| 1. |
- Simán, Henrik, et al.
(author)
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Association between Helicobacter pylori and gastric carcinoma in the city of Malmo, Sweden. A prospective study
- 1997
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In: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 1502-7708 .- 0036-5521. ; 32:12, s. 1215-1221
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Journal article (peer-reviewed)abstract
- BACKGROUND: We have investigated the association between Helicobacter pylori and gastric carcinoma through a nested case-control study in a single city. METHODS: From a cohort of 32,906 residents recruited from 1974 through 1992, 56 cases of gastric adenocarcinoma and 224 matched controls were selected. The mean interval between serum collection and diagnosis was 5.7 years. Frozen serum or plasma samples were analysed for IgG antibodies against H. pylori with an enzyme-linked immunosorbent assay. RESULTS: The overall seropositivity prevalence in gastric cancer cases was 82%, compared with 49% in controls, giving an odds ratio (OR) of 5.0 (95% confidence interval (CI), 2.2-11.5). Partial gastrectomy because of peptic ulcer 5 to 36 year before diagnosis of gastric cancer could be a confounding factor. With exclusion of 10 such cases, H. pylori seropositivity among cases was 78%, as compared with 50% in matched controls (OR, 3.9; 95% CI, 1.7-9.2). Tumours of the cardia were not associated with H. pylori (OR, 0.92; 95% CI, 0.23-3.7), which is in contrast to tumours of the fundus, corpus, and antrum, which were significantly associated (OR, 11.1; 95% CI, 2.4-71.8). This difference in location was significant (P < 0.01). CONCLUSION: There is a significant association between prior infection with H. pylori and later development of gastric carcinoma, and the association is related to noncardia gastric cancer.
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| 2. |
- Ekström, Ulf, et al.
(author)
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An individual with a healthy phenotype in spite of a pathogenic LDL receptor mutation (C240F)
- 1999
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In: Clinical Genetics. - : Wiley. - 0009-9163. ; 55:5, s. 332-339
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Journal article (peer-reviewed)abstract
- Familial hypercholesterolemia (FH) is caused by a defect in the function of the low density lipoprotein (LDL) receptor and inherited in an autosomal, codominant way. In this study we present a 13-year-old girl, compound heterozygote for the LDL receptor mutations C240F and Y167X. Fibroblasts from the patient showed very low cholesterol esterification rate, LDL uptake, and degradation compared to normal fibroblasts (< 2%, 8%, and < 2%, respectively). The C240F mutant was expressed in LDL receptor deficient CHOMldlA7 cells. Analysis of cell extracts by immunoblotting demonstrated delayed processing of the mutated LDL receptor, which was accumulated as a precursor protein of normal size. A high molecular weight form of the receptor was also detectable in these cells, which probably reflects cross-linking through the unpaired cysteine residue in the binding domain. Cells expressing the C240F mutant protein were unable to mediate uptake and degradation of LDL. The two siblings of the index case also carried the C240F mutation, but surprisingly one of them (a 17-year-old brother) showed no signs of hypercholesterolemia. This observation is consistent with the view that there may be cholesterol lowering mechanisms that can be activated, perhaps by mutations in known or hitherto unknown genes.
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| 3. |
- Ekström, Ulf, et al.
(author)
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Mutations in the low-density lipoprotein receptor gene in Swedish familial hypercholesterolaemia patients: clinical expression and treatment response
- 1998
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In: European Journal of Clinical Investigation. - : Wiley. - 0014-2972. ; 28:9, s. 740-747
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Journal article (peer-reviewed)abstract
- BACKGROUND: Familial hypercholesterolaemia, an autosomal co-dominant disorder caused by defects in the low-density lipoprotein receptor gene, is strongly associated with premature development of cardiovascular disease. METHODS: In this study, we have applied a gene screening method in a population of familial hypercholesterolaemia patients in order to describe the genetic background of the disease in southern Sweden. These patients were studied with the aim of relating the presence of the different mutations to the clinical expression of the disease and to the response to pharmacological treatment. RESULTS: In 16 out of 21 patients, potentially disease-causing low-density lipoprotein receptor gene defects were found, including five not previously described alterations (C240-->F, C122-->stop, C356-->Y, 785insG, 165delG). No defects in apolipoprotein B were found. One group of patients (n = 4) carried the mutation C122-->stop and another group of patients (n = 4) a mutation causing the substitution W66-->G. Patients in the two genotype subgroups were very similar with respect to lipid levels before treatment. CONCLUSION: A tendency towards differential susceptibility to treatment with statins was observed for the patient groups, encouraging further comparative studies of heterozygous FH patients.
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| 4. |
- Florén, Claes-Henrik, et al.
(author)
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Bone mineral density in patients with Crohn's disease during long-term treatment with azathioprine
- 1998
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In: Journal of Internal Medicine. - 1365-2796. ; 243:2, s. 123-126
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Journal article (peer-reviewed)abstract
- OBJECTIVES: To ascertain whether patients with Crohn's disease treated with azathioprine maintained bone mineral mass better than patients treated with steroids alone. DESIGN: Retrospective study. SETTING: University Hospital of Malmo, Sweden. SUBJECTS: A total of 59 patients with ileocolonic, ileocaecal or colonic Crohn's disease. METHODS: Bone mass was assessed by dual photon X-ray absorptiometry at the level of L2-L4. RESULTS: Patients treated with a high lifetime dose of steroids (> 5 g prednisolone) had significantly (P = 0.011) lower Z-score of L2-L4 (-0.87 +/- 1.11; 11 SD) than steroid-treated patients, who had received a low dose of prednisolone (< 5 g) (0.08 +/- 1.16 SD). Azathioprine did not negatively influence the steroid effect on bone mineral density. CONCLUSIONS: Azathioprine does not seem to affect bone mineral density by itself. However, by being steroid-saving, it seems to conserve bone mineral mass in patients with Crohn's disease.
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| 5. |
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| 6. |
- Solvig, J, et al.
(author)
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Ultrasound examination of the small bowel: comparison with enteroclysis in patients with Crohn disease
- 1995
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In: Abdominal Imaging. - 0942-8925. ; 20:4, s. 323-326
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Journal article (peer-reviewed)abstract
- BACKGROUND: Screening for inflammatory small bowel disease has hereto relied on barium examination, usually performed after duodenal intubation. A noninvasive technique for imaging of the small bowel in such patients would be preferable. METHODS: A total of 59 patients were included in the study. A small bowel barium examination (SBE) was performed after duodenal intubation using a barium and air double-contrast technique. Ultrasound (US) of the right lower quadrant was performed with a 3.5- or 5-MHz transducer. The patients fasted overnight. RESULTS: In 37 of 39 patients with a normal SBE, US was also normal. In 20 patients, SBE showed lesions compatible with Crohn disease and in 18 of these the US study showed thickening of the bowel wall. One of these patients later tested positive for Yersinia enterocolitica. There were two false-positive and two false-negative US examinations. For detection of inflammatory disease of the small bowel, US was calculated to have a sensitivity of 0.95, specificity of 0.93, accuracy of 0.93, predictive value of a positive test was 0.90, and a predictive value of a negative test was 0.95. CONCLUSIONS: US, therefore, seems to be a reliable method in the workup of patients suspected of having inflammatory small bowel disease. Thereby, US probably can select patients for SBF.
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