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Pelayo Correa

Publications and source records attributed to Pelayo Correa.

49 records · Page 3Linked to original sources
PubMed2003

Increased reflux symptoms after calcium carbonate supplementation and successful anti-Helicobacter pylori treatment.

We used data from a randomized placebo-controlled clinical trial to examine the relationship between Helicobacter pylori and reflux symptoms in nonulcer dyspepsia patients randomly assigned anti-Helicobacter pylori triple therapy alone, calcium carbonate alone, or in combination with triple therapy, tetracycline, or placebo. We compared risk differences for posttreatment Helicobacter pylori status and increased reflux symptoms from crude, multivariable and stratified multivariable analyses. In crude analyses, 54% of subjects without Helicobacter pylori after-treatment reported an increase in reflux compared to 41% of those with persistent infection (risk difference = 13%; P = 0.07). Only subjects with multifocal atrophic gastritis assigned to calcium carbonate reported an increase in reflux symptoms more frequently when Helicobacter pylori was absent versus when it persisted (risk difference = 52%; P = 0.0001). Therefore, the interaction of calcium carbonate use, chronic multifocal atrophic gastritis, and the absence of Helicobacter pylori may increase reflux symptoms.

Adult↗
PubMed2003

MUC1 polymorphism confers increased risk for intestinal metaplasia in a Colombian population with chronic gastritis.

Gastric cancer (GC) stands as the second most common cause of cancer death for males worldwide, and intestinal metaplasia (IM) is a lesion that precedes GC development. In previous works it was shown that polymorphisms of MUC1 gene are associated with increased risk for GC and IM. The aim of the present study was to evaluate MUC1 gene polymorphism in patients with chronic gastritis from Colombia. A Portuguese population of patients with chronic gastritis was used for comparative purposes. A total of 67 Colombian cases and 52 Portuguese cases were analysed by restriction analysis and Southern blotting. MUC1 allele frequencies were significantly different between the two populations, with an overall prevalence of smaller alleles in Colombian samples. Colombian cases showed a lower prevalence of individuals homozygous for small MUC1 mucins in cases without IM (62.5%) when compared with cases with IM (86.0%). The same trend, although not statistically significant, is observed in the Portuguese population. In conclusion, our study shows that Colombian patients with chronic gastritis have a significantly higher prevalence of small MUC1 alleles than the Portuguese population. Our study also shows that small MUC1 genotypes are associated with increased risk for IM development in Colombian patients.

Chronic Disease↗
PubMed2003

Histopathology of gastritis in Helicobacter pylori-infected children from populations at high and low gastric cancer risk.

Infection with Helicobacter pylori has been recognized as a cause of gastric carcinoma. Although the neoplasia is always detected in adults, the infection starts in childhood. It has been reported that early age at first infection is a determinant of gastric cancer risk. In this study, we examined the histopathology of the gastric mucosa in infected children from a population at high risk for gastric cancer (Pasto, Colombia) and compared it with that of a lower-risk population (New Orleans, LA). Gastric biopsies obtained from antrum and corpus were stained with hematoxylin and eosin and Steiner's silver method. Immunohistochemical stains were used to identify B lymphocytes (CD20), T lymphocytes (CD3 and CD8), macrophages (CD68), and polymorphonuclear neutrophil myeloperoxidase. Morphometric techniques were used to evaluate the immunohistochemical stains. In both populations, the inflammatory lesions were seen predominantly in the antrum. Compared with children from the lower-risk populations, children from the higher-risk population exhibited more severe polymorphonuclear neutrophil infiltration, stromal and intraepithelial lymphocyte infiltration, mucus depletion, and H. pylori colonization density. Regenerative activity was significantly more marked in the lower-risk population. Morphometric analysis of immunohistochemical stains showed increased representation of T lymphocytes and macrophages in the higher-risk population. Most T lymphocytes stained positive for CD8, a marker of suppressor/cytotoxic cells. B lymphocytes were relatively more abundant in the lower-risk population. The possibility that the aforementioned characteristics of H. pylori infection in children are related to cancer risk in adults is discussed.

B-Lymphocytes↗
PubMed2003

Impact of Helicobacter pylori infection on growth of children: a prospective cohort study.

OBJECTIVE: The aim of this study was to prospectively follow a cohort of children without Helicobacter pylori infection and to compare growth velocity in the children who become infected during follow-up with that of children who remained infection-free. METHODS: Three hundred forty-seven children in general good health, aged 12 to 60 months, who tested negative for H. pylori by the 13C-urea breath test, from three daycare centers in a lower-middle class borough of Cali, Colombia, were monitored for 2.5 years. Anthropometric measurements were performed every 2 months and breath tests every 4 months. Linear mixed models were used to analyze growth velocity in relation to onset of H. pylori infection. RESULTS: One hundred five (30.3%) children who were uninfected at the start of the study became infected during follow-up. Growth velocity in infected children was reduced by 0.042 +/- 0.014 cm/mo (P = 0.003) (approximately 0.5 cm/yr) after adjusting for age. The rate of deceleration in growth velocity was relatively constant over time. CONCLUSIONS: Among these lower-middle class children aged 12 to 60 months from a population with high prevalence of H. pylori infection, a new and sustained infection was followed by significant growth retardation.

Body Height↗
PubMed2003

Comparison of genotyping of Helicobacter pylori cagA and vacA virulence genes from gastric biopsies and stool specimens.

BACKGROUND: We compared results of genotyping of Helicobacter pylori cagA and vacA virulence genes in DNA from gastric biopsies, both paraffin-embedded and frozen, and from stool samples, in order to evaluate the comparative sensitivity of the stool assay. METHODS: Genomic DNA from paraffin-embedded biopsies, unfixed frozen biopsies, and stool samples of the same 20 patients was amplified for the cagA gene, an empty site (which provides a positive signal for cagA negative strains) and for the s and m alleles of the vacA gene. Composite genotypes were determined by combining data from analysis of all three materials. RESULTS: Analysis of none of the materials taken singly showed all of the genotypes revealed by all three materials taken together, probably because of sampling error. Analysis of paraffin biopsies revealed 83.5%, that of frozen biopsies revealed 74.7% and that of stools revealed 75.9% of the genotypes. There was no significant difference in the percentage of the H. pylori genotypes identified from the three materials. Analysis of combinations of frozen biopsies and stools revealed 89.9% of the composite genotypes, and that of paraffin biopsies and stools revealed 96.2% of the composite genotypes. Evidence of multiple genotypes was found in 10 of 20 (50%) of the cases. CONCLUSIONS: Any one of the investigated biological materials can be used for detection of cagA and vacA genes, but no single assay provided a complete genotype. The use of a combination of two materials may generate a more accurate representation of H. pylori genotypes in each individual.

Adult↗
PubMed2003

[Microsatellite instability and loss of heterozygosity in neoplastic and preneoplastic gastric lesions].

BACKGROUND: Gastric cancer is the leading cause of cancer deaths in the general population in Chile, with mortality rates as high as 33.7 per 105 in males in the IX region. A chain of genetic and morphological events precedes the intestinal type of gastric carcinoma. One of them is the called multifocal atrophic gastritis often associated with intestinal metaplasia. AIM: To study the frequency of microsatellite instability (MSI) and loss of heterocigozity (LOH) in neoplastic and preneoplastic lesions of gastric carcinoma, especially intestinal metaplasia. MATERIAL AND METHODS: Ninety four gastric cancer biopsies were studied using laser capture microdissection, to obtain well defined cell populations from paraffin-embedded tissues: lymphocytes (control DNA), intestinal metaplasia and gastric cancer areas. Primer flanking microsatellite 15 highly polymorphic regions were used to study MSI and LOH. Radioactive PCR products were electrophoresed and exposed for autoradiography. RESULTS: LOH was observed in 83% of gastric carcinomas and in 54% areas containing intestinal metaplasia. The most commonly altered regions were the CA repeat associated with the p53 gene and the 3p21 region. High grade MSI was observed in 11.7% of gastric cancer preparations and 17% of intestinal metaplasia associated to cancer with MSI-H phenotype. CONCLUSIONS: MSI and LOH were frequently observed in intestinal metaplasia glands in patients with gastric carcinoma. The frequency of MSI-H phenotype in gastric patients was slightly lower than the one described in sporadic colorectal cancer not associated to HNPCC. The high incidence of genetic lesions in intestinal metaplasia area, support the idea that intestinal metaplasia is a genetically highly unstable cell population.

Adenocarcinoma↗
PubMed2002

Delayed rise in incidence of gastric cancer in females results in unique sex ratio (M/F) pattern: etiologic hypothesis.

BACKGROUND: The age-standardized and cumulative incidence rates of gastric cancer (GCA) are twice as high in males as in females. METHODS: Based on age-group-specific (5-year age groups) annual incidence data of GCA among males and females published by 18 cancer registries worldwide, and on a consecutive series of 938 GCAs from Finland, we explored how the male predominance of GCA has changed over the decades and how this male predominance may possibly vary worldwide between populations with high and low gastric cancer incidence. RESULTS: It appeared that the age-group-specific male-to-female (M/F) ratio of the annual GCA incidence is not constant but increases with age, reaches a peak at age around 60, and decreases thereafter. This special form of the M/F curve is not seen in other gastrointestinal (GI) cancer types (colon, rectum, pancreas). This "low-high-low" form of the M/F curve is related to a 10- to 15-year delay in the appearance and onset of GCA of the intestinal type in females compared with males. The age-group-specific M/F ratio rises as the GCA of the intestinal subtype prevails in males and is rare in females before age 60 and starts to decrease after age 60 as the GCA of the intestinal subtype begins to be common also in females. This special form of the M/F curve is globally consistent and similar in countries or populations of high and low GCA incidence. The data from the Finnish Cancer Registry indicate that the age group-specific M/F curve of the annual GCA incidence has, in addition, remained unchanged over the decades (from the 1950s) in spite of a decrease in the annual GCA incidence of more than 70%. In order to examine the role of gastritis-related diseases as a cause of the sex difference in GCA, 1700 consecutive endoscopied outpatients were studied in Finland. In this series, the age-group-specific prevalences of Helicobacter pylori gastritis, atrophic gastritis, or intestinal metaplasia were proportionally as common in males as in females in all age groups except for the youngest one (20-49 years), in which H. pylori nonatrophic gastritis was slightly more common in males than in females. CONCLUSION: The male predominance of GCA is a global phenomenon, and is similar in populations with high and low GCA incidence, and this predominance is related to a 10- to 15-year delay in the appearance and onset of GCA of the intestinal subtype in females compared with males. It is suggested that sex hormones (estrogens) protect women against GCA, and that GCA begins to be as prevalent in females as in males only after the menopausal age. Another possibility is that a later acquisition of H. pylori gastritis in females than in males causes the relative delay in the appearance and onset of new GCA cases in females compared with males.

Adult↗
PubMed2002

Gastric neoplasia.

This review summarizes the significant recent advances in our understanding of the clinical, epidemiologic, and pathologic aspects of gastric adenocarcinoma, gastrointestinal stromal tumors (GISTs), and mucosa-associated lymphoid tissue (MALT) lymphoma. Most of the advances in distal gastric adenocarcinoma are in its etiology and pathogenesis. The modulation of the inflammatory response to Helicobacter pylori organisms has been determined to be at the center of the precancerous process. These advances in the understanding of the pathogenesis of H. pylori-related carcinogenesis are relevant to the design of prevention strategies in high-risk populations. New markers of GISTs have focused on the cell of origin and have made possible the development and monitoring of new drugs that are effective even in metastatic tumors. MALT lymphomas have been causally associated with H. pylori infection. Molecular markers are useful to distinguish tumors that respond to H. pylori eradication from those requiring classic chemotherapy.

Adenocarcinoma↗
PubMed2002

Food groups and risk of lung cancer in Uruguay.

The objective of the present study was to estimate the risk of lung cancer associated with several food groups. The study included 1,032 cases with lung cancer and 1,030 hospitalized controls, admitted to the Cancer Institute of Montevideo in the period 1988-2000. Total meat intake was directly associated with lung cancer (OR 1.6, 95% CI 1.2-2.2) whereas total vegetables and total fruits were inversely associated with lung cancer risk. When vegetable and fruit intakes were further adjusted for smoking status, years since quit, cigarettes/day and age at start, the protective effect was attenuated for plant foods (total vegetables and fruits). Also, the effect of vegetables and fruits was closest to the null among smokers of black tobacco and hand-rolled cigarettes. Thus, the present study is consistent in showing moderate associations with major food groups (meat, vegetables and fruits), and strongly suggests that the stringent control of tobacco smoking is mandatory in studies dealing with diet and lung cancer risk.

Adult↗
PubMed2002

Alcohol intake and risk of adenocarcinoma of the lung. A case-control study in Uruguay.

In order to examine in detail the relationship between alcohol drinking and risk of adenocarcinoma of the lung, a case-control study involving 160 cases of this cell type and 520 hospitalized controls was conducted in Uruguay in the time period January 1998-July 2000. Total alcohol intake was not associated with risk of adenocarcinoma of the lung (OR 1.2, 95% CI 0.6-2.1). Also beer drinking was not associated with risk of carcinoma (OR 0.6, 95% CI 0.3-1.6). On the other hand, wine drinking displayed a marginally significant reduction in risk (OR 0.4, 95% CI 0.2-1.1). On the contrary, hard liquor intake was associated with a 40% increase in risk of adenocarcinoma of the lung. These findings suggest that wine drinking has a protective effect in adenocarcinoma of the lung, whereas hard liquor increases moderately the risk of this cell type of lung cancer.

Adenocarcinoma↗
PubMed2002

Virulence-associated genotypes of Helicobacter pylori: do they explain the African enigma?

OBJECTIVES: The aim of this study was to compare the distribution of virulence-associated genotypes of Helicobacter pylori in two Colombian populations with contrasting gastric cancer risk but with similar H. pylori infection prevalence. METHODS: Gastric biopsies were taken from 241 subjects from the high gastric cancer risk area of Pasto and from 93 subjects from the low risk area of Tumaco. Four gastric biopsies from each patient were fixed in 10% buffered formalin for histopathologic analysis, and one was frozen immediately in liquid nitrogen and used for genotyping. CagA and vacA genotypes were determined by multiplex polymerase chain reaction and reverse hybridization on a line probe assay. RESULTS: In patients from the population with high risk for gastric cancer, statistically significant higher relative frequencies of cagA positive and vacA s1 and ml genotypes were found as compared to the population from the low risk area. CONCLUSIONS: Although H. pylori infection has been recognized as a cause of gastric cancer in humans, some large populations with high prevalence of infection have low gastric cancer rates. This so-called "African enigma" so far remains unexplained. Our findings suggest that virulence-associated genes of H. pylori may partially explain the African enigma. Other factors, including human genetic polymorphisms and diet, are also suspected to play a major role. Further investigations are needed to test this hypothesis.

Africa↗