Biomedical subjects
Publications and source records attributed to D Boixeda.
Two cases are reported of spontaneous ascitic fluid Candida albicans peritonitis in two patients with liver cirrhosis secondary to HBV. In non of the two cases was there evidence of findings associated with secondary peritonitis, where ascitic fluid Candida infection has usually been reported.
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BACKGROUND: Serology is a good alternative, minimally invasive, diagnostic and screening test for Helicobacter pylori infection. Several immunoglobulin G (IgG) enzyme-linked immunosorbent assay (ELISA) commercial kits have been evaluated. Information on IgA ELISAs is relatively poor, and on the combined use of IgG and IgA ELISAs very scarce. OBJECTIVE: We intended to evaluate the sensitivity, specificity and predictive values of two quantitative commercial IgG and IgA ELISAs (Helico-G and GAP, respectively) and more particularly the accuracy of their combined use. PATIENTS AND METHODS: Serum samples and gastric biopsy specimen culture findings from 400 patients were evaluated. RESULTS: The sensitivity, specificity, positive and negative predictive values of the IgG ELISA Helico-G test in detecting IgG antibodies to H. pylori were 97.2, 85.4, 98.3 and 77.8%, respectively, when compared with those of the reference method used. The corresponding findings for detection of IgA antibodies with the GAP test were 96.4, 80.5, 97.7 and 71.1%, respectively. When considering a patient infected with H. pylori when both tests were positive, the sensitivity, specificity, positive and negative predictive values were 94.1, 85.3, 98.2 and 62.5%, respectively. On the other hand, when at least one test was positive, the corresponding values were 99, 80, 97 and 94%, respectively. CONCLUSION: The IgG ELISA Helico-G and IgA ELISA GAP, taken separately, are good and reliable tests for the detection of antibodies to H. pylori. Furthermore, the combined use of both serological methods provided more useful information compared with single IgG and IgA determinations.
BACKGROUND: To study basal gastrin levels in duodenal ulcer patients and in those with normal endoscopy, according to Helicobacter pylori infection. METHODS: Eighty-four duodenal ulcer patients and 164 with normal endoscopy were studied. Biopsy specimens were taken from gastric antrum and body, and investigated for microbiology (Gram stain and culture) and histology (hematoxilin-eosin stain). Basal gastrin levels were measured (RIA). RESULTS: In duodenal ulcer patients the percentage of chronic gastritis was higher (p < 0.001) than in patients with normal endoscopy without H. pylori infection, and similar to patients infected by H. pylori. In patients with normal endoscopy (n = 164), those infected with H. pylori (n = 115) had higher (p = 0.02) gastrin levels (mean +/- SD) than non-infected (64 +/- 34 vs 51 +/- 14 pg/ml) and similar to duodenal ulcer patients (62 +/- 20 pg/ml). In the multiple regression model analysis H. pylori infection was the only variable which correlated with gastrin levels (regression coefficient 9.48 [SE = 4.59]; multiple correlation coefficient 0.22 [p = 0.008]). Additional variables (age, sex, duodenal ulcer) were not correlated with gastrin levels. Patients with chronic gastritis had higher gastrin levels (p < 0.01) than those with normal histologic mucosa. CONCLUSIONS: In patients with normal endoscopy, those infected with H. pylori had significantly higher basal gastrin levels than non-infected individuals, and similar to duodenal ulcer patients. Therefore, hypergastrinaemia seems to be associated with H. pylori infection, and is not a distinctive feature of duodenal ulcer disease.
BACKGROUND: The aim of this study was to describe the prevalence of Helicobacter pylori infection in patients with gastric ulcer in addition to study its relationship with the ingestion of non steroid antiinflammatory drugs (NSAIDS). METHODS: One hundred sixty-one patients (mean age 54 years, 70% males) in whom gastric ulcer was endoscopically demonstrated were studied. Biopsies of the antrum and gastric body (hematoxillin-eosin, Gram staining and culture) were obtained during endoscopy. RESULTS: H. pylori was detected in 83% (CI = 78-89%) of the cases. In the patients not taking NSAIDS positivity was 87% (CI = 81-93%) while in those with NSAIDS this was only 63% (CI = 43-79%) (p = 0.008). The percentage of patients without H. pylori infection or NSAIDS intake represented 11% (CI = 6-16%). On multivariant analysis the only variable correlated with H. pylori infection was NSAIDS intake (OR = 0.25; CI = 0.09-0.66; chi 2 model = 7.27; p = 0.007) while the remaining variables (sex, age, smoking, alcohol and ulcer site) did not show a significant correlation. The percentage of chronic gastritis was higher (p < 0.001) in H. pylori positive patients in comparison with those who were uninfected (97% versus 67% in the antrum and 78% versus 41% in the gastric body). CONCLUSIONS: The prevalence of infection by Helicobacter pylori in patients with gastric ulcer is greater in those without non steroid antiinflammatory drug (NSAIDS) intake in comparison with those who have this history. The percentage of patients without H. pylori infection or NSAIDS ingestion was very low (11%), and thus it may be deduced that these elements represent pathogenic factors of major importance in gastric ulcer disease since the appearance of this entity in the absence of both is infrequent.
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The aim of our study was to demonstrate the effect of Helicobacter pylori eradication on basal and stimulated serum gastrin levels and gastric acid output 5 months after therapy of patients with duodenal ulcer. Thirty-two patients (24 men and eight women with a mean age of 45 years) who had had endoscopy and were diagnosed as having duodenal ulcer entered the study. In all patients three biopsy specimens were taken from the duodenal bulb, gastric antrum, body, and fundus. These specimens were then sent for microbiological and histological examination. Triple therapy consisting of bismuth, metronidazole, and tetracycline was administered. Endoscopy was repeated 1 and 5 months after therapy, and biopsy specimens were again taken from the gastric antrum and body. Before treatment, serum samples were taken to measure basal and stimulated (90 min) gastrin levels after ingestion of two beef cubes, and basal and stimulated acid outputs (after pentagastrin) were studied. Measurements of gastrin and gastric acid output were repeated 5 months after therapy. H. pylori was eradicated in 26 patients (81.3%). Basal gastrin levels (mean +/- SD) at diagnosis and after eradication were 44 +/- 12 and 35.8 +/- 2 pg/ml, respectively (p < 0.05). Similarly, stimulated gastrin levels (integrated values) decreased from 5,303 +/- 1,526 pg/ml/min before therapy to 3,779 +/- 1,204 pg/ml/min after eradication (p < 0.001). However, basal (4.9 +/- 4mEq/h) and stimulated (28.5 +/- 10mEq/h) acid output did not vary after eradication (3.9 +/- 4 mEq/h and 26.2 +/- 12 mEq/h, respectively). We conclude that basal and stimulated gastric acid output are not changed by H. pylori eradication in duodenal ulcer patients 5 months after therapy, in spite of its association with a significant decrease in basal and stimulated gastrin levels.
We made a retrospective study of 233 episodes of spontaneous bacterial peritonitis that were treated at our Service between January 1980 and September 1996 in order to analyze the clinical presentation, microbiological data, possible pathogenic factors, treatment, and evolution of this clinical entity. Ascites, abdominal pain, and fever were the most frequent symptoms. Only 3.43% of the episodes developed asymptomatically. Thirty-six episodes resulted in the patient's death (15.45%) and, of all the factors analyzed, only a prothrombin time of < 35%, bilirubin > 8 mg/dl, and serum creatinine > 2.1 mg/dl were statistically correlated with a higher death rate. The culture of the ascitic fluid gave a positive result in 47.6% of the cases, whereas no clinical differences were noticed between these patients and those with negative results. The most frequently isolated microorganisms turned out to be Gram negative (49.54%). A proportion of 71.24% of the episodes were treated with cephotaxime (i.v.), whereas 28.76% were treated with other drugs or pharmacological combinations. The death rate was much lower with cephotaxime (4.81% vs. 41.79%, p < 0.01%).
OBJECTIVE: To determine the seroprevalence of Helicobacter pylori infection in healthy individuals in Spain and its relationship with different epidemiological features. PATIENTS AND METHODS: The study was conducted on a large group of healthy individuals without ulcer disease antecedents or other gastrointestinal disease; moreover, information, was obtained on symptoms attributable to the gastrointestinal tract, smoking, alcohol consumption, non-steroidal anti-inflammatory drug (NSAID) use as well as the presence of peptic ulcer disease antecedents among first-degree relatives. The H. pylori infection status was ascertained by immunoglobulin G (IgG) antibody determination, using a quantitative enzyme-linked immunosorbent assay. RESULTS: Three hundred and eighty-one individuals (138 males and 243 females) were included in the study (mean age: 34.3 +/- 12.9 years; range: 5-77). Two hundred and two individuals (53%) were positive for H. pylori IgG antibodies. A consistent increase in H. pylori infection seroprevalence with increasing age was observed. No association was observed between H. pylori infection and consumption of alcohol, NSAID use or smoking. On the other hand, the presence of digestive symptoms and peptic ulcer disease antecedents among first-degree relatives were associated with a higher prevalence of infection in a given individual (P < 0.05). CONCLUSION: H. pylori infection seroprevalence in healthy individuals in Spain is similar to that in countries with high socio-economic standards and other Western countries. Digestive symptoms and previous antecedents of peptic ulcer disease in first-degree relatives were associated with a higher prevalence of Helicobacter pylori infection.
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BACKGROUND: We wanted to demonstrate the effect of Helicobacter pylori eradication on basal and stimulated pepsinogen-I levels in duodenal ulcer patients and to verify whether modification of such levels is a useful method for determining the success of eradication therapy. METHODS: Thirty-two patients (24 men; mean age, 45 years) with active duodenal ulcer were studied. In all patients three biopsy specimens were taken from the duodenal bulb, gastric antrum, body and fundus for microbiologic and histologic examination. Triple therapy consisting of bismuth, metronidazole, and tetracycline was administered. Endoscopy was repeated 1 month after completing therapy, and biopsy specimens were again taken from the gastric antrum and body. Serum samples were taken at initial and repeat endoscopies, to measure basal and stimulated (120 min) pepsinogen-I levels after injection of pentagastrin. RESULTS: H. pylori was eradicated in 26 patients (81%). Significant histologic improvement, in both the antrum and body, was observed (p < 0.001). Basal pepsinogen-I levels (mean and 95% confidence interval) at diagnosis and after eradication were 106 (92-119) and 87 (74-100) ng/ml, respectively (P < 0.001). Similarly, stimulated pepsinogen-I levels (integrated values) decreased from 4790 (4199-5381) before therapy to 3970 (3383-4557) ng/ml.min after eradication (P < 0.001). Pepsinogen I levels did not change in patients in whom H. pylori was not eradicated. The area under the receiver operating characteristic curve for decreased basal and stimulated pepsinogen-I levels was 0.77 (SE, 0.09) and 0.79 (SE, 0.1), respectively. CONCLUSION: H. pylori eradication in duodenal ulcer patients was associated with a significant decrease in basal and stimulated pepsinogen-I levels. Measurement of these levels could determine how successful response to therapy has been in both the eradication and resolution of associated gastritis. Other advantages of this procedure are that it has low cost and results are evident at an early stage.
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AIM: To study basal pepsinogen I levels in patients with duodenal ulcer and in subjects with normal endoscopy, depending on Helicobacter pylori status. METHODS: One-hundred and one patients with duodenal ulcer and 74 controls with normal endoscopy were studied. Mean age and gender distribution were: 46 vs 42 years, and 74% vs 43% males, respectively. At endoscopy biopsies from the gastric antrum and body were obtained for histologic (H&E) and microbiologic (Gram and culture) study. Basal levels of serum pepsinogen I were measured (RIA). RESULTS: Among the subjects with a normal endoscopy, those with H. pylori infection had higher pepsinogen I levels (m +/- SD) than non-infected patients (77 +/- 27 vs 62 +/- 28 ng/ml; p < 0.05). Basal levels in duodenal ulcer patients were 107 +/- 38 ng/ml, higher (p < 0.001) than in the group with normal endoscopy (both with and without H. pylori). In multivariate analysis pepsinogen I levels were correlated with H. pylori infection (regression coef.= 17; SE= 8.1), duodenal ulcer (regr. coef.= 22; SE= 5.8) and smoking habit (regr. coef.= 24; SE= 5.2). CONCLUSION: Basal pepsinogen I levels were significantly higher in duodenal ulcer patients than in H. pylori infected subjects with normal endoscopy. The lowest levels corresponded to non-infected patients. Therefore, an additional factor other than H. pylori infection is likely involved in the hyperpepsinogenemia classically reported in duodenal ulcer patients.
AIM: To study the influence of various factors on duodenal ulcer healing, specially the success or failure of Helicobacter pylori eradication. METHODS: One-hundred and nine patients with duodenal ulcer and H. pylori infection were studied. At endoscopy biopsies were obtained from the gastric antrum and body, and processed by microbiological (Gram stain and culture) and histological methods (haematoxylin-eosin); also, a 13C breath test was performed. A < > triple therapy (bismuth, tetracycline, metronidazole) or omeprazole plus amoxicillin was administered. Endoscopy and breath test were repeated one month after completing therapy. Eradication was defined as the absence of H. pylori by all diagnostic methods. RESULTS: H. pylori eradication was achieved in 60 patients (55%). In the multivariate analysis H. pylori eradication was the only variable which correlated with ulcer healing (regr. coef. = 2.4; OR = 10.6). Additional variables (age, sex, smoking, time of evolution, ulcer size, and type of therapy) were not significantly correlated. Ulcer healing was achieved in 92% of patients after H. pylori eradication, and in 51% of therapy failures (p < 0.001). CONCLUSION: H. pylori eradication accelerates ulcer healing, which represents an additional argument for employing eradicating therapy in patients with duodenal ulcer disease.
AIM: To evaluate the efficiency of omeprazole (20 mg/12 h) plus amoxycillin (1 gr/12 h) in eradicating Helicobacter pylori in duodenal ulcer patients studied in four hospitals in our country. METHODS: One-hundred and four patients (mean age: 49 +/- 16 years, 67% males) attended at four general hospitals in Spain, who had a duodenal ulcer demonstrated by endoscopy. These patients were infected with H. pylori demonstrated by urease test and histologic methods, and in 32 by a breath test and 18 by culture. Omeprazole 20 mg b.i.d. plus amoxycillin 1 gr b.i.d. was administered for 2 weeks. Endoscopy was repeated 1 month after completing therapy, and the aforementioned diagnostic methods were performed again. RESULTS: Eradication was achieved in 29% of cases (n = 30). In multiple logistic regression analysis, duration of ulcer disease was the only variable which correlated with success in H. pylori eradication (chi(2) = 7.2; p = 0.02). Additional variables (age, sex, smoking, pre-treatment with omeprazole, AINEs or H2 antagonist, ulcer size, and antral histologic gastritis) were not correlated with H. pylori eradication. Ulcer healing was demonstrated in 80% of patients (n = 83), and the healing rate was higher when eradication was achieved (97%) than in H. pylori-positive patients (73%) (p < 0.01). Compliance was good in all cases. No adverse effects were observed. CONCLUSION: [corrected] Disappointing results were obtained with omeprazole (20 mg b.i.d.) plus amoxycillin (1 gr b.i.d.) on H. pylori eradication. This combination cannot be recommended in our country at the doses employed in this study.
AIM: To describe the prevalence of Helicobacter pylori infection in patients with gastric adenocarcinoma, and compare it with that of patients with chronic gastritis. METHODS: Fifty-four patients with endoscopically diagnosed gastric cancer (later confirmed histologically as gastric adenocarcinoma), and 60 patients with histologic chronic gastritis were studied. Age and sex distribution was similar in both groups. At endoscopy biopsy specimens were taken from antrum and body (H&E stain, Gram stain and culture). RESULTS: H. pylori was found in 95% (95%CI = 86-98%) of patients with chronic gastritis, and in 41% (CI = 29-54%) of patients with gastric adenocarcinoma (p < 0.001). H. pylori was present in malignant tissue in 13% (CI = 6-24%) of cases, a significant lower (p < 0.01) percentage than in the gastric antrum and body. CONCLUSION: The prevalence of H. pylori infection diagnosed by microbiologic and histologic methods in patients with gastric adenocarcinoma (41%) is significantly lower than in patients with chronic gastritis, its premalignant lesion. H. pylori was present less frequently in malignant tissue than in endoscopically normal mucosa.
AIM: To study different factors influencing the success of classic triple therapy in Helicobacter pylori eradication. METHODS: Fifty-seven duodenal ulcer patients infected with H. pylori were prospectively studied. At endoscopy biopsy specimens were taken from the gastric antrum and body (H & E, Gram stain, and culture). Classic triple therapy was administered (bismuth, tetracyclin, metronidazole). Patients were investigated endoscopically one month after completing therapy, and repeated biopsy specimens from the antrum and body were also obtained. RESULTS: H. pylori eradication was achieved in 42 patients (74%). In multiple logistic regression analysis metronidazole susceptibility (regr. coef. = 3.4; OR = 29.3) and previous therapy with omeprazol plus amoxycillin (regr. coef. = -1.7; OR = 0.18) were the only variables which correlated with success in H. pylori eradication (chi 2 model = 21; p < 0.001). Additional variables (age, sex, smoking, histologic lesion and ulcer history) were no correlated with H. pylori infection. H. pylori was susceptible to metronidazole in 36 patients (79%). Eradication rates for metronidazole-susceptible and metronidazole-resistant H. pylori isolates were 87% and 25%, respectively (p < 0.001). When previous therapy with omeprazole plus amoxycillin had been administered the eradication rate was lower (61%) than in patients without previous therapy (82%). CONCLUSION: Success of classic triple therapy in H. pylori eradication is higher when the organism is metronidazole-susceptible, and lower when previous therapy with omeprazole plus amoxycillin has been administered. This factor, although not fully elucidated, lends no support to choosing triple therapy when eradicating therapy with omeprazole plus amoxycillin fails.
PURPOSE: To study a possible correlation between the urea breath test values prior to treatment and the response to Helicobacter pylori eradication therapy in patients with duodenal ulcer. METHODS: Seventy-seven patients with duodenal ulcer were retrospectively studied (mean age: 46 +/- 13 years; 71% males). Initially, an endoscopy with biopsy samples (H&E stain) taken from antrum and body was performed, and a 13C-urea breath test (measuring 13C difference: delta 13CO2) was also performed. Both procedures were repeated one month after completing therapy ("classic" triple therapy [n = 25], and omeprazole plus amoxycillin [n = 52]). RESULTS: Eradication was achieved in 40% of cases (n = 32), and it was higher in patients treated with "classic" triple therapy (60%) than in those treated with omeprazole plus amoxycillin (31%) (p = 0.017). Mean delta 13CO2 level was 25 +/- 15. There were no differences when comparing values of patients with successful eradication (24 +/- 18) or therapy failure (25.6 +/- 13). No differences were observed when considering both therapies separately or when comparing eradication rates depending upon breath test levels prior to therapy. Breath test values did not influence the eradication in the logistic regression model. Mean delta 13CO2 values after therapy in patients with eradication failure ran in parallel with those observed previously. CONCLUSION: No correlation was observed between urea breath test values before treatment and the response to H. pylori eradication therapy in patients with duodenal ulcer. Thus, we conclude that quantification of this diagnostic method is not useful to predict the success or failure of eradicating therapy.