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Biomedical subjects

A S Taha

Publications and source records attributed to A S Taha.

At least 19 recordsLinked to original sources
PubMed2006

Clinical outcome in upper gastrointestinal bleeding complicating low-dose aspirin and antithrombotic drugs.

BACKGROUND: The current risk stratification systems in upper gastrointestinal bleeding do not correct for the intake of low-dose aspirin and other antithrombotic drugs. AIM: To test the Blatchford scores in evaluating the clinical outcome in bleeders using these drugs. METHODS: We calculated the Blatchford scores in 510 bleeders, including 123 on low-dose aspirin, 44 on other antithrombotic drugs, and 68 on non-steroidal anti-inflammatory drugs. RESULTS: The median clinical scores distributed according to aetiological risk factors were as follows: no risk factors, 5; non-steroidal anti-inflammatory drugs, 8; aspirin, 7; other antithrombotics, 6; excess alcohol, 4; multiple risk factors, 7; (P = 0.003, Kruskal-Wallis test). Scores correlated positively with the duration of admission in the entire group (r(s) = 0.285; P < 0.001) and in those taking aspirin and antithrombotics (r(s) = 0.211; P = 0.029). The median scores in patients requiring the blood transfusion were 10 in the entire group and 11 in users of aspirin or antithrombotics, compared with 3 and 4, respectively, in those not transfused (P < 0.001). CONCLUSIONS: The Blatchford scores are significantly elevated in users of non-steroidal anti-inflammatory drugs, low-dose aspirin, and other antithrombotic drugs. They correlate positively with the duration of admission and the need for blood transfusion.

Aspirin↗
PubMed2006

Upper gastrointestinal mucosal abnormalities and blood loss complicating low-dose aspirin and antithrombotic therapy.

BACKGROUND: Little is known about the site and nature of bleeding lesions related to low-dose aspirin and other antithrombotic agents. AIM: To describe the mucosal abnormalities in patients presenting with upper gastrointestinal bleeding while being treated with these drugs. METHODS: The endoscopic findings and clinical details were analysed in all patients presenting with haematemesis and/or melaena at a single centre during three calendar years. Associations between endoscopic findings and risk factors, including the intake of non-steroidal anti-inflammatory drugs, low-dose aspirin (75 mg daily) and other antithrombotic drugs including warfarin, clopidogrel, and dipyridamole, were assessed by logistic regression analysis. RESULTS: In 674 upper gastrointestinal bleeders, we found that the odds ratio for the presence of erosive oesophagitis in aspirin users was 2 (95% CI, 1-3; P = 0.03) and 3 (2-5; P = 0.0003) in patients taking other antithrombotic agents. In 41 patients with oesophagitis and taking these drugs, 36 (88%) had cardiovascular disease and only 4 (10%) had peptic symptoms. CONCLUSIONS: Erosive oesophagitis is common in patients with upper gastrointestinal bleeding taking low-dose aspirin or antithrombotic agents, and could potentially be confused with the coexisting heart disease.

Adult↗
PubMed2005

Upper gastrointestinal haemorrhage associated with low-dose aspirin and anti-thrombotic drugs - a 6-year analysis and comparison with non-steroidal anti-inflammatory drugs.

BACKGROUND: Low-dose aspirin and other anti-thrombotic therapy has been increasingly used for vascular protection. AIM: To assess the possibility that the incidence of upper gastrointestinal blood loss has changed in subjects using these agents in comparison with non-steroidal anti-inflammatory drugs. METHODS: We studied the characteristics of all patients with acute upper gastrointestinal haemorrhage and attending a single hospital at 3 points over a 6-year period: 1996 (n = 204), 1999 (n = 224) and in 2002 (n = 252). RESULTS: The incidence of haemorrhage in subjects taking low-dose aspirin rose from 15 per 100 000 of the population per annum in 1996, to 18 in 1999 and 27 in 2002 (P = 0.004). The respective incidence in subjects taking other anti-thrombotic drugs was 4, 8, and 12 (P < 0.001). No significant change was detected in non-steroidal anti-inflammatory drug users. However, acute myocardial infarction mortality was 216 per 100 000 in 1996, 221 in 1999 and fell to 169 in 2002 (P < 0.001). CONCLUSIONS: The incidence of upper gastrointestinal haemorrhage in users of low-dose aspirin and other anti-thrombotic drugs has been steadily rising. This has been paralleled by a fall in cardiac mortality.

Adult↗
PubMed2005

Gastric epithelial anti-microbial peptides--histological correlation and influence of anatomical site and peptic ulcer disease.

BACKGROUND AND AIMS: Natural anti-microbial peptides are increasingly recognised for their protective effects in mucosal surfaces. We, therefore, aimed at investigating their expression in the human stomach in a range of peptic conditions. METHODS: We assessed the expression of epithelial secretory leukocyte protease inhibitor, human beta-defensins (HBD1 and HBD2), and alpha-defensin (HD5) in gastric biopsies taken from 52 patients, median age of 55 years. Expression of peptide mRNA was determined using real-time quantitative polymerase chain reaction. The activity of gastritis was graded on a 0-3 scale. RESULTS: The antrum had a median secretory leukocyte protease inhibitor of 0.93 and HBD1 of 0.42, compared with 0.13 (P = 0.001) and 0.08 units (P = 0.002) respectively in the gastric body. The antral histological scores correlated positively with HBD2 expression (r = 0.69; P< 0.001) and negatively with HBD1 (r = -0.47; P = 0.006) particularly in the absence of aspirin. Patients with Helicobacter pylori gastritis, gastric or duodenal ulcers had lower expression of HBD1 and greater expression of HBD2 than in controls. The intake of aspirin by patients infected with H. pylori was associated with marked rise in the expression of HD5 and less expression of secretory leukocyte protease inhibitor. CONCLUSIONS: Gastric epithelial anti-microbial peptides are influenced by anatomical site, grade of gastritis, peptic ulceration, and can be modulated by aspirin.

Adolescent↗
PubMed2003

Reflux and Barrett's oesophagitis after gastric surgery--long-term follow-up and implications for the roles of gastric acid and bile in oesophagitis.

BACKGROUND: The role of gastric acid is difficult to separate from that of bile in oesophageal reflux, and the complications of this can take many years to develop. Gastric surgery patients provide a good model for both significant bile reflux and marked gastric acid inhibition. AIM: To study the oesophageal abnormalities in gastric surgery patients undergoing long-term follow-up, compared with patients with intact stomachs. METHODS: Two hundred and forty adult patients were endoscoped regardless of their age, sex or type of surgical procedure. Oesophageal damage was graded on a scale of 0-5, and biopsies were taken to exclude neoplasia, to diagnose Barrett's oesophagus and to identify Helicobacter pylori. RESULTS: Of the 240 patients studied, 140 had undergone gastric surgery 27 years (19-31 years) [median (interquartile range)] prior to endoscopy, and these patients had milder oesophageal scores and fewer cases of Barrett's oesophagitis. Of the 119 patients with post-surgical bile reflux gastritis, 31 (26%) had oesophagitis, two (1.7%) had Barrett's oesophagitis and oesophageal scores of 0 (0-1) were found. These results compared with corresponding values of 37 (37%; P = 0.11), 11 (11%; P = 0.007) and 0 (0-2) (P = 0.046), respectively, in 100 patients with intact stomachs. In addition, of the 83 patients with vagotomy, 19 had oesophagitis (23%; P = 0.05), none had Barrett's oesophagitis and lower oesophageal scores (P = 0.02) were found. CONCLUSIONS: The prevalence and severity of reflux and Barrett's oesophagitis are not increased in patients with a long history of gastric surgery, particularly after vagotomy, and despite being at risk of bile reflux.

Aged↗
PubMed2003

Oesophagitis and bile reflux gastritis--clinical and histological assessments.

BACKGROUND AND AIMS: Little is known concerning the relationship between oesophagitis and bile reflux (chemical) gastritis despite the numerous studies on gastritis related to Helicobacter pylori. Given the importance of bile in the pathogenesis of both gastric and oesophageal disorders, we aimed at assessing the chemical gastritis score in patients with or without oesophagitis. METHODS: Chemical/bile reflux gastritis score and bile reflux index were assessed in gastric biopsies taken from patients with oesophagitis and gastric surgery (group 1, n=9), gastric surgery without oesophagitis (group 2, n= 11), and oesophagitis without gastric surgery (group 3, n= 10). Endoscopic oesophageal damage was also graded on a 0-5 scale. RESULTS: Group 1 had a median (interquartile range) chemical score of 6 (4-9) compared with 8 (6-10) in group 2, and 1 (0-2) in group 3 (p=0.001; Kruskal-Wallis test for multiple group comparisons). Both the reflux gastritis score and bile reflux index were lowest in patients with intact stomachs. However, the oesophageal scores were 2 (1-2) in group 1 compared with 3 (2-5) in group 3 (p=0.01). CONCLUSION: Patients with post-surgical stomachs have similar chemical and related scores regardless of the presence or absence of oesophagitis. Despite the higher chemical gastritis scores, patients with gastric surgery, exposed mainly to bile reflux, have milder oesophagitis than those with intact stomachs, exposed to both gastric acid and bile.

Aged↗
PubMed2003

Urinalysis for interleukin-8 in the non-invasive diagnosis of acute and chronic inflammatory diseases.

BACKGROUND AND AIMS: Given its role in mediating inflammation, the use of urinary interleukin-8 (IL-8) was assessed in the non-invasive diagnosis of acute and chronic inflammatory diseases. METHODS: IL-8 was measured by an enzyme linked immunosorbent assay in random urine samples (1 ml each) carrying code numbers and taken from 208 patients: 177 adults and 31 children presenting with a range of active or inactive inflammatory conditions. RESULTS: In the appropriate controls and in patients with inactive inflammation, the median urinary IL-8 levels ranged from 7-12 pg/ml, compared with 104 pg/ml in active ulcerative colitis (p = 0.002), 54 in active Crohn's disease (p = 0.025), 93 in active rheumatoid arthritis (p = 0.001), 107 in acute cholecystitis (p<0.0001), 127 in acute appendicitis (p = 0.0001), and 548 pg/ml in urinary tract infection (p<0.0001). Children with non-viral inflammation/infection also had higher IL-8 values (median, 199 pg/ml; p = 0.0001) than those with viral infection (median, 7 pg/ml) or non-specific conditions (median, 10 pg/ml). In the study group as a whole urinary IL-8 values correlated positively with peripheral blood white cell count (r = 0.32; p < 0.001), erythrocyte sedimentation rate (r = 0.41; p<0.001), and C-reactive protein (r = 0.33; p<0.001). CONCLUSION: Taking the appropriate clinical situation into account, urinary IL-8 measurement helps in the non-invasive assessment of active inflammation in at least a number of common acute and chronic conditions.

Acute Disease↗
PubMed1999

Neutrophils, Helicobacter pylori, and nonsteroidal anti-inflammatory drug ulcers.

BACKGROUND & AIMS: Gastric injury by nonsteroidal anti-inflammatory drugs (NSAIDs) is minimal in neutropenic animals. This study examined peptic ulcer development in the presence or absence of gastric neutrophils in patients requiring long-term use of NSAIDs. METHODS: Gastric histology, neutrophils, and Helicobacter pylori were assessed in 120 patients randomized to receive placebo or 20 or 40 mg famotidine twice daily as prophylaxis against NSAID-related ulcers and who underwent endoscopy at 0, 4, 12, and 24 weeks. RESULTS: In 43 patients without gastric neutrophils, ulcers developed in 1 of 14 (7.7%) taking placebo, 2 of 16 (12.5%) taking 20 mg famotidine, and none of 13 taking 40 mg famotidine. However, in 77 patients with neutrophils, ulcers developed in 13 of 28 (47. 4%) taking placebo (P < 0.001), 3 of 26 (12.6%) taking 20 mg famotidine, and 3 of 23 (13%) taking 40 mg famotidine. Eight of 46 patients (17%) without H. pylori had neutrophils compared with 69 of 74 (93%) with both H. pylori and neutrophils (P < 0.001). CONCLUSIONS: Gastric neutrophils increase the incidence of ulceration in long-term NSAID users. Because neutrophils exist with H. pylori, eradicating this infection might prevent NSAID-related peptic ulcers.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1999

Non-steroidal anti-inflammatory drug gastropathy and Helicobacter pylori infection.

The interest in the interaction between NSAIDs and Helicobacter pylori derives its importance from its potential to provide a different strategy to combat the common problem of NSAID-related peptic ulcers and their life threatening complications. Studies assessing this subject have differed in almost every aspect of their methodology, including the definition of a NSAID user as well as the types, doses, duration, and the indications for NSAID use. They also differed in their end points, the tests for the assessment of Helicobacter pylori, and the regimes used for its eradication. However, NSAIDs and Helicobacter pylori are known to share a number of important pathogenic mechanisms, and the prevalence of the infection is high in cohorts of ulcer patients taking NSAIDs. Eradication of Helicobacter pylori using bismuth-based regimes has also been more successful and beneficial in preventing the occurrence or relapse of NSAID-related ulcers than regimes using proton pump inhibitors.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1998

Reduced gastric mucosal vascularity in patients with chronic gastritis.

OBJECTIVES/DESIGN: Chronic inflammation is increasingly being linked to ischaemia, but the mechanism is poorly understood, and little is known about its effect on local gastric endothelial microvessels. We aimed at studying the number and surface area of gastric mucosal endothelial microstructures in the presence or absence of chronic gastritis. METHODS: Immunohistochemical assessments were carried out on gastric antral and body biopsies taken from patients with chronic gastritis and others with normal histology. The primary antibody (QB-END/10) was raised against CD34 antigen within the endothelial cell membranes. A computer attached to a microscope was used to count the number and measure the surface area of mucosal endothelial entities. RESULTS: In patients with Helicobacter pylori gastritis (n = 19), the median number of endothelial microstructures per section was 43 in the antrum and 86 in the gastric body, compared with 205 (P = 0.00004) and 165 (P = 0.002), respectively, in subjects with normal gastric histology (n = 11). The median surface area of the endothelial microstructures was also reduced in patients with gastritis. The normal gastric antrum had more endothelial entities than the normal body (median of 205 vs 165; P = 0.007). CONCLUSIONS: Within the normal stomach, the antrum is more richly vascularized than the gastric body. However, active chronic gastritis is associated with reduction in both the number and surface area of mucosal endothelial microstructures, with the reduction being more marked in the antrum. This is different from acute inflammation, and is relevant to our understanding of the natural history of mucosal defence, particularly the greater susceptibility of the gastric antrum to ulceration, compared with the gastric body.

Adult↗
PubMed1997

Famotidine for healing and maintenance in nonsteroidal anti-inflammatory drug-associated gastroduodenal ulceration.

BACKGROUND & AIMS: Nonsteroidal anti-inflammatory drugs (NSAIDs) are strongly associated with gastroduodenal ulceration. How to manage patients with NSAID-associated ulcers is a common clinical dilemma. High-dose famotidine in the healing and maintenance of NSAID-associated gastroduodenal ulceration was therefore evaluated. METHODS: One hundred four patients with rheumatoid or osteoarthritis who had gastroduodenal ulceration received famotidine, 40 mg twice daily. Sixteen patients stopped and 88 continued their NSAID treatment. Ulcer healing was assessed endoscopically at 4 and 12 weeks. Seventy-eight NSAID users with healed ulcers were then randomized to receive 40 mg twice daily famotidine or placebo and underwent endoscopy at 4, 12, and 24 weeks. RESULTS: Cumulative ulcer healing rates at 12 weeks were 89.0% (95% confidence interval [CI], 82.3%-95.7%) for patients who continued NSAID treatment and 100% (95% CI, 82.9%-100.0%) for those who stopped. The subsequent estimated cumulative gastroduodenal ulcer relapse over 6 months for NSAID users who took placebo was 53.5% (95% CI, 36.6%-70.3%). This was reduced to 26.0% (12.1%-39.9%) in patients taking famotidine (P = 0.011). CONCLUSIONS: High-dose famotidine is effective ulcer healing therapy in patients who stop or continue NSAID treatment and significantly reduced the cumulative incidence of gastroduodenal ulcer recurrence compared with placebo when given as maintenance therapy.

Adult↗
PubMed1996

Famotidine for the prevention of gastric and duodenal ulcers caused by nonsteroidal antiinflammatory drugs.

BACKGROUND: Acid suppression with famotidine, a histamine H2-receptor antagonist, provides protection against gastric injury in normal subjects receiving short courses of aspirin or naproxen. The efficacy of famotidine in preventing peptic ulcers in patients receiving long-term therapy with nonsteroidal antiinflammatory drugs (NSAIDs) is not known. METHODS: We studied the efficacy of two doses of famotidine (20 mg and 40 mg, each given orally twice daily), as compared with placebo, in preventing peptic ulcers in 285 patients without peptic ulcers who were receiving long-term NSAID therapy for rheumatoid arthritis (82 percent) or osteoarthritis (18 percent). The patients were evaluated clinically and by endoscopy at base line and after 4, 12, and 24 weeks of treatment. The evaluators were unaware of the treatment assignment. The primary end point was the cumulative incidence of gastric or duodenal ulceration at 24 weeks. RESULTS: The cumulative incidence of gastric ulcers was 20 percent in the placebo group, 13 percent in the group of patients receiving 20 mg of famotidine twice daily (P = 0.24 for the comparison with placebo), and 8 percent in the group receiving 40 mg of famotidine twice daily (P = 0.03 for the comparison with placebo). The proportion of patients in whom duodenal ulcers developed was significantly lower with both doses of famotidine than with placebo (13 percent in the placebo group, 4 percent in the low-dose famotidine group [P = 0.04], and 2 percent in the high-dose famotidine group [P = 0.01]). Both doses of famotidine were well tolerated. CONCLUSIONS: Treatment with high-dose famotidine significantly reduces the cumulative incidence of both gastric and duodenal ulcers in patients with arthritis receiving long-term NSAID therapy.

Adult↗
PubMed1996

Insulin-like growth factor-I in Helicobacter pylori gastritis and response to eradication using bismuth based triple therapy.

AIMS: To measure insulin-like growth factor-I (IGF-I) concentrations in the presence and absence of Helicobacter pylori infection and in response to eradication of the organism. METHODS: An enzyme linked immunosorbent assay was used to measure gastric and fasting serum concentrations of IGF-I in 17 patients with and 11 without H pylori infection. Repeat assessments were performed in the infected patients six weeks after they received a two week course of bismuth chelate, metronidazole, and amoxycillin. RESULTS: IGF-I was detected at very low concentrations in gastric juice and in mucosal incubates. The median serum IGF-I concentration was 88 micrograms/l in the patients infected with H pylori compared with 90 micrograms/l in the non-infected controls; IGF-I concentrations dropped to 77 micrograms/l following eradication therapy (p = 0.014). CONCLUSION: The similarity in baseline IGF-I concentrations in the presence and absence of H pylori suggests that their subsequent drop after treatment is more likely to be due to the treatment.

Adult↗
PubMed1996

Gastric mucosal hepatocyte growth factor in Helicobacter pylori gastritis and peptic ulcer disease.

OBJECTIVES: Hepatocyte growth factor (HGF) is increasingly recognized for its role in a variety of hepatic and systemic diseases. Its relationship to gastritis has not been studied. We aimed at measuring gastric mucosal HGF levels in the presence or absence of Helicobacter pylori gastritis, in peptic ulcers, and in response to H. pylori eradication. METHODS: Fifty one patients were studied. Patients were not entered if they had liver disease, malignancy, or any systemic illness. HGF was measured in gastric antral incubates using an enzyme-linked immunosorbent assay. Assessments were repeated 6 wk after a 2-wk course of anti-H. pylori triple therapy in 12 patients. Code numbers were used for blinding. RESULTS: The median gastric mucosal HGF level was 36 ng/gm/tissue in patients with H. pylori gastritis (n = 33) compared with 19 ng/gm in 18 negative controls (p = 0.0024), 18 ng/gm after the eradication of H. pylori (p = 0.021), 23 ng/gm in all patients with ulcers (n = 10), and 26 ng/gm/tissue in H. pylori-positive ulcers (n = 7). CONCLUSIONS: Gastric mucosal HGF levels were elevated in H. pylori gastritis and reduced by its eradication. These results are relevant to our understanding of the increased gastric cell proliferation in patients with H. pylori-related gastritis.

Adult↗
PubMed1996

Altered urinary interleukin-8/creatinine ratio in peptic ulcer disease: pathological and diagnostic implications.

OBJECTIVES AND METHODS: To assess its clinicopathological and diagnostic significance, interleukin-8 (IL-8) was measured by radioimmunoassay in fasting urine specimens and in gastric mucosal incubates taken from 54 patients with dyspepsia. The presence of Helicobacter pylori, the activity of gastritis, and urine creatinine levels were also assessed. RESULTS: The median urinary IL-8/creatinine ratio was 0.1 x 10(-6) in patients with current peptic ulcers (n = 13) and 0.2 x 10(-6) in patients with a history of ulcers (n = 8), compared with 0.4 x 10(-6) (p < 0.0001) in patients without ulcers who were infected with H. pylori (n = 20) or not infected (n = 13). The activity of gastritis had a positive correlation with gastric IL-8 (r = 0.5870, p < 0.01) and a negative correlation with urinary IL-8/creatinine ratio (r = -0.6447, p < 0.005). The improvement in the activity of gastritis in 20 patients given anti-H. pylori triple therapy was associated with a significant fall in gastric mucosal IL-8 and a rise in urinary IL-8/creatinine ratio. CONCLUSIONS: An inverse relationship seems to exist between urinary IL-8 and the activity of gastritis and gastric IL-8. This may represent another concept in the pathogenesis of peptic ulcers and can assist in the noninvasive diagnosis of peptic ulcer disease.

Adult↗
PubMed1996

Histopathological aspects of mucosal injury related to non-steroidal anti-inflammatory drugs.

As the majority of patients with chronic arthritis are treated, for many years, with non-steroidal anti-inflammatory drugs (NSAID), it is only natural to expect the long-term use of these agents to be associated with a range of oesophago-gastro-duodenal histopathological changes. We have demonstrated that oesophagitis (defined as basis of papillary length, basal cell hyperplasia and inflammatory cell infiltration) is less prevalent in patients taking NSAID. This phenomenon can be utilised in the treatment of certain conditions such as post-irradiation oesophagitis and Barrett's oesophagitis. It also implies that NSAID-related oesophageal ulceration is due to lodging of tablets in the oesophagus and is, in turn, preventable by swallowing of some fluids or solids after taking NSAID. In the stomach, long-term use of NSAID is associated with a specific entity known as chemical or reactive gastritis in about 25% of cases. This is frequently associated with ulceration. Chronic active superficial gastritis, in the presence of Helicobacter pylori, can be found in about 70% of cases. Not unlike oesophagitis, the prevalence of active duodenitis is low in chronic NSAID users. Local ulceration still takes place. This implies that duodenitis is not required in at least some cases of NSAID-related duodenal ulcers, and demonstrates the multi-factorial nature of the pathogenesis of mucosal damage in long-term users of a NSAID.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1995

Mucosal erosions in longterm non-steroidal anti-inflammatory drug users: predisposition to ulceration and relation to Helicobacter pylori.

The importance of erosions in longterm non-steroidal anti-inflammatory drug (NSAID) users, their relevance to ulceration and their relation to Helicobacter pylori are unclear. This study assessed the incidence of peptic ulcers in the presence or absence of erosions or H pylori in a group of longterm NSAID users (n = 50), undergoing endoscopy at 0, 4, 12, and 24 weeks while continuing with NSAIDs. Ulcers diagnosed at baseline endoscopy were excluded. Ulcers developed in nine of 23 patients (39%) with pre-existing erosions compared with six of 27 (22%) without erosions (p < 0.05). The group infected with H pylori (n = 30) had a total of 18 patients (60%) with erosions, a total of 12 ulcers (40%), and eight ulcers (27%) complicating previous erosions, compared with five (25%, p < 0.01), three (15%, p < 0.05), and one (5%, p < 0.01) respectively in patients not infected with H pylori (n = 20). Ulcer development was not influenced by the initial number of erosions but strongly associated with H pylori positive duodenal erosions. It is concluded that ulcers are more likely to develop in longterm NSAID users who have mucosal erosions or H pylori, or both.

Adult↗