The Experts below are selected from a list of 15 Experts worldwide ranked by ideXlab platform
Hanan Abdel Hafez - One of the best experts on this subject based on the ideXlab platform.
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predictive value of non invasive Blood Ammonia Level for the presence of oesophageal varices in egyptian patients with liver cirrhosis
Journal of gastroenterology and hepatology research, 2015Co-Authors: Hanan Abdel HafezAbstract:AIM: Although recent guidelines recommend screening of cirrhotic patients by upper endoscopy for oesophageal varices prediction, Non-invasive parameters are needed due to high endoscopy cost and burden on endoscopic units particularly in poor countries. The aim of this study is to evaluate the accuracy of using Ammonia Blood Level as potential non-invasive predictor of oesophageal varices in cirrhotic patients. Methods: This prospective study was conducted on 150 Egyptian participants. Patients were categorized as group I which included 100 with oesophageal varices and group II included 30 patients without varices. There were 20 healthy control participants served as a control group (group III). All patients underwent for full clinical and laboratory workup, abdominal ultrasound and upper gastrointestinal endoscopy. Venous Ammonia Blood Levels were calculated for all the contributors of this study. Results: The mean Ammonia Level was higher in group I (88.29±42.82 µmol/L) than in group II (82.77±49.76 µmol/L) with no statistical significant difference between the two groups (p=0.34). Ammonia Level in group III was 73.37±30.36 µmol/L with no statistical significant difference with the other groups (p>0.05). In group I; Ammonia Level is positively correlated with the splenic vein diameter with r = 0.22 (p=0.026) but did not correlate with the grade of oesophageal varices r =0.031 (p-value=0.762). In multivariate analysis; Ammonia combined with platelets, Age, PT and PC shared in a significant prediction model (I) for esophageal varices grading (p=0.002). Prediction model (II) including portal and splenic veins diameters and the liver size was developed (p=0.016). Conclusion: Non-invasive means could be used to monitor cirrhotic patients and consider treatment. Ammonia Level can not be used alone but its use within a significant prediction model can help restricting the use of endoscopic screening in patients with a high probability of esophageal varices.
Seymour Packman - One of the best experts on this subject based on the ideXlab platform.
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Hyperammonemia in urea cycle disorders: Role of the nephrologist
American Journal of Kidney Diseases, 2001Co-Authors: Robert Mathias, Dana Kostiner, Seymour PackmanAbstract:Hyperammonemia associated with inherited disorders of amino acid and organic acid metabolism is usually manifested by irritability, somnolence, vomiting, seizures, and coma. Although the majority of these patients present in the newborn period, they may also present in childhood, adolescence, and adulthood with failure to thrive, persistent vomiting, developmental delay, or behavioral changes. Persistent hyperammonemia, if not treated rapidly, may cause irreversible neuronal damage. After the diagnosis of hyperammonemia is established in an acutely ill patient, certain diagnostic tests should be performed to differentiate between urea cycle defects and other causes of hyperammonemic encephalopathy. In a patient with a presumed inherited metabolic disorder, the aim of therapy should be to normalize Blood Ammonia Levels. Recent experience has provided treatment guidelines that include minimizing endogenous Ammonia production and protein catabolism, restricting nitrogen intake, administering substrates of the urea cycle, administering compounds that facilitate the removal of Ammonia through alternative pathways, and, in severe cases, dialysis therapy. Initiation of dialysis in the encephalopathic patient with hyperammonemia is indicated if the Ammonia Blood Level is greater than three to four times the upper limit of normal. Hemodialysis is the most effective treatment for rapidly reducing Blood Ammonia Levels. Continuous hemofiltration and peritoneal dialysis are also effective modalities for reducing Blood Ammonia Levels. An improved understanding of the metabolism of Ammonia and neurological consequences of hyperammonemia will assist the nephrologist in providing optimal care for this high-risk patient population.
Robert Mathias - One of the best experts on this subject based on the ideXlab platform.
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Hyperammonemia in urea cycle disorders: Role of the nephrologist
American Journal of Kidney Diseases, 2001Co-Authors: Robert Mathias, Dana Kostiner, Seymour PackmanAbstract:Hyperammonemia associated with inherited disorders of amino acid and organic acid metabolism is usually manifested by irritability, somnolence, vomiting, seizures, and coma. Although the majority of these patients present in the newborn period, they may also present in childhood, adolescence, and adulthood with failure to thrive, persistent vomiting, developmental delay, or behavioral changes. Persistent hyperammonemia, if not treated rapidly, may cause irreversible neuronal damage. After the diagnosis of hyperammonemia is established in an acutely ill patient, certain diagnostic tests should be performed to differentiate between urea cycle defects and other causes of hyperammonemic encephalopathy. In a patient with a presumed inherited metabolic disorder, the aim of therapy should be to normalize Blood Ammonia Levels. Recent experience has provided treatment guidelines that include minimizing endogenous Ammonia production and protein catabolism, restricting nitrogen intake, administering substrates of the urea cycle, administering compounds that facilitate the removal of Ammonia through alternative pathways, and, in severe cases, dialysis therapy. Initiation of dialysis in the encephalopathic patient with hyperammonemia is indicated if the Ammonia Blood Level is greater than three to four times the upper limit of normal. Hemodialysis is the most effective treatment for rapidly reducing Blood Ammonia Levels. Continuous hemofiltration and peritoneal dialysis are also effective modalities for reducing Blood Ammonia Levels. An improved understanding of the metabolism of Ammonia and neurological consequences of hyperammonemia will assist the nephrologist in providing optimal care for this high-risk patient population.
Dana Kostiner - One of the best experts on this subject based on the ideXlab platform.
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Hyperammonemia in urea cycle disorders: Role of the nephrologist
American Journal of Kidney Diseases, 2001Co-Authors: Robert Mathias, Dana Kostiner, Seymour PackmanAbstract:Hyperammonemia associated with inherited disorders of amino acid and organic acid metabolism is usually manifested by irritability, somnolence, vomiting, seizures, and coma. Although the majority of these patients present in the newborn period, they may also present in childhood, adolescence, and adulthood with failure to thrive, persistent vomiting, developmental delay, or behavioral changes. Persistent hyperammonemia, if not treated rapidly, may cause irreversible neuronal damage. After the diagnosis of hyperammonemia is established in an acutely ill patient, certain diagnostic tests should be performed to differentiate between urea cycle defects and other causes of hyperammonemic encephalopathy. In a patient with a presumed inherited metabolic disorder, the aim of therapy should be to normalize Blood Ammonia Levels. Recent experience has provided treatment guidelines that include minimizing endogenous Ammonia production and protein catabolism, restricting nitrogen intake, administering substrates of the urea cycle, administering compounds that facilitate the removal of Ammonia through alternative pathways, and, in severe cases, dialysis therapy. Initiation of dialysis in the encephalopathic patient with hyperammonemia is indicated if the Ammonia Blood Level is greater than three to four times the upper limit of normal. Hemodialysis is the most effective treatment for rapidly reducing Blood Ammonia Levels. Continuous hemofiltration and peritoneal dialysis are also effective modalities for reducing Blood Ammonia Levels. An improved understanding of the metabolism of Ammonia and neurological consequences of hyperammonemia will assist the nephrologist in providing optimal care for this high-risk patient population.
M. Arakawa - One of the best experts on this subject based on the ideXlab platform.
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Clinical factors that affect Blood gases in non-smoking women with chronic liver disease.
Respiratory Medicine, 1998Co-Authors: K. Fujimori, M. ArakawaAbstract:Abstract Chronic liver disease is often accompanied by hypoxaemia. We investigated the clinical factors that were related to the arterial oxygen tension ( P aO 2 ) in 40 women, all non-smokers with chronic liver disease. They were positive for hepatitis C virus (HCV) antibody and had no evidence of cardiopulmonary disease. Arterial Blood was collected from patients at rest (>15 min) for analysis of Blood gases. We determined the correlation between Blood gas tension and the clinical variables, i.e. the presence or absence of skin manifestations such as cutaneous spider nevi and palmar erythema, the presence or absence of splenomegaly, vital capacity, forced expiratory volume in one second, V 25 /body height, serum alanine aminotransferase (AST), serum asparate aminotransferase (ALT), serum cholinesterase, serum γ-globulin/total protein, excretion of indocyanine green at 15 min (15-min retention rate, ICG Level), Blood Level of Ammonia, Blood Level of endotoxin, plasma Level of glucagon and the serum Level of type IV collagen-7S. The mean Level of P aO 2 was 78 ± 11 (range: 43–95) torr. The mean alveolar-arterial oxygen tension gradient ( A - aD O 2 ) was 19 ± 13 (range: 2–60) torr. Multiple regression analysis used P aO 2 and A - aD O 2 as objective variables, and the clinical findings as explanatory variables. The explanatory variables that were significantly correlated with Blood gas values were ICG Level, Blood Level of endotoxin and presence of skin manifestations. The ICG Level showed a high correlation with Blood gas values; the ICG Level increased, the P aO 2 decreased ( r = − 0·69), while the A - aD O 2 showed a high positive correlation ( r = + 0·78, P
