Scielo RSS http://scielo.isciii.es/rss.php?pid=1130-010820060007&lang=es vol. 98 num. 7 lang. es http://scielo.isciii.es/img/en/fbpelogp.gif http://scielo.isciii.es http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000700001&lng=es&nrm=iso&tlng=es http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000700002&lng=es&nrm=iso&tlng=es Background: the objective of our paper is to report on the long-term results of patients with gastric cancer treated by mini-invasive surgery with "intention-to-treat" laparoscopy. Patients and methods: between June 1993 and January 2006, 130 patients comprising 94 men and 36 women with gastric adenocarcinoma were prospectively selected by two surgical teams in three hospitals based on a prior agreement (CHU Charleroi, Belgium, Centre Hospitalier de Luxembourg and Zumárraga Hospital, Spain). Patients with adenocarcinoma of the cardia were excluded. Mean age of patients was 68 years (range, 37-85 years). Results: post-operative mortality within 60 days of operation was 6 patients; 109 patients were therefore properly followed up for an average of 49 months (range, 2-153 months). Average survival time for 10 non-resected patients was 4.5 months. Average survival rate for all 14 palliatively resected patients was 6.9 months. Actuarial 5-year survival rate for R0-type surgery was 35%. Global actuarial 5-year survival rate after resective surgery was 31%. Conclusions: laparoscopic gastrectomy with any kind of lymphadenectomy is a major but safe operation with acceptable mortality and morbility rates in patients with advanced gastric cancer, usually in poor general condition. Laparoscopic gastrectomy for locally advanced cancers is equivalent to laparotomy as far as long-term oncological results are concerned. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000700003&lng=es&nrm=iso&tlng=es Objective: the causal relation between rosacea and Helicobacter pylori infection is discussed. We evaluated the clinical evolution of rosacea after infection eradication. Patients and methods: we have prospectively studied 44 patients diagnosed with rosacea. Helicobacter pylori infection was determined, and infected patients were treated with eradication therapy. The evolution of dermatological symptoms in a subgroup of 29 infected patients in whom eradication had been achieved was followed during 16.8 (± 17.8) months. Median age was 50.6 (± 14.1) years for 22 women (75.9%) and 7 men (24.1%). Clinical response according to gender and clinical subtype of rosacea was evaluated. Results: complete improvement was observed in 10 patients (34.5%; 95% CI: 18.6-54.3%), relevant improvement in 9 (31.1%; 95% CI: 16-51%), poor improvement in 5 (17.2%; 95% CI: 6.5-36.4%), and absence of improvement in 5 cases (17.2%; 95% CI: 6.5-36.4%). No significant differences in dermatological evolution according to sex were observed. Regarding subtype of rosacea there was a relevant improvement in 83.3% (95% CI: 64.1-93.8%) of cases with papulopustular type as opposed to 36.5% (95% CI: 20-56.1%) of cases with erythematous predominance, p = 0.02. Conclusions: based on these results, the relation between Helicobacter pylori and rosacea is supported, and infection should be investigated in these patients because an appreciable percentage of patients diagnosed with rosacea and Helicobacter pylori infection can benefit from eradication therapy, mainly in the papulopustular subtype. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000700004&lng=es&nrm=iso&tlng=es Background: patients with inflammatory bowel disease may suffer one or more extraintestinal manifestations during the course of their condition, these being more frequent in Crohn's disease. The aim of our study was to evaluate the prevalence of extraintestinal manifestations in patients with Crohn's disease in our healthcare area, and to assess the relationship between its presence and diverse clinical-evolutionary variables. Material and methods: extraintestinal manifestations in 157 patients diagnosed with Crohn's disease in our center were retrospectively studied. The clinical-evolutionary characteristics of this population were compared with respect to the presence or absence of different extraintestinal manifestations. Results: seventy-two patients (46%) presented at least with one extraintestinal manifestation. Thirty-one percent were colitis-related manifestations (22% rheumatologic, 13% muco-cutaneous, 4% ophthalmologic), 11% cholelithiasis, 8% nephrolithiasis, 3% thromboembolic illness, and other manifestations were less frequent. Fourteen percent presented with more than one extraintestinal manifestation. Rheumatologic and muco-cutaneous manifestations were significantly more frequent in patients with disease confined to the colon. Cholelithiasis was significantly associated to those over 40 and also to males. Nephrolithiasis was also significantly associated to those over 40, and thromboembolic illness was linked to females. Conclusions: forty-six percent of patients with Crohn's disease presented at least with one extraintestinal manifestation. Thirty-one percent presented with colitis-related manifestations, rheumatologic and muco-cutaneous manifestations being the most frequent, whereas hepatic manifestations were infrequent. Rheumatologic and muco-cutaneous manifestations were more frequent in patients with disease confined to the colon. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000700005&lng=es&nrm=iso&tlng=es Objectives: to estimate the impact of gastroesophageal reflux (GER) symptoms on the utilization of healthcare services and work absenteeism in Spain. Methods: a cross-sectional study on 2,500 subjects representative of the Spanish population from 40 to 79 years of age. Data were collected via a telephone interview in January 2002 using Locke's questionnaire after its cross-cultural adaptation and validation for telephone use in Spain. Results: GER is responsible for 296.8 doctor consultations (95% CI: 245.3-348.7) per 1,000 inhabitants per year, for 24 esophagogastrointestinal radiographic studies per 1,000 inhabitants per year (95% CI: 18-30), for 32.4 (95% CI: 25.5-39.3) high digestive endoscopies per 1,000 inhabitants per year, and for the loss of 201 (95% CI: 0-411.1) working days per 1,000 employed inhabitants with GER per year. In relation to medication intake, GER resulted in 4,092 (95% CI: 3,300-5,133) treatment days with H2 antagonists per 1,000 inhabitants per year, 9,030 (95% CI: 7,846-10,332) treatment days with proton pump inhibitors per 1,000 inhabitants per year, and 1,082 (95% CI: 519-1,549) treatment days with prokinetics per 1,000 inhabitants per year. Conclusions: GER has a large impact on the utilization of healthcare resources and work absenteeism in Spain, in contrast to the widespread belief that it is an illness of little importance. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000700006&lng=es&nrm=iso&tlng=es The formation of new blood vessels seen in conditions commonly associated with Helicobacter pylori (H. pylori) infection, including gastritis, peptic ulcer, and gastric carcinoma, prompts consideration of a potential relationship between mucosal colonization by this organism and the angiogenic process. H. pylori directly or indirectly damages endothelial cells, which induces a number of changes in the microvasculature of the gastric mucosa. In H. pylori-associated conditions, that is, in gastritis, peptic ulcer and gastric carcinoma, there is an increased concentration of angiogenic factors, and subsequently a formation of new blood vessels. However, this early angiogenesis -which is activated to repair the gastric mucosa- is subsequently inhibited in patients with peptic ulcer, and ulcer healing is thus delayed. This may be due to the antiproliferative action of this organism on endothelial cells. While the angiogenic process becomes inhibited in infected patients with peptic ulcer, it remains seemingly active in those with gastritis or gastric cancer. This fact is in support of the notion suggested by various studies that peptic ulcer and gastric cancer are mutually excluding conditions. In the case of gastric cancer, neoangiogenesis would enhance nutrient and oxygen supply to cancer cells, and thus tumor growth and metastatic spread. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000700007&lng=es&nrm=iso&tlng=es The formation of new blood vessels seen in conditions commonly associated with Helicobacter pylori (H. pylori) infection, including gastritis, peptic ulcer, and gastric carcinoma, prompts consideration of a potential relationship between mucosal colonization by this organism and the angiogenic process. H. pylori directly or indirectly damages endothelial cells, which induces a number of changes in the microvasculature of the gastric mucosa. In H. pylori-associated conditions, that is, in gastritis, peptic ulcer and gastric carcinoma, there is an increased concentration of angiogenic factors, and subsequently a formation of new blood vessels. However, this early angiogenesis -which is activated to repair the gastric mucosa- is subsequently inhibited in patients with peptic ulcer, and ulcer healing is thus delayed. This may be due to the antiproliferative action of this organism on endothelial cells. While the angiogenic process becomes inhibited in infected patients with peptic ulcer, it remains seemingly active in those with gastritis or gastric cancer. This fact is in support of the notion suggested by various studies that peptic ulcer and gastric cancer are mutually excluding conditions. In the case of gastric cancer, neoangiogenesis would enhance nutrient and oxygen supply to cancer cells, and thus tumor growth and metastatic spread. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000700008&lng=es&nrm=iso&tlng=es The formation of new blood vessels seen in conditions commonly associated with Helicobacter pylori (H. pylori) infection, including gastritis, peptic ulcer, and gastric carcinoma, prompts consideration of a potential relationship between mucosal colonization by this organism and the angiogenic process. H. pylori directly or indirectly damages endothelial cells, which induces a number of changes in the microvasculature of the gastric mucosa. In H. pylori-associated conditions, that is, in gastritis, peptic ulcer and gastric carcinoma, there is an increased concentration of angiogenic factors, and subsequently a formation of new blood vessels. However, this early angiogenesis -which is activated to repair the gastric mucosa- is subsequently inhibited in patients with peptic ulcer, and ulcer healing is thus delayed. This may be due to the antiproliferative action of this organism on endothelial cells. While the angiogenic process becomes inhibited in infected patients with peptic ulcer, it remains seemingly active in those with gastritis or gastric cancer. This fact is in support of the notion suggested by various studies that peptic ulcer and gastric cancer are mutually excluding conditions. In the case of gastric cancer, neoangiogenesis would enhance nutrient and oxygen supply to cancer cells, and thus tumor growth and metastatic spread. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000700009&lng=es&nrm=iso&tlng=es The formation of new blood vessels seen in conditions commonly associated with Helicobacter pylori (H. pylori) infection, including gastritis, peptic ulcer, and gastric carcinoma, prompts consideration of a potential relationship between mucosal colonization by this organism and the angiogenic process. H. pylori directly or indirectly damages endothelial cells, which induces a number of changes in the microvasculature of the gastric mucosa. In H. pylori-associated conditions, that is, in gastritis, peptic ulcer and gastric carcinoma, there is an increased concentration of angiogenic factors, and subsequently a formation of new blood vessels. However, this early angiogenesis -which is activated to repair the gastric mucosa- is subsequently inhibited in patients with peptic ulcer, and ulcer healing is thus delayed. This may be due to the antiproliferative action of this organism on endothelial cells. While the angiogenic process becomes inhibited in infected patients with peptic ulcer, it remains seemingly active in those with gastritis or gastric cancer. This fact is in support of the notion suggested by various studies that peptic ulcer and gastric cancer are mutually excluding conditions. In the case of gastric cancer, neoangiogenesis would enhance nutrient and oxygen supply to cancer cells, and thus tumor growth and metastatic spread. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000700010&lng=es&nrm=iso&tlng=es The formation of new blood vessels seen in conditions commonly associated with Helicobacter pylori (H. pylori) infection, including gastritis, peptic ulcer, and gastric carcinoma, prompts consideration of a potential relationship between mucosal colonization by this organism and the angiogenic process. H. pylori directly or indirectly damages endothelial cells, which induces a number of changes in the microvasculature of the gastric mucosa. In H. pylori-associated conditions, that is, in gastritis, peptic ulcer and gastric carcinoma, there is an increased concentration of angiogenic factors, and subsequently a formation of new blood vessels. However, this early angiogenesis -which is activated to repair the gastric mucosa- is subsequently inhibited in patients with peptic ulcer, and ulcer healing is thus delayed. This may be due to the antiproliferative action of this organism on endothelial cells. While the angiogenic process becomes inhibited in infected patients with peptic ulcer, it remains seemingly active in those with gastritis or gastric cancer. This fact is in support of the notion suggested by various studies that peptic ulcer and gastric cancer are mutually excluding conditions. In the case of gastric cancer, neoangiogenesis would enhance nutrient and oxygen supply to cancer cells, and thus tumor growth and metastatic spread. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000700011&lng=es&nrm=iso&tlng=es The formation of new blood vessels seen in conditions commonly associated with Helicobacter pylori (H. pylori) infection, including gastritis, peptic ulcer, and gastric carcinoma, prompts consideration of a potential relationship between mucosal colonization by this organism and the angiogenic process. H. pylori directly or indirectly damages endothelial cells, which induces a number of changes in the microvasculature of the gastric mucosa. In H. pylori-associated conditions, that is, in gastritis, peptic ulcer and gastric carcinoma, there is an increased concentration of angiogenic factors, and subsequently a formation of new blood vessels. However, this early angiogenesis -which is activated to repair the gastric mucosa- is subsequently inhibited in patients with peptic ulcer, and ulcer healing is thus delayed. This may be due to the antiproliferative action of this organism on endothelial cells. While the angiogenic process becomes inhibited in infected patients with peptic ulcer, it remains seemingly active in those with gastritis or gastric cancer. This fact is in support of the notion suggested by various studies that peptic ulcer and gastric cancer are mutually excluding conditions. In the case of gastric cancer, neoangiogenesis would enhance nutrient and oxygen supply to cancer cells, and thus tumor growth and metastatic spread. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000700012&lng=es&nrm=iso&tlng=es The formation of new blood vessels seen in conditions commonly associated with Helicobacter pylori (H. pylori) infection, including gastritis, peptic ulcer, and gastric carcinoma, prompts consideration of a potential relationship between mucosal colonization by this organism and the angiogenic process. H. pylori directly or indirectly damages endothelial cells, which induces a number of changes in the microvasculature of the gastric mucosa. In H. pylori-associated conditions, that is, in gastritis, peptic ulcer and gastric carcinoma, there is an increased concentration of angiogenic factors, and subsequently a formation of new blood vessels. However, this early angiogenesis -which is activated to repair the gastric mucosa- is subsequently inhibited in patients with peptic ulcer, and ulcer healing is thus delayed. This may be due to the antiproliferative action of this organism on endothelial cells. While the angiogenic process becomes inhibited in infected patients with peptic ulcer, it remains seemingly active in those with gastritis or gastric cancer. This fact is in support of the notion suggested by various studies that peptic ulcer and gastric cancer are mutually excluding conditions. In the case of gastric cancer, neoangiogenesis would enhance nutrient and oxygen supply to cancer cells, and thus tumor growth and metastatic spread. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000700013&lng=es&nrm=iso&tlng=es The formation of new blood vessels seen in conditions commonly associated with Helicobacter pylori (H. pylori) infection, including gastritis, peptic ulcer, and gastric carcinoma, prompts consideration of a potential relationship between mucosal colonization by this organism and the angiogenic process. H. pylori directly or indirectly damages endothelial cells, which induces a number of changes in the microvasculature of the gastric mucosa. In H. pylori-associated conditions, that is, in gastritis, peptic ulcer and gastric carcinoma, there is an increased concentration of angiogenic factors, and subsequently a formation of new blood vessels. However, this early angiogenesis -which is activated to repair the gastric mucosa- is subsequently inhibited in patients with peptic ulcer, and ulcer healing is thus delayed. This may be due to the antiproliferative action of this organism on endothelial cells. While the angiogenic process becomes inhibited in infected patients with peptic ulcer, it remains seemingly active in those with gastritis or gastric cancer. This fact is in support of the notion suggested by various studies that peptic ulcer and gastric cancer are mutually excluding conditions. In the case of gastric cancer, neoangiogenesis would enhance nutrient and oxygen supply to cancer cells, and thus tumor growth and metastatic spread. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000700014&lng=es&nrm=iso&tlng=es The formation of new blood vessels seen in conditions commonly associated with Helicobacter pylori (H. pylori) infection, including gastritis, peptic ulcer, and gastric carcinoma, prompts consideration of a potential relationship between mucosal colonization by this organism and the angiogenic process. H. pylori directly or indirectly damages endothelial cells, which induces a number of changes in the microvasculature of the gastric mucosa. In H. pylori-associated conditions, that is, in gastritis, peptic ulcer and gastric carcinoma, there is an increased concentration of angiogenic factors, and subsequently a formation of new blood vessels. However, this early angiogenesis -which is activated to repair the gastric mucosa- is subsequently inhibited in patients with peptic ulcer, and ulcer healing is thus delayed. This may be due to the antiproliferative action of this organism on endothelial cells. While the angiogenic process becomes inhibited in infected patients with peptic ulcer, it remains seemingly active in those with gastritis or gastric cancer. This fact is in support of the notion suggested by various studies that peptic ulcer and gastric cancer are mutually excluding conditions. In the case of gastric cancer, neoangiogenesis would enhance nutrient and oxygen supply to cancer cells, and thus tumor growth and metastatic spread. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000700015&lng=es&nrm=iso&tlng=es The formation of new blood vessels seen in conditions commonly associated with Helicobacter pylori (H. pylori) infection, including gastritis, peptic ulcer, and gastric carcinoma, prompts consideration of a potential relationship between mucosal colonization by this organism and the angiogenic process. H. pylori directly or indirectly damages endothelial cells, which induces a number of changes in the microvasculature of the gastric mucosa. In H. pylori-associated conditions, that is, in gastritis, peptic ulcer and gastric carcinoma, there is an increased concentration of angiogenic factors, and subsequently a formation of new blood vessels. However, this early angiogenesis -which is activated to repair the gastric mucosa- is subsequently inhibited in patients with peptic ulcer, and ulcer healing is thus delayed. This may be due to the antiproliferative action of this organism on endothelial cells. While the angiogenic process becomes inhibited in infected patients with peptic ulcer, it remains seemingly active in those with gastritis or gastric cancer. This fact is in support of the notion suggested by various studies that peptic ulcer and gastric cancer are mutually excluding conditions. In the case of gastric cancer, neoangiogenesis would enhance nutrient and oxygen supply to cancer cells, and thus tumor growth and metastatic spread. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000700016&lng=es&nrm=iso&tlng=es The formation of new blood vessels seen in conditions commonly associated with Helicobacter pylori (H. pylori) infection, including gastritis, peptic ulcer, and gastric carcinoma, prompts consideration of a potential relationship between mucosal colonization by this organism and the angiogenic process. H. pylori directly or indirectly damages endothelial cells, which induces a number of changes in the microvasculature of the gastric mucosa. In H. pylori-associated conditions, that is, in gastritis, peptic ulcer and gastric carcinoma, there is an increased concentration of angiogenic factors, and subsequently a formation of new blood vessels. However, this early angiogenesis -which is activated to repair the gastric mucosa- is subsequently inhibited in patients with peptic ulcer, and ulcer healing is thus delayed. This may be due to the antiproliferative action of this organism on endothelial cells. While the angiogenic process becomes inhibited in infected patients with peptic ulcer, it remains seemingly active in those with gastritis or gastric cancer. This fact is in support of the notion suggested by various studies that peptic ulcer and gastric cancer are mutually excluding conditions. In the case of gastric cancer, neoangiogenesis would enhance nutrient and oxygen supply to cancer cells, and thus tumor growth and metastatic spread.