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A S Taha

Publications and source records attributed to A S Taha.

At least 37 records · Page 2Linked to original sources
PubMed1994

Predicting NSAID related ulcers--assessment of clinical and pathological risk factors and importance of differences in NSAID.

Although ulcers are often associated with non-steroidal anti-inflammatory drugs (NSAIDs) little is known about the feasibility of predicting their development in patients taking NSAIDs. In addition, the ulcerogenic potentials of the newer NSAIDs, taken on long term basis, have not been compared with those of more established preparations. The aim of this study was to identify the clinical and pathological characteristics of patients at a higher risk of NSAID induced ulcers, measure the ulcerogenic potential of a variety of NSAIDs, and test the effect of these potentials on the predictability of ulceration. Altogether 190 long term NSAID users were studied. The presence of abdominal complaints, previous history of ulcers, arthritis related physical disability, anaemia, gastritis, and Helicobacter pylori status were all assessed as possible risk factors. NSAIDs were classified into established drugs (group I), and newer agents (group II). Group I included naproxen, indomethacin, diclofenac, ketoprofen, piroxicam, and flurbiprofen. Group II included fenbufen, nabumetone, ibuprofen, etodolac, azapropazone, and tiaprofenic acid. Of 63 ulcers identified in the study group, 51 (81%) were seen in group I NSAID patients (51 of 132, 39%) compared with 12 ulcers in group II (12 of 58, 21%), p < 0.02; estimated relative risk (ERR): 2.41). In group I, 25 ulcers were found in 38 patients with abdominal pain (25 of 38, 66%, p < 0.01, ERR: 5.03); 18 in 25 (72%) patients with a previous history of ulcers (p < 0.001, ERR: 5.77), 26 in 44 (59%) patients with debilitating arthritis (p < 0.001, ERR 3.64), and 35 in 73 (48%) patients with H pylori associated gastritis (p < 0.01, ERR: 2.48). The presence of these factors in group II patients did not influence the risk of ulceration. Group I NSAIDs were more likely to be associated with chemical gastritis and to intensify H pylori related damage. Although silent ulcers are not uncommon in patients taking NSAIDs, recognition of the risk factors might helps predict a significant number (up to 81%), especially in those receiving group I NSAIDs.

Aged↗
PubMed1994

Oesophageal histology in long term users of non-steroidal anti-inflammatory drugs.

AIMS: To study the oesophageal histological changes in long term users of non-steroidal anti-inflammatory drugs (NSAIDs) compared with patients not receiving these drugs. METHODS: Ninety eight patients were studied, 53 of whom had taken NSAIDs for three years; 45 had not. Oesophageal biopsy specimens were taken from healthy-looking mucosa in the lower third of oesophagus. The papillary length, the thickness of the basal cell layer, and the intensity of cells infiltrating the epithelium were all assessed blind. RESULTS: The NSAID group included four (7%) cases of papillary elongation and two (4%) cases of basal cell hyperplasia, compared with 13 (29%; p < 0.01) and eight (18%; p < 0.02), respectively, in patients not taking NSAIDs. The total histological scores were also lower in patients treated with NSAIDs. CONCLUSION: Long term NSAID users have fewer oesophageal histological abnormalities than patients not receiving NSAIDs. Macroscopic damage related to NSAID use is, therefore, unlikely to require pre-existing histological oesophagitis for its development.

Aged↗
PubMed1993

The Health Assessment Questionnaire as a predictor of non-steroidal peptic ulceration.

To assess the possibility of a relationship between the degree of physical disability in arthritic patients and non-steroidal peptic ulceration, patients were endoscoped immediately after performing their arthritic functional assessments. The Health Assessment Questionnaire was used and patients were classified into three main groups: I, scoring 0-1; II, 1.1-2; and III, 2.1-3. Ulcers, found in 36 out of 89 patients studied (36/89, 40%), were distributed as follows: 15/22 (68%) in group III compared with 9/28 (32%) in group I (chi 2 = 5.2, P < 0.02), and 12/39 (31%) in group II (chi 2 = 7.24, P < 0.01). Patients with debilitating arthritis appear to have a higher prevalence of non-steroidal peptic ulceration. This finding might be relevant to the process of selecting patients for prophylactic anti-ulcer therapy.

Adult↗
PubMed1993

Gastric and duodenal mucosal blood flow in patients receiving non-steroidal anti-inflammatory drugs--influence of age, smoking, ulceration and Helicobacter pylori.

Using laser Doppler flowmetry, we measured gastric and duodenal mucosal blood flow in 70 patients who had taken non-steroidal anti-inflammatory drugs (NSAIDs) for longer than 4 weeks, and studied the correlation with demographic factors, ulceration, and Helicobacter pylori. Blood flow was also measured in 17 other subjects not taking any drugs. Measurements were taken from healthy-looking mucosa in the gastric antrum and the first part of the duodenum. Both gastric and duodenal blood flow values were significantly lower in patients taking NSAID than in those who did not. In the NSAID group, the median duodenal mucosal blood flow was 150 perfusion units in smokers (n = 29) compared with 175 in non-smokers (P = 0.024), 123 units in patients with duodenal ulcers (n = 12) compared with 160 in those without duodenal ulcers (P = 0.020), 135 units in patients with H. pylori (n = 30) compared with 168 in patients without H. pylori (P = 0.033), and 118 in smokers infected with H. pylori compared with 175 units in non-smokers not infected with H. pylori (F = 13.4, P = 0.0005). There was no correlation with age. Gastric blood flow was not significantly influenced by any of the above variables. These results suggest that chronic NSAID intake is associated with reduced blood flow in both the stomach and duodenum. However, amongst NSAID patients, duodenal, but not gastric, mucosal blood flow is reduced in smokers, and in those with duodenal ulcers and H. pylori.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1993

The gold plated stomach?

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Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1993

Serological diagnosis of Helicobacter pylori--evaluation of four tests in the presence or absence of non-steroidal anti-inflammatory drugs.

The host's humoral immune response to Helicobacter pylori has been used in the diagnosis of active infection with these organisms. Several commercial tests are available but there are few and unconfirmed reports of their efficacy. This study aimed to assess and compare the efficacy of the following H pylori serological tests in patients treated or not treated with non-steroidal anti-inflammatory drugs (NSAID): Pyloriset Latex, Helico-G, Biolab Malakit, and Bio-Rad GAP Test IgG. Venous blood was tested at random in 124 patients, 64 of whom had received NSAID and 60 who had not. H pylori IgG antibodies were detected by latex agglutination (Pyloriset), or by ELISA (the remaining tests). Endoscopic gastric antral biopsy specimens were also obtained for urease activity, culture, and histology. Detection of H pylori by at least two of these was considered as a true positive, and its absence in all biopsy specimens as a true negative. The sensitivity values in the presence (or absence) of NSAID were: Pyloriset Latex, 59 (60)%; Helico-G, 79 (74)%; Biolab Malakit, 85 (81)%; and Bio-Rad GAP Test IgG, 100 (95)%. The respective specificity values were: 50 (71)%, 47 (59)%, 50 (65)%, and 30 (29)%. The Bio-Rad GAP Test IgG has the highest sensitivity and the lowest specificity values regardless of NSAID intake. The sensitivity of the other tests, however, is less than that of the standard biopsy related tests and their specificity is even lower in chronic NSAID users.

Adult↗
PubMed1993

Duodenal histology, ulceration, and Helicobacter pylori in the presence or absence of non-steroidal anti-inflammatory drugs.

Duodenitis and gastric metaplasia, which is often colonised by Helicobacter pylori (H pylori), are increasingly recognised for their importance in the pathogenesis of duodenal ulcers. The situation is not clear in patients receiving non-steroidal anti-inflammatory drugs (NSAIDs), who have a higher risk of peptic ulceration. The aim of this study was to identify the duodenal histological abnormalities in the presence or absence of NSAIDs, H pylori, and duodenal ulceration. Endoscopic duodenal biopsy specimens were taken from healthy looking mucosa of 172 patients (74 took NSAIDs, and 98 did not). Duodenitis was graded according to the degree of neutrophilic and plasma cell infiltration, villus height, Brunner's gland prolapse, and gastric metaplasia. The activity of duodenitis was dependent on the neutrophilic infiltration. A global score covering all the above factors was constructed, and H pylori in both the stomach and duodenum, was also assessed. The results showed that duodenitis with varying degrees of neutrophilic infiltration and gastric metaplasia was found in 20 patients (27%) taking NSAIDs, compared with 56 patients (57%) not taking NSAIDs (chi 2 = 16.24, p < 0.001). This degree of duodenitis was also found in 20 of 25 patients (80%) with duodenal ulcers, regardless of NSAID intake (chi 2 = 15.38, p < 0.001). Gastric metaplasia was identified in 20 patients (27%) receiving NSAIDs and 38 (39%) not receiving NSAIDs. Duodenal H pylori was only seen in patients with gastric metaplasia 10 (50%) receiving NSAIDs, and 34 (89%) not receiving NSAIDs. H pylori positive gastritis, and the combination of active duodenitis and gastric metaplasia were independent predictors of duodenal ulceration. It is concluded that active duodenitis is less common in patients taking NSAIDs but is strongly associated with gastric metaplasia, H pylori positive gastritis, and duodenal ulceration. These findings are relevant to the pathogenesis and treatment of duodenal ulcers in patients taking NSAIDs.

Adult↗
PubMed1992

Chemical gastritis and Helicobacter pylori related gastritis in patients receiving non-steroidal anti-inflammatory drugs: comparison and correlation with peptic ulceration.

AIMS: To evaluate the prevalence and significance of chemical gastritis, in comparison with gastritis related to Helicobacter pylori in patients receiving non-steroidal anti inflammatory drugs (NSAIDs). METHODS: Two hundred and eighteen patients were studied, 174 of whom were taking NSAIDs. Chemical gastritis was defined as the presence of foveolar hyperplasia, muscle fibres in the lamina propria, oedema and vasodilation, in the absence of a chronic inflammatory cell infiltrate. RESULTS: Chemical gastritis was found in 46 (26%) patients taking NSAIDs, and three (7%) in subjects not taking these drugs (p less than 0.01). H pylori was detected in 56 (32%) subjects taking NSAIDs compared with 22 (50%) not taking these agents (p less than 0.02). Ulcers were found in 16 out of 72 patients (22%) taking NSAIDs and without H pylori infection or chemical gastritis compared with 27 out of 56 (48%) with H pylori related gastritis (p less than 0.01), and 25 out of 46 (54%) with chemical gastritis (p less than 0.01). CONCLUSIONS: Peptic ulcers associated with the use of NSAIDs seem to occur more commonly in patients with chemical gastritis or H pylori infection. Patients taking NSAIDs also seem to have a greater prevalence of chemical gastritis but a lower prevalence of H pylori than those not taking these drugs.

Adult↗
PubMed1992

Diagnostic tests for Helicobacter pylori: comparison and influence of non-steroidal anti-inflammatory drugs.

AIMS: To evaluate the efficacy of culture, histology, CLO-test, Helico-G and Pyloriset tests in diagnosing Helicobacter pylori in the presence or absence of non-steroidal anti-inflammatory drugs (NSAIDs). METHODS: Of 134 patients studied, 75 had taken NSAIDs. At endoscopy, biopsy specimens were taken for culture, histology, and CLO-test. Blood was also taken for enzyme linked immunosorbent assay (ELISA) (Helico-G) and latex agglutination (Pyloriset) tests. RESULTS: The sensitivity, specificity, and predictive values of histology and CLO-test, compared with culture, ranged from 90% to 97%, regardless of NSAID intake. In the 59 patients not taking NSAIDs Helico-G had a sensitivity of 75% (p < 0.05) and a specificity of 61%; Pyloriset's sensitivity and specificity were, respectively, 63% (p < 0.05) and 67%. In the 75 patients taking NSAIDs the sensitivity of Helico-G was 81% and its specificity 45% (p < 0.05); Pyloriset had a sensitivity of 61% (p < 0.05) and a specificity of 50% (p < 0.05). CONCLUSION: These findings suggest that H pylori is more reliably diagnosed by culture, histology, and CLO-test than by the serological tests used in this study, especially in patients treated with NSAIDs.

Adult↗
PubMed1992

Vocal cord paralysis and oesophago-broncho-aortic fistula complicating foreign body-induced oesophageal perforation.

A 61 year old man died after presenting with a 24 h history of haematemesis and haemoptysis, and one year history of hoarseness of voice. Post-mortem examination showed a dental plate eroding through the mid-oesophagus into a bronchus and into the descending arch of the aorta, with scarring suggestive of old perforation. An organized haematoma also involved the left recurrent laryngeal nerve. Vocal cord paralysis may be a manifestation of foreign body-induced oesophageal perforation, which can lead to death from an oesophago-broncho-aortic fistula. Both complications of oesophageal perforation from a foreign body have not to our knowledge been previously reported.

Aorta, Thoracic↗
PubMed1992

Helicobacter pylori and peptic ulcers in rheumatoid arthritis patients receiving gold, sulfasalazine, and nonsteroidal anti-inflammatory drugs.

The conflicting reports on gold and Helicobacter pylori could be related to the use of serological tests of unproven value in NSAID patients, and to the lack of the appropriate control groups. More important is the fact that the endoscopic consequences of the possible effect of gold on H. pylori have not been investigated. We therefore decided to assess the prevalence of H. pylori and peptic ulcers in rheumatoid patients being treated with gold sodium thiomalate (GST) plus NSAID, sulfasalazine plus NSAID, or NSAID only. Eighty-five patients receiving treatment for at least 6 months were endoscoped, and H. pylori was studied in gastric antral biopsies by both culture and histology. Endoscopic abnormalities were classified into ulcers (measuring 5 mm in diameter or more) and erosions (smaller lesions). H. pylori (and ulcers) were found in 17 (12 ulcers) of 31 patients on NSAID only and 21 (9 ulcers) of 27 patients on sulfasalazine plus NSAID, compared with nine (3 ulcers) of 27 patients receiving GST plus NSAID, p < 0.05, analysis of variance. Patients treated with GST and NSAID had the lowest prevalence of detectable H. pylori. This could explain the apparent reduction in the prevalence of peptic ulcers in this group and, if confirmed in larger randomized studies, might have therapeutic implications.

Aged↗
PubMed1991

Inhibition of human gastric cyclic AMP production by Helicobacter pylori protein--possible involvement of mucosal prostaglandin E2.

The effect of Helicobacter pylori protein on cAMP and prostaglandin (PGE2) production was studied in incubates of human gastric fundic mucosa. At 24 hours, specimens incubated in the control fluid had a median cAMP value of 81 pmol/mg protein, compared to 28 pmol/mg (P less than 0.05) when incubated in H. pylori protein, 155 pmol/kg (P less than 0.006) in histamine, and 23 pmol/kg (P less than 0.05) in histamine plus H. pylori protein. A similar trend was observed at 48 hours. Although H. pylori protein had no direct effect on mucosal PGE2, it intensified the inhibitory effect of indomethacin and prevented the stimulatory effect of histamine on both PGE2 and cAMP production. Given the role of cAMP in various physiological responses, these results suggest that H. pylori protein might alter those functional aspects of the human gastric mucosa which rely on cAMP as a second messenger. Assuming that PGE2 is involved in mediating such effect, its role would appear to be either partial or indirect.

Bacterial Proteins↗
PubMed1991

Nonsteroidal peptic damage in rheumatoid patients receiving second-line drugs.

Using endoscopy, we assessed the prevalence of peptic ulceration in 281 rheumatoid patients receiving nonsteroidal antiinflammatory drugs alone, or in combination with second-line agents. Ulcers were found in 33 of 96 patients who took nonsteroidals only (33/96, 34%), compared with 8/33 (24%) on hydroxychloroquine, 10/30 (33%) on penicillamine, 13/46 (28%) on sulphasalazine, but only 11/76 (14%) on intramuscular gold plus nonsteroidals (chi 2 = 7.95, 0.001 less than p less than 0.01, p less than 0.05 using Bonferroni correction). Second-line drugs do not seem to increase the prevalence of ulcers related to nonsteroidal antiinflammatory drugs; on the contrary, fewer ulcers were found in patients receiving gold therapy, and this might have therapeutic implications.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1990

The interaction between Helicobacter pylori culture filtrate and indomethacin: effects on the integrity of human gastric antral mucosa and its prostaglandin E2 production in vitro.

Histopathological methods and radioimmunoassay were used to assess the microstructure and prostaglandin E2 production by paired specimens of human gastric antral mucosa; the specimens were studied after 48 h of incubation in base-line tissue culture medium, Helicobacter pylori culture filtrate, H. pylori culture control fluid, indomethacin, and H. pylori culture filtrate plus indomethacin. When applied alone, the filtrate did not affect the structure of the mucosal tissue or its prostaglandin E2 synthesis. In the overall group (n = 21), specimens incubated with the mixture of H. pylori filtrate and indomethacin had a median histological grade of 1 and prostaglandin E2 of 29 pg/mg tissue, compared to 2 pg/mg (P = 0.04) and 60 pg/mg (P = 0.0007) respectively, in specimens incubated with indomethacin alone. These results indicate that an interaction may exist between indomethacin and a factor contained in H. pylori culture filtrate. Such interaction is damaging to the human gastric antral mucosa, and its understanding might have therapeutic implications.

Adult↗
PubMed1990

Effect on gastric and duodenal mucosal prostaglandins of repeated intake of therapeutic doses of naproxen and etodolac in rheumatoid arthritis.

The synthesis of gastric and duodenal mucosal prostaglandin E2, prostaglandin I2, and thromboxane B2 during a 60 minute incubation of biopsy specimens, the degree of endoscopic and histological damage, and the anti-inflammatory response were all studied after a four week, double blind study of therapeutic doses of two non-steroidal anti-inflammatory drugs, naproxen and etodolac, received by 27 patients with active rheumatoid arthritis (13 receiving naproxen, 14 etodolac). Prostaglandin values after treatment did not differ from the baseline levels when all the patients were analysed as one group. Subgroup analysis showed that naproxen suppressed gastric prostaglandin E2 from a median of 29 to 9 ng/mg protein, duodenal prostaglandin E2 from 34 to 11 ng/mg, and duodenal prostaglandin I2 from 62 to 15 ng/mg protein. No overall suppression occurred with etodolac. Also, on the second assessment patients receiving naproxen had lower gastric and duodenal prostaglandin E2 and prostaglandin I2, but higher values of duodenal thromboxane B2, than patients receiving etodolac. Both drugs had comparable anti-arthritic activity and caused microscopic gastritis in similar proportions of patients. No correlation was detected between prostaglandin values and the mucosal damage which developed in seven patients receiving naproxen (54%) and three receiving etodolac (21%). These findings indicate that, unlike naproxen, etodolac does not seem to affect gastric or duodenal prostaglandin synthesis; other mechanisms of injury need to be considered.

Adolescent↗
PubMed1990

Gastric mucosal prostaglandin synthesis in the presence of Campylobacter pylori in patients with gastric ulcers and non-ulcer dyspepsia.

It is unclear how Campylobacter pylori (CP) interacts with gastric mucosal prostaglandins (PG). In a double-blind study we measured gastric PG synthesis in 22 patients with benign gastric antral ulcers (GU) and 26 with non-ulcer dyspepsis (NUD). CP status was determined by histology and bacteriology: 26 (16 GU plus 10 NUD) were CP positive, and 22 (6 GU plus 16 NUD) were CP negative. Patients with severe gastritis regardless of CP status) had significantly higher PGE2 and PGI2 values than those with mild gastritis. Severe gastritis was found in 36% of CP-negative subjects and 77% of the CP-positive patients (chi 2 = 8.64, p less than 0.01), but no significant differences in PG values were found between CP-positive or -negative patients.

Adult↗