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  • 1
    Electronic Resource
    Electronic Resource
    Type I Allergy to Normal Cellular Constituents in Chronic Inflammatory Bowel Disease? (1984)
    Oxford, UK : Blackwell Publishing Ltd
    Allergy 39 (1984), S. 0 
    Details
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The possibility of autoimmune type I reactions to cellular constituents was investigated in 22 patients with ulcerative colitis, 12 with Crohn's disease, and in 22 healthy volunteers Nuclear components and colon mucosa fragments were tested as potential antigens by the basophil histamine release technique One of 12 patients with ulcerative colitis responded to sonicated leukocyte nuclei and one of 12 patients with Crohn's disease responded to both nuclei and RNA. Increased serum levels of total IgE and antinuclear antibodies of IgE class were found in one and three of the 24 patients, respectively Histamine release caused by colon mucosa fragments was not observed in a separate study consisting of 10 ulcerative colitis patients and 10 healthy volunteers. Autoimmune type I allergy to cellular‘constituents does not seem to be of significance for chronic inflammatory bowel disease and thus could not explain the involvement of tissue mast cells and eosinophils in this condition
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1398-9995.1984.tb01929.x
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  • 2
    Electronic Resource
    Electronic Resource
    Inhibition of intestinal macrophage chemotaxis to leukotriene B4 by sulphasalazine, olsalazine, and 5-aminosalicylic acid (1988)
    Oxford, UK : Blackwell Publishing Ltd
    Alimentary pharmacology & therapeutics 2 (1988), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Purified intestinal macrophages obtained at resections for colonic neoplasms were investigated for chemotaxis to leukotriene B4 (LTB4) by the Millipore filter assay and leading front technique. Possible inhibition by drugs effective in the treatment of chronic inflammatory bowel disease (sulphasalazine, olsalazine, its active moiety 5-aminosalicylic acid (5-ASA), and the 5-ASA metabolite N-acetylated-5-ASA (ac-5-ASA)) was tested at therapeutic colonic concentrations of 0.01–10 mm. Leukotriene B4 at a dose of 10 nm was equipotent with casein (5 g litre—1) as regards chemoattraction of macrophages. Sulphasalazine, olsalazine and 5-ASA were potent inhibitors of macrophages chemotaxis to LTB4 with IC50 values of 0.43, 0.39 and 0.24 mm, respectively. These concentrations are below the lowest concentration of 5—ASA (2 mm) in the colonic lumen during conventional sulphasalazine treatment of patients with chronic inflammatory bowel disease. The inhibition of macrophage chemotaxis by these drugs may be important for this limitation of the local inflammatory process in chronic inflammatory bowel disease, and may in part explain the beneficial effect of systemic and local treatment with sulphasalazine. Leukotriene B4 appears to be an important inflammatory mediator for the activation of macrophages in colonic inflammation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2036.1988.tb00689.x
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Effects of antirheumatic drugs on endogenous arachidonate metabolism and chemotaxis in human neutrophil granulocytes (1989)
    Springer
    Inflammation research 26 (1989), S. 233-234 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Conclusion Calcium ionophore A23187 was chosen for these studies, since 5-lipoxygenase exhibits an absolute requirement for calcium, and A23187 is assumed to produce the maximal synthesis of leukotrienes in response to calcium influx. The sensitivity of the present 5-lipoxygenase assay did not allow quantification of the markedly lower synthesis of 5-lipoxygenase products from PMNs challenged with physiologic stimuli. The present results suggest that local recruitment and activation of PMNs may be inhibited by timegadine and auranofin, leading to a minimized production of tissue destructive and pro-inflammatory mediators, such as LTB4 and 5-HETE. Inflammation may be further reduced by timegadine and auranofin because PMNs, apart from producing inflammatory active eicosanoids, also have the potential for release of tissue destructive oxygen free radicals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02126622
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  • 4
    Electronic Resource
    Electronic Resource
    Elevated serum parathyroid hormone concentration during treatment with high ceiling diuretics (1980)
    Springer
    European journal of clinical pharmacology 18 (1980), S. 363-364 
    Details
    ISSN: 1432-1041
    Keywords: furosemide ; bumetanide ; serum parathyroid hormone ; serum calcium ; serum alkaline phosphatase ; bone remodelling
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Serum concentrations of parathyroid hormone (s-PTH) calcium, phosphorus and alkaline phosphatase were measured during treatment with furosemide or bumetanide for congestive heart failure. Significant elevations both of s-PTH and alkaline phosphatase were found, whereas serum calcium concentration was descreased. The changes were not related to the dose of drug or to the duration of treatment. It is concluded that treatment with furosemide or bumetanide may cause hypocalcaemia, resulting in elevation of s-PTH. The increased concentration of alkaline phosphatase may indicate accelerated bone remodelling, as found in primary hyperparathyroidism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00561397
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  • 5
    Electronic Resource
    Electronic Resource
    Lack of adrenergic influence on renin release after furosemide in normal man (1981)
    Springer
    European journal of clinical pharmacology 20 (1981), S. 339-342 
    Details
    ISSN: 1432-1041
    Keywords: furosemide ; propranolol ; sympathetic nervous system ; plasma renin concentration ; plasma catecholamines ; renin release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The role of the sympathetic nervous system in furosemide-induced renin release was investigated in six normal subjects. After intravenous administration of furosemide, plasma renin concentrations increased more than two-fold within 15 min. Neither replacement of urinary fluid loss by intravenous infusion of saline nor pharmacological betablockade with d,1-propranolol changed the renin response to furosemide. The activity of the sympathetic nervous system, as estimated by measurement of plasma catecholamine concentrations, remained at the reference level after furosemide. It is concluded that the sympathetic nervous system is not involved in renin release after intravenous administration of furosemide.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00615402
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  • 6
    Electronic Resource
    Electronic Resource
    Inhibition of 5-lipoxygenase pathway of arachidonic acid metabolism in human neutrophils by sulfasalazine and 5-aminosalicylic acid (1987)
    Springer
    Digestive diseases and sciences 32 (1987), S. 577-582 
    Details
    ISSN: 1573-2568
    Keywords: 5-aminosalicylic acid ; sulfasalazine ; leukotrienes ; Crohn's disease ; ulcerative colitis ; neutrophils
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The possible effect of sulfasalazine, 5-aminosalicylic acid, and acetyl-5-aminosalicylic acid on endogenous arachidonic acid release and metabolism was studied in human polymorphonuclear leukocytes (PMNs). A newin vitro assay was used by which [1-14C]arachidonic acid is incorporated by purified peripheral PMNs until steady state was obtained (5 hr). After preincubation with the test drugs prior to activation with calcium ionophore A23187, the released eicosanoids were isolated by extraction and thin-layer chromatography (TLC) and quantitated by autoradiography and laser densitometry. Median drug concentrations needed for 50% inhibition of leukotriene B4 and 5-hydroxyeicosatetraenoic acid (5-HETE) release was 4–5 mM (range 1–9 mM) for both sulfasalazine and 5-aminosalicylic acid. The acetylated derivative of 5-aminosalicylic acid was ineffective. The present data suggest that inhibition of arachidonic acid lipoxygenation may be an essential action of sulfasalazine and its active metabolite, 5-aminosalicylic acid. Interference with lipoxygenase enzymes, rather than a steroid-like inhibition of arachidonic acid release from intracellular phospholipids, seems to be the mode of action.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01296156
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