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Biomedical subjects

C Martín de Argila

Publications and source records attributed to C Martín de Argila.

At least 19 recordsLinked to original sources
PubMed2001

[Basal concentrations of gastrin and pepsinogen I and II in gastric ulcer: influence of Helicobacter pylori infection and usefulness in the control of the eradication].

AIM: To study the influence of Helicobacter pylori eradication on basal gastrin and pepsinogen I and II levels in patients with gastric ulcer over a 1-year follow-up period, and to assess the usefulness of these values in confirming H. pylori eradication after treatment. METHODS: Fifty-six patients with gastric ulcer and H. pylori infection were prospectively studied. At the beginning of the study, endoscopy with biopsies for histologic examination and urease testing was carried out, as were 13C-urea breath test and blood samples for determination of gastrin and pepsinogen I and II values by radioimmunoassay and serology. Histologic study, 13C-urea breath test and laboratory determinations were repeated at months 1, 6 and 12 after completion of eradication treatment. RESULTS: H. pylori infection was eradicated in 82.1% of patients. In patients with successful H. pylori eradication, the initial mean gastrin value was 75.5 +/- 39.1 pg/ml, while at 1 month after treatment this value decreased to 49.2 +/- 21 pg/ml (p < 0.0001). No further reductions were noted. Initial pepsinogen I and II values were 104 +/- 58 and 15.8 +/- 10 ng/ml, respectively, whereas at month 1 after treatment these values were 77 +/- 42 and 7.3 +/- 4 ng/ml, respectively (p < 0.0001) and were 72 +/- 41 and 6.7 +/- 3 ng/ml respectively at month 6 (p < 0.01); no further variations were observed thereafter. The area under the ROC curve which reveals eradication through reductions in hormonal values was 0.70 for gastrin, 0.78 for pepsinogen I, 0.93 for pepsinogen II and 0.92 for the pepsinogen I/II ratio. At months 6 and 12 after treatment completion, differences in mean gastrin and pepsinogen I and II values between the patients with normal histologic findings and those with chronic gastritis were significant (p < 0.05). CONCLUSIONS: a) H. pylori eradication is associated with an early fall in basal gastrin values and a progressive decrease in basal pepsinogen I and II values. b) In patients with gastric ulcer, determination of the decrease in basal pepsinogen II levels is a useful and early non-invasive method for confirming eradication. c) Determination of gastrin and pepsinogen I and II values may be useful for assessing improvement in gastritis 6 months after treatment completion.

Area Under Curve↗
PubMed2000

[Effects of Helicobacter pylori eradication on the recurrence of gastric ulcer during a 12-month follow up].

BACKGROUND: To study the influence of Helicobacter pylori eradication on the incidence of ulcer recurrence during 12 months of follow-up in gastric ulcer patients. PATIENTS AND METHOD: Seventy-three patients with gastric ulcer were prospectively studied. At endoscopy two biopsies from both antrum and body for haematoxylin-eosin staining and one for rapid urease test were obtained. Likewise, serology and 13C-urea breath test were carried out. Fifty-six H. pylori infected patients were monitored after giving an eradication therapy with omeprazole, clarithromycin and amoxicillin. A first control endoscopy was performed immediately after completing treatment to confirm ulcer healing. A second control endoscopy (with histologic study) and a breath test were performed one month after completing therapy (eradication was defined as the absence of H. pylori by both methods). Finally, an endoscopy was repeated at 6 and 12 months to study ulcer recurrences. RESULTS: Mean age was 54 +/- 13 years (69% males). Cumulative ulcer recurrence rate for 12 months, respectively for patients with eradication success and failure, was 2.3% (95% CI, 0-12%) and 70% (34-93%) (chi 2: 23.9; p < 0.0001). Comparison between Kaplan-Meier curves for ulcer recurrence depending on H. pylori eradication showed significant differences (log-rank test; chi 2: 33.8; p < 0.0001). A patient successfully treated underwent ulcer recurrence while receiving treatment with acetylsalicylic acid, without recurrence of the infection. CONCLUSIONS: H. pylori eradication is associated with a dramatic reduction on the recurrence of gastric ulcer, with a cumulative recurrence rate during 12 months of only 2.3%, which suggests that definitive cure of gastric ulcer disease is possible by means of microorganism eradication.

Adult↗
PubMed1999

[Antral biopsy is sufficient to confirm Helicobacter pylori eradication with the "new" one-week long triple treatments].

BACKGROUND: To evaluate whether antral biopsies are enough for confirming Helicobacter pylori eradication with the "new" one week triple therapies with omeprazole. PATIENTS AND METHODS: 229 duodenal ulcer patients were treated with omeprazole for 7 days plus two antibiotics. Eradication was confirmed with histology (two biopsies from both gastric antrum and body) and 13C-urea breath test one month after the end of therapy. RESULTS: H. pylori eradication was achieved in 76.9% of the patients (95% CI: 71-82%). Histology at antrum was highly reliable to detect eradication failure: in all but in one case in which H. pylori was observed at gastric body, was the microogranism also observed at antrum. Infection prevalences at both locations were not homogeneous (McNemar: 6.4; p < 0.05). Concordance between antral biopsies and breath test for H. pylori diagnosis after therapy was excellent (kappa: 0.91; SE: 0.07), and both prevalences were homogeneous (McNemar: 1.3; p > 0.05). CONCLUSIONS: Taking antral biopsies is enough for confirming H. pylori eradication with the "new" one week triple therapies.

Amoxicillin↗
PubMed1999

[Helicobacter pylori and digestive hemorrhage due to duodenal ulcer: the prevalence of the infection, the efficacy of 3 triple therapies and the role of eradication in preventing a hemorrhagic recurrence].

BACKGROUND: To report the prevalence of Helicobacter pylori in patients with bleeding duodenal ulcer and to verify the effect of eradication on hemorrhage recurrence. To evaluate the efficacy on H. pylori eradication and on ulcer healing of three one-week triple therapies and to compare their efficacy with that of a dual therapy. PATIENTS AND METHODS: One-hundred and eleven patients with bleeding duodenal ulcer not taking gastroerosive drugs were prospectively studied. At endoscopy, biopsies from gastric antrum and body were obtained (haematoxylin-eosin), and a 13C-urea breath test was also performed. Both diagnostic methods were repeated one month after completing one of the following treatments (randomized study): omeprazole (20 mg/12 h), amoxycillin (1 g/12 h) and clarithromycin (500 mg/12 h) (OAC, n = 27); omeprazole (20 mg/12 h), clarithromycin (500 mg/12 h) and metronidazole (500 mg/12 h) (OCM, n = 27); lansoprazole (30 mg/12 h), amoxycillin (1 g/12 h) and clarithromycin (500 mg/12 h) (LAC, n = 27); and lansoprazole (30 mg/12 h) and clarithromycin (500 mg/8 h) (LC, n = 27). The first three therapies were administered for one week, and LC for two weeks. Once eradication was confirmed no antisecretory therapy was administered. A breath test was performed in the follow-up at 6 months and at one year. RESULTS: The prevalence of H. pylori infection was 97.3% (95% CI: 92-99%). Five patients were lost from the study during follow-up. The eradication efficacy (intention-to-treat) was: OAC, 89% (72-96%); OCM: 93% (77-98%); LAC, 93% (77-98%), and LC, 70% (51-84%). Overall triple therapy efficacy was higher than that of dual therapy (91% vs 70%; p < 0.05). Thirteen patients needed a 2nd or 3rd therapy, and eradication success was finally achieved in all cases. The type of therapy was the only variable which influenced on H. pylori eradication (OR: 4.5; 95% CI: 1.4-14%; p < 0.01) and H. pylori eradication was the only variable which influenced on ulcer healing (OR: 4.7; 95% CI: 1.2-19%; p < 0.05). The yearly reinfection rate was 2.8% (0.9-7.8%). No hemorrhage recurrences occurred during the one year follow-up period. CONCLUSIONS: H. pylori prevalence in bleeding doudenal ulcer is almost 100%. These patients will be spared of hemorrhage recurrence at least for one year if infection is eradicated. Therefore, eradication therapy is the therapy of choice, and maintenance therapy with antisecretory drugs is no longer needed. One-week triple therapies with a proton pump inhibitor and two antibiotics (clarithromycin plus amoxycillin or metronidazole) have a high efficacy in patients with bleeding duodenal ulcer.

Anti-Bacterial Agents↗
PubMed1999

Re-treatment after Helicobacter pylori eradication failure.

AIM: Currently, highly effective Helicobacter pylori eradication therapies are used, and although eradication failures still appear in a considerable proportion of cases, the therapeutic efficacy in such refractory cases has been only exceptionally studied. Therefore, our aim was to evaluate the appropriate attitude when eradication therapy fails. METHODS: In 127 duodenal ulcer patients, several therapies with omeprazole (O) plus one or two antibiotics [amoxycillin (A), clarithromycin (C), metronidazole (M)] had failed to eradicate H. pylori. Re-treatment was administered depending on initial therapy; in no case was the same regimen repeated, and antibiotics with resistance risk (as C or M) were only re-administered using combination regimens with bismuth (B): O + A + C + B (when C was re-administered) and O + bismuth triple therapy (BTT) (when M was re-administered). RESULTS: First therapy and eradication rates, with the corresponding second therapy, were: CONCLUSION: BTT re-treatment in O + A failure achieves a relatively low eradication rate, probably lower than BTT for the first time, suggesting that other regimens should be tried. The following re-treatments are recommended in H. pylori eradication failure: in O + A failure, BTT (or O + BTT, as BTT re-treatment could be less effective than the initial BTT treatment); in O + C failure, O + A + M; in O + A + C failure, O + BTT; in O + A + M failure, O + A + C; and, finally, in O + C + M failure, O + BTT (or O + A + C + B).

Adult↗
PubMed1999

Mutations in 23S rRNA in Helicobacter pylori conferring resistance to erythromycin do not always confer resistance to clarithromycin.

Mutations conferring resistance to erythromycin or clarithromycin in Helicobacter pylori were studied. Mutation A2142G was consistently associated with clarithromycin MIC of > 256 micrograms/ml, whereas mutants carrying A2143G had MICs ranging from < or = 0.016 to > 256 micrograms/ml, suggesting that additional factors account for the observed multiple levels of resistance to clarithromycin.

Anti-Bacterial Agents↗
PubMed1998

[new one-week triple therapies with metronidazole for the eradication of Helicobacter pylori: clarithromycin or amoxycillin as the second antibiotic].

BACKGROUND: To compare the efficacy of two "new" one-week triple therapies (with omeprazole, metronidazole and clarithromycin or amoxycillin) for the eradication of Helicobacter pylori and healing duodenal ulcer. METHODS: Randomised therapeutic trial. Eighty-eight consecutive duodenal ulcer patients with H. pylori infection were studied. At endoscopy, biopsies from both gastric antrum and body were obtained for histologic study (H&E). Two different therapies were administered for one week: omeprazole (O) (20 mg b.i.d.) and metronidazole (M) (500 mg b.i.d.) associated with clarithromycin (C) (500 mg b.i.d.) (group OMC, n = 44) or amoxycillin (A) (1 g b.i.d.) (group OMA, n = 44). Endoscopy with biopsies was repeated one month after completing therapy, and a 13C-urea breath test was also performed. Compliance was evaluated by tablet count. Analysis of data: multiple logistic regression, intention-to-treat. Eradication was defined as the absence of H. pylori by all diagnostic methods. RESULTS: Mean age (standard deviation) was 45(14) years, 75% males. Distribution of variables was similar in both therapeutic groups. Forty-two patients in each group completed the protocol. Eradication was achieved in 90.5% (95% CI = 78-96%) in group OMC and in 57% (42-71%) in group OMA (p < 0.001). In the multivariate analysis the type of therapy was the only variable which influenced on H. pylori eradication (OR = 7.1; CI = 2.2-24; p = 0.001). Ulcer healing was demonstrated in 88% (75-95%) of patients in group OMC and in 71% (56-83%) in group OMA (p = 0.1). Ulcer healing was higher when eradication was achieved (90%; 80-95%) than in H. pylori-positive patients (50%; 31-69%) (p < 0.001). Eradication of H. pylori was the only variable which influenced on ulcer healing (OR = 9.3; CI = 2.8-31; p < 0.001). CONCLUSION: The "new" triple therapy with omeprazole, metronidazole and clarithromycin (administered in a twice-a-day basis and only for one week) had an excellent efficacy for the eradication of H. pylori, significantly higher than that obtained with amoxycillin instead of clarithromycin. Both therapies achieved a high ulcer healing rate when H. pylori was eradicated, even with omeprazole administered only for one week.

Adult↗
PubMed1998

ABO blood groups, rhesus factor and Helicobacter pylori.

BACKGROUND: The aim of this study was to demonstrate an association between Helicobacter pylori infection, ABO blood groups and Rhesus factor; providing the association between duodenal ulcer and O group blood as well as the former and H. pylori infection. METHODS: Three-hundred and one healthy subjects were prospectively studied. In all of them ABO blood groups and Rhesus factor were determined by standard techniques. Systemic IgG antibodies against H. pylori were assayed using a quantitative enzyme-linked immunosorbent assay technique (Helico-G, Porton, Cambridge, UK). RESULTS: The overall seroprevalence was 52.2%. H. pylori infection distribution was similar among ABO blood groups and Rhesus factor. No statistically significant differences were observed in mean values of IgG antibodies among different blood groups. CONCLUSIONS: Distribution of H. pylori seroprevalence does not differ between different ABO or Rhesus factor blood groups. This excludes a possible link between this microorganism and the high ulcer prevalence in O blood group.

ABO Blood-Group System↗
PubMed1998

[Gastroduodenal lesions and non-steroidal anti-inflammatory agents. What role does Helicobacter pylori play in this relationship?].

Helicobacter pylori infection and non-steroidal anti-inflammatory drugs (NSAIDs) are the two most important causal factors in gastroduodenal ulcer disease. The coincidence of both occurs frequently and, therefore, demonstration of a possible relationship, and the consequent attitude (giving or not eradication therapy) would have important implications. The lower H. pylori prevalence in gastric ulcer, in comparison with duodenal ulcer, seems to be due greatly to NSAIDs intake, although in a low number of patients this ulcer is not explained by either of these factors. Therefore, the finding of a gastroduodenal ulcer in an H. pylori-negative patient should suggest other possible causes, and among them NSAIDs outstands. Histologic gastritis found in a patient with NSAIDs intake is related to the subjacent presence of H. pylori and not with NSAIDs. It is not clear whether, in patients taking NSAIDs, the infection favors the appearance of dyspeptic symptoms. The possibility of H. pylori and NSAIDs having a synergistic effect on gastroduodenal ulcer disease is a debatable issue. H. pylori eradication in patients taking NSAIDs does not confer a clear advantage in ulcer healing, and the possible protecting effect of eradication on the development of an ulcer in subjects taking NSAIDs is doubtful. In an H. pylori-positive patient in whom an ulcer occurs while taking NSAIDs, it is not possible to know for sure whether the ulcer has been caused by the organism, by NSAIDs, or by both, and therefore it seems logical to administrate an eradication therapy. However, H. pylori eradication with the intention of preventing appearance of gastroduodenal lesions is not so evident. Finally, indications of traditional preventive treatment (with antisecretory drugs or mysoprostol) should not be influenced by the concomitant administration of H. pylori eradication therapy.

Anti-Inflammatory Agents, Non-Steroidal↗