ASA Users Research Articles

Genotypes of Helicobacter pylori obtained from gastric ulcer patients taking or not taking NSAIDs

OBJECTIVE: Whether Helicobacter pylori infection and use of nonsteroidal antiinflammatory drugs (NSAIDs) are independent risk factors for ulcerogenesis remains unclear. We undertook this study to evaluate H. pylori isolates from gastric ulcer patients to determine whether the genotype of the infecting isolate could be correlated with the use or nonuse of NSAIDs. METHODS: Fifty-two patients presenting with gastric ulcer and infected with H. pylori were included; 26 patients were taking NSAIDs or aspirin (ASA) regularly at the time of ulcer diagnosis. Polymerase chain reaction (PCR) was employed to assess the presence and mosaicism of the following H. pylori genes: cagA, vacA, iceA, and picB. RESULTS: We found no statistical differences in the presence of these genes in H. pylori isolates from gastric ulcer patients taking or not taking prescription NSAIDs or ASA. A 297-bp fragment of the cagA gene was detected in 96% of the isolates from the NSAID and ASA users and 100% from the non-NSAID users ( p = 1.0). A larger and more variable region of the cagA gene was detected more frequently among the isolates from non-NSAID users than those from NSAID users ( p = 0.05). Ninety-two percent of the isolates were identified as vacA genotype s1. The dominant vacA subtype was s1b, 76.9% and 65.4% in isolates from non-NSAID–taking or NSAID–taking patients, respectively ( p = 0.4). iceA1 genotype was not correlated with gastric ulcer as this allele was only detected in 17.3% of all isolates. CONCLUSIONS: No significant differences in the presence of the candidate virulence genes vacA, cagA, picB, or iceA were detected in isolates from gastric ulcer patients taking prescription NSAIDs or ASA, compared with those not taking these drugs, indicating that single gene presence does not allow discrimination of isolates that may be important in NSAID-induced ulcerogenesis. A variable region of the cagA gene was more frequently detected in isolates from patients not taking NSAIDs or ASA, suggesting that this gene may be modified by NSAID- or ASA-related factors or that certain strains may be selected for in patients taking these medications.

Genotypes of Helicobacter pylori obtained from gastric ulcer patients taking or not taking NSAIDs.

Whether Helicobacter pylori infection and use of nonsteroidal antiinflammatory drugs (NSAIDs) are independent risk factors for ulcerogenesis remains unclear. We undertook this study to evaluate H. pylori isolates from gastric ulcer patients to determine whether the genotype of the infecting isolate could be correlated with the use or nonuse of NSAIDs. Fifty-two patients presenting with gastric ulcer and infected with H. pylori were included; 26 patients were taking NSAIDs or aspirin (ASA) regularly at the time of ulcer diagnosis. Polymerase chain reaction (PCR) was employed to assess the presence and mosaicism of the following H. pylori genes: cagA, vacA, iceA, and picB. We found no statistical differences in the presence of these genes in H. pylori isolates from gastric ulcer patients taking or not taking prescription NSAIDs or ASA. A 297-bp fragment of the cagA gene was detected in 96% of the isolates from the NSAID and ASA users and 100% from the non-NSAID users (p = 1.0). A larger and more variable region of the cagA gene was detected more frequently among the isolates from non-NSAID users than those from NSAID users (p = 0.05). Ninety-two percent of the isolates were identified as vacA genotype s1. The dominant vacA subtype was s1b, 76.9% and 65.4% in isolates from non-NSAID-taking or NSAID-taking patients, respectively (p = 0.4). iceA1 genotype was not correlated with gastric ulcer as this allele was only detected in 17.3% of all isolates. No significant differences in the presence of the candidate virulence genes vacA, cagA, picB, or iceA were detected in isolates from gastric ulcer patients taking prescription NSAIDs or ASA, compared with those not taking these drugs, indicating that single gene presence does not allow discrimination of isolates that may be important in NSAID-induced ulcerogenesis. A variable region of the cagA gene was more frequently detected in isolates from patients not taking NSAIDs or ASA, suggesting that this gene may be modified by NSAID- or ASA-related factors or that certain strains may be selected for in patients taking these medications.

NSAID injury to the small intestine.

To identify the clinical and radiologic findings in patients with diaphragm-like strictures in the small bowel. We reviewed the histories, radiologic findings, and pathologic findings in two men and two women, all in their sixties, with a history of long-term nonsteroidal antiinflammatory drug (NSAID) or aspirin (ASA) usage and one or more radiologically demonstrated diaphragm-like strictures in the small bowel. Two patients had long histories of NSAID usage, and two of ASA usage. One NSAID user had a long segment of jejunal involvement, and the other three had short segments of duodenal involvement. The ASA users presented with symptoms of esophageal disease, the small bowel lesions were unexpected, and ASA usage was not initially elicited. In one NSAID user and one ASA user, broader strictures with humps rather than diaphragms were also seen producing a lifesaver-like or bagel-like configuration. Multiple diaphragm-like strictures can occur in NSAID injury and are pathognomonic except in the rare patient with ulcerative enteritis complicating celiac disease. Single or few diaphragm-like strictures can occur in NSAID injury and peptic ulceration. ASA should be considered an NSAID with regard to small-bowel toxicity. A careful medication history is required when an unexplained small bowel abnormality is seen radiologically, and a dedicated small bowel examination is required when NSAID injury is suspected.

Significant Role of Aspirin Use in Patients With Esophagitis

This study determines objectively the extent of nonsteroidal anti-inflammatory drug (NSAID) use in upper gastrointestinal (GI) mucosal acid-peptic diseases by supplementing the conventional interview with two tests of current aspirin (ASA) use--high-performance liquid chromatography (HPLC) for the presence of salicylates in serum and platelet cyclooxygenase activity, which detects ASA use within 5 days of testing. Of 186 consecutive patients undergoing upper endoscopy, 62% of 55 patients with esophagitis had evidence of current NSAID use, vs. 26% of 42 control patients with normal endoscopy (p less than 0.001), 12% of 17 patients with recently healed peptic ulcer (p less than 0.001), and 36% of 25 patients who had an active peptic ulcer (p less than 0.05), five of whom had concomitant esophagitis. Another 52 patients were ineligible for this analysis. Testing for platelet cyclooxygenase activity uncovered 26% more ASA users than history alone. In considering age, sex, smoking and drinking habits, arthritis, and ASA use by logistic regression, ASA use was the only factor contributing to esophagitis; ASA could not be further associated with severity, stricture or symptoms, however. In these patients, 95% of NSAID use was chronic, and 84% of that was ASA. These data show a previously unreported, strong association of ASA use with esophagitis, which suggests that ASA may be a significant factor in the resistance of esophagitis to current therapies as well as the frequently rapid relapse after therapy is withdrawn.