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J M Pajares

Publications and source records attributed to J M Pajares.

At least 73 records · Page 4Linked to original sources
PubMed2000

Helicobacter pylori infection, gastric metaplasia in the duodenum and the relationship with ulcer recurrence.

OBJECTIVE: To study the prevalence of Helicobacter pylori (H. pylori) infection and gastric metaplasia (GM) in the duodenum a large group of patients with duodenal ulcer was evaluated to determine whether these factors are related to the number of ulcer recurrences. METHODS: Three hundred and seven patients diagnosed by endoscopy as having active duodenal ulcers were studied. At endoscopy, all patients had gastric biopsies taken for histology, the rapid urease test and culture. Three duodenal biopsies were also taken and processed for histology (haematoxylin & eosin, Giemsa, Warthin-Starry, and PAS stain). RESULTS: GM and H. pylori in the duodenum was identified in 73% (68-78%) and 66% (60-71%) of the cases, respectively. All patients with H. pylori in the duodenum also had GM at this location, while areas with GM but without H. pylori were described. The kappa statistic for concordance between GM and H. pylori at the duodenum was 0.82. The prevalence of GM and H. pylori, depending on the number of ulcer recurrences, was: 1st episode, 34% and 27%, respectively; 2nd episode, 84% and 80%; and > or = 3rd episode, 90% and 79% (P < 0.001 when comparing 1st vs 2nd or > or = 3rd episode). In the multivariate analysis, age and number of ulcer recurrences correlated both with GM and with H. pylori in the duodenum. Chronic duodenitis was demonstrated in all duodenal biopsies, 87% being active chronic duodenitis. H. pylori in the duodenum was more frequent in patients with active duodenitis (73%) than in those with inactive duodenitis (13%) (P < 0.001). CONCLUSIONS: Patients with recurrent ulcer disease have a higher prevalence of both GM and H. pylori infection in the duodenum, suggesting that these two factors are related with the chronicity and recurrence of duodenal ulcer disease. H. pylori infection in the duodenum always appears in areas of GM, although GM is not necessarily colonized by the organism. H. pylori infection cannot be excluded based only on the results of duodenal biopsies, as false negative results at this area are frequent.

Adult↗
PubMed2000

["Rapid" serology for the diagnosis of Helicobacter pylori infection. Evaluation of its accuracy compared with a gold-standard and its concordance with "classic" serology].

AIM: To prospectively evaluate the validity of a rapid office-based diagnostic serological test (using capillary blood) in our population, taking as reference a combination of standard diagnostic methods, as well as to compare the results of this technique with those of "classic" serological tests (using venous blood). PATIENTS AND METHODS: We prospectively studied 39 consecutive patients with symptoms of the upper digestive tract who had undergone oral gastroscopy. Gastric biopsies were taken for histology and rapid urease testing, and a 13C-urea breath test was performed. An enzyme-linked immunoassay that detects IgG antibodies against Helicobacter pylori was used as a "classic" serological test and the commercial kit FlexPack HP was used as a "rapid" serological test. The endoscopist, the pathologist and those responsible for reading the rapid urease test, the 13C-urea breath test and both serological tests did not know the results of the other diagnostic methods. Patients were considered H. pylori positive when at least two of the three validated tests (rapid urease test, histology, and 13C-urea breath test) revealed infection and were considered free of infection when all tests were negative. RESULTS: Thirty-nine patients were studied. Thirty-eight per cent were male (mean age 48 +/- 15 years). The prevalence of H. pylori infection detected by the gold standard was 69.2%. The sensitivity and specificity of the "classic" serological test was 96% 95% (CI: 79-99) and 91% (59-100). "Rapid" serological testing was positive in nine patients, negative in 28 and indeterminate in two. A single digital puncture was sufficient in 80% of the patients, 15% needed two and 5% needed three. Most patients (77%) had no preference for either type of serological test while 20.5% preferred digital puncture and 2.5% venous puncture. The sensitivity, specificity, positive predictive value and negative predictive value were 31% (16-50), 91% (59-100), 89% (52-100) and 36% (19-56) respectively. Sensitivity was unaffected by age but specificity was lower in patients older than 40 years (89% vs. 100%; McNemar's test: 8; p < 0.01). Kappa's coefficient between the "classic" and the "rapid" serological tests was 0.16 (SE 0.1) and McNemar's test was 12.2 (p < 0.001), which indicates that the prevalence of infection diagnosed by both methods was not homogeneous. CONCLUSION: The "rapid" office-based serological test used in our study is of insufficient diagnostic accuracy to be used in clinical practice to identify H. pylori infection.

Enzyme-Linked Immunosorbent Assay↗
PubMed1999

H. pylori-negative duodenal ulcer prevalence and causes in 774 patients.

The prevalence of H. pylori infection has been reported to be very high in duodenal ulcer (DU) disease, but the precise frequency and causes of H. pylori-negative DU are not well known. In some geographical regions, however, a relatively low prevalence of the infection has been described. Our aim was to study the frequency and causes of H. pylori-negative DU and to evaluate whether empirical H. pylori eradication therapy without confirmation of the infection is justified. In all 774 consecutive patients with an endoscopic diagnosis of DU were studied prospectively. Exclusion criteria were associated diseases and previous gastric surgery. The use of NSAIDs, antibiotics (during the last month), and proton pump inhibitors (during the last month) was evaluated by means of a specific questionnaire. At endoscopy, two biopsies from both antrum and corpus were obtained in all 774 patients for histologic study (H&E stain). One sample from the antrum for rapid urease test, one sample each from the antrum and corpus for culture, and two duodenal biopsies for histologic study were also obtained in the first 307 patients. A [13C] urea breath test was carried out in the remaining 467 patients. Patients were considered infected if any of the diagnostic tests were positive and noninfected when all tests performed were negative. Age (mean +/- SD) was 46+/-12 years, 70% were males. NSAID, antibiotic, and proton pump inhibitor use was described, respectively, in 8.9%, 5.8%, and 6.3% of the cases. H. pylori infection was demonstrated, overall, in 95.3% (95% CI: 93.6-96.6%) of the patients. H. pylori prevalence increased up to 99.1% (98.1-99.6%) if patients taking NSAIDs and/or antibiotics were excluded. Among the 36 H. pylori-negative patients, 20 (55%) were taking NSAIDs, 9 (25%) were taking antibiotics, and 1 (3%) both of them. Therefore, in only 6/774 patients (0.8%) could DU disease be considered truly "idiopathic." Differences were demonstrated between H. pylori-positive and -negative patients (univariate study; chi2) with regard to NSAID intake (7% vs 58%; P < 0.0001) and previous antibiotic use (5% vs 28%; P < 0.0001). In the multivariate analysis (logistic regression), NSAID use (OR: 0.06; CI: 0.03-0.13; P < 0.001) and antibiotic use (OR: 0.23; CI: 0.09-0.59; P < 0.01) were the only variables that correlated with H. pylori infection. The most important factors associated with H. pylori-negative DU are NSAIDs and prior antibiotic use, and if these agents are excluded, the prevalence of infection in our area is as high as 99%. Therefore, in DU patients not taking NSAIDs and living in areas where previous studies have shown the prevalence of the infection in DU disease to be very close to 100%, empirical H. pylori eradication therapy without confirmation of the infection may be justified.

Anti-Bacterial Agents↗
PubMed1999

Seven-day 'rescue' therapy after Helicobacter pylori treatment failure: omeprazole, bismuth, tetracycline and metronidazole vs. ranitidine bismuth citrate, tetracycline and metronidazole.

BACKGROUND: Eradication therapy with omeprazole (O), amoxycillin (A) and clarithromycin (C) is used extensively, although it often fails. A 'rescue' therapy with a quadruple combination of O, bismuth (B), tetracycline (T) and metronidazole (M) has been recommended. AIM: : To assess ranitidine bismuth citrate (Rbc) instead of O and B for treatment failure. METHODS: Sixty consecutive patients (13 duodenal ulcer, 47 non-ulcer dyspepsia) in whom a previous eradication trial with O, A and C had failed were randomized to receive one of two regimens for 7 days: O (20 mg b.d.), B (120 mg q. d.s.), T (500 mg q.d.s.) and M (250 mg q.d.s.) (group OBTM, n=30); or Rbc (400 mg b.d.), T (500 mg q.d.s.) and M (250 mg q.d.s.) (group RbcTM, n=30). Eradication was defined as a negative 13C-urea breath test 1 month after completing therapy. RESULTS: Mean age +/- s.d. was 45 +/- 12 years, 47% were males. Distribution of studied variables (age, sex, smoking, duodenal ulcer/non-ulcer dyspepsia) was similar in both therapeutic groups. Per protocol eradication was achieved in 17 out of 29 patients (59%) in group OBTM and in 25 out of 29 patients (86%) in group RbcTM (P < 0.05). Intention-to-treat eradication was achieved, respectively, in 17 out of 30 (57%) and in 25 out of 30 (83%) (P < 0.05). In the multivariate analysis the variables which influenced on H. pylori eradication were the type of therapy (odds ratio, OR=3.9; 95%CI: 1.02-15; P < 0.05) and diagnosis (duodenal ulcer/non-ulcer dyspepsia) (OR=0.1; CI: 0.02-0.4). Adverse effects were infrequent and mild with both regimens. CONCLUSION: Therapy with RbcTM is a promising option after H. pylori eradication failure with OCA, achieving a higher efficacy than quadruple therapy with OBTM.

Adult↗
PubMed1998

Recurrence of Helicobacter pylori infection after eradication: incidence and variables influencing it.

BACKGROUND: Our aim was to study the incidence of Helicobacter pylori recurrence in our country and to assess the different variables that might influence it. METHODS: We studied prospectively 331 duodenal ulcer patients (mean age, 48 +/- 14 years, 71% male) in whom H. pylori had been eradicated. Several therapies were used, classified as low-efficacy (omeprazole + amoxycillin, 32% eradication rate; omeprazole + amoxycillin + metronidazole, 56%) and high-efficacy therapies (omeprazole + clarithromycin + amoxycillin or metronidazole, 88%; bismuth triple therapy, 77%). One month after completion of therapy an endoscopy with biopsies and/or 13C-urea breath test was performed. A breath test was carried out again at 6 months, 1 year, and 2 years, to study H. pylori recurrences. Endoscopy (with biopsies) was performed only to confirm recurrences. Multiple logistic regression analysis was used. Differences between Kaplan-Meier curves were evaluated with the log-rank test. RESULTS: Sixty-seven patients were followed up for 6 months, 136 for 1 year, and 128 for 2 years, giving 425 patient-years of follow-up. A total of 18 H. pylori recurrences was observed (12 at 6 months, 4 at 1 year, and 2 after 2 years), yielding a yearly recurrence of 4.2% patient-years(-1). The respective risk of H. pylori recurrence for each period was 3.6% (95% confidence interval (CI), 2.1%-6.2%), 1.5% (0.6%-3.8%), and 1.5% (0.4%-5.5%). The probability of being H. pylori-negative at 6 months, 1 year, and 2 years was, respectively, 96.4% (94.4%-98.4%), 94.9% (92.5%-97.4%), and 93.4% (90.3%-96.6%). Duodenal ulcer was found in half of the reinfected patients. The recurrence rate at 6 months was 10.3% (5.7%-18%) in patients <40 years old and only 0.85% (0.2%-3.1%) in those > or =40 years old (P = 0.0002). Of the patients who became reinfected at 6 months 27% (6%-61%) had delta breath test values between 3 per thousand and 5 per thousand 1 month after therapy, whereas only 4.6% (2.7%-7.7%) of non-reinfected patients had delta after eradication > or =3 per thousand (P = 0.0097). H. pylori recurrence at 6 months was 8.2% (4.5%-15%) in patients previously treated with low-efficacy therapies and only 1.7% (0.7%-4.3%) when high efficacy therapies were used (P = 0.0098). In the multivariate analysis age (odds ratio (OR), 0.9; 95% CI, 0.8-0.96; P = 0.0008), the delta breath test value after therapy (OR, 2.2; CI, 1.2-4.1; P = 0.0076), and therapy regimen (OR, 6.4; CI, 1.5-27; P = 0.0109) were the only variables that correlated with H. pylori recurrence at 6 months. Differences were observed when Kaplan-Meier curves were compared, depending on age (<40 or > or =40 years; P = 0.0054), breath test value (delta) 1 month after therapy (<3 or > or =3 per thousand; P = 0.0089), and therapy regimen (high or low efficacy; P = 0.0006). CONCLUSIONS: Risk of post-eradication H. pylori recurrence is higher during the first 6 months, which suggests that most recurrences during this period are recrudescences and not true reinfections. Patients who have H. pylori recurrence tend to be younger and have higher delta 13C-urea breath test values after therapy, which suggests that a 'negative' value between 3 per thousand and 5 per thousand needs to be confirmed. Recurrence of H. pylori is more frequent in patients treated with low-efficacy therapies but is exceptional when high-efficacy therapies are used, in which case post-therapy eradication can be safely confirmed at 4 weeks. Finally, recurrence of H. pylori is clinically relevant, as ulcer recurrence is observed in a considerable proportion of these patients.

Adult↗
PubMed1998

An increased number of follicles containing activated CD69+ helper T cells and proliferating CD71+ B cells are found in H. pylori-infected gastric mucosa.

OBJECTIVE: An immune response occurring in Helicobacter pylori-infected gastric mucosa could have a direct implication for associated pathologies. In the present study we analyzed the expression of the immune activation, proliferation, and phenotype markers by immune cell subpopulations in H. pylori-infected and uninfected gastric samples. METHODS: Antral gastric biopsies from both H. pylori-positive and -negative patients were processed by immunohistochemistry; gastric epithelial cells were isolated from biopsy tissue and analyzed by flow cytometry. RESULTS: Ten of the 13 biopsies that contained follicles were H. pylori positive. Follicular CD69 was expressed mainly by CD4+ T cells and the central core of follicles showed double immunopositivity for the B-cell marker CD19 and transferrin receptor. Also detected was an increase in the percentage of epithelial cells from H. pylori-positive samples expressing HLA-DR and beta2 microglobulin, compared to negative samples (61 +/- 15% vs 9 +/- 9%, p = 0.003 and 93 +/- 7% vs 52 +/- 18%, p = 0.002, respectively), whereas no variation on class I HLA was detected. CONCLUSIONS: These results suggest that chronic H. pylori infection could facilitate the persistence of follicles on which continuous follicular helper T-cell activation could lead to uncontrolled follicular B-cell proliferation. Furthermore, beta2 microglobulin expression by epithelial cells in a nonparallel way to class I HLA may indicate the possibility of nonclassical class I MHC expression on the basal surface of the epithelium.

Adult↗
PubMed1998

Helicobacter pylori disrupts epithelial barrier function in a process inhibited by protein kinase C activators.

Helicobacter pylori colonizes the gastric mucosa, and the infection is related to the development of diverse gastric pathologies, possibly by directly or indirectly affecting epithelial-cell function. We analyzed the influence of the bacteria on transepithelial electrical resistance (TER) on a model tight epithelium, T84, grown to confluence in permeable filters. H. pylori sonicates produced a dramatic decrease in TER after 1 to 2 h of exposure, while sonicates from other bacteria did not induce a significant reduction of TER. The effect induced by sonicates was mimicked by a water-soluble fraction from the bacterial surface, was not reproducible with isolated lipopolysaccharide, and was concomitant with a significant increase in the paracellular permeability of the marker molecule [14C]mannitol. Furthermore, H. pylori sonicates also provoked a significant increase in permeability to [14C]mannitol across rat gastric mucosa in vitro. The sonicate-induced decrease in TER in T84 monolayers was inhibited by the protein kinase C (PKC) activator phorbol myristate acetate. As PKC is directly involved in tight junction regulation, we suggest that H. pylori may induce intracellular signalling events counteracting PKC effects. Following long-term H. pylori stimulation, epithelial monolayers regained baseline resistance values slowly after 24 h. The resistance recovery process was inhibited by cycloheximide, indicating its dependency upon protein synthesis. No association between resistance variation and E-cadherin protein levels was observed. These results indicate that H. pylori alters in vitro the barrier properties of the epithelium, probably by generating cell signalling events counteracting the normal function of PKC. This increased permeability may provide a potential mechanism by which H. pylori antigens can reach the gastric lamina propria, thereby activating the mucosal immune system.

Animals↗
PubMed1998

H pylori infection is associated with downregulation of E-cadherin, a molecule involved in epithelial cell adhesion and proliferation control.

Extracellular matrix proteins and proteins involved in epithelial adhesion are essential for maintenance of tissue structure. Helicobacter pylori is the major aetiological agent in peptic ulcer disease and has been shown to increase gastric cancer risk up to ninefold. In this study, changes induced by H pylori on the expression of extracellular matrix proteins (collagen IV, fibronectin, and laminin) as well as two essential proteins for cell-basement and cell-cell adhesion (alpha 6-integrin and E-cadherin) were assessed. Immunohistochemistry was performed in antral biopsy sections obtained from infected and non-infected patients, and light microscopy was used to determine the distribution and intensity of specific staining. The results showed that the infection was significantly associated with downregulation of E-cadherin, an essential protein for maintenance of solid tissues and differentiation, but did not induce changes in the expression of alpha 6-integrin or the extracellular matrix proteins.

Cadherins↗
PubMed1998

Eradication and follow-up of Helicobacter pylori infection in hemodialysis patients.

It is currently accepted that Helicobacter pylori (Hp) infection is crucial in the pathogenesis of peptic ulcer. Therefore, we developed a prospective study to assess the prevalence of Hp infection by the 13C Urea Breath Test (13C UBT) in 52 hemodialysis patients, and we evaluated the efficacy of two consecutive eradication regimens in 23 positive patients with dyspepsia and/or on a transplantation list. The correlation between anti-Hp serology and 13C UBT results was also analyzed in 34 patients who were followed up during 18 months. The Hp prevalence by 13C UBT was 63.5% (33/52). The eradication rate after the first cycle of therapy (amoxicillin 500 mg/8 h and omeprazole 20 mg/12 h, 14 days) was 60.8% (14/23). After the second cycle (clarithromycin 500 mg/12 h plus omeprazole 20 mg/12 h, 14 days), the eradication rate reached 82.6% (19/23). The serological procedure showed a good correlation with 13C UBT (about 80% sensitive and specific) when very restrictive diagnostic and eradication criteria were adopted. We conclude that an eradication rate higher than 80% can be reached after two consecutive cycles of dual therapy in hemodialysis patients. Anti-Hp serological tests must be cautiously interpreted in these patients.

Aged↗
PubMed1997

Ranitidine versus colloidal bismuth subcitrate in combination with amoxicillin and metronidazole for eradicating Helicobacter pylori in patients with duodenal ulcer.

One hundred twenty-two patients were randomly assigned to three groups of treatment (A, B, and C), with (1) ranitidine (300 mg q.d. for 6 weeks), (2) ranitidine (300 mg q.d. for 6 weeks) with amoxicillin (500 mg t.i.d.) and metronidazole (500 mg b.i.d.) for the first 12 days, or (3) colloidal bismuth subcitrate (120 mg q.i.d. for 6 weeks) with amoxicillin and metronidazole (at same dosages as in the latter group). Six weeks after the beginning of treatment, an endoscopy showed that ulcers had healed in 49 of 52 patients (94.2%) from whom Helicobacter pylori had been eradicated and in 59 of 70 patients (84.3%) from whom it had not (NS). The rates of H. pylori eradication in groups A, B, and C were zero, 47.5%, and 86.8%, respectively. At 6, 12, and 18 months, an endoscopy was repeated for monitoring ulcer recurrence and H. pylori status. Reinfection rates at 6 months were 42.1% and 15.1% in groups B and C, respectively (P < .05). At 18 months, ulcers recurred in 82.9% (63) of 76 patients with noneradicated H. pylori infection, vs. 5.7% (2) of 35 patients without H. pylori infection (P < .001). We conclude that colloidal bismuth subcitrate is more effective for eradication of H. pylori than ranitidine when given with amoxicillin plus metronidazole for the treatment of duodenal ulcer, as both early reinfection and ulcer recurrence are diminished.

Adolescent↗