Rheumatoid Arthritis: Mangge H

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A digest of articles written 1999 and later, on the topic "Arthritis, Rheumatoid," originating from Planet Earth —» Mangge H.  Display:  All Citations ·  All Abstracts
1 Review Beyond cholesterol--inflammatory cytokines, the key mediators in atherosclerosis. 2004

Mangge H, Hubmann H, Pilz S, Schauenstein K, Renner W, März W. · Clinical Institute of Medical and Chemical Laboratory Diagnosis, Medical University of Graz, Graz, Austria. · Clin Chem Lab Med. · Pubmed #15202781 No free full text.

Abstract: The development of atherosclerotic lesions encompasses a cascade of cellular and molecular responses that can at best be characterized as an inflammatory process, and exhibits striking similarities to autoimmune diseases, such as rheumatoid arthritis. Chemokines, cytokines and their receptors are critically involved in initiation and perpetuation of atherosclerosis, and they play important roles at all levels in the pathogenesis of this disease. In the present article, the currently available information on cytokines and chemokines as key mediators in atherosclerosis is reviewed. Furthermore, based on recent experiences of our own with very early stages of atherosclerosis, possible new ways to make use of these parameters toward improved early detection, prevention and treatment of this disease are indicated.

2 Review Do chemokines spark autoimmunity in juvenile and adult rheumatic disease? 2002

Mangge H, Vojinovic J, Schauenstein K. · Department of Laboratory Medicine, University of Graz, Austria. · Immunobiology. · Pubmed #12437075 No free full text.

Abstract: The recent increase in knowledge on chemokines contributes substantially to the understanding of autoimmune inflammatory diseases, as cell migration is an essential prerequisite for the local immune reaction. The purpose of this review is to summarize the essential functions of chemokines in immune activation and to examine their role(s) in the initiation and perpetuation of autoimmunity in juvenile idiopathic arthritis and adult rheumatic disease. The possible relevance of chemokines as therapeutical targets will be discussed.

3 Review Diet and rheumatoid arthritis--a review. 1999

Mangge H, Hermann J, Schauenstein K. · Department of Medical and Chemical Laboratory Diagnosis, School of Medicine, University of Graz, Austria. · Scand J Rheumatol. · Pubmed #10503555 No free full text.

This publication has no abstract.

4 Clinical Conference Long-term follow-up of cytokines and soluble cytokine receptors in peripheral blood of patients with juvenile rheumatoid arthritis. 1999

Mangge H, Gallistl S, Schauenstein K. · Department of Pediatrics, University of Graz, School of Medicine, Austria. · J Interferon Cytokine Res. · Pubmed #10505742 No free full text.

Abstract: Plasma levels of interleukin-1beta (IL-1beta), IL-2, soluble IL-2 receptor (sIL-2R), IL-6, IL-8, tumor necrosis factor-alpha (TNF-alpha), and the p60 soluble TNF receptor (sTNFR) were repeatedly determined by enzyme-linked immunosorbent assays (ELISA) in 35 patients with different subtypes of juvenile rheumatoid arthritis (JRA) during an observation period of up to 36 months. The data were related to conventional inflammatory parameters and disease activity. Patients with systemic disease showed the most pronounced elevations of plasma cytokines, followed by polyarticular and pauciarticular JRA. Soluble receptors sIL-2R and sTNFR were consistently elevated in patients of all JRA subtypes and indicated disease activity even in patients with normal C-reactive protein (CRP). In contrast, the determination of IL-1beta, IL-2, IL-8, and TNF-alpha revealed strikingly different individual profiles in patients of the same clinical subtype of JRA and irrespective of disease activity. It is concluded that the determination of sIL-2R and sTNFR may be relevant for monitoring JRA, as they indicate disease activity also in cases with unaltered conventional inflammatory parameters. The different individual cytokine profiles of patients within identical subtypes of disease suggest JRA to be even more heterogeneous than hitherto assumed. The data should be considered in attempts to develop anticytokine strategies in the therapy of JRA.

5 Article Fatal occlusive vessel disease in a patient with systemic juvenile idiopathic arthritis. 2004

Mangge H, Heinzl B, Grubbauer HM, Aschauer M, Tillich M. · Clinical Institute of Medical and Chemical Laboratory Diagnosis and Pediatric Rheumatology/Immunology, University of Graz, Graz, Austria. · J Rheumatol. · Pubmed #14760814 No free full text.

This publication has no abstract.

6 Article Atopic dermatitis as a side effect of anti-tumor necrosis factor-alpha therapy. 2003

Mangge H, Gindl S, Kenzian H, Schauenstein K. · Clinical Institute of Medical and Chemical Laboratory Diagnosis, University of Graz, A-8036 Graz, Austria. · J Rheumatol. · Pubmed #14677200 No free full text.

This publication has no abstract.

7 Article Therapeutic experience with infliximab in a patient with polyarticular juvenile idiopathic arthritis and uveitis. 2003

Mangge H, Heinzl B, Grubbauer HM, El-Shabrawi Y, Schauenstein K. · Clinical Institute of Medical and Chemical Laboratory Diagnosis, University Clinic of Graz, 8036 Graz, Austria. · Rheumatol Int. · Pubmed #12687288 No free full text.

Abstract: A pediatric patient with prolonged seronegative polyarticular juvenile idiopathic arthritis (JIA) and concomitant aggressive, anterior uveitis refractory to any conventional antirheumatic therapy was treated with infliximab. Arthritis and C-reactive protein (CRP) values showed prompt positive effects but, after 6 weeks, returned gradually to initial values despite ongoing therapy. In contrast, a more sustained therapeutic effect was observed on the uveitis, with increased visual acuity and reduced inflammatory signs of the affected eye. However, this benefit was also lost at week 30, after which infliximab had to be discontinued due to side effects. To conclude, in polyarticular seronegative JIA, infliximab showed a transient beneficial effect which was more pronounced on uveitis than arthritis.

8 Article Cystatin C, an early indicator for incipient renal disease in rheumatoid arthritis. 2000

Mangge H, Liebmann P, Tanil H, Herrmann J, Wagner C, Gallistl S, Schauenstein K, Erwa W. · Department of Laboratory Medicine (Blocklabor III) and Pediatric Immunology/Rheumatology, University of Graz, School of Medicine, A-8036, Graz, Austria. · Clin Chim Acta. · Pubmed #10958875 No free full text.

Abstract: Rheumatoid arthritis (RA) is a chronic disease requiring potential nephrotoxic therapy with nonsteroidal antiinflammatory drugs (NSAIDs) and disease modifying antirheumatic drugs (DMARDs). The rationale of our study was to examine the renal status of patients suffering from prolonged RA by means of plasma cystatin C, a new parameter of renal function. Fifty-six patients affected with RA for more than 5 years, and treated with NSAIDs for more than 50 months, were included in the study. Besides conventional markers of renal function (i.e. plasma creatinine, estimated glomerular filtration rate, creatinine clearance), we analysed plasma cystatin C by an automated, nephelometric immunoassay on a Behring nephelometer. Sixty percent of the RA patients exhibited elevated levels of plasma cystatin C, whereas only three out of 56 patients showed an elevated plasma creatinine, even though the creatinine clearance was decreased in 57% of these patients. Cystatin C exhibited a by far better correlation with creatinine clearance than plasma creatinine. In conclusion, patients with prolonged RA for more than 50 months, show a disturbed renal function despite normal plasma creatinine. Elevated cystatin C indicates such incipient renal disease, and is, not least because of a simple, well reproducible technique, more recommendable for screening purposes than tedious clearance determinations.

9 Article Early rheumatoid arthritis is associated with diminished numbers of TH1 cells in stimulated peripheral blood. 1999

Mangge H, Felsner P, Herrmann J, el-Shabrawi Y, Liebmann P, Schauenstein K. · Department of Laboratory Medicine (Blocklabor III), University of Graz, School of Medicine, Austria. · Immunobiology. · Pubmed #10416135 No free full text.

Abstract: Rheumatoid arthritis (RA) has been associated with an altered TH1/TH2 balance. Here we present first results with a technique to quantitate stimulated TH1 and TH2 subsets in whole blood by means of cytofluorimetric detection of intracytoplasmic TH1 and TH2 cytokines. A group of 10 patients suffering from initial stages of RA exhibited a significantly reduced percentage of TH1 cells (11.0 +/- 2.0%) in the peripheral blood as compared to 13 healthy, age matched controls (28.8 +/- 2.0%). The TH2 response, as determined by intracellular expression of IL-4, remained unchanged. The data may indicate a defect in the TH0-TH1 differentiation or/and a selective trapping of TH1 cells into the affected joints.