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I Llorca

Publications and source records attributed to I Llorca.

4 recordsLinked to original sources

Diagnostic value of C-reactive protein in exudative pleural effusions.

BACKGROUND: Tests able to help in the diagnostic work-up of pleural exudates are needed. C-reactive protein (CRP) may be useful for distinguishing between benign and malignant exudates. METHODS: A total of 123 consecutive patients diagnosed as having exudative pleural effusion (60 associated with malignancy and 63 benign effusions) were included in the study. Sensitivity, specificity, positive and negative predictive values (PV+, PV-), and positive and negative likelihood ratios (LR+, LR-) were established at different cut-off points. RESULTS: Pleural fluid CRP level was 23+/-12 mg/l (mean+/-S.D.) in pleural exudates associated with malignancy and 50+/-33 mg/l in benign effusions (P<0.001). With a cut-off point below 20 mg/l for malignancy, sensitivity of CRP was 0.50, specificity 0.89, PV+ 0.81, PV- 0.65, LR+ 4.50, and LR- 0.65. With a cut-off point above 45 mg/l for benign diseases, sensitivity was 0.44, specificity 0.95, PV+ 0.90, PV- 0.62, LR+ 8.89, and LR- 0.58. CONCLUSIONS: The pleural CRP level provides useful information for the study of pleural exudates. A level below 20 mg/l suggests a malignant origin and a level above 45 mg/l virtually rules out this possibility. Additional advantages of measuring CRP level are that it is an inexpensive test and is easy to perform.

Journal Article↗

Helicobacter pylori and bleeding duodenal ulcer: prevalence of the infection and role of non-steroidal anti-inflammatory drugs.

BACKGROUND: Several authors have reported low prevalence of Helicobacter pylori infection in patients with upper gastrointestinal bleeding (UGIB). Our aim was to study the prevalence of H. pylori in bleeding duodenal ulcer (DU), with both invasive and non-invasive methods, and to assess the role of non-steroidal anti-inflammatory drugs (NSAIDs). METHODS: Ninety-two patients with bleeding DU were prospectively studied. The use of NSAIDs was evaluated by specific questionnaire. As a control group, 428 patients undergoing outpatient evaluation for the investigation of dyspepsia and found to have a DU at endoscopy were included. At endoscopy, two antral biopsies were obtained (H&E stain). A 13C-urea breath test was carried out in all patients. Breath test was repeated in patients treated with omeprazole during the hospitalization if H. pylori was not detected with the first test. RESULTS: Gastric biopsies could be obtained in 39 patients with UGIB. Three patients with UGIB treated with omeprazole and being H. pylori-negative with the first breath test were finally considered infected with the second test. Overall, 92.4% (95% CI, 85%-96%) of the patients with UGIB were infected (89.7% with histology and 92.4% with breath test (P = 0.15)). Concordance kappa value for both diagnostic tests was 0.64. NSAID intake was more frequent in patients with UGIB (34%) than in those without UGIB (5.6%) (P < 0.001), while H. pylori infection was less frequent in patients with UGIB (92.4% (85%-96%)) than in those without UGIB (99.1% (98%-100%); P < 0.001). Even in patients with UGIB, NSAID intake was the only risk factor in 5% of cases. The proportion of cases without H. pylori infection and without NSAID intake was very low in both bleeding and non-bleeding ulcers (2% and 0.5%, respectively; P = 0.146). H. pylori prevalence in bleeding ulcers was of 84% (67%-93%) in patients with NSAID intake, and 96.7% (89%-99%) when patients taking NSAIDs were excluded. In the multivariate analysis, NSAID intake (odds ratio, 9.8 (5.2-18.4)) correlated with UGIB; however, neither H. pylori status nor the interaction between H. pylori infection and NSAID intake correlated with UGIB. In the multivariate analysis in the subgroup of patients with UGIB, NSAID use was the only variable which correlated with H. pylori prevalence (odds ratio, 0.18 (0.03-0.97)). CONCLUSIONS: The most important factor associated with H. pylori-negative bleeding DU is NSAID use, and if this factor is excluded prevalence of infection is almost 100% (97%), similar to that found in patients with non-bleeding DU (and without NSAID intake). Bleeding DU patients with neither H. pylori infection nor NSAID use are extremely rare (only 2%), which suggests that the pathogenesis of bleeding DU is similar to that of non-complicated DU disease.

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