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Objective A prevailing hypothesis for neuropsychiatric involvement in systemic lupus erythematosus (SLE) and primary Sjögren’s syndrome is that brain reactive autoantibodies enter the brain through a disrupted blood–brain barrier. Our aim was to investigate whether TNF-like weak inducer of apoptosis (TWEAK) plays a role in cerebral involvement in human SLE and primary Sjögren’s syndrome, and whether an impaired blood–brain barrier is a prerequisite for neuropsychiatric manifestations. Methods TWEAK was measured in the cerebrospinal fluid and serum and compared with markers of blood–brain barrier permeability (Q-albumin and MRI contrast-enhanced lesions) and S100B, an astrocyte activation marker in 50 SLE and 52 primary Sjögren’s syndrome patients. Furthermore, we estimated the general intrathecal B-cell activation (IgG index), measured anti-NR2 antibodies in cerebrospinal fluid, and explored whether these variables were associated with neuropsychiatric manifestations. Results No associations were found between TWEAK in the cerebrospinal fluid or serum and neuropsychiatric manifestations in SLE nor in primary Sjögren’s syndrome patients. Furthermore, no associations were found between neuropsychiatric manifestations and indicators of blood–brain barrier integrity or astroglial activity. Anti-NR2 antibodies were associated with impaired visuospatial processing (odds ratio 4.9, P = 0.03) and motor functioning (odds ratio 6.0, P = 0.006). Conclusion No clinical neuropsychiatric manifestations could be attributed to impaired integrity of the blood–brain barrier, or to TWEAK levels in cerebrospinal fluid or serum in either patient group. The TWEAK concentration was considerably higher in the cerebrospinal fluid than in blood, which indicates intrathecal production. We hypothesize that increased TWEAK and S100B result from immunological stress caused by brain-reactive antibodies produced by brain residing immune cells. [ABSTRACT FROM AUTHOR]

Background : Iron deficiency is a common complication of inflammatory bowel disease. Oral iron therapy may reinforce intestinal tissue injury by catalyzing production of reactive oxygen species. Aim : To compare the effects of ferrous sulphate and non-ionic iron–polymaltose complex on markers of oxidative tissue damage and clinical disease activity in patients with inflammatory bowel disease. Methods : Forty-one patients with inflammatory bowel disease and iron deficiency were randomized to treatment with ferrous sulphate 100 mg twice a day or iron–polymaltose complex 200 mg once a day for 14 days. Results : Following ferrous sulphate, plasma malondialdehyde increased ( P = 0.02), while urine 8-isoprostaglandin F2 α and plasma antioxidants did not change significantly. Iron–polymaltose complex did not change plasma malondialdehyde, urine 8-isoprostaglandin F2 α or plasma antioxidants. Comparing the two treatments, changes in plasma malondialdehyde tended to differ ( P = 0.08), while urine 8-isoprostaglandin F2 α and plasma antioxidants did not differ. Neither ferrous sulphate nor iron–polymaltose complex altered clinical disease activity indices. Conclusions : Ferrous sulphate increased plasma malondialdehyde, a marker of lipid peroxidation. Comparing treatment with ferrous sulphate and iron–polymaltose complex, changes in plasma malondialdehyde tended to differ. Clinical disease activity was unchanged after both treatments. [ABSTRACT FROM AUTHOR]

Objectives: The production of magnesium is a well known source of both aliphatic and aromatic chlorinated compounds, among others the polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs). The aim of this study was to establish whether increased concentrations of PCDDs and PCDFs could be found in the blood of workers in a magnesium plant.Methods: Blood plasma from 10 workers, employed at a magnesium plant for 10 to 36 years, and from a control group consisting of nine people who had no direct contact with the production were studied. Isomer specific analyses of PCDDs and PCDFs by means of high resolution gas chromatography/high resolution mass spectrometry (HRGC/HRMS) techniques were performed.Results: A significant increase was found in the concentrations of some of the congeners, mainly PCDFs, in the workers compared with the control group. Octachlorodibenzofuran (OCDF) is the congener that most strongly correlates with occupational exposure in the magnesium plant. Low concentrations of 1,2,3,4,6,8,9-heptachlorodibenzofuran were found in seven of the workers. Such isomers--that is, not 2,3,7,8-substituted--are rarely found in human samples.Conclusion: Due to the long biological half lives and lipid solubility of PCDDs and PCDFs, blood analyses may serve as an index of past cumulative occupational exposure and a means of assessing a person's exposure situation. [ABSTRACT FROM AUTHOR]