Publications by authors named "Al-Mardini H"

Background: The epidemiology of hepatitis C virus infection has been well characterized in Western Europe, North America and Japan. Less is known about it in other regions of the world. In order to fully understand the relationship between host and virus, it is important to study the effect of virus infection in all regions of the world.

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Background/aims: The pathogenesis of hepatic encephalopathy (HE) is controversial. We have therefore studied the effect of induced hyperammonaemia in man.

Patients And Methods: 108 g of an amino acid mixture was given orally to 18 cirrhotics and 11 control subjects and changes in blood ammonia, EEG and plasma amino acids were observed.

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Background: It is well known that portacaval shunting ultimately leads to a decrease in liver volume and hepatic function, but the mechanism is uncertain. The aim of the present study was to evaluate the effect of portacaval shunting (PCS) upon the morphological changes that occur in the liver in rats after port caval anastomosis.

Materials And Methods: Sixty-six male rats underwent either PCS (n = 35) or sham operations (n = 31).

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Background: The role of Helicobacter pylori (H. pylori) eradication in non-steroidal anti inflammatory drug (NSAID) users with peptic ulcer disease is controversial especially in countries with a high prevalence of the infection. Furthermore the value of low dose omeprazole for maintenance of remission is not yet known.

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Hepatic encephalopathy is a frequent complication of cirrhosis. Abnormalities of 5-hydroxytryptamine (5-HT) and its metabolites are recognized and may contribute to its pathogenesis. We therefore studied the effect of an oral tryptophan load (6-18 g) upon psychometric test scores and analyzed EEG's in alcoholic cirrhotic patients.

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Background/aims: To mimic episodic hepatic encephalopathy after gastrointestinal bleeding under controlled conditions, cirrhotic patients were challenged with an amino acid mixture of comparable composition to haemoglobin.

Methods: Basal EEG, psychometric score (HE test), reaction times and venous blood ammonia were recorded. Following a 54 or 108 gm oral amino acid challenge, blood ammonia levels and EEG were recorded at 30-min intervals, and psychometric testing was repeated at 180 min.

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Background: Hepatic fibrosis is one of the main consequences of liver disease. Both fibrosis and steatosis may be seen in some patients with chronic hepatitis C and alcoholic liver disease (ALD).

Aims: To quantitate fibrosis and steatosis by stereological and morphometric techniques in patients with chronic hepatitis C and compare the results with a control group of patients with ALD.

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Background And Aim: An oral glutamine load in cirrhotic patients awaiting liver transplantation was shown to cause a rise in blood ammonia and psychometric abnormalities which were reversed by hepatic transplantation. L-Ornithine-L-aspartate (LOLA) has been shown to reduce ammonia and improve psychometric function in patients with hepatic encephalopathy. The aim of the present study was to assess the effect of LOLA in healthy patients with cirrhosis and no evidence of clinical encephalopathy after challenging the central nervous system by administration of oral glutamine.

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Aim: To assess the topographical relation between gastric glands, using the minimum spanning tree (MST), to derive both a model of neighbourhood and quantitative representation of the tissue's architecture, to assess the characteristic features of gastric atrophy, and to assess the grades of gastric atrophy.

Methods: Haematoxylin and eosin stained sections from corporal and antral biopsy specimens (n = 139) from normal patients and from patients with nonatrophic gastritis and atrophic gastritis of grades 1, 2, and 3 (Sydney system) were assessed by image analysis system (Prodit 5.2) and 11 syntactic structure features were derived.

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To evaluate the differential effects of portacaval shunting (PCS) on the morphological changes that occur in humans with portal-systemic encephalopathy, male rats underwent either PCS (13) or sham operations (10). Normal adult rats (6) were used as controls. All animals were killed 5 to 7 weeks after the surgery.

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Latent or sub-clinical hepatic encephalopathy is a recognized complication of cirrhosis and is thought to represent one end of the spectrum of neuropsychiatric impairment, which occurrs as a result of portal-systemic shunting. We studied the psychometric, analyzed electroencephalography (EEG), and venous blood ammonia responses to an oral glutamine challenge in 17 patients with cirrhosis and in 4 normal controls. The cirrhotics were attending for liver transplant assessment and had no clinical evidence of hepatic encephalopathy.

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Dysfunction of excitatory glutamatergic neurotransmission has been implicated in the cause of hepatic encephalopathy. Brain microdialysis studies in various animal models of portal systemic encephalopathy (PSE) and encephalopathy associated with acute liver failure, have established that an increase in extracellular glutamate occurs but the mechanisms of this are unclear. We have measured oxygen consumption, citrate synthase activity (as indices of energy state and mitochondrial content, respectively), calcium-dependent glutamate release, and high-affinity, sodium-dependent glutamate uptake by synaptosomes prepared from rats with thioacetamide-induced encephalopathy.

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Background/aims: Quinolinic acid is an endogenous neuroexcitant derived from tryptophan. Brain quinolinic acid concentrations are reportedly elevated in chronic liver failure. The aim of this study was to determine if brain quinolinic acid levels correlate with the severity of hepatic encephalopathy.

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A method for the analysis of 1,2-diacylglycerols in biological samples is presented. After tissue extraction and derivatisation with 3,5-dinitrobenzoyl chloride, samples are analysed by normal phase HPLC, using a 3.9 x 300 mm microPorasil column, and ultraviolet detection at 254 nm.

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The neurotransmitter serotonin has a profound effect on the control of sleep; thus excess serotonin activity in the brain could be responsible for impaired consciousness in hepatic encephalopathy. Furthermore, an increased brain level of 5-hydroxy-indoleacetic acid has been a consistent finding in various animal models of the condition. In this study, using high-performance liquid chromatography with fluorometric detection, we examined levels of brain serotonin (5-hydroxytryptamine) and its precursors and metabolites in 16 patients dying with hepatic encephalopathy complicating acute and chronic liver disease and 9 control subjects matched for age, sex, postmortem delay in brain retrieval and length of frozen tissue storage.

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In a significant proportion of cases of community acquired diarrhoea no recognised pathogen is detected. Verocytotoxin producing Escherichia coli (VTEC) are associated with haemorrhagic colitis and the haemolytic uraemic syndrome but their role in community acquired diarrhoea is not fully understood. Using a method of toxin enhancement in mixed faecal culture, 175 stools negative on culture for recognised pathogens were tested for the presence of cytotoxin and 28% were found to be positive.

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The number of verocytotoxin producing Escherichia coli (VTEC) present in the faeces during an infection may be very low, making their detection difficult. We report a method for enhancing toxin production by VTEC using mitomycin C as an inducing agent with the aim of improving the detection of VTEC. In pure culture, mitomycin C enhanced toxin production up to 100-fold.

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Thirty-seven patients suffering an attack of acute distal ulcerative colitis of mild or moderate severity were randomized in a double-blind, double-dummy fashion to receive either 800 mg oral mesalazine four times daily (18 patients) or steroid enemas twice daily (19 patients) for 4 weeks. Both treatments were well tolerated with no adverse effects. Three patients in each group were withdrawn because of clinical deterioration but both treatments produced significant clinical improvement with decreases in stool frequency and scores for urgency, bleeding and tenesmus.

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The value of lactulose treatment in hepatic encephalopathy is widely recognised but its mode of action remains controversial. Much evidence supports a role for gamma-aminobutyric acid in hepatic encephalopathy, and lactulose could alter its bacterial production in the gut. Using the rat synaptic membrane assay and gas chromatography mass spectrometry, the production of gamma-aminobutyric acid by faecal Escherichia coli, with and without the addition of albumin, haemoglobin, whole blood, and lactulose under aerobic and anaerobic conditions was determined.

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Although gluten withdrawal is likely to remain the mainstay of treatment for adult coeliac disease, many patients find the diet inconvenient and unpalatable and compliance among asymptomatic patients is often poor. Oral corticosteroids have been used for patients who seem to be resistant to gluten withdrawal but preparations with low systemic bioavailability might be preferable. We have given a new glucocorticoid (fluticasone propionate) to 12 adults with untreated coeliac disease for six weeks while they were on a normal diet.

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Morphometric measurements were performed on rectal biopsy specimens from 10 normal control subjects and 33 patients with a relapse of distal ulcerative colitis before and after treatment for four weeks in a double blind controlled trial with oral eudragit S coated 5 amino salicylic acid (n = 12) or rectal prednisolone enemas (n = 15). Measurements were assessed using a computer aided measuring system and a counting technique. When untreated patients were compared with the control group there were significant decreases in the area and height of the surface epithelium, in the area of crypt epithelium, and in the ratios of goblet cells to epithelial cells and of surface epithelium to lamina propria.

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In five patients with cirrhosis given an oral methionine load, blood mercaptan concentrations were not significantly affected by neomycin and metronidazole therapy. Methanethiol and dimethyl sulphide rose after methionine to levels encountered in hepatic encephalopathy but in stable cirrhotics no neurological abnormalities were evident. In one patient with chronic hepatic encephalopathy there was no significant change in methanethiol, dimethyl sulphide or ammonia concentration 4 h after methionine when conscious state had deteriorated by two stages of encephalopathy.

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The validation of a new assay for the leucine degradion product isovaleraldehyde in biological fluids is described. A gas purge technique was used with trapping of volatile constituents in a Tenax cartridge followed by automated thermal desorption and gas chromatographic analysis. The concentration of isovaleraldehyde during the course of hepatic encephalopathy (80 observations in 48 patients; 25 cirrhotic, 23 fulminant hepatic failure) was significantly increased compared to control subjects (0.

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In order to determine the specificity of abnormalities of alcohol metabolism in patients with alcoholic liver disease, blood acetaldehyde concentrations after oral ethanol challenge and the activities of alcohol metabolising enzymes in liver biopsy samples have been determined in patients with alcoholic liver disease and a wide variety of non-alcoholic liver disorders. Significant decreases in hepatic cytosolic aldehyde dehydrogenase activity were associated with significant increases in acetaldehyde concentrations after ethanol in both patient groups compared with control subjects. There was a significant correlation between hepatic cytosolic aldehyde dehydrogenase and mean blood acetaldehyde concentration 30-180 min after ethanol ingestion (y = 17.

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