Efficacy of levofloxacin, amoxicillin and a proton pump inhibitor in the eradication of Helicobacter pylori in Brazilian patients with peptic ulcers.

OBJECTIVES: The eradication of Helicobacter (H.) pylori allows peptic ulcers in patients infected with the bacteria to be cured. Treatment with the classic triple regimen (proton pump inhibitor, amoxicillin and clarithromycin) has shown decreased efficacy due to increased bacterial resistance to clarithromycin. In our country, the eradication rate by intention to treat with this regimen is 83%. In Brazil, a commercially available regimen for bacterial eradication that uses levofloxacin and amoxicillin with lansoprazole is available; however, its efficacy is not known. Considering that such a treatment may be an alternative to the classic regimen, we aimed to verify its efficacy in H. pylori eradication. METHODS: Patients with peptic ulcer disease infected with H. pylori who had not received prior treatment were treated with the following regimen: 30 mg lansoprazole bid, 1,000 mg amoxicillin bid and 500 mg levofloxacin, once a day for 7 days. RESULTS: A total of 66 patients were evaluated. The patients' mean age was 52 years, and women comprised 55% of the sample. Duodenal ulcers were present in 50% of cases, and gastric ulcers were present in 30%. The eradication rate was 74% per protocol and 73% by intention to treat. Adverse effects were reported by 49 patients (74%) and were mild to moderate, with a prevalence of diarrhea complaints. CONCLUSIONS: Triple therapy comprising lansoprazole, amoxicillin and levofloxacin for 7 days for the eradication of H. pylori in Brazilian peptic ulcer patients showed a lower efficacy than that of the classic triple regimen.

Efficacy of levofloxacin, amoxicillin and a proton pump inhibitor in the eradication of Helicobacter pylori in Brazilian patients with peptic ulcers

OBJECTIVES: The eradication of Helicobacter (H.) pylori allows peptic ulcers in patients infected with the bacteria to be cured. Treatment with the classic triple regimen (proton pump inhibitor, amoxicillin and clarithromycin) has shown decreased efficacy due to increased bacterial resistance to clarithromycin. In our country, the eradication rate by intention to treat with this regimen is 83%. In Brazil, a commercially available regimen for bacterial eradication that uses levofloxacin and amoxicillin with lansoprazole is available; however, its efficacy is not known. Considering that such a treatment may be an alternative to the classic regimen, we aimed to verify its efficacy in H. pylori eradication. METHODS: Patients with peptic ulcer disease infected with H. pylori who had not received prior treatment were treated with the following regimen: 30 mg lansoprazole bid, 1,000 mg amoxicillin bid and 500 mg levofloxacin, once a day for 7 days. RESULTS: A total of 66 patients were evaluated. The patients’ mean age was 52 years, and women comprised 55% of the sample. Duodenal ulcers were present in 50% of cases, and gastric ulcers were present in 30%. The eradication rate was 74% per protocol and 73% by intention to treat. Adverse effects were reported by 49 patients (74%) and were mild to moderate, with a prevalence of diarrhea complaints. CONCLUSIONS: Triple therapy comprising lansoprazole, amoxicillin and levofloxacin for 7 days for the eradication of H. pylori in Brazilian peptic ulcer patients showed a lower efficacy than that of the classic triple regimen. .

Molecular markers of mucosa harboring gastric adenomas.

CONTEXT: Gastric adenoma is a precursor lesion of the adenocarcinoma. OBJECTIVE: To characterize gastric adenomas according to the mucin immunoexpression and to evaluate the immunoexpression of p53, p16ink4a, BCL-2, cyclin D, Ki-67, in the adenoma and in the gastric mucosa harboring adenoma. METHODS: Forty gastric specimens from 20 patients were classified as intestinal (MUC2-goblet cell mucin) or foveolar (MUC5AC-gastric-foveolar mucin) adenomas. Immunohistochemistry was performed using streptavidin-biotin-complex method. RESULTS: Twelve (60%) patients were men. The mean age was 67.9±12.9 years-old. Intestinal adenomas were detected in 13 (65%) patients and gastric type in 7 (35%). Low-grade dysplasia was present in 13 (65%) of the adenomas, high-grade in 3 (15%), and adenocarcinoma within the polyp in 4 (20%). Six (30%) patients had synchronous adenocarcinoma. p53 immunoexpression was observed in 6/20 (30%) of adenomas, and in 2/6 (33.3%) of synchronous tumors. There was an association between p53 immunoexpression and intestinal type of adenoma/tumor, P=0.04. There was no association between p16ink4a, Bcl-2, cyclin D and Ki-67 and adenoma clinicopathological characteristics. CONCLUSION: Immunohistochemistry may be useful to classify the adenomas subtypes and may define the pathway of adenoma to carcinoma sequence.

A possible role of IL-1RN gene polymorphism in the outcome of gastrointestinal diseases associated with H. pylori infection.

OBJECTIVE: To verify whether the variable number of tandem repeat (VNTR) polymorphism in the IL-1RN gene that encodes the interleukin (IL)-1 receptor antagonist (IL-1Ra) plays a role in the outcome of gastrointestinal diseases associated with Helicobacter pylori (H. pylori) infection. METHODS: Patients with normal endoscopy (n = 71), inflammation of the upper gastrointestinal tract only (n = 196), gastric ulcer (n = 28), duodenal ulcer (n = 76), and gastric cancer (n = 19) were studied. H. pylori infection was diagnosed by the urease test, histological examination, and polymerase chain reaction. The IL-1 receptor antagonist gene (IL-1RN intron 2 VNTR) was analyzed by polymerase chain reaction. Gastritis was scored according to the updated Sydney system of classification. RESULTS: H. pylori infection was an independent risk factor for mild (odds ratio [OR] = 5.53 [95% confidence interval [CI] = 2.63-11.64; P < 0.05]), moderate (OR = 83.93 [95% CI = 29.7-237.18; P < 0.05]) and marked (OR = 47.47 [95% CI = 5.39-418.05; P < 0.05]) gastritis. The carriage of IL-1RN*2/*2 had a significant protective effect of H. pylori infection (OR = 0.31 [95% CI = 0.17-0.57; P < 0.05]). H. pylori infection was identified as an independent risk of inflammation, duodenal ulcer, and gastric ulcer. The carriage of IL-1RN*2/*2 was an independent risk factor for gastric cancer (OR = 5.81 [95% CI = 1.06-31.98; P < 0.05]); nonetheless, the carriage of allele 2 (IL-1RN*2/*2 plus IL-1RN*L/*2) had an independent protective effect on duodenal ulcer (OR = 0.45 [95% CI = 0.22-0.91; P < 0.05]). CONCLUSIONS: Allele 2 of the VNTR IL-1RN polymorphism had a protective effect against duodenal ulcer and H. pylori infection; however, it increased the risk of gastric cancer.

Molecular markess of mucosa harboring gastric adenoass

Context Gastric adenoma is a precursor lesion of the adenocarcinoma. Objective To characterize gastric adenomas according to the mucin immunoexpression and to evaluate the immunoexpression of p53, p16ink4a, BCL-2, cyclin D, Ki-67, in the adenoma and in the gastric mucosa harboring adenoma. Methods Forty gastric specimens from 20 patients were classified as intestinal (MUC2 - goblet cell mucin) or foveolar (MUC5AC - gastric-foveolar mucin) adenomas. Immunohistochemistry was performed using streptavidin-biotin-complex method. Results Twelve (60%) patients were men. The mean age was 67.9 ± 12.9 years-old. Intestinal adenomas were detected in 13 (65%) patients and gastric type in 7 (35%). Low-grade dysplasia was present in 13 (65%) of the adenomas, high-grade in 3 (15%), and adenocarcinoma within the polyp in 4 (20%). Six (30%) patients had synchronous adenocarcinoma. p53 immunoexpression was observed in 6/20 (30%) of adenomas, and in 2/6 (33.3%) of synchronous tumors. There was an association between p53 immunoexpression and intestinal type of adenoma/tumor, P = 0.04. There was no association between p16ink4a, Bcl-2, cyclin D and Ki-67 and adenoma clinicopathological characteristics. Conclusion Immunohistochemistry may be useful to classify the adenomas subtypes and may define the pathway of adenoma to carcinoma sequence. .

Contexto Adenoma gástrico é uma lesão precursora do adenocarcinoma. Objetivo Melhor caracterizar os adenomas de acordo com a imunoexpressão de mucinas e avaliar a imunoexpressão de p53, p16ink4a, BCL-2, cyclin D, Ki-67, nos adenomas e na mucosa gástrica adjacente. Métodos Quarenta espécimes gástricos provenientes de 20 pacientes portadores de adenomas foram classificados como do tipo intestinal (MUC2 – mucina presente nas células caliciformes) ou gástrico (MUC5AC – mucinas de padrão foveolar). Realizou-se imunoistoquímica para p53, p16ink4a, BCL-2, cyclin D e Ki-67 pelo método do complexo da estreptavidina-biotina. Resultados Doze (60%) pacientes eram homens e a média de idade foi de 67,9 ± 12,9 anos. Os adenomas foram classificados como do tipo intestinal em 13 (65%) pacientes e do tipo gástrico em 7 (35%). Displasia (neoplasia intraepitelial) de baixo grau estava presente em 13 (65%), displasia de alto grau em 3 (15%), e adenocarcinoma no pólipo adenomatoso em 4 (20%) pacientes. Observou-se immunoexpressão do p53 em 6/20 (30%) adenomas, e em 2/6 (33,3%) dos tumores sincrônicos. Houve associação entre imunoexpressão do p53 e adenoma/tumor tipo intestinal, P = 0.04. Não houve associação entre imunoexpressão do p16ink4a, Bcl-2, ciclina D e Ki-67 e as características clinicopatológicas dos adenomas. Conclusão Imunoistoquímica pode ser utilizada para caracterizar os subtipos de adenoma e talvez indicar o caminho de carcinogênese. .

Application of real-time PCR stool assay for Helicobacter pylori detection and clarithromycin susceptibility testing in Brazilian children.

BACKGROUND: Helicobacter pylori ClariRes assay is a novel commercially available real-time PCR assay allowing H. pylori detection and clarithromycin susceptibility testing in either gastric biopsy or stool specimens. OBJECTIVE: The aim of this study was to validate the novel biprobe real-time assay in stool specimens from 217 dyspeptic children. METHODS: DNA from gastric biopsies and stool specimens were obtained and submitted to the biprobe real time assay for H. pylori detection and clarithromycin susceptibility testing. RESULTS: The sensitivity, specificity, and test accuracy were 69, 100 and 93.9% for the detection of H. pylori infection and 83.3, 100 and 95.6%, for detection of clarithromycin resistance. CONCLUSION: This assay proved to be appropriate for H. pylori clarithromycin susceptibility testing, particularly in children populations where a high prevalence of clarithromycin-resistant strains is suspected.

High prevalence of clarithromycin resistance and cagA, vacA, iceA2, and babA2 genotypes of Helicobacter pylori in Brazilian children.

We isolated 45 Helicobacter pylori strains from 217 child patients. Resistance to clarithromycin, metronidazole, amoxicillin, and tetracycline was detected in 27%, 13%, 4%, and 0% of strains, respectively. The A2143G mutation was the most prevalent (67%) among clarithromycin-resistant strains. In addition, strain genotyping revealed a significant association between gastritis severity and the simultaneous presence of cagA, vacA s1m1, iceA2, and babA2 genes.

Preoperative gastric acid secretion and the risk to develop Barrett's esophagus after esophagectomy for chagasic achalasia.

INTRODUCTION: The aim of this study was to determine the contribution of preoperative gastric secretory and hormonal response, to the appearance of Barrett's esophagus in the esophageal stump following subtotal esophagectomy. METHODS: Thirty-eight end-stage chagasic achalasia patients submitted to esophagectomy and cervical gastric pull-up were followed prospectively for a mean of 13.6 +/- 9.2 years. Gastric acid secretion, pepsinogen, and gastrin were measured preoperatively in 14 patients who have developed Barrett's esophagus (Group I), and the results were compared to 24 patients who did not develop Barrett's esophagus (Group II). RESULTS: In the group (I), the mean basal and stimulated preoperative gastric acid secretion was significantly higher than in the group II (basal: 1.52 vs. 1.01, p = 0.04; stimulated: 20.83 vs. 12.60, p = 0.01). Basal and stimulated preoperative pepsinogen were also increased at the Group I compared to Group II (Basal = 139.3 vs. 101.7, p = 0.02; stimulated = 186.0 vs. 156.5, p = 0.07. There was no difference in preoperative gastrin between the two groups. Gastritis was present during endoscopy in 57.1% of the Group I, while it was detected in 16.6% of the Group II, p = 0.014. CONCLUSIONS: Barrett's esophagus in the esophageal stump was associated to high preoperative levels of gastric acid secretion, serum pepsinogen, and also gastritis in the transposed stomach.

Mucin pattern reflects the origin of the adenocarcinoma in Barrett's esophagus: a retrospective clinical and laboratorial study.

BACKGROUND: Mucin immunoexpression in adenocarcinoma arising in Barrett's esophagus (BE) may indicate the carcinogenesis pathway. The aim of this study was to evaluate resected specimens of adenocarcinoma in BE for the pattern of mucins and to correlate to the histologic classification. METHODS: Specimens were retrospectively collected from thirteen patients who underwent esophageal resection due to adenocarcinoma in BE. Sections were scored for the grade of intestinal metaplasia. The tissues were examined by immunohistochemistry for MUC2 and MUC5AC antibodies. RESULTS: Eleven patients were men. The mean age was 61 years old (varied from 40 to 75 years old). The tumor size had a mean of 4.7 +/- 2.3 cm, and the extension of BE had a mean of 7.7 +/- 1.5 cm. Specialized epithelium with intestinal metaplasia was present in all adjacent mucosas. Immunohistochemistry for MUC2 showed immunoreactivity in goblet cells, while MUC5AC was extensively expressed in the columnar gastric cells, localizing to the surface epithelium and extending to a variable degree into the glandular structures in BE. Tumors were classified according to the mucins in gastric type in 7/13 (MUC5AC positive) and intestinal type in 4/13 (MUC2 positive). Two tumors did not express MUC2 or MUC5AC proteins. The pattern of mucin predominantly expressed in the adjacent epithelium was associated to the mucin expression profile in the tumors, p = 0.047. CONCLUSION: Barrett's esophagus adenocarcinoma shows either gastric or intestinal type pattern of mucin expression. The two types of tumors developed in Barrett's esophagus may reflect the original cell type involved in the malignant transformation.

Prognostic significance of occult lymph node micrometastasis in gastric cancer: a histochemical and immunohistochemical study based on 1997 UICC TNM and 1998 JGCA classifications / Significância prognóstica das micrometástases ocultas em linfonodos no câncer gástrico: estudo histoquímico e imunoistoquímico baseado nas classificações UICC TNM de 1997 e JCGCA de 1998

BACKGROUND: Micrometastasis is a single or a cluster of malignant cells inside the lymph node that are not detected by routine histopathological sections. Micrometastasis is related to poorer prognosis in many gastric cancer studies the real significance of these cells is still controversial. AIM: To evaluate if lymph node micrometastasis is a significant independent prognostic factor and important risk factor for recurrence in gastric cancer. METHODS: A total of 1290 lymph nodes from 28 patients with gastric cancer, since 1998 until 2003, treated by radical resection (D2 and modified D3 lymphadenectomies) were studied. Three sections per lymph node were stained by Hematoxilin-Eosin, histochemical (AB-PAS) and immunohistochemical (AE1-AE3) techniques. Kaplan-Meier's survival curves and Log-rank/Cox tests were used in order to compares lymph node micrometastasis positivity, depth (pT) and location of tumor in gastric wall, histologic type, lymphatic, vascular and perineural invasion, lymph node status (pN) and stage. RESULTS: There were worse prognosis and recurrence in patients with positive lymph node micrometastasis related to vascular and perineural invasions, advanced lymph node status and advanced stages. CONCLUSION: Lymph node micrometastasis seems to be a significant independent prognostic factor and important risk factor for recurrence in gastric cancer, in a context of radical D2 lymphadenectomy.

RACIONAL: Micrometástases são um conjunto de células malignas dentro de linfonodo que não são detectadas pelos exames histopatológicos de rotina. Elas são relacionadas a prognóstico mais pobre em muitos estudos sobre câncer gástrico, mas a real significância dessas células permanece controversa. OBJETIVO: Avaliar se micrometástase linfonodal é um fator independente de prognóstico e importante para detectar a recurrência do câncer gástrico. MÉTODOS: Um total de 1290 lifonodos de 28 pacientes com câncer gástrico, de 1998 a 2003, tratados com operações radicais (D2 e D3 modificadas) foram revistos. Três secções por linfonodo foram corados por Hematoxilina-Eosina, histoquímica (AB-PAS) e imunoistoquímica (AE1-AE3). Curvas de sobrevida de Kaplan-Meyer e teste de Log-rank/Cox foram usados para comparar positividade das imcrometástases, profundidade (pT) e localização tumoral na parede gástrica, tipo histológico, invasão linfática, vascular e perineural, estado linfonodal (pN) e estádio onde se encontra a doença. RESULTADOS: Houve pior prognóstico e recurrência nos pacientes com linfonodos com micrometástases relacionadas às invasões vascular e perineural , avançado estado de invasão linfática e estadiamento mais elevado. CONCLUSÃO: Micrometástase parece ser importante e independente fator de risco para recurrência no câncer gástrico no contexto das linfadenectomias radicais D2.

Secondary lymphangiectasia of the small bowel: utility of double balloon enteroscopy for diagnosis and management.

Sporadic lymphangiectasias are commonly found throughout the small bowel and are considered to be normal. Not uncommonly, lymphangiectasias are pathologic and can lead to mid-gastrointestinal bleeding, abdominal pain and protein-losing enteropathy. Pathologic lymphangiectasias of the small bowel include primary lymphangiectasia, secondary lymphangiectasia and lymphaticovenous malformations. In this report we present three different cases of small bowel lymphangiectasia detected by double balloon enteroscopy. The patients were diagnosed with South American blastomycosis, tuberculosis and primary small bowel lymphangioma.

Trends in tumor location in gastric carcinoma over a 28-year period.

BACKGROUND/AIMS: Gastric cancer is still a leading cause of cancer death in the world and in Brazil. Historically a majority of gastric tumors were located in the distal third of the stomach. However, several studies have shown a shift in tumor location towards the proximal third. METHODOLOGY: Japanese rules for gastric cancer treatment were followed. All patients that were submitted to surgical resection for gastric cancer between 1971 and 1998 were included. These patients were divided into 3 time periods and classifled according to tumor location. RESULTS: 1021 patients underwent gastric resection for adenocarcinoma. The distal third of the stomach (53.7%) was the most common site. The proportion of tumors located in the proximal and middle thirds of the stomach increased significantly from 8.1% to 15% and 16.2 to 29.8% respectively at the last decade. CONCLUSIONS: The findings of this study suggest an increase in the incidence of tumors to the proximal third of the stomach. However the high incidence of these tumors reported in literature is not confirmed.

What to expect in the excluded stomach mucosa after vertical banded Roux-en-Y gastric bypass for morbid obesity.

Mucosal alterations after vertical banded Roux-en-Y gastric bypass have not been clearly evaluated. The aim of this paper was to analyze the histological findings and the presence of Helicobacter pylori in the excluded stomach. Forty consecutive patients who underwent Roux-en-Y gastric bypass longer than 36 months were selected for double-balloon enteroscopy. The excluded stomach was reached in 35/40 patients (88%). Morphological alterations were analyzed through hematoxilin and eosin and the presence of H. pylori was confirmed with Giemsa staining. Thirty patients (86%) were female, and the mean age was 43 years old. The mean postoperative time was 78 months (36-110 months). Histologically, all patients had chronic gastritis in the bypassed stomach, with pangastritis in 33/35 (94%). Five cases (5/35, 14%) presented atrophy and four of them also had intestinal metaplasia. Helicobacter pylori was detected in 7/35 (20%) of the excluded stomach and in 12/35 (34%) of the functional pouch. All patients positive for H. pylori in the excluded stomach were also positive in the functional pouch, p = 0.0005. Helicobacter pylori is still present in the excluded stomach after Roux-en-Y gastric bypass and might be considered for treatment. Histological findings indicated high prevalence of atrophy and intestinal metaplasia in this selected population.

Prognostic value of immunohistochemistry in gastric neuroendocrine (carcinoid) tumors.

UNLABELLED: Three subtypes of enterochromaffin-like cell tumors (carcinoids) have been described: type I, associated with chronic atrophic gastritis; type II, multiple endocrine neoplasia 1 and Zollinger-Ellison syndrome; and type III, sporadic tumors. OBJECTIVES: (i) To investigate the immunoexpression of Ki-67, p53 and Bcl-2 proteins in enterochromaffin-like cell (carcinoid) tumors and (ii) to evaluate the prognostic value of these markers. METHODS: Fifty-four samples from 21 patients with gastric carcinoid tumors were sectioned and immunostained using avidin-biotin peroxidase method. RESULTS: The mean age was 62.2+/-11.4 years (36-83 years-old) and 13 (61.9%) were women. Type I lesions were detected in 61.9% and type III in 38.1%. Tumors were single in 10 (47.6%) and were multiple and/or multicentric in 11 (52.4%). Nuclear p53 immunoreactivity was observed in 6/21 patients (28.6%), and all of them were type III tumors (6/8), compared with no p53 expression in type I (0/13), P=0.0002. p53 expression was also associated with high degree of cell proliferation (Ki-67-positive nuclear cells), P=0.00001. Bcl-2 expression was either unreactive or weakly positive in all tumor lesions. The mean follow-up period was 50.4 months (SD=45.2), varying from 6 to 144 months. Overall survival time of patients with positive p53 expression and high proliferative rate was significantly lower than that of negative patients (14.4 vs 123 months, P=0.0007). CONCLUSIONS: (i) p53 immunoexpression associated with high proliferative rate was useful to distinguish between type I and type III gastric carcinoid tumors and (ii) these markers were able to predict a shorter survival.

Helicobacter pylori cag pathogenicity island genes: clinical relevance for peptic ulcer disease development in Brazil.

The purpose of this study was to verify whether the presence of any of the Helicobacter pylori cagPAI genes or segments--cagA, cagA promoter, cagE, cagM, tnpB, tnpA, cagT and the left end of the cag II (LEC) region--would be a useful marker for the risk of peptic ulcer disease development. H. pylori DNA extracted from positive urease tests of 150 peptic ulcer patients and 65 dyspeptic controls was analysed by PCR. Duodenal ulcers were present in 110, gastric ulcers in 23 and both gastric and duodenal ulcers in 17 patients. A significant association (P <0.001) was found between a conserved cagPAI and peptic ulcer disease (34 %). The positivity of the cagA gene varied according to the region of the gene that was amplified. The region near to the promoter was present in almost all of the H. pylori isolates (97.2 %). The segment from nt 1764 to 2083 and the extreme right end were frequently deleted in the isolates from the controls (P <0.01). The positivity of the promoter region of cagA and cagT, cagE, cagM and LEC showed a significant difference between the isolates from peptic ulcer patients and from the controls (P <0.01). Patients usually had moderate gastritis; however, the intensity of the active inflammation was higher in the peptic ulcer group (P <0.001). cagT, cagM, LEC and the right end terminus of the cagA-positive H. pylori isolates were associated with a 27-fold, 8-fold, 4-fold and 4-fold risk of peptic ulcer disease, respectively, and may be useful markers to identify individuals at higher risk of peptic ulcer disease development in Brazil.

Lugol staining and histological evaluation of esophageal mucosa in achalasia.

BACKGROUND/AIMS: Esophageal cancer in achalasia is often diagnosed in the advanced stage, which makes for a poor prognosis. Therefore, the aim of this study was to evaluate the macroscopic and histological features of the esophageal mucosa in order to improve the early detection of cancer. METHODOLOGY: We studied the macroscopic features of esophageal mucosa using Lugol's solution and compared them with histological analysis of the entire mucosa in 20 esophagectomy specimens resected for achalasia. Intraepithelial neoplasia, when detected, was selected for DNA ploidy analysis through static cytometry. RESULTS: Macroscopically, the mucosa showed opacification and/or diffuse irregularities in 19 specimens. Advanced squamous cell carcinoma was diagnosed in 2 cases. Using Lugol, the esophageal mucosa acquired irregular brownish color. Clear unstained areas were circumscribed in 5 esophagi. They were macroscopically defined as ulcer, neoplasia (2 cases) and mucosal irregularities (2 cases). The histological analysis showed ulcer, squamous cell carcinoma (2 cases), Barrett's esophagus and esophagitis, respectively. The histological study of the stained mucosa revealed minute foci of DNA aneuploid intraepithelial neoplasia in 4 cases. CONCLUSIONS: Macroscopic examination using Lugol failed to identify minute foci of early carcinoma. The stained mucosa does not exclude the esophageal cancer risk in achalasia.

No correlation of babA2 with vacA and cagA genotypes of Helicobacter pylori and grading of gastritis from peptic ulcer disease patients in Brazil.

BACKGROUND: The babA2 gene, which encodes a blood-group antigen-binding adhesin that mediates attachment of Helicobacter pylori to human Lewis(b) antigens on gastric epithelial cells, has been associated with a higher risk of peptic ulcer and gastric cancer. The purpose of this study was to ascertain the frequency of babA2 genotype in H. pylori strains of patients with peptic ulcer and to correlate with other virulence factors. MATERIALS AND METHODS: vacA, cagA, and babA2 genotypes of H. pylori were determined by using polymerase chain reaction (PCR). DNA was extracted from positive urease test gastric samples of 150 patients with peptic ulcer. Antrum and corpus biopsies were taken for histologic examination according to the updated Sydney system classification. RESULTS: babA2 genotype was present in 104 (69.3%) and cagA in 113 (75.3%) gastric samples. No significant correlation was observed between babA2 and vacAs1 genotype or between babA2 and cagA status. The correlation of vacAs1 genotype with positive cagA was statistically significant ( p < .001). The babA2-positive strain was more frequently found from the gastric samples of men, than of women (p = .01). Strains harboring cagA, vacAs1, and babA2 genotypes had no association to the grading of gastritis, presence of glandular atrophy, or intestinal metaplasia. The simultaneous presence of cagA, vacAs1, and babA2 was found in 32.6% of the H. pylori strains. CONCLUSIONS: babA2 genotype is frequently found in H. pylori strains from peptic ulcer disease in Brazil, although it has no significant correlation to the worsening of the gastritis and to other virulence markers such as vacAs1 and cagA.

Origin of adenocarcinoma in Barrett's esophagus: p53 and Ki67 expression and histopathologic background.

UNLABELLED: Barrett's esophagus is the substitution of squamous epithelium of the distal esophagus by columnar epithelium. Intestinal metaplasia in Barrett's esophagus is considered to be the main risk factor for the development of adenocarcinoma. Diffuse adenocarcinoma and Barrett's esophagus without intestinal metaplasia are rare, and reports on the subject are scarce. PURPOSE AND METHOD: To estimate the prevalence of adenocarcinoma in 297 patients with Barrett's esophagus, during the period of 1990 to 2002, and in 13 patients undergoing surgery, to conduct detailed macroscopic and microscopic analysis, with performance of immunohistochemical tests for p53 and Ki67, correlating the type of tumor with its adjacent epithelium. RESULTS: In our patients with Barrett's esophagus, there was a prevalence of 5.7% of adenocarcinoma. The tumors developed only when the Barrett's esophagus segment was long (>3.0 cm). Tumors were located close to the squamous-columnar junction. The histological study revealed 2 patients (15.4%) with Barrett's esophagus adjacent to a tumor with gastric metaplasia without the presence of intestinal metaplasia. Tumors were classified according to Nakamura's classification (23% differentiated pattern, and 77% undifferentiated pattern) and to Lauren's classification (61% intestinal and 39% diffuse). The difference is due to the migration of microtubular and foveolar tumors of undifferentiated (gastric) pattern in Nakamuras classification to the Lauren's intestinal type. The immunohistochemical test for Ki67 was strongly positive in all the patients, thus evidencing intense cell proliferation in both the columnar epithelium and tumor. Expression of p53 was negative in 67% of the adjacent columnar epithelia and 42% of the tumors, without any correlation between the tissue types. CONCLUSION: Adenocarcinoma develops from mixed columnar epithelium, either intestinal or gastric, showing both the gastric and the intestinal patterns; thus, tumors can also grow in columnar epithelium without intestinal metaplasia. Barrett's esophagus should be followed up for the possibility of progression to malignancy, especially when the segment is longer than 3 cm.

Origin of adenocarcinoma in Barrett's esophagus: P53 and Ki67 expression and histopathologic background

O esôfago de Barrett é definido como a substituição do epitélio escamoso do esôfago distal por epitélio colunar. A metaplasia intestinal no esôfago de Barrett é considerada por muitos como o principal fator de risco para o desenvolvimento do adenocarcinoma. Embora já descrito, o adenocarcinoma do tipo difuso e o esôfago de Barrett sem metaplasia intestinal, são raros e pouco estudados. OBJETIVO E MÉTODO: O presente estudo objetivou o cálculo da prevalência do adenocarcinoma no esôfago de Barrett, assim como a análise macroscópica e microscópica detalhada de treze pacientes operados no período de 1990 a 2002, com realização de estudo imunohistoquímico do p53 e Ki67, correlacionando o tipo de tumor com o epitélio adjacente a este. RESULTADOS: Obtivemos uma prevalência de 5,7% de adenocarcinoma em pacientes internados para tratamento cirúrgico de esôfago de Barrett . Encontraram-se tumores relativamente grandes, com média de 4,67 ± 2,28 cm, e sempre em esôfago de Barrett longo, com média de 7,71 ± 1,5 cm. Observou-se tendência de os tumores se localizarem próximos à transição escamo-colunar. O estudo histológico mostrou dois pacientes (15,4%) que apresentavam esôfago de Barrett adjacente ao tumor do tipo juncional sem presença de metaplasia intestinal. Classificaram-se os tumores segundo a classificação japonesa de Nakamura (23% de padrão diferenciado ou intestinal e 77% de padrão indiferenciado ou gástico) e pela classificação de Laurén (61% intestinais e 39% difusos). A diferença decorre da migração dos tumores microtubulares e foveolares do padrão gástrico para o tipo intestinal de Laurén. O estudo do Ki67 foi fortemente positivo em todos os pacientes, mostrando o alto índice de proliferação celular no epitélio colunar e no tumor. O p53 mostrou-se negativo em 66,7% dos pacientes no epitélio colunar e 41,7% no tumor, não mostrando correlação entre os dois materiais. CONCLUSAO: O adenocarcinoma se desenvolve sobre o esôfago de Barrett a partir do epitélio colunar misto, intestinal, bem como do juncional, apresentando padrão tanto gástrico como intestinal; portanto tumores podem se desenvolver em epitélio colunar sem metaplasia intestinal o qual também deve ser seguido, principalmente quando for extenso.