Scielo RSS http://scielo.isciii.es/rss.php?pid=1130-010820060006&lang=es vol. 98 num. 6 lang. es http://scielo.isciii.es/img/en/fbpelogp.gif http://scielo.isciii.es http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000600001&lng=es&nrm=iso&tlng=es http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000600002&lng=es&nrm=iso&tlng=es Background: the widespread of serologic diagnosis for celiac disease has brought about an epidemiologic shift. Little up-to-date information is available on relevant epidemiologic issues regarding diagnosis, information, and therapy. Objective: to examine forms of presentation, diagnostic difficulties, follow-up, information sources, and treatment-related issues regarding celiac disease. Method: a cross-sectional observational study using a self-completed questionnaire. Results: seventy-three adult patients were included; 15.0% of cases were diagnosed over 60 years of age. Most were non-smokers (91.8%). The rate of first-degree relatives with celiac sprue was 10.9%. The disease had a classic presentation in only 54.7% of cases. A functional gastrointestinal disorder was initially suspected in 42.4% of patients. Diet adherence is adequate, with unintentional lack of compliance in 15.5% of patients. Diet results in absent or improved symptoms in virtually all patients, but most of them consider compliance a challenge. Forty percent had difficulty finding gluten-free food, and 50.8% had problems in labelling recognition. Conclusions: celiac disease presents at any age, has a great variety of manifestations, and responds very well to gluten-free diet. It is crucial that patients be highly motivated and informed, and that they know for certain which foods and manufactured products are to be to used. Therefore, adequate control will result from coordination and cooperation regarding all resources involved, including medical care, and information provided by associations and other sources such as the Web. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000600003&lng=es&nrm=iso&tlng=es Objectives: the aim of this retrospective study was to evaluate early experience with laparoscopic restorative proctocolectomy by analyzing the perioperative results of surgical treatment. Patients and methods: seven major surgeries were performed in six patients with familial adenomatous polyposis and ulcerative colitis. All procedures were performed under laparoscopy at our third-level hospital from June 2003 to October 2004. Results: mean surgical time was 287.5 ± 80.7 min, and median blood loss was 300 ± 249.0 cc. There were no conversions; return of peristalsis began at 32 ± 12.4 h; average time to first oral intake was 64.0 ± 32.8 h, and mean duration of hospital stay was 9.3 ± 1.2 days. There was one case of perineal sepsis due to ileal pouch-anal anastomotic leakage, which was successfully treated with oral intake restriction, parenteral nutrition, and intra-rectal drainage. The most common postoperative complication was postoperative ileus. Conclusions: we believe that the laparoscopic approach to restorative proctocolectomy may be considerably improved in our center. Particular aspects for improvement include efforts to achieve lower operating and hospitalization times to equate our results with those reported by multicenter studies for laparoscopic colon cancer surgery. In our opinion, learning and further training opportunities should be encouraged to improve surgeon experience in the field of laparoscopy, preferably at centers specializing in restorative proctocolectomy. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000600004&lng=es&nrm=iso&tlng=es Zenker's diverticulum arises in the posterior wall of the pharynx, above the cricopharyngeal muscle, secondary to a functional cricopharyngeal disorder. We describe our experience with the management of Zenker's diverticulum from 1985 to this day in a third-level hospital. We review clinical data from 27 patients (78% males) with a mean age of 60.4 years. The most common clinical manifestations were dysphagia, regurgitation, syalorrhea, cough, and weight loss. All cases were diagnosed using an esophagogram. A diverticulectomy with cricopharingeal myotomy was performed in 74% of patients. Complications developed in 5 cases (21%), and the recurrence rate was 4% (1 of 3 cases, where myotomy was not performed). http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000600005&lng=es&nrm=iso&tlng=es Aim: when programming a medical test such as capsule endoscopy (CE), finding the closest point between the patient's experience and his/her expectation is essential to improve any further explorations. For this purpose we designed a form which tries to collect the information required. Material and methods: from December 2003 to January 2005 we examined the small intestine of 98 patients with the help of CE. Later they were sent an anonymous questionnaire in July 2005, which included 10 questions upon the origin and previous knowledge of the patient about this technique, their tolerance to it, and the value they attached to it with regard to finding a new diagnosis and assigning different treatments, and also the incidence in the positive or negative evolution of their disease in particular and of medicine in general. Results: answer rate reached 58% and was slightly higher among women and people over 70 years; 80% of repliers had been informed about CE by a physician, while nearly all the rest had received previous information from the media; 37% had had symptoms for more than 12 months, while only 17% had suffered them for one month before the exploration. A bit over 30% did not know what the specific diagnostic field of the test was (most of them women and young people), although most of them were not surprised by the procedure. Over 75% showed "acceptable" or "excellent" tolerance, while 5.5% (most of them young people) found it hard to bear. The opinion about its utility in the diagnosis was 37%, and although 70% thought that CE had revealed nothing new about their pathology, over 60% declared feeling better after the test; 84% pointed out that it had achieved a breakthrough for their quality of life (most of them men and very old people), and only 13% thought it was worthless. However, nearly all the answers agreed in that CE was an "important" or "very important" diagnostic device. Conclusions: after the test using CE, the diagnostic benefit detected by the patient is not the same as that shown by technical studies. Nevertheless, the test can be highly satisfactory for the patient in particular, and also in an overall view. CE is a well-tolerated test, applied in our setting to chronic diseases and that, contrary to what we supposed, is explained to patients mainly by a physician. Most of them are not familiar with its specific indications. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000600006&lng=es&nrm=iso&tlng=es Objective: to determine the incidence of constipation in Albacete province and its relation with diet and lifestyle. Patients and methods: cross-sectional population survey. We studied 414 participants over 50 years of age in Albacete province. 445 persons over 50 years of age were included in the study. All participants were selected by systematic random sampling; 414 participants filled in the questionnaire correctly. Main measures: age, weight and height, marital status, level of education and occupation; presence of a disease, number of sleep hours a day, physical exercise, smoking, alcohol intake, drug intake (anti-inflammatories and laxatives); bowel habit, diet, meal frequency and place; food intake frequency per week, daily intake of water, coffee, tea and herbal beverages; vitamin and fiber supplements; presence of cancer in the family. Results: 56.9% of participants were women. Mean age 67.07 years. In Albacete province, 4.4% of the population over 50 years have a bowel habit consistent with constipation. Most participants had three meals a day (breakfast, lunch, and supper), while 50% had another meal in the morning or afternoon. These meals took place, habitually, in the domicile. There was a preponderance in daily intake of the following foods: milk (83.7%), bread (95.1%), vegetables (68.8%), fruit (91.8%), and virgin olive oil (96.6%). Fish was eaten every one to two days, and pulses and meat every three to six days. 44.4% of participants drank one to two liters of water a day. Only 3.9% of participants took some supplement; 35% of participants were on a diet. It was observed that 97.7% of participants with more than three defecations a week had a high intake of virgin olive oil; 65.7% of participants did some physical exercise customarily; 70.2% of participants were non-smokers, 10.2% were smokers, and 18.4% were ex-smokers. With regard to alcohol, the percentage of drinkers was 35.1%. The main class of medications taken by participants was NSAIDs -14.5%; 79.7% took neither NSAIDs nor laxatives. Only 2.7% of participants took laxatives regularly. Conclusions: Most participants had relatively healthy eating habits. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000600007&lng=es&nrm=iso&tlng=es Liver disease is a major cause of illness and death worldwide. A central component in the complex network leading to the development of alcoholic liver disease is the activation of Kupffer cells by endotoxin and other soluble mediators. Alcohol consumption induces a state of ‘leaky gut' increasing plasma and liver endotoxin levels. When Kupffer cells become activated, they interact with a complex of proteins located on the extracellular membrane signaling to produce a wide array of soluble factors, including cytokines, chemokines, growth factors, cyclooxygenase and lipoxygenase metabolites, and reactive oxygen species such as superoxide anion, hydrogen peroxide, and nitric oxide, all of which provide physiologically diverse and pivotal paracrine effects on all other liver cell types and, ultimately, liver injury. Kupffer cells are also central to the liver homeostatic response to injury as upon cellular degenerative changes, they immediately respond to the insult and release mediators to orchestrate inflammatory and reparative responses. Thus, the homeostatic responses are initiated by Kupffer cell-derived mediators at the cellular level and underlie the liver's defense and reparative mechanisms against injury. In order to understand better the role of Kupffer cells in the onset of liver injury, animal models in which Kupffer cells are inactivated, and cell culture settings (e.g. co-cultures) are being used with promising results that advance our understanding of alcoholic liver disease. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000600008&lng=es&nrm=iso&tlng=es Liver disease is a major cause of illness and death worldwide. A central component in the complex network leading to the development of alcoholic liver disease is the activation of Kupffer cells by endotoxin and other soluble mediators. Alcohol consumption induces a state of ‘leaky gut' increasing plasma and liver endotoxin levels. When Kupffer cells become activated, they interact with a complex of proteins located on the extracellular membrane signaling to produce a wide array of soluble factors, including cytokines, chemokines, growth factors, cyclooxygenase and lipoxygenase metabolites, and reactive oxygen species such as superoxide anion, hydrogen peroxide, and nitric oxide, all of which provide physiologically diverse and pivotal paracrine effects on all other liver cell types and, ultimately, liver injury. Kupffer cells are also central to the liver homeostatic response to injury as upon cellular degenerative changes, they immediately respond to the insult and release mediators to orchestrate inflammatory and reparative responses. Thus, the homeostatic responses are initiated by Kupffer cell-derived mediators at the cellular level and underlie the liver's defense and reparative mechanisms against injury. In order to understand better the role of Kupffer cells in the onset of liver injury, animal models in which Kupffer cells are inactivated, and cell culture settings (e.g. co-cultures) are being used with promising results that advance our understanding of alcoholic liver disease. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000600009&lng=es&nrm=iso&tlng=es Liver disease is a major cause of illness and death worldwide. A central component in the complex network leading to the development of alcoholic liver disease is the activation of Kupffer cells by endotoxin and other soluble mediators. Alcohol consumption induces a state of ‘leaky gut' increasing plasma and liver endotoxin levels. When Kupffer cells become activated, they interact with a complex of proteins located on the extracellular membrane signaling to produce a wide array of soluble factors, including cytokines, chemokines, growth factors, cyclooxygenase and lipoxygenase metabolites, and reactive oxygen species such as superoxide anion, hydrogen peroxide, and nitric oxide, all of which provide physiologically diverse and pivotal paracrine effects on all other liver cell types and, ultimately, liver injury. Kupffer cells are also central to the liver homeostatic response to injury as upon cellular degenerative changes, they immediately respond to the insult and release mediators to orchestrate inflammatory and reparative responses. Thus, the homeostatic responses are initiated by Kupffer cell-derived mediators at the cellular level and underlie the liver's defense and reparative mechanisms against injury. In order to understand better the role of Kupffer cells in the onset of liver injury, animal models in which Kupffer cells are inactivated, and cell culture settings (e.g. co-cultures) are being used with promising results that advance our understanding of alcoholic liver disease. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000600010&lng=es&nrm=iso&tlng=es Liver disease is a major cause of illness and death worldwide. A central component in the complex network leading to the development of alcoholic liver disease is the activation of Kupffer cells by endotoxin and other soluble mediators. Alcohol consumption induces a state of ‘leaky gut' increasing plasma and liver endotoxin levels. When Kupffer cells become activated, they interact with a complex of proteins located on the extracellular membrane signaling to produce a wide array of soluble factors, including cytokines, chemokines, growth factors, cyclooxygenase and lipoxygenase metabolites, and reactive oxygen species such as superoxide anion, hydrogen peroxide, and nitric oxide, all of which provide physiologically diverse and pivotal paracrine effects on all other liver cell types and, ultimately, liver injury. Kupffer cells are also central to the liver homeostatic response to injury as upon cellular degenerative changes, they immediately respond to the insult and release mediators to orchestrate inflammatory and reparative responses. Thus, the homeostatic responses are initiated by Kupffer cell-derived mediators at the cellular level and underlie the liver's defense and reparative mechanisms against injury. In order to understand better the role of Kupffer cells in the onset of liver injury, animal models in which Kupffer cells are inactivated, and cell culture settings (e.g. co-cultures) are being used with promising results that advance our understanding of alcoholic liver disease. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000600011&lng=es&nrm=iso&tlng=es Liver disease is a major cause of illness and death worldwide. A central component in the complex network leading to the development of alcoholic liver disease is the activation of Kupffer cells by endotoxin and other soluble mediators. Alcohol consumption induces a state of ‘leaky gut' increasing plasma and liver endotoxin levels. When Kupffer cells become activated, they interact with a complex of proteins located on the extracellular membrane signaling to produce a wide array of soluble factors, including cytokines, chemokines, growth factors, cyclooxygenase and lipoxygenase metabolites, and reactive oxygen species such as superoxide anion, hydrogen peroxide, and nitric oxide, all of which provide physiologically diverse and pivotal paracrine effects on all other liver cell types and, ultimately, liver injury. Kupffer cells are also central to the liver homeostatic response to injury as upon cellular degenerative changes, they immediately respond to the insult and release mediators to orchestrate inflammatory and reparative responses. Thus, the homeostatic responses are initiated by Kupffer cell-derived mediators at the cellular level and underlie the liver's defense and reparative mechanisms against injury. In order to understand better the role of Kupffer cells in the onset of liver injury, animal models in which Kupffer cells are inactivated, and cell culture settings (e.g. co-cultures) are being used with promising results that advance our understanding of alcoholic liver disease. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000600012&lng=es&nrm=iso&tlng=es Liver disease is a major cause of illness and death worldwide. A central component in the complex network leading to the development of alcoholic liver disease is the activation of Kupffer cells by endotoxin and other soluble mediators. Alcohol consumption induces a state of ‘leaky gut' increasing plasma and liver endotoxin levels. When Kupffer cells become activated, they interact with a complex of proteins located on the extracellular membrane signaling to produce a wide array of soluble factors, including cytokines, chemokines, growth factors, cyclooxygenase and lipoxygenase metabolites, and reactive oxygen species such as superoxide anion, hydrogen peroxide, and nitric oxide, all of which provide physiologically diverse and pivotal paracrine effects on all other liver cell types and, ultimately, liver injury. Kupffer cells are also central to the liver homeostatic response to injury as upon cellular degenerative changes, they immediately respond to the insult and release mediators to orchestrate inflammatory and reparative responses. Thus, the homeostatic responses are initiated by Kupffer cell-derived mediators at the cellular level and underlie the liver's defense and reparative mechanisms against injury. In order to understand better the role of Kupffer cells in the onset of liver injury, animal models in which Kupffer cells are inactivated, and cell culture settings (e.g. co-cultures) are being used with promising results that advance our understanding of alcoholic liver disease. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000600013&lng=es&nrm=iso&tlng=es Liver disease is a major cause of illness and death worldwide. A central component in the complex network leading to the development of alcoholic liver disease is the activation of Kupffer cells by endotoxin and other soluble mediators. Alcohol consumption induces a state of ‘leaky gut' increasing plasma and liver endotoxin levels. When Kupffer cells become activated, they interact with a complex of proteins located on the extracellular membrane signaling to produce a wide array of soluble factors, including cytokines, chemokines, growth factors, cyclooxygenase and lipoxygenase metabolites, and reactive oxygen species such as superoxide anion, hydrogen peroxide, and nitric oxide, all of which provide physiologically diverse and pivotal paracrine effects on all other liver cell types and, ultimately, liver injury. Kupffer cells are also central to the liver homeostatic response to injury as upon cellular degenerative changes, they immediately respond to the insult and release mediators to orchestrate inflammatory and reparative responses. Thus, the homeostatic responses are initiated by Kupffer cell-derived mediators at the cellular level and underlie the liver's defense and reparative mechanisms against injury. In order to understand better the role of Kupffer cells in the onset of liver injury, animal models in which Kupffer cells are inactivated, and cell culture settings (e.g. co-cultures) are being used with promising results that advance our understanding of alcoholic liver disease. http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000600014&lng=es&nrm=iso&tlng=es Liver disease is a major cause of illness and death worldwide. A central component in the complex network leading to the development of alcoholic liver disease is the activation of Kupffer cells by endotoxin and other soluble mediators. Alcohol consumption induces a state of ‘leaky gut' increasing plasma and liver endotoxin levels. When Kupffer cells become activated, they interact with a complex of proteins located on the extracellular membrane signaling to produce a wide array of soluble factors, including cytokines, chemokines, growth factors, cyclooxygenase and lipoxygenase metabolites, and reactive oxygen species such as superoxide anion, hydrogen peroxide, and nitric oxide, all of which provide physiologically diverse and pivotal paracrine effects on all other liver cell types and, ultimately, liver injury. Kupffer cells are also central to the liver homeostatic response to injury as upon cellular degenerative changes, they immediately respond to the insult and release mediators to orchestrate inflammatory and reparative responses. Thus, the homeostatic responses are initiated by Kupffer cell-derived mediators at the cellular level and underlie the liver's defense and reparative mechanisms against injury. In order to understand better the role of Kupffer cells in the onset of liver injury, animal models in which Kupffer cells are inactivated, and cell culture settings (e.g. co-cultures) are being used with promising results that advance our understanding of alcoholic liver disease.