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1.
Ugeskr Laeger ; 162(31): 4145-9, 2000 Jul 31.
Article in Danish | MEDLINE | ID: mdl-10962915

ABSTRACT

To evaluate MRI for assessment of inflammation, destruction and prognosis in rheumatoid arthritis (RA), 26 RA patients, randomized to disease-modifying anti-rheumatic drug (DMARD) therapy alone or in combination with oral prednisolone, were followed for one year with contrast-enhanced MRI of the dominant wrist (months zero, three, six and 12), conventional radiography and clinical and biochemical examinations. Significant synovial membrane volume reductions were observed in both groups, earliest in the DMARD + prednisolone group. The rate of erosive progression on MRI was highly correlated with baseline and area-under-curve (AUC)-values of synovial membrane volume, but not with baseline or AUC-values of local or global clinical or biochemical parameters, nor with +/- prednisolone. MRI was more sensitive than radiography as regards detection of progressive bone destruction (22 versus 12 new bone erosions). MRI may prove valuable as marker of joint disease activity and destruction and, perhaps, prognosis in RA.


Subject(s)
Arthritis, Rheumatoid , Magnetic Resonance Imaging/methods , Wrist Joint/pathology , Adult , Aged , Anti-Inflammatory Agents/administration & dosage , Antirheumatic Agents/administration & dosage , Arthritis, Rheumatoid/diagnosis , Arthritis, Rheumatoid/drug therapy , Arthritis, Rheumatoid/pathology , Follow-Up Studies , Humans , Middle Aged , Prednisolone/administration & dosage , Prognosis , Synovial Membrane/pathology
2.
Ugeskr Laeger ; 159(25): 3956-61, 1997 Jun 16.
Article in Danish | MEDLINE | ID: mdl-9214070

ABSTRACT

Volumes of synovial membrane and joint effusion were determined by MRI in 36 knees with gonarthritis and five healthy knees. In 18 knees MRI was performed before and immediately after arthrocentesis. The difference between MRI-determined and syringe-determined volumes of aspirated joint fluid was 0-7 ml, median 2 ml, corresponding to 0-18%, median 7%, of the pre-aspiration effusion volume. Synovial membrane volumes, determined before and after arthrocentesis varied 0-10 ml, median 3 ml (0-17%, median 7%). No significant systematic misinterpretation of the borderline between joint fluid and synovium was found. The interobserver variation was < 15% in all measurements of synovial volumes > 10 ml and effusion volumes > 5 ml. Patient repositioning resulted in variations < 10%. The synovial volumes in clinically active, clinically inactive and healthy knees were statistically significantly different (median 79 ml, 21 ml and 3 ml, respectively). We conclude that effusion volumes, and in all probability also synovial membrane volumes, can be determined by MRI with a maximal error of approximately 20%. The synovial volume is related to the inflammatory activity of the joint. The results encourage further studies of the value of effusion and synovial membrane volumes as markers of the activity and/or severity of joint inflammation.


Subject(s)
Arthritis, Rheumatoid/diagnosis , Knee Joint/pathology , Synovial Fluid/physiology , Synovial Membrane/pathology , Arthritis, Rheumatoid/physiopathology , Cross-Sectional Studies , Humans , Knee Joint/physiopathology , Magnetic Resonance Imaging , Observer Variation
3.
Eur J Clin Invest ; 25(1): 15-8, 1995 Jan.
Article in English | MEDLINE | ID: mdl-7705381

ABSTRACT

This paper assesses alterations in collagen metabolism following thrombolytic therapy of acute myocardial infarction with tissue-plasminogen activator. Sequential serum measurements of the amino-terminal propeptide of type III procollagen (S-PIIINP) and the carboxyterminal propeptide of type I collagen (S-PICP) in patients suspected of acute myocardial infarction randomized to tissue-plasminogen activator or placebo were used. S-PIIINP increased at 3 h in patients with acute myocardial infarction treated with tissue-plasminogen activator (P < 0.05). S-PIIINP was higher in patients treated with tissue-plasminogen activator compared with placebo-treated patients at 3 and 6 h (P < 0.05). S-PICP decreased independently of therapy and diagnosis. Tissue-plasminogen activator, therefore, induces breakdown of collagen, some of which is located in the wall of atheromatous arteries. Vascular patency following thrombolytic therapy may partly be mediated by breakdown of thrombogenic collagen in the vessel wall. The findings may suggest a role for S-PIIINP as a non-invasive indicator of the risk of reocclusion.


Subject(s)
Collagen/metabolism , Myocardial Infarction/drug therapy , Myocardial Infarction/metabolism , Thrombolytic Therapy , Tissue Plasminogen Activator/therapeutic use , Adolescent , Adult , Aged , Biomarkers/blood , Collagen/drug effects , Female , Humans , Male , Middle Aged , Peptide Fragments/blood , Procollagen/blood , Tissue Plasminogen Activator/metabolism
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