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Sökning: (hsv:(MEDICIN OCH HÄLSOVETENSKAP) hsv:(Klinisk medicin) hsv:(Gastroenterologi)) srt2:(2000-2009) > (2006)

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1.
  • Laurell, Helena, et al. (författare)
  • Acute abdominal pain among elderly patients
  • 2006
  • Ingår i: Gerontology. - : S. Karger AG. - 0304-324X .- 1423-0003. ; 52:6, s. 339-344
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Diagnosis of acute abdominal pain in older persons is a challenge, with the age-related increase in concurrent diseases. In most western countries the number of elderly people is constantly rising, which means that an increasing proportion of patients admitted for abdominal pain at the emergency department are elderly. Objective: To characterize differences in clinical presentation and diagnostic accuracy between younger and more elderly patients with acute abdominal pain. Methods: Patients admitted to Mora Hospital with abdominal pain of up to seven days' duration were registered according to a detailed schedule. From 1st February 1997 to 1st June 2000, 557 patients aged 65-79 years and 274 patients aged ≥80 years were registered. Patients aged 20-64 years (n = 1,458) served as a control group. Results: A specific diagnosis, i.e. other than 'non-specific abdominal pain', was established in 76 and 78% of the patients aged 65-79 and ≥80 years respectively, and in 64% of those aged 20-64 (p < 0.001). Pain duration before admission increased with age (p < 0.003), as did frequency and duration of hospitalization (p < 0.0001). Hospital stay increased from 170 days per 100 emergency admissions in the control group to 320 and 458 days in the younger and older study groups, respectively. At the emergency department, older patients were more often misdiagnosed than control patients (52 vs. 45%; p = 0.002). At discharge the diagnosis was more accurate in the control group (86 vs. 77%; p < 0.0001). Hospital mortality was higher among older patients (23/831 vs. 2/1,458; p < 0.001). The admission-to-surgery interval was increased (1.8 vs. 0.9 days, p < 0.0001) in patients ≥65 years. Rebound tenderness (p < 0.0001), local rigidity (p = 0.003) and rectal tenderness (p = 0.004) were less common in the older than in the control patients with peritonitis. In patients ≥65 years, C-reactive protein did not differ between patients operated on and those not, contrary to the finding in patients <65 years (p<0.0001). Conclusion: Both the preliminary diagnosis at the emergency department and the discharge diagnosis were less reliable in elderly than in younger patients. Elderly patients more often had specific organic disease and arrived at the emergency department after a longer history of abdominal pain compared to younger patients.
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3.
  • Bergquist, Annika, et al. (författare)
  • Perinatal events and the risk of developing primary sclerosing cholangitis
  • 2006
  • Ingår i: World Journal of Gastroenterology. - : Baishideng Publishing Group Inc.. - 1007-9327 .- 2219-2840. ; 12:37, s. 6037-6040
  • Tidskriftsartikel (refereegranskat)abstract
    • AIM: To investigate whether perinatal events, intrauterine or postpartum, are associated with the development of primary sclerosing cholangitis (PSC) later in life.METHODS: Birth records from 97 patients with adult PSC in Sweden were reviewed. Information on perinatal events including medications and complications during pregnancy, gestation length, birth weight and length were collected. Two control children of the same sex were selected for each subject. Conditional multiple logistic regression was used to assess associations of the perinatal measures with development of PSC.RESULTS: No significant associations were found between gestational age, birth length, breastfeeding, and the majority of medical complications including infections or medication during pregnancy for the mothers or postpartum for the children. Vaginal bleeding and peripheral oedema showed associations with PSC, with matched odds ratios of 5.70 (95% CI, 1.13-28.83) and 2.28 (95% CI, 1.04-5.03), respectively. CONCLUSION: The associations of vaginal bleeding and oedema with subsequent PSC cannot readily be explained, so our findings do not strongly support the hypothesis of a significant role of perinatal events as a risk for the development of PSC later in life.
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4.
  • Ludvigsson, Jonas F., et al. (författare)
  • Coeliac disease in the father and risk of adverse pregnancy outcome : a population-based cohort study
  • 2006
  • Ingår i: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 0036-5521 .- 1502-7708. ; 41:2, s. 178-185
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE:The risk of adverse foetal outcomes was investigated in offspring to men with coeliac disease (CD) diagnosed prior to infant birth and in offspring to men who did not receive a diagnosis of CD until after the delivery.MATERIAL AND METHODS:A cohort study was based on national registry data restricted to women aged 15-44 years with singleton live-born infants, with linkage between the Swedish national birth registry (1973-2001) and the national inpatient registry (1964-2001). A total of 1059 offspring to men who had received a diagnosis of CD were included: 554 offspring to men diagnosed prior to birth and 505 offspring to men diagnosed after infant birth.RESULTS:Undiagnosed CD in the father was associated with an increased risk of caesarean section (adjusted odds ratio (AOR)=1.83; 95% confidence interval (CI) for AOR=1.13-2.95; p=0.014) but was otherwise not linked to adverse pregnancy outcome: (intrauterine growth retardation (OR=1.37; 95% CI=0.91-2.07), low birth-weight (OR=1.41; 95% CI=0.93-2.12), very low birth-weight (OR=1.21; 95% CI=0.39-3.77), preterm birth (OR=1.10; 95% CI=0.74-1.62), and very preterm (OR=0.62; 95% CI=0.09-4.40)). A paternal diagnosis of CD made before infant birth was not associated with adverse foetal outcome.CONCLUSIONS:CD in the father is not a risk factor for unfavourable foetal outcome. The increased risk for caesarean section in offspring to men with undiagnosed CD in this study may be due to multiple comparisons.
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5.
  • Van Odijk, Jenny, 1969, et al. (författare)
  • Measurements of eosinophil activation before and after food challenges in adults with food hypersensitivity
  • 2006
  • Ingår i: Int Arch Allergy Immunol. - : S. Karger AG. - 1018-2438 .- 1423-0097. ; 140:4, s. 334-41
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Objective assessment of inflammatory reactions in the gastrointestinal tract could be useful in the diagnosis of food hypersensitivity. The aim of the present study was to investigate the involvement of eosinophils and mast cells in the inflammatory response of patients with food hypersensitivity before and after food challenges. METHODS: Eleven patients (4 with IgE-mediated allergy and 7 without) with food hypersensitivity and positive double-blind, placebo-controlled food challenge were subjected to food challenge in a single-blinded fashion. Four subjects with no known food hypersensitivity were recruited as controls. Placebo was given after a 1-week washout period followed by an active dose. Stool, urinary and serum samples were collected and symptoms were recorded in a diary. Fecal samples were analyzed for eosinophil protein X (F-EPX) and tryptase; urinary samples for EPX (U-EPX) and leukotriene E4 (U-LTE4) and serum samples were analyzed for eotaxin and food-specific IgE antibodies. RESULTS: Patients with IgE-mediated food allergy had increased levels of F-EPX compared to controls and tended to have lower serum levels of eotaxin compared to non-allergic patients and controls. U-LTE4 was significantly higher in allergic patients compared to non-allergic patients after challenge. Moreover, F-EPX correlated to U-LTE4 (p = 0.011). Reported symptoms, abdominal pain, distension, flatulence and nausea were similar in the allergic and non-allergic patients. CONCLUSION: The results strongly indicate that eosinophils are activated in the gastrointestinal tract of food-allergic patients but not in patients with non-allergic food hypersensitivity. Due to the inconsistent pattern of symptoms after placebo and active food challenge, it was not possible to relate the levels of inflammation markers to the recorded symptoms.
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6.
  • Bruck, Wolfram M, et al. (författare)
  • Effects of bovine alpha-lactalbumin and casein glycomacropeptide-enriched infant formulae on faecal microbiota in healthy term infants
  • 2006
  • Ingår i: Journal of Pediatric Gastroenterology and Nutrition - JPGN. - Philadelphia : Lippincott Williams & Wilkins. - 0277-2116 .- 1536-4801. ; 43:5, s. 673-679
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: Certain milk factors may promote the growth of a host-friendly gastrointestinal microbiota, for example, one that is predominated by bifidobacteria, a perceived healthpromoting genus. This may explain why breast-fed infants experience fewer intestinal infections than their formula-fed counterparts who are believed to have a more diverse microbiota, which is similar to that of adults. The effects of formulas supplemented with 2 such ingredients from bovine milk, a-lactalbumin (alpha-lac) and casein glycomacropeptide (GMP), on gut flora were investigated in this study.Patients and Methods: Six-week-old (4-8 wk), healthy term infants were randomised to a standard infant formula or 1 of 2 test formulae enriched in alpha-Jac with higher or lower GMP until 6 months. Faecal bacteriology was determined by the culture-independent procedure fluorescence in situ hybridisation.Results: There was a large fluctuation of bacterial counts within groups with no statistically significant differences between groups. Although all groups showed a. predominance of bifidobacteria, breast-fed infants had a small temporary increase in counts. Other bacterial levels varied in formula-fed groups, which overall showed an adult-like faecal microflora.Conclusions: It can be speculated that a prebiotic effect for alpha-lac and GMP is achieved only with low starting populations of beneficial microbiota (eg, infants not initially breast-fed).
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7.
  • Ludvigsson, Jonas F., et al. (författare)
  • Effect of HLA DQ2, dietary exposure and coeliac disease on the development of antibody response to gliadin in children
  • 2006
  • Ingår i: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 0036-5521 .- 1502-7708. ; 41:8, s. 919-928
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: To study the effect of HLA DQ2, dietary history and development of coeliac disease (CD) on the induction of antibody response to wheat gliadin and cow's milk, beta-lactoglobulin between 1 and 2.5 years of age in children who developed CD and in healthy children. MATERIAL AND METHODS: Infants participating in a birth cohort study (the ABIS study) in Sweden were studied. Thirty-nine children developed CD (=cases), confirmed through biopsy, during follow-up until 2.5-5 years of age. A total of 181 healthy control children were matched for duration of exclusive breast-feeding, birth-weight, gender, maternal smoking and season of birth. IgG and IgA antigliadin and anti-beta-lactoglobulin antibodies were measured using enzyme immunoassay (EIA). The effects of HLA-risk genotypes, DQ2 and DQ8, on CD were also considered. RESULTS: Children who developed CD had higher IgG and IgA antigliadin and anti-beta-lactoglobulin antibody levels at 1 year of age than controls (all comparisons: p<0.001). Similar differences were seen between cases with as yet undiagnosed CD by 1 year of age and controls, and also when cases were compared with HLA-matched controls. Higher levels of IgG and IgA antibodies to beta-lactoglobulin (p=0.003; p=0.001), but not to gliadin, were found in treated cases versus controls at 2.5 years of age. HLA-DQ2-positive healthy children had lower levels of IgG and IgA antigliadin antibodies than HLA-DQ2 negative controls at 1 year of age (p=0.004; p=0.012). CONCLUSIONS: Enhanced humoral response emerging not only to gliadin, but also to other food antigens seems to be primarily associated with CD. Poor induction of antibody response to wheat gliadin in healthy children with the HLA-DQ2 risk molecule could at least partly explain the genetic predisposition to gluten intolerance and CD.
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9.
  • Larsson, Susanna C., et al. (författare)
  • Folate intake, MTHFR polymorphisms, and risk of esophageal, gastric, and pancreatic cancer : A meta-analysis
  • 2006
  • Ingår i: Gastroenterology. - Karolinska Inst, Natl Inst Environm Med, Div Nutr Epidemiol, SE-17177 Stockholm, Sweden. Harvard Univ, Sch Med, Boston, MA USA. Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA. : W B SAUNDERS CO-ELSEVIER INC. - 0016-5085 .- 1528-0012. ; 131:4, s. 1271-1283
  • Tidskriftsartikel (refereegranskat)abstract
    • Background & Aims: Increasing evidence suggests that a low folare intake and impaired folate metabolism may be implicated in the development of gastrointestinal cancers. We conducted a systematic review with meta-analysis of epidemiologic studies evaluating the association of folate intake or genetic polymorphisms in S,10-methylenetetrahydrofolate reductase (MTHFR), a central enzyme in folate metabolism, with risk of esophageal, gastric, or pancreatic cancer. Methods: A literature search was performed using MEDLINE for studies published through March 2006. Study-specific relative risks were weighted by the inverse of their variance to obtain random-effects summary estimates. Results: The summary relative risks for the highest versus the lowest category of dietary folate intake were 0.66 (9S% confidence interval [CI], 0.53-0.83) for esophageal squamous cell carcinoma (4 case-control), 0.50 (9S% CI, 0.39-0.65) for esophageal adenocarcinoma (3 casecontrol), and 0.49 (95% CI, 0.3S-0.67) for pancreatic cancer (I case-control, 4 cohort); there was no heterogeneity among studies. Results on dietary folate intake and risk of gastric cancer (9 case-control, 2 cohort) were inconsistent. In most studies, the MTHFR 677TT (variant) genotype, which is associated with reduced enzyme activity, was associated with an increased risk of esophageal squamous cell carcinoma, gastric cardia adenocarcinoma, noncardia gastric cancer, gastric cancer (all subsites), and pancreatic cancer; all but one of 22 odds ratios were > 1, of which 13 estimates were statistically significant. Studies of the MTHFR A1298C polymorphism were limited and inconsistent. Conclusions: These findings support the hypothesis that folare may play a role in carcinogenesis of the esophagus, stomach, and pancreas.
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10.
  • Acosta, Stefan, et al. (författare)
  • Fatal colonic ischaemia : A population-based study
  • 2006
  • Ingår i: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 0036-5521 .- 1502-7708. ; 41:11, s. 1312-1319
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives. To estimate the incidence of fatal colonic ischaemia (CI) and the cause-specific mortality of CI, and to describe the localization and extension of colonic infarction and quantify the risk factors associated with CI. Material and methods. Between 1970 and 1982 the autopsy rate in Malmo, Sweden, was 87%, creating the possibilities for a population-based study. Out of 23,446 clinical autopsies, 997 cases were coded for intestinal ischaemia in a database. In addition, 7569 forensic autopsy protocols were analysed. In a case-control study nested in the clinical autopsy cohort, four CI-free controls, matched for gender, age at death and year of death, were identified for each fatal CI case in order to evaluate the risk factors. Results. The cause-specific mortality ratio was 1.7/1000 autopsies. The overall incidence of autopsy-verified fatal CI was 1.7/100,000 person years, increasing with age up to 23/100,000 person years in octogenarians. Fatal cardiac failure (odds ratio (OR) 5.2), fatal valvular disease (OR 4.3), previous stroke (OR 2.5) and recent surgery (OR 3.4) were risk factors for fatal CI. Narrowing/occlusion of the inferior mesenteric artery (IMA) at the aortic origin was present in 68% of the patients. The most common segments affected by transmural infarctions were the sigmoid (83%) and the descending (77%) colon. Conclusions. Heart failure, atherosclerotic occlusion/stenoses of the IMA and recent surgery were the main risk factors causing colonic hypoperfusion and infarction. Segments of transmural infarctions were observed within the left colon in 94% of the patients. Awareness of the diagnosis and its associated cardiac comorbidities might help to improve survival.
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