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Frequency of antibiotic-associated diarrhoea in 2462 antibiotic-treated hospitalized patients : a prospective study
- 2001
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Ingår i: Journal of Antimicrobial Chemotherapy. - : Oxford University Press (OUP). - 0305-7453 .- 1460-2091. ; 47:1, s. 43-50
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Tidskriftsartikel (refereegranskat)abstract
- The frequency of antibiotic-associated diarrhoea (AAD) and Clostridium difficile-associated diarrhoea (CdAD) was prospectively determined in a population of 2462 patients recruited from five Swedish hospitals, including divisions for infectious diseases, orthopaedics, surgery, geriatrics, nephrology and internal medicine. AAD developed in 4.9% of the treated patients. Faecal samples were obtained from 69% of patients with AAD and 55.4% were positive for C. difficile cytotoxin B. The frequency of AAD varied from 1.8 to 6.9% at the participating centres (P < 0.001). The frequency of AAD also varied considerably between medical disciplines and wards within different hospitals and was highest in the nephrology and geriatric units (6.7 and 7.1%, respectively). There was no difference in frequency of AAD when analysed with respect to gender or age. Medical interventions (laxative treatment, endoscopy and abdominal surgery) or presence of one concomitant disease (diabetes, malignancy, chronic renal disease and inflammatory bowel disease) did not significantly affect the frequency of AAD, whereas patients suffering from two or more of these illnesses had significantly (P = 0.001) higher frequencies of AAD. Patients treated with antibiotics for 3 days had a significantly (P = 0.009) lower frequency of AAD than those treated for longer periods. Treatment with cephalosporins, clindamycin or broad-spectrum penicillins was associated with an increased risk of AAD. With specimens from one centre, 62.5% of tested patients with AAD and 33.8% of asymptomatic patients were positive for cytotoxin B. Although C. difficile cytotoxin B in stool samples was significantly associated with AAD IP = 0.003), the causal relationship with diarrhoea is not always evident.
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- Jensen-Urstad, K, et al.
(författare)
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Cardiac valvular abnormalities are frequent in systemic lupus erythematosus patients with manifest arterial disease
- 2002
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Ingår i: Lupus. - : SAGE Publications. - 0961-2033 .- 1477-0962. ; 11:11, s. 744-752
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Tidskriftsartikel (refereegranskat)abstract
- The objective of this study was to study cardiac valve morphology and function and ventricular function in systemic lupus erythematosus(SLE) patients with and without co-existingcardiovascular disease (CVD) and in populationcontrols.Twenty-six women (52§ 8.2 years) with SLE (SLE cases) and a history of CVD (angina pectoris, myocardial infarction, cerebral infarction or intermittent claudication) were compared with 26 age-matched women with SLE but without manifest CVD (SLE controls) and 26 age-matched control women (population controls). Echocardiography was performed to assess valvular abnormalities and manifestations of ischaemic heart disease. Thirteen of the 26 SLE cases but only one of the SLE controls and one of the population controls had cardiac valvularabnormalities.Three of the SLE cases had already undergonevalve replacement and another had significant aortic insufficiency; the other nine had thickening of mainly mitral leaflets without hemodynamic significance. Among SLE cases, patients with valvular abnormalities had higher homocysteine (P < 0.001) and triglyceride (P=0.02) concentrations than patients without valvular disease. In contrast atherosclerosis as determined by IMT, oxidized LDL as measured by the monoclonal antibody E06, autoantibodiesagainst epitopesof OxLDL (aOxLDL) or phospholipids (aPL), disease duration or activity, or acute phase reactants did not differ between SLE cases with or without valvular abnormalities.Valvular abnormalitieswere not more common in SLE cases with stroke as compared to those with myocardial infarction, angina or claudication. In conclusion, valvular abnormalities are strongly associated with CVD in SLE. Raised levels of homocysteine and triglycerides characterize patients with cardiac valve abnormalities.
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- Prokunina, Ludmila, et al.
(författare)
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A regulatory polymorphism in PDCD1 is associated with susceptibility to systemic lupus erythematosus in humans
- 2002
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Ingår i: Nature Genetics. - : Springer Science and Business Media LLC. - 1061-4036 .- 1546-1718. ; 32:4, s. 666-669
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Recension (övrigt vetenskapligt/konstnärligt)abstract
- Systemic lupus erythematosus (SLE, OMIM 152700) is a complex autoimmune disease that affects 0.05% of the Western population, predominantly women. A number of susceptibility loci for SLE have been suggested in different populations, but the nature of the susceptibility genes and mutations is yet to be identified. We previously reported a susceptibility locus (SLEB2) for Nordic multi-case families. Within this locus, the programmed cell death 1 gene (PDCD1, also called PD-1) was considered the strongest candidate for association with the disease. Here, we analyzed 2,510 individuals, including members of five independent sets of families as well as unrelated individuals affected with SLE, for single-nucleotide polymorphisms (SNPs) that we identified in PDCD1. We show that one intronic SNP in PDCD1 is associated with development of SLE in Europeans (found in 12% of affected individuals versus 5% of controls; P = 0.00001, r.r. (relative risk) = 2.6) and Mexicans (found in 7% of affected individuals versus 2% of controls; P = 0.0009, r.r. = 3.5). The associated allele of this SNP alters a binding site for the runt-related transcription factor 1 (RUNX1, also called AML1) located in an intronic enhancer, suggesting a mechanism through which it can contribute to the development of SLE in humans.
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- Svenungsson, E, et al.
(författare)
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TNF-alpha: a link between hypertriglyceridaemia and inflammation in SLE patients with cardiovascular disease
- 2003
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Ingår i: Lupus. - : SAGE Publications. - 0961-2033 .- 1477-0962. ; 12:6, s. 454-461
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Tidskriftsartikel (refereegranskat)abstract
- Patients with systemic lupus erythematosus (SLE) are at high risk of cardiovascular disease (CVD). Tumour necrosisfactor-a (TNF-α) has been implicatedin the pathophysiologicalprocessesof both SLE and CVD. This study focuses on the role of TNF-α and its soluble receptors in SLE-related CVD. In summary, 26 women (52 + 8.2 years) with SLE and a history of CVD (SLE cases)were compared with 26 age-matched women with SLE and no clinical manifestations of CVD (SLE controls) and 26 age-matched population-based control women (population controls). Plasma concentrations of circulating TNF-α, TNF-α receptor 1 (sTNFR1) and TNF-α receptor 2 (sTNFR2) were determined by ELISA. TNF-α, sTNFR1 and sTNFR2 were raised in SLE cases as compared to SLE controls ( P = 0.009; P = 0.001; P = 0.001, respectively), and SLE controls had higher levels than population controls ( P = 0.001; P = 0.02; P = 0.001, respectively). Exclusively in the SLE case group there was a striking positivecorrelationbetweenTNF-α and plasma triglycerides( r = 0.57, P < 0.002), VLDL triglycerides ( r = 0.54, P = 0.004) and VLDL cholesterol ( r = 0.58, P = 0.002). Furthermore, TNF-α correlated with the waist-hip ratio but not with estimated insulin resistance. TNF-α may thus be a major factor in SLE-related CVD acting both by contributing to hypertriglyceridaemia and by promoting atherosclerosis-relatedinflammation. sTNFR1 and sTNFR2 are strongly associated with CVD in SLE but their exact roles in disease development remain to be elucidated.
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- Trysberg, Estelle, 1960, et al.
(författare)
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Decreased levels of soluble amyloid beta-protein precursor and beta-amyloid protein in cerebrospinal fluid of patients with systemic lupus erythematosus
- 2004
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Ingår i: Arthritis Res Ther. - : Springer Science and Business Media LLC. - 1478-6362 .- 1465-9905. ; 6:2
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Tidskriftsartikel (refereegranskat)abstract
- Symptoms originating from the central nervous system (CNS) frequently occur in patients with systemic lupus erythematosus (SLE). These symptoms are extremely diverse, including a state of dementia. The aim of this study was to examine the cerebrospinal fluid (CSF) content of soluble molecules indicating axonal degeneration and amyloidogenesis.One hundred and fourteen patients with SLE and age-matched controls were evaluated clinically, with magnetic resonance imaging of the brain and CSF analyses. Levels of tau, amyloid precursor protein (APP), beta-amyloid protein (Abeta42), and transforming growth factor beta (TGF-beta) were all determined using sandwich ELISAs.APP and Abeta42 levels were significantly decreased in SLE patients irrespective of their CNS involvement, as compared with healthy controls. Patients with neuropsychiatric SLE who underwent a second lumbar puncture following successful cyclophosphamide treatment showed further decreases of Abeta42. CSF-tau levels were significantly increased in SLE patients showing magnetic resonance imaging-verified brain pathology as compared with SLE patients without such engagement. Importantly, tau levels displayed significant correlation to Abeta42 levels in the CSF. Finally, TGF-beta levels were significantly increased in patients with neuropsychiatric SLE as compared with those without.Low intrathecal levels of Abeta42 found in SLE patients seem to be a direct consequence of a diminished production of APP, probably mediated by heavy anti-inflammatory/immuno-suppressive therapy. Furthermore, our findings suggest that CSF tau can be used as a biochemical marker for neuronal degeneration in SLE. Finally, the increased TGF-beta levels observed may support a notion of an ongoing anti-inflammatory response counteracting tissue injury caused by CNS lupus.
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