Hemosuccus pancreaticus in a heterotopic jejunal pancreas.

Heterotopic pancreas is a congenital anomaly defined as pancreatic tissue occurring outside its normal anatomical location, lacking both anatomic and vascular connections. Ninety percent of heterotopic pancreas is found in the upper part of the gastrointestinal tract. Symptoms, when present, are normally non-specific and include abdominal pain, nausea, vomiting and bleeding. However, aberrant pancreas is not often recognized as patients are usually symptom-free. We report on a 29 year-old man with acute and severe gastrointestinal hemorrhage through the duct of an aberrant pancreas located in the upper jejunum, without clinical or histological evidence of pancreatic inflammation. We believe that our case is the first description of a pancreatic ductal hemorrhage in an aberrant pancreas.

Basal and stimulated gastrin and pepsinogen levels after eradication of Helicobacter pylori: a 1-year follow-up study.

AIM: A decrease in gastrin and pepsinogen (PG) levels 1 month after Helicobacter pylori eradication has been described repeatedly, but the long-term progression of such a decrease has been scarcely studied. We therefore studied the effect of H. pylori eradication on basal and stimulated gastrin and PG levels for 1 year. Initially, the usefulness of measuring these parameters for the noninvasive diagnosis of H. pylori eradication was validated. Furthermore, an assessment was made of the association between H. pylori reinfection and a re-increase in gastrin and PG values. Finally, an evaluation was made of the variables influencing gastrin and PG concentration, with particular attention to H. pylori infection and histological lesions of gastric mucosa. METHODS: Two-hundred and twenty-two patients with duodenal ulcer were studied prospectively. Exclusion criteria were the administration of antibiotics, H2 antagonists, omeprazole or bismuth prior to endoscopy. In all patients serum basal levels of gastrin, PGI, and PGII were measured before and 1 month after completing eradication therapy. In the successfully eradicated patients, gastrin, PGI, and PGII were also measured at 6 and 12 months. In 80 patients stimulated measurements of gastrin (after ingestion of two beef cubes) and PGI (after injection of pentagastrin) were also performed. H. pylori-negative patients after therapy underwent a urea breath test at 6 and 12 months, and patients who had stimulated gastrin and PG concentration measured had also an endoscopy performed at 6 months. RESULTS: H. pylori was eradicated in 73% of patients. A histological improvement was observed 1 month after completing H. pylori eradication therapy, both at gastric antrum and body (P < 0.001), while a further improvement at antrum was demonstrated at 6 months (P < 0.01). With regard to the different cut-off points for decreased basal and stimulated measurements for diagnosing H. pylori eradication, the best results were obtained, respectively, with PGII (sensitivity of 90% and specificity of 76%) and PGI 30 min after stimulation (sensitivity and specificity of 82%), with an area under the ROC curve of 0.87 in both cases. In the multiple regressions analysis H. pylori status correlated with gastrin, PGI and PGII after therapy (P < 0.001), while histological lesions correlated only with gastrin levels (P < 0.05). A decrease in basal and stimulated serum parameters was demonstrated immediately after eradication (Wilcoxon test, P < 0.001), and an additional decrease (at 6 months) was observed just in PGI (Friedman test, P < 0.01). However, gastrin and PGII values remained unchanged after the first month post-eradication. Seven patients were reinfected with H. pylori during follow-up. Quantitation of basal and stimulated gastrin and PGI levels was not reliable as a reinfection marker. Regarding basal PGII, the parallelism was strong at 6 months (re-increase in all four reinfected patients), although only in one out of three with reinfection at 1 year did PGII rise at that stage. CONCLUSIONS: (1) Measurement of gastrin and PG levels (especially basal PGII values) is a useful non-invasive method to confirm H. pylori eradication after therapy. (2) H. pylori eradication is associated with a significant decrease in basal and stimulated gastrin levels and in basal PGII levels that is detected immediately (1 month) after finishing treatment, and remains unchanged for 1 year. However, the decrease in basal and stimulated PGI levels occurs progressively for 6 months, although such levels remain also unchanged afterwards. (3) Measurement of gastrin and PGI concentrations has a limited usefulness in the diagnosis of H. pylori reinfections after successful eradication, although PGII determination could be more useful in this situation.

Unhealed duodenal ulcers despite Helicobacter pylori eradication.

BACKGROUND: Our aims were 1) to study the influence of several factors (age, sex, smoking, previous ulcer disease, ulcer size, chronic gastritis, serum gastrin and pepsinogen I levels, therapy regimen and, especially, eradication of Helicobacter pylori) on duodenal ulcer healing; 2) to evaluate the frequency of duodenal ulcer healing failure despite eradication of H. pylori, to study why this failure occurs, and to verify its evolution without antisecretory therapy; and 3) to confirm whether a week's prescription of omeprazole is sufficient to obtain ulcer healing. METHODS: Three-hundred and eight patients (mean age, 45 +/- 13 years; 71% males) with duodenal ulcer and H. pylori infection were studied prospectively. Biopsy specimens were obtained at initial endoscopy, and serum gastrin and pepsinogen I levels were measured. A repeat endoscopy (with biopsies) was performed 1 month after eradication therapy had been completed, and a 13C-urea breath test was also carried out. Three eradication therapies were used: omeprazole plus amoxycillin for 2 weeks (OA group, n = 61); 'classic' triple therapy (with bismuth; CTT group, n = 65); and 'new' triple therapies for 1 week (NTT group, n = 182): omeprazole plus two of the following antibiotics: clarithromycin, metronidazole, and amoxycillin. When the ulcer did not heal despite successful H. pylori eradication, antacids were prescribed on an as-needed basis, and endoscopy was repeated 1 month later (2nd control endoscopy). If the ulcer was still present, the acid output (basal and pentagastrin-stimulated) was measured, a secretin test was performed, and a final endoscopy (3rd control endoscopy) was carried out after an additional month. The statistical method used was multiple logistic regression. RESULTS: Overall eradication was achieved in 69% (n = 212) of the patients, and ulcer healing in 76% (n = 233): 57% in the OA group, 80% in the CTT group, and 81% in the NTT group (P < 0.01 when comparing the OA group with the others). Ulcer healing was achieved in 90% of H. pylori-eradicated patients and in only 45% of patients with eradication therapy failure (P < 0.001). Similar results were obtained when only patients treated with NTT were considered: ulcer healing in 90% of patients with the organisms eradicated. Eradication of H. pylori (odds ratio (OR), 11.8; 95% confidence interval (CI), 6.3-22) and sex (OR, 2.5; 95% CI, 1.2-5.1) were the only variables that correlated with ulcer healing in the multivariate analysis. The ulcer persisted despite successful eradication of H. pylori in 22 patients. The duodenal ulcer had healed spontaneously in 73% of these patients at the 2nd control endoscopy. Finally, by the 3rd control endoscopy, only three patients still had duodenal ulcer. Therefore, ulcer healing was finally achieved in 98.1% (95-99%) of patients in whom H. pylori was eradicated. Gastrin, pepsinogen I, acid output, and the secretin test had normal values in all patients. CONCLUSIONS: Eradication of H. pylori favours ulcer healing, which is achieved in most patients in whom the organism is eradicated. Just 1 week of omeprazole therapy (that is, the antibiotic administration period in the new triple therapies) is enough to obtain a high ulcer healing rate. Most duodenal ulcers that do not heal initially despite H. pylori eradication will ultimately do so after several weeks without additional therapy.

[One-week treatment with omeprazole, clarithromycin and amoxicillin: high efficacy in the eradication of Helicobacter pylori and cicatrization of duodenal ulcer]. / Tratamiento con omeprazol, claritromicina y amoxicilina durante una semana: elevada eficacia en la erradicación de Helicobacter pylori y en la cicatrización de la úlcera duodenal.

BACKGROUND: To evaluate the efficacy of one-week therapy with omeprazole, clarithromycin and amoxycillin in eradicating Helicobacter pylori and healing duodenal ulcer. PATIENTS AND METHODS: One-hundred and thirty-four consecutive duodenal ulcer patients (mean age 47 +/- 13 yrs, 66% males) with H. pylori infection were prospectively studied. At endoscopy, biopsies from both gastric antrum and body were obtained for histologic study (H/E). A 15C-urea breath test was also performed in 98 patients. Omeprazole 20 mg b.i.d., amoxycillin 1 g b.i.d., and clarithromycin 500 mg b.i.d. were administered only for 1 week, and no therapy was administered thereafter. Endoscopy with biopsies and breath test were repeated 1 month after completing therapy. RESULTS: Eradication was achieved in 87.3% of patients (n = 93; 95% CI = 82-93%). In the multivariate analysis the variables which influenced H. pylori eradication were: time of evolution of ulcer disease (p = 0.002) and active chronic gastritis in the antrum (p = 0.04) (chi 2 model = 15.8; p = 0.001). Ulcer healing was demonstrated in 89.5% of patients (84-95%), and healing rate was higher when eradication was achieved (94%; 90-98%) than in H. pylori-positive patients (59%; 36-78%) (p < 0.001). In the multivariate analysis the variables which influenced ulcer healing were: age (p = 0.02) and H. pylori eradication (p = 0.001) (chi 2 model = 21.2; p = 0.0001). An improvement of histologic gastritis was observed when eradication was achieved (p < 0.001). Compliance of therapy was complete in all patients but one and no relevant adverse effects were reported. CONCLUSION: One-week triple therapy with omeprazole, clarithromycin and amoxycillin administered on a twice daily basis achieves a high efficacy in eradicating H. pylori and healing duodenal ulcer. Moreover, this therapy regimen is simple and is associated with a low incidence of adverse effects and a low cost.

[Isolated colonic tuberculosis]. / Tuberculosis colónica aislada.

Two cases of colonic tuberculosis (TB) isolated in two elderly, not HIV seropositive women, presenting unspecific clinical manifestations (constitutional syndrome, fever, abdominal pain and diarrhea) and stenosis of the colon in diagnostic imaging techniques are presented. In the second case, endoscopy showed stenosis of the colonic lumen and inflammatory mucosa, the biopsy of which demonstrated granulation tissue with no signs of specificity (in the first case, technical problems did not allow the colonoscopy to reach the affected site). In both cases, diagnosis was performed postoperatively by study of the surgical pieces. Biopsy showed granulomas with acid-alcohol resistant bacilli. Both patients responded favorably to tuberculostatic treatment.

[Erradicating treatment of Helicobacter pylori with lansoprazole and amoxicillin in duodenal ulcer patients]. / Tratamiento erradicador de Helicobacter pylori con lansoprazol y amoxicilina en pacientes ulcerosos duodenales.

OBJECTIVE: To study the efficiency of the combination lansoprazole and amoxicillin on the eradication of Helicobacter pylori and duodenal ulcer healing. METHODS: Twenty-nine duodenal ulcer patients infected with H. pylori were prospectively studied (mean age, 46 +/- 11 years, 90% males). During endoscopy biopsies were obtained from gastric antrum and body for histologic examination (H & E); a urea breath test with 13C was also performed. Therapy with lansoprazole 30 mg/12 h and amoxicillin 500 mg/6 h for two weeks was prescribed. One month after completing therapy another endoscopy was performed (with biopsies obtained from gastric antrum and body) and again a urea breath test performed. Eradication was defined as the absence of H. pylori by both diagnostic methods. RESULTS: Eradication was achieved in 48% of patients (n = 14). Ulcer healing was obtained in 62% of cases (n = 18). When eradicating therapy was successful the percentage of healing reached 100%, versus 27% in those patients with persisting infection (p < 0.001). In patients with eradication obtained an histological improvement was noted both at gastric antrum and body, whereas when therapy failed no significant changes were observed. In all cases compliance with therapy was completed, and in no patient were secondary effects observed. CONCLUSION: The association of lansoprazole and amoxicillin at the administered doses has a low efficiency on H. pylori eradication in duodenal ulcer patients. Further studies are warranted to definitely assess the eradicating efficiency of such combination and also to determine the optimal dose of its components, the minimal duration of therapy and the ideal moment for its administration.

[Prevalence of Helicobacter pylori infection in gastric adenocarcinoma and chronic gastritis]. / Prevalencia de la infección por Helicobacter pylori en el adenocarcinoma gástrico y en la gastritis crónica.

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.

[Breath test in the diagnosis of Helicobacter pylori infection: concordance with histological methods and correlation with anatomopathological lesions of the gastric mucosa]. / Prueba del aliento para el diagnóstico de infección por Helicobacter pylori: concordancia con los métodos histológicos y correlación con las lesiones anatomopatológicas de la mucosa gástrica.

PURPOSE: To study the concordance between 13C-urea breath test and histology in the diagnosis of Helicobacter pylori infection, and to evaluate whether there is a correlation between breath test values and histologic lesions of the gastric mucosa. METHODS: Sixty-nine patients with duodenal ulcer were prospectively studied. An endoscopy with biopsy samples (H&E stain) taken from the antrum and body was performed, and a 13C-urea breath test (measuring 13C difference: delta 13CO2) was also done. Both procedures were repeated one month after completing therapy ["classic" triple therapy (n = 28), and omeprazole+amoxycillin (n = 41)]. Eradication was defined as the absence of H. pylori both by histological and breath test methods. RESULTS: At the beginning of the study, 94.2% of patients (n = 65) were H. pylori positive by histological methods, and 98.6% (n = 68) were positive by the breath test (ratio of positive agreement = 0.96). Kappa for H. pylori diagnosis after therapy was 0.83 (95% CI: 0.69-0.96). A correlation between delta 13CO2 and histologic lesions was observed, both in the antrum at before treatment (Spearman coef = 0.34; p = 0.007) and after therapy in both the gastric antrum (0.63; p < 0.001) and body (0.35; p = 0.005). A significant difference was observed when comparing mean delta 13CO2 in patients with different degrees of histologic gastritis, both before treatment (antrum: W Kruskal-Wallis = 6; p < 0.05) and after therapy (antrum: W = 17; p < 0.001; body: W = 10; p < 0.05). CONCLUSION: A high concordance was observed between the 13C-urea breath test and histology in the diagnosis of H. pylori infection. A correlation exists between breath test values and histologic lesions of the gastric mucosa.

[Helicobacter pylori infection and basal levels of serum gastrins in patients with duodenal ulcer and subjects with normal endoscopy]. / Infección por Helicobacter pylori y concentraciones basales de gastrina sérica en pacientes con úlcera duodenal y en individuos con endoscopia normal.

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.

[What factors influence healing of duodenal ulcer when Helicobacter pylori eradication treatment is used?]. / De qué factores depende la cicatrización ulcerosa duodenal cuando empleamos un tratamiento erradicador de Helicobacter pylori?

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.

[Helicobacter pylori, gastric ulcer and non-steroidal anti-inflammatory agents]. / Helicobacter pylori, úlcera gástrica y antiinflamatorios no esteroides.

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.

[Is there any association between Helicobacter pylori infection and peptic esophagitis?]. / Existe alguna relación entre la infección por Helicobacter pylori y la esofagitis péptica?

BACKGROUND: To describe the prevalence of Helicobacter pylori infection in patients with reflux esophagitis, and compare it with that in patients with normal endoscopy. METHODS: Fifty-five patients with endoscopic peptic esophagitis and 55 symptomatic patients with normal endoscopy were studied. Age and sex distribution were similar in both groups. At endoscopy biopsy specimens were taken from gastric antrum and body (H & E, Gram stain and culture). RESULTS: H. pylori was found in 74.5% (95% CI = 62-84%) of patients with reflux esophagitis, and in 76.4% (CI = 64-86%) of cases with normal endoscopy (a non-significant difference). In patients with esophagitis and H. pylori infection normal histologic antral mucosa was observed in 7.3% of cases (CI = 2.5-19.4%). In patients with normal endoscopy the corresponding figure was 4.8% (CI = 1.3-15.8%) (a non-significant difference). At gastric body from infected patients the percentages of patients with normal histologic mucosa was 29.3% (n = 12) and 23.8% (n = 10), in both groups respectively. CONCLUSIONS: The prevalence of H. pylori infection in patients with reflux esophagitis was 74.5%, and no difference was observed when comparing with infection rate in patients with normal endoscopy (76.4%). Therefore, a non-significant association was found between this esophageal disorder and H. pylori infection.

[Is measurement of basal levels of serum pepsinogen II useful in proving the eradication of Helicobacter pylori by treatment?]. / Es útil la determinación de las concentraciones basales de pepsinógeno II sserico para comprobar la erradicación de Helicobacter pylori con el tratamiento?

BACKGROUND: The aim of this study was to demonstrate the influence of the eradication of Helicobacter pylori on the basal concentrations of serum pepsinogen II in patients with duodenal ulcer. METHODS: Thirty-two patients with active duodenal ulcer were prospectively studied. A triple therapy was used consisting in bismuth, metronidazole and tetracycline. At the time of initial endoscopy and in those performed 5 months later on completion of the treatment, biopsies of the gastric mucosa were taken for histologic and microbiologic studies, and the basal concentrations of serum pepsinogen II are also determined. RESULTS: The eradication of H. pylori was accompanied by a significant pathologic improvement (p < 0.001) in both the antrum and the gastric body. On eradication of H. pylori, the basal pepsinogen II value (m +/- SD) decreased from 9.2 +/- 2.7 ng/ml to 6.4 +/- 1.7 ng/ml after treatment (p < 0.001). However, when eradication was not achieved, these values increased (11.8 ng/ml) with respect to the initial determination (9.3 ng/ml) (p < 0.05). The area under the ROC curve was 0.99 (SE 0.01) with a sensitivity of 92% and specificity of 100% with respect to the diagnosis of infection eradication (cut off point of the decrease of pepsinogen levels O). CONCLUSIONS: The eradication of Helicobacter pylori in patients with duodenal ulcer is associated with a significant decrease in the basal concentrations of serum pepsinogen II measured 5 months after completion of treatment. The verification of this decrease constitutes a useful, inexpensive non invasive method to prove the eradication of H. pylori with treatment.

[The importance of obtaining biopsies of the gastric body in the follow-up after eradicating treatment of Helicobacter pylori]. / Importancia de la obtencion de biopsias del cuerpo gástrico en el seguimiento después del tratamiento erradicador de Helicobacter pylori.

BACKGROUND: The aim of the present was to study the usefulness of performing biopsies of the gastric body in addition to those normally obtained of the antrum in the control of the eradication of Helicobacter pylori after treatment. METHODS: Sixty-four patients with duodenal ulcer and infection by H. pylori were prospectively studied. Two therapeutic schedules were used: amoxycillin/clavulanic associated with omeprazole (n = 32) and the classical triple therapy (bismuth, metronidazole, tetracycline) (n = 32). At the time of initial endoscopy and one month after completion of the treatment biopsies of the antrum and gastric body were taken for histologic (hematoxylin-eosin) and microbiologic (Gram and culture) studies. A patient was considered to have H. pylori infection when its presence was demonstrated by histologic or microbiologic methods in either of the localizations. RESULTS: The eradication of H. pylori was globally achieved in 64% (n = 41) of the cases. In the patients in whom eradication was not achieved (n = 23), H. pylori was detected only in the antrum in 70% (30% false negatives) while this was seen in the gastric body in 96% of the cases (p < 0.05). CONCLUSIONS: Carrying-out biopsies of only the antrum after eradicating H. pylori treatment is associated with a high percentage of false negative diagnosis of infection. Therefore, additional biopsies of the gastric body are recommended.

[Course of histological lesions of the gastric mucosa after eradication of H. pylori in patients with duodenal ulcer. Initial study and 6-month follow-up]. / Evolución de las lesiones histológicas de la mucosa gástrica tras la erradicación de H. pylori en pacientes con úlcera duodenal. Estudio inicial y a los 6 meses.

UNLABELLED: Helicobacter pylori is the major etiologic agent of chronic active gastritis, and it may be isolated from the gastric mucosa in a high proportion of patients with duodenal ulcer. AIM: To study, in duodenal ulcer patients, the histological changes associated with H. pylori infection in gastric antrum and body, and the improvement of such lesions after eradication, at an early stage and after 6 months. METHODS: 76 patients with duodenal ulcer disease were investigated prospectively. Biopsy specimens taken by endoscopy from the duodenal bulb, antrum, body and gastric fundus were analyzed by microbiological and histological methods. A patient was considered to be H. pylori-positive when microbiology or/and histology demonstrated colonization in any of the locations. An endoscopy with biopsy samples from the antrum and gastric body was performed 1 month after therapy and 4 months later. Different therapy regimens were used: amoxicillin/clavulanic plus omeprazole or ranitidine; triple therapy; and omeprazole or ranitidine alone. RESULTS: All patients were positive by microbiology. Eradication was reached as a whole in 47% (N = 36). In those patients, in gastric antrum, rates of chronic gastritis/chronic active gastritis previous to treatment and 2 and 6 months later were 100%/96%; 38%/23% and 16%/5.6% respectively. At gastric body they were: 54%/38%; 12%/12% and 12%/5.6% respectively. A favourable histologic evolution, globally and of the acute inflammatory component, was observed 1 month after therapy (p < 0.001). Six months later, there was further improvement which did not reach a statistically significant difference compared with the results obtained at the first month. No differences were observed when eradication failed. CONCLUSION: An improvement of antral and gastric body gastritis is associated with H. pylori eradication in duodenal ulcer patients. This successful evolution is observed immediately after eradication, and it is confirmed six months after the diagnosis.

[Decrease of basal levels of gastrin following H. pylori eradication]. / Descenso de los niveles basales de gastrina tras la erradicación de H. pylori.

UNLABELLED: Hypergastrinemia has long been considered an important factor in the pathophysiology of duodenal ulcer. Moreover, H. pylori infection has been reported in virtually all duodenal ulcers. AIM: To demonstrate the influence of H. pylori eradication on the basal levels of serum gastrin in patients with duodenal ulcer. METHODS: Seventy-six patients with endoscopically proved duodenal ulcer were prospectively studied. At endoscopy three biopsy samples each were taken from duodenal bulb, gastric antrum, corpus and fundus. Two samples from every location were submitted for conventional histological examination and the other for microbiological examination (Gram staining and culture). Endoscopy was repeated one month after the end of therapy, when endoscopy samples were again obtained from the gastric antrum and corpus. Basal levels of gastrin were measured both at initial and repeat endoscopies. Different therapeutic regimes were used: Amoxycillin/Clavulanate plus omeprazole or ranitidine, and triple therapy. RESULTS: H. pylori eradication was associated with a significant histological improvement (p < 0.001), both in antrum and corpus. In those patients with eradicated H. pylori the differences in basal gastrin levels both at diagnosis and after therapy were 45.4 +/- 11 pg/ml and 36.7 +/- 10 pg/ml, respectively; these differences were statistically significant (p < 0.001). When eradication was not achieved differences were not significant. The area under the ROC curve constructed from the different cutoff points for the gastrin decreases was 0.68 (EE 0.06). CONCLUSION: H. pylori eradication in patients with duodenal ulcer was associated with a significant decrease in basal levels of serum gastrin. Although the verification of such a decrease doesn't have an optimal relationship between sensitivity and specificity, it could be an aid as a useful non-invasive method to monitor the efficiency of therapy, both in H. pylori eradication and in the resolution of the associated gastritis. This procedure is also associated with early results and a low cost.

Solitary plasmacytoma of the rectum: report of a case treated by endoscopic polypectomy and radiotherapy.

Solitary extramedullary plasmacytoma (EMP) of the rectum is an exceedingly rare entity. We report the fourth case of solitary EMP of the rectum and the first one treated by endoscopic polypectomy and radiotherapy. The patient showed no signs of local recurrence or dissemination of the disease after a 12-month follow-up. This case report is presented along with a review of the literature dealing with solitary plasmacytomas of the rectum.