Mahmoud Abd El Hafez M. Adam

n/a

Background: This study was carried out to compare the haemodynamic and respiratory effects of low-pressure and conventional pressure pneumoperitoneum during robotically assisted laparoscopic splenectomy in children. Methods: Twenty children aged 2-6 years were randomly assigned into two equal groups. Group I received low-pressure pneumoperitoneum [intra-abdominal pressure (IAP) = 5-8 mm Hg] while group II received conventional pressure pneurnoperitoneum [IAP = 10-13 mm Hg]. Anaesthesia was standardized for the two groups, consisting of halothane, fentanyl and atracurium. Mechanical ventilation was adjusted to obtain an end-tidal C02 (ETC02) of 30-35 mm Hg before insufflation, and ventilatory parameters were unchanged thereafter. Heart rate (HR), mean arterial pressure (MAP), ETC02, peak inspiratory pressure (PIP) and blood gas analysis were recorded before insufflation; 30 and 60 min after insufflation with C02, and 10 min after desfullation. Results: A significant increase in HR, MAP, ETCO2 and PaC02 and a significant decrease in arterial blood pH were noted relative to baseline in both groups after insufflation, but the changes were significantly more in group II than group I (P < 0.05 Or all parameters). PIP increased significantly (P < 0.05) relative to baseline in group II, but not in group I. Arterial oxygen saturation was not significantly changed in either group. Conclusion: The use of low-pressure pneumoperitoneum in the more prolonged robotically assisted laparoscopic surgery in children produces less physiological alterations during abdominal C02 insufflation and seems more favourable than the use of conventional pressure pneumoperitoneum.

The outcome of hepatitis C virus (HCV) infection acquired in childhood is uncertain because of the diversity of the epidemiological and clinical features of infection and disease. The aim of this study was to determine the outcome of HCV infection in 105 Egyptian children who tested positive for HCV antibody (anti-HCV). The data of 105 anti-HCV-positive children presenting to the Pediatric Hepatology Unit, Cairo University Children's Hospital, between 1995 and 2002, were retrospectively analysed for risk factors. Seventy-four children with available polymerase chain reaction results were further analysed clinically, serologically and histologically. The age range was 1.3-22 years, with a mean of 11.2 +/- 4.9 years. History of blood transfusion was found in 81 children (77%). HCV RNA was detected in 58.1% of 74 children. Persistently elevated alanine aminotransferase (ALT) levels were present in 40 patients (54.1%). Hepatitis B virus markers (HBsAg and/or anti-HBc) were detected in 18 patients (24.3%). Twenty-six of the 43 HCV RNA-positive children underwent a diagnostic liver biopsy that showed chronic hepatitis in 19 patients (73.1%), cirrhosis in one case only (3.8%), and normal biopsy findings in seven children (26.9%). Blood transfusion remains a major risk of HCV transmission among Egyptian children. HCV infection is not always benign in the childhood period. ALT levels remain elevated in half of the children and histological abnormalities are detected in three quarters of HCV RNA-positive cases.

The outcome of hepatitis C virus (HCV) infection acquired in childhood is uncertain because of the diversity of the epidemiological and clinical features of infection and disease. The aim of this study was to determine the outcome of HCV infection in 105 Egyptian children who tested positive for HCV antibody (anti-HCV). The data of 105 anti-HCV-positive children presenting to the Pediatric Hepatology Unit, Cairo University Children's Hospital, between 1995 and 2002, were retrospectively analysed for risk factors. Seventy-four children with available polymerase chain reaction results were further analysed clinically, serologically and histologically. The age range was 1.3-22 years, with a mean of 11.2 +/- 4.9 years. History of blood transfusion was found in 81 children (77%). HCV RNA was detected in 58.1% of 74 children. Persistently elevated alanine aminotransferase (ALT) levels were present in 40 patients (54.1%). Hepatitis B virus markers (HBsAg and/or anti-HBc) were detected in 18 patients (24.3%). Twenty-six of the 43 HCV RNA-positive children underwent a diagnostic liver biopsy that showed chronic hepatitis in 19 patients (73.1%), cirrhosis in one case only (3.8%), and normal biopsy findings in seven children (26.9%). Blood transfusion remains a major risk of HCV transmission among Egyptian children. HCV infection is not always benign in the childhood period. ALT levels remain elevated in half of the children and histological abnormalities are detected in three quarters of HCV RNA-positive cases.

The outcome of hepatitis C virus (HCV) infection acquired in childhood is uncertain because of the diversity of the epidemiological and clinical features of infection and disease. The aim of this study was to determine the outcome of HCV infection in 105 Egyptian children who tested positive for HCV antibody (anti-HCV). The data of 105 anti-HCV-positive children presenting to the Pediatric Hepatology Unit, Cairo University Children's Hospital, between 1995 and 2002, were retrospectively analysed for risk factors. Seventy-four children with available polymerase chain reaction results were further analysed clinically, serologically and histologically. The age range was 1.3-22 years, with a mean of 11.2 +/- 4.9 years. History of blood transfusion was found in 81 children (77%). HCV RNA was detected in 58.1% of 74 children. Persistently elevated alanine aminotransferase (ALT) levels were present in 40 patients (54.1%). Hepatitis B virus markers (HBsAg and/or anti-HBc) were detected in 18 patients (24.3%). Twenty-six of the 43 HCV RNA-positive children underwent a diagnostic liver biopsy that showed chronic hepatitis in 19 patients (73.1%), cirrhosis in one case only (3.8%), and normal biopsy findings in seven children (26.9%). Blood transfusion remains a major risk of HCV transmission among Egyptian children. HCV infection is not always benign in the childhood period. ALT levels remain elevated in half of the children and histological abnormalities are detected in three quarters of HCV RNA-positive cases.

The outcome of hepatitis C virus (HCV) infection acquired in childhood is uncertain because of the diversity of the epidemiological and clinical features of infection and disease. The aim of this study was to determine the outcome of HCV infection in 105 Egyptian children who tested positive for HCV antibody (anti-HCV). The data of 105 anti-HCV-positive children presenting to the Pediatric Hepatology Unit, Cairo University Children's Hospital, between 1995 and 2002, were retrospectively analysed for risk factors. Seventy-four children with available polymerase chain reaction results were further analysed clinically, serologically and histologically. The age range was 1.3-22 years, with a mean of 11.2 +/- 4.9 years. History of blood transfusion was found in 81 children (77%). HCV RNA was detected in 58.1% of 74 children. Persistently elevated alanine aminotransferase (ALT) levels were present in 40 patients (54.1%). Hepatitis B virus markers (HBsAg and/or anti-HBc) were detected in 18 patients (24.3%). Twenty-six of the 43 HCV RNA-positive children underwent a diagnostic liver biopsy that showed chronic hepatitis in 19 patients (73.1%), cirrhosis in one case only (3.8%), and normal biopsy findings in seven children (26.9%). Blood transfusion remains a major risk of HCV transmission among Egyptian children. HCV infection is not always benign in the childhood period. ALT levels remain elevated in half of the children and histological abnormalities are detected in three quarters of HCV RNA-positive cases.

The outcome of hepatitis C virus (HCV) infection acquired in childhood is uncertain because of the diversity of the epidemiological and clinical features of infection and disease. The aim of this study was to determine the outcome of HCV infection in 105 Egyptian children who tested positive for HCV antibody (anti-HCV). The data of 105 anti-HCV-positive children presenting to the Pediatric Hepatology Unit, Cairo University Children's Hospital, between 1995 and 2002, were retrospectively analysed for risk factors. Seventy-four children with available polymerase chain reaction results were further analysed clinically, serologically and histologically. The age range was 1.3-22 years, with a mean of 11.2 +/- 4.9 years. History of blood transfusion was found in 81 children (77%). HCV RNA was detected in 58.1% of 74 children. Persistently elevated alanine aminotransferase (ALT) levels were present in 40 patients (54.1%). Hepatitis B virus markers (HBsAg and/or anti-HBc) were detected in 18 patients (24.3%). Twenty-six of the 43 HCV RNA-positive children underwent a diagnostic liver biopsy that showed chronic hepatitis in 19 patients (73.1%), cirrhosis in one case only (3.8%), and normal biopsy findings in seven children (26.9%). Blood transfusion remains a major risk of HCV transmission among Egyptian children. HCV infection is not always benign in the childhood period. ALT levels remain elevated in half of the children and histological abnormalities are detected in three quarters of HCV RNA-positive cases.

Chronic kidney disease (CKD) is a worldwide public health problem. There is an increasing incidence and prevalence of patients with kidney failure requiring replacement therapy, with poor outcomes and high cost. There is an even higher prevalence of patients in earlier stages of CKD, with adverse outcomes such as kidney failure, cardiovascular disease, and premature death. Patients at earlier stages of CKD can be detected through laboratory testing and their treatment is effective in slowing the progression to kidney failure and reducing cardiovascular events. The science and evidence-based care of these patients are universal and independent of their geographic location. There is a clear need to develop a uniform and global public health approach to the worldwide epidemic of CKD. It is to this end that a new initiative "Kidney Disease: Improving Global Outcomes" has been established. Its stated mission is "Improve the care and outcomes of kidney disease patients worldwide through promoting coordination, collaboration and integration of initiatives to develop and implement clinical practice guidelines."

Iatrogenic obstruction of the vas deferens within the inguinal canal can be managed by direct on-site vasovasostomy. However, in cases with large defect of the vas, the anastomosis may be under tension. Dissecting through the site of a previous hernia repair is tedious, and may lead to recurrence of the hernia. The present work reports an, first of a kind, alternative technique that avoids the latter drawbacks. Fifteen cases were operated upon. Under laparoscopic vision, the pelvic vas was dissected and the lateral-most end was clipped, cut and extruded from the abdomen through a port in the external inguinal ring. End-to-end vasovasostomy and microsurgical anastomosis for the vasal vessels were performed, bridging the retrieved stump of the pelvic vas with the scrotal vas. There were positive results in the form of sperm count ranging from 1.5 to 15 million ml(-1), an average of 7.25 (SD 5.44) in nine of 15 cases (60%), within the first 6 months following surgery. "Pelvi-scrotal vasovasostomy" can be offered as a cost-effective and successful alternative or supplement to intracytoplasmic sperm injection, for cases with iatrogenic large defects of the vas deferens within the inguinal canal.

We aimed to assess the right atrial performance in patients after surgical correction of tetralogy of Fallot, and to clarify the relationship between the pump function of the right atrium and right ventricular systolic function. We included in the study 50 asymptomatic patients following corrective surgery of tetralogy of Fallot, comparing them to 30 normal subjects. Right atrial areas were measured by echocardiography, and the active fractional area of emptying was expressed, in percentages, as the area measured at the onset of atrial contraction, minus the minimal area, divided by the area at the onset of atrial contraction. We used this value to assess the atrial pump function. Right atrial peak strain rates were measured by tissue Doppler imaging. Compared to controls, patients with tetralogy of Fallot had a significantly reduced right atrial active fractional area of emptying (p = 0.005), along with a reduced peak late diastolic strain rate (p = 0.002). Among 20 patients who underwent magnetic resonance tomographic examination, a relatively higher right atrial peak late diastolic strain rate was shown in patients with a right ventricular ejection fraction of less than 50% (p = 0.021). Right atrial performance is reduced in patients after surgical correction of tetralogy of Fallot. When facing right ventricular systolic dysfunction, nonetheless, the right atrial pump function may be relatively enhanced. Tissue Doppler derived strain rate can provide quantitative analysis of regional right atrial performance.

BACKGROUND: Bladder cancer manifests many different forms ranging from superficial to aggressive muscle invasive stages, which suggests that various genetic alterations are involved. Several attempts have been made to establish correlations between specific genetic alterations and various stages of the disease. At the National Cancer Institute (NCI), Cairo, bladder cancer constitutes 30.3% of all cancers. Bladder cancer observed among Egyptians has a clinico-pathological profile that differs from transitional cell carcinoma (TCC) seen in the western world.

PATIENTS AND METHODS: We used fluorescence in situ hybridization to detect numerical chromosome changes in 25 patients presenting with carcinoma in situ and Ta lesions. Twenty-four cases had transitional cell carcinoma and one case had squamous cell carcinoma.

RESULTS: Five out of 24 TCC cases had diploid chromosome count with all the probes. Numerical chromosome aberrations were detected in 19 cases (79%). In eight cases, a loss of chromosome 9 was observed. In one case, an additional loss of chromosome 17 was detected. One case demonstrated a loss of chromosome 17, whereas another three cases showed a gain of chromosome 7. Loss of chromosome Y was observed in nine of the 22 male cases studied (40.9%). The only case with SCC had normal diploid chromosome count with all the probes used.

CONCLUSION: When the genetic basis of bilharzial related bladder cancer is fully understood, new diagnostic and therapeutic strategies will be developed, which in turn may promote better clinical management by pathologists and urologists. A theory of bilharzial related bladder cancer pathogenesis is suggested.

BACKGROUND: Gene amplifications are common events in different tumor types and may confer diagnostic, prognostic, or therapeutic information for patient management. Fluorescence in situ hybridization (FISH) represents a standard methodologic approach for testing for this genetic alteration, as it is rapid, reproducible and extremely reliable in detecting presence of C-erb-B2 gene amplification for clinical utility.

PATIENTS AND METHODS: In this study, FISH is used in a series of archival human bilharzial bladder cancer specimens to evaluate for the presence of cerbB-2 gene alterations in the most common malignant tumor in bilharzial endemic areas, e.g., Egypt and some other countries. The study included 40 cases, 30 males and 10 females. Their ages ranged between 30 years and 76 years (median: 51 years). Twenty-one cases had squamous cell carcinoma, 16 had transitional cell carcinoma, two had adenocarcinoma, and one case had undifferentiated carcinoma.

RESULTS: Thirteen out of 40 tumor samples (32.5%) show evidence of true C-erb-B2 gene amplification. Of the remaining samples, 24 (60%) show no gene amplification and three (7.5%) fall into the borderline category with a ratio between one and two C-erb-B2 genes/cell relative to chromosome 17 centromeres. No evidence of chromosome 17 polysomy was found in any cases scored as single copy with the C-erb-B2 probe.

CONCLUSION: No significant association was found between gene amplification and any of the tested clinicopathologic parameters or tumor recurrence except for tumor grade where higher tumor grades tended to be associated with more C-erb-B2 gene amplification (P = 0.01) thus reflecting more tumor aggressiveness. So, the amplification of C-erb-B2 in bilharzial associated bladder cancer is probably not independently related to clinical outcome of patients.

Expression and storage of breast milk is way to maintain breastfeeding when mother and infant are separated, if the nutritional value can be conserved. Three expressed breast milk samples were collected from 61 healthy lactating mothers in Cairo, Egypt, for determination of total protein, fat, lactose and zinc content, as well as vitamins C, A and E concentrations. One sample was analysed immediately without storage, 1 after storage for 24 hours in a refrigerator (4 degrees C) and 1 after storage for 1 week in a home freezer (-4 degrees C to -8 degrees C). Refrigeration and freezing of breast milk caused a statistically significant decline in levels of vitamins C, A and E. Nevertheless, the values of all nutrients were still within the international reference ranges for mature breast milk.

No identifiable cause can be found in more than half of the cases of portal vein thrombosis (PVT). Our aim was to assess the prevalence of factor V Leiden mutation and other thrombophilic factors as risk factors in the development of PVT in the pediatric age group. From March 2001 to January 2002, 40 children with PVT were enrolled in the study, in addition to 20 age-matched and sex-matched controls. Protein C, protein S, antithrombin III, and activated protein C resistance (APCR) were assayed. Molecular study of factor II and factor V mutations was carried out. Of the patients, 25 had detectable hereditary thrombophilia (62.5%), 12 had factor V Leiden mutation (30%), 11 had protein C deficiency (27.5%), 6 had factor II mutation (15%), 1 had antithrombin III deficiency (2.5%), and none had protein S deficiency. Five children had concurrence of more than one defect. Factor V Leiden mutation is the most common hereditary thrombophilia associated with PVT and the relative risk of factor V Leiden mutation, as a cause of PVT, was six times more than in controls (odds ratio=6). Concurrence of more than one hereditary thrombophilic factor was seen in 12.5% of our patients. Circumstantial risk factors (neonatal sepsis, umbilical sepsis, umbilical catheterization) were not more significantly prevalent among patients with hereditary thrombophilia than among those with no detectable abnormalities in anticoagulation.

No identifiable cause can be found in more than half of the cases of portal vein thrombosis (PVT). Our aim was to assess the prevalence of factor V Leiden mutation and other thrombophilic factors as risk factors in the development of PVT in the pediatric age group. From March 2001 to January 2002, 40 children with PVT were enrolled in the study, in addition to 20 age-matched and sex-matched controls. Protein C, protein S, antithrombin III, and activated protein C resistance (APCR) were assayed. Molecular study of factor II and factor V mutations was carried out. Of the patients, 25 had detectable hereditary thrombophilia (62.5%), 12 had factor V Leiden mutation (30%), 11 had protein C deficiency (27.5%), 6 had factor II mutation (15%), 1 had antithrombin III deficiency (2.5%), and none had protein S deficiency. Five children had concurrence of more than one defect. Factor V Leiden mutation is the most common hereditary thrombophilia associated with PVT and the relative risk of factor V Leiden mutation, as a cause of PVT, was six times more than in controls (odds ratio=6). Concurrence of more than one hereditary thrombophilic factor was seen in 12.5% of our patients. Circumstantial risk factors (neonatal sepsis, umbilical sepsis, umbilical catheterization) were not more significantly prevalent among patients with hereditary thrombophilia than among those with no detectable abnormalities in anticoagulation.

No identifiable cause can be found in more than half of the cases of portal vein thrombosis (PVT). Our aim was to assess the prevalence of factor V Leiden mutation and other thrombophilic factors as risk factors in the development of PVT in the pediatric age group. From March 2001 to January 2002, 40 children with PVT were enrolled in the study, in addition to 20 age-matched and sex-matched controls. Protein C, protein S, antithrombin III, and activated protein C resistance (APCR) were assayed. Molecular study of factor II and factor V mutations was carried out. Of the patients, 25 had detectable hereditary thrombophilia (62.5%), 12 had factor V Leiden mutation (30%), 11 had protein C deficiency (27.5%), 6 had factor II mutation (15%), 1 had antithrombin III deficiency (2.5%), and none had protein S deficiency. Five children had concurrence of more than one defect. Factor V Leiden mutation is the most common hereditary thrombophilia associated with PVT and the relative risk of factor V Leiden mutation, as a cause of PVT, was six times more than in controls (odds ratio=6). Concurrence of more than one hereditary thrombophilic factor was seen in 12.5% of our patients. Circumstantial risk factors (neonatal sepsis, umbilical sepsis, umbilical catheterization) were not more significantly prevalent among patients with hereditary thrombophilia than among those with no detectable abnormalities in anticoagulation.

No identifiable cause can be found in more than half of the cases of portal vein thrombosis (PVT). Our aim was to assess the prevalence of factor V Leiden mutation and other thrombophilic factors as risk factors in the development of PVT in the pediatric age group. From March 2001 to January 2002, 40 children with PVT were enrolled in the study, in addition to 20 age-matched and sex-matched controls. Protein C, protein S, antithrombin III, and activated protein C resistance (APCR) were assayed. Molecular study of factor II and factor V mutations was carried out. Of the patients, 25 had detectable hereditary thrombophilia (62.5%), 12 had factor V Leiden mutation (30%), 11 had protein C deficiency (27.5%), 6 had factor II mutation (15%), 1 had antithrombin III deficiency (2.5%), and none had protein S deficiency. Five children had concurrence of more than one defect. Factor V Leiden mutation is the most common hereditary thrombophilia associated with PVT and the relative risk of factor V Leiden mutation, as a cause of PVT, was six times more than in controls (odds ratio=6). Concurrence of more than one hereditary thrombophilic factor was seen in 12.5% of our patients. Circumstantial risk factors (neonatal sepsis, umbilical sepsis, umbilical catheterization) were not more significantly prevalent among patients with hereditary thrombophilia than among those with no detectable abnormalities in anticoagulation.

No identifiable cause can be found in more than half of the cases of portal vein thrombosis (PVT). Our aim was to assess the prevalence of factor V Leiden mutation and other thrombophilic factors as risk factors in the development of PVT in the pediatric age group. From March 2001 to January 2002, 40 children with PVT were enrolled in the study, in addition to 20 age-matched and sex-matched controls. Protein C, protein S, antithrombin III, and activated protein C resistance (APCR) were assayed. Molecular study of factor II and factor V mutations was carried out. Of the patients, 25 had detectable hereditary thrombophilia (62.5%), 12 had factor V Leiden mutation (30%), 11 had protein C deficiency (27.5%), 6 had factor II mutation (15%), 1 had antithrombin III deficiency (2.5%), and none had protein S deficiency. Five children had concurrence of more than one defect. Factor V Leiden mutation is the most common hereditary thrombophilia associated with PVT and the relative risk of factor V Leiden mutation, as a cause of PVT, was six times more than in controls (odds ratio=6). Concurrence of more than one hereditary thrombophilic factor was seen in 12.5% of our patients. Circumstantial risk factors (neonatal sepsis, umbilical sepsis, umbilical catheterization) were not more significantly prevalent among patients with hereditary thrombophilia than among those with no detectable abnormalities in anticoagulation.

Sufficient data relating urinary iodine excretion in children to other iodine deficiency indicators are lacking in Egypt. We assayed urinary iodine concentration and serum levels of thyroid stimulating hormone (TSH), thyroglobulin, free triiodothyronine (T3) and free tetraiodothyronine in 99 school-aged Egyptian children. Goitre was found in 25 children. Median urinary iodine concentration was 70 microg/L. We found mild iodine deficiency (50-99 microg/L) in 60.6 % of the children and moderate to severe deficiency (< 50 microg/L) in 31.3%. The latter showed a high frequency of goitre and elevated mean serum free T3, TSH and thyroglobulin levels. Individual urinary iodine excretion rates vary, therefore these other indicators could help in screening for iodine deficiency at an individual level, especially in moderate to severe deficiency.