out of 88 (44.3%), followed by Thrombasthenia (21/88; 23.9%). ADP receptor defect was present in 17/88(19.3%), 9 cases had Storage pool disease (10.3%), one case had Collagen receptor defect (1.1%) and one case had Bernard Soulier syndrome (1.1%).

The inherited qualitative platelet disorders (IPFD) are important causes of bleeding, and there is considerable heterogeneity in their features. This heterogeneity poses diagnostic challenges because the specialized testing needed to evaluate platelet disorders is often restricted to tertiary referral centers, and there are no simple tests that adequately detect or sub-categorize all forms of congenital platelet disorders. The aim of this study was to assess inherited qualitative platelet disorders in Upper Egypt. This study was carried out at the Clinical Pathology Department at Assiut University Hospitals in the period from January 2015 to December 2015. Platelet function defects could be detected by Light Transmission Aggregometry (LTA) in the presence of normal screening tests of haemostasis after exclusion of acquired platelet function disorders in the presence of normal liver and kidney function. The diagnosis was considered as primary diagnosis of IPFD in 88 patients out of 404 patients (21.7%) presented with bleeding tendency to the Haemostasis laboratory, Clinical Pathology Department at Assiut University Hospitals. The age of IPFD patients ranged from 1 month up to 60 years, forty six (52.3%) of them were less than 10 years, female patients represented 55.7% (49/88). Positive family history for qualitative platelet disorders was present only in 5 (5.7%) patients. The IPFDs detected in the studied patients were enzyme deficiency (cyclooxygenase or thromboxane synthetase deficiency) which was found in 39 cases out of 88 (44.3%), followed by Thrombasthenia (21/88; 23.9%). ADP receptor defect was present in 17/88(19.3%), 9 cases had Storage pool disease (10.3%), one case had Collagen receptor defect (1.1%) and one case had Bernard Soulier syndrome (1.1%).

The inherited qualitative platelet disorders (IPFD) are important causes of bleeding, and there is considerable heterogeneity in their features. This heterogeneity poses diagnostic challenges because the specialized testing needed to evaluate platelet disorders is often restricted to tertiary referral centers, and there are no simple tests that adequately detect or sub-categorize all forms of congenital platelet disorders. The aim of this study was to assess inherited qualitative platelet disorders in Upper Egypt. This study was carried out at the Clinical Pathology Department at Assiut University Hospitals in the period from January 2015 to December 2015. Platelet function defects could be detected by Light Transmission Aggregometry (LTA) in the presence of normal screening tests of haemostasis after exclusion of acquired platelet function disorders in the presence of normal liver and kidney function. The diagnosis was considered as primary diagnosis of IPFD in 88 patients out of 404 patients (21.7%) presented with bleeding tendency to the Haemostasis laboratory, Clinical Pathology Department at Assiut University Hospitals. The age of IPFD patients ranged from 1 month up to 60 years, forty six (52.3%) of them were less than 10 years, female patients represented 55.7% (49/88). Positive family history for qualitative platelet disorders was present only in 5 (5.7%) patients. The IPFDs detected in the studied patients were enzyme deficiency (cyclooxygenase or thromboxane synthetase deficiency) which was found in 39 cases out of 88 (44.3%), followed by Thrombasthenia (21/88; 23.9%). ADP receptor defect was present in 17/88(19.3%), 9 cases had Storage pool disease (10.3%), one case had Collagen receptor defect (1.1%) and one case had Bernard Soulier syndrome (1.1%).