Low-dose prednisolone in early rheumatoid arthritis inhibits collagen type I degradation by matrix metalloproteinases as assessed by serum 1CTP--a possible mechanism for specific inhibition of radiological destruction

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Fältnamn	Indikatorer	Metadata
000		04463naa a2200565 4500
001		oai:DiVA.org:umu-82922
003		SwePub
008		131113s2013 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
009		oai:gup.ub.gu.se/170664
009		oai:prod.swepub.kib.ki.se:126459716
024	7	a https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-829222 URI
024	7	a https://doi.org/10.1093/rheumatology/kes3692 DOI
024	7	a https://gup.ub.gu.se/publication/1706642 URI
024	7	a http://kipublications.ki.se/Default.aspx?queryparsed=id:1264597162 URI
040		a (SwePub)umud (SwePub)gud (SwePub)ki
041		a engb eng
042		9 SwePub
072	7	a ref2 swepub-contenttype
072	7	a art2 swepub-publicationtype
100	1	a Engvall, Inga-Lillu Karolinska Institutet4 aut
245	1 0	a Low-dose prednisolone in early rheumatoid arthritis inhibits collagen type I degradation by matrix metalloproteinases as assessed by serum 1CTP--a possible mechanism for specific inhibition of radiological destruction
264		c 2012-12-28
264	1	b Oxford University Press (OUP),c 2013
338		a print2 rdacarrier
520		a OBJECTIVE: To study the effects of low-dose prednisolone on the osteoclast-regulating proteins osteoprotegerin (OPG) and RANK ligand (RANKL) and on markers of bone resorption, 1CTP generated by MMPs and CTX-1 generated by cathepsin K, in patients with early RA in relation to inflammation and joint destruction.METHODS: In 225 patients, who at the start of the first DMARD had been randomized to 7.5 mg prednisolone daily for 2 years, the P-group, or no prednisolone, the NoP-group, OPG and RANKL were analysed at 0-24 months and 1CTP and CTX-1 at 0-12 months. Radiographs of hands and feet were assessed at 0, 1 and 2 years using the modified Sharp-van der Heijde score and radiological progression defined as increase in total Sharp score above 5.8. Data were analysed with a mixed linear model and by the GENMOD procedure.RESULTS: In the P-group, RANKL and the ratio OPG/RANKL were stable between baseline and 24 months, whereas in the NoP-group, RANKL increased and the ratio OPG/RANKL decreased. CTX-1 decreased significantly more in the P-group. 1CTP decreased over time in both groups, but more in the P-group, P < 0.001, a difference also present in the subgroups of patients in remission. The decrease in 1CTP was associated with less radiological progression after 2 years and displayed a significant interaction with treatment. CONCLUSION: Low-dose prednisolone may inhibit progression of joint destruction by interfering with MMP activity, seen as a marked decrease in 1CTP, as well as by impairing osteoclast activation, shown by a stable OPG/RANKL ratio.
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Odontologi0 (SwePub)302162 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Dentistry0 (SwePub)302162 hsv//eng
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Reumatologi och inflammation0 (SwePub)302102 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Rheumatology and Autoimmunity0 (SwePub)302102 hsv//eng
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Endokrinologi och diabetes0 (SwePub)302052 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Endocrinology and Diabetes0 (SwePub)302052 hsv//eng
653		a rheumatoid arthritis
653		a prednisolone
653		a joint destruction
653		a OPG
653		a RANKL
653		a 1CTP
653		a CTX-1
700	1	a Svensson, Björn4 aut
700	1	a Boonen, Annelies4 aut
700	1	a van der Heijde, Désirée4 aut
700	1	a Lerner, Ulf Hu Gothenburg University,Göteborgs universitet,Umeå universitet,Institutionen för odontologi,Centre for Bone and Arthritis Research4 aut0 (Swepub:gu)xlerul
700	1	a Hafström, Ingiäldu Karolinska Institutet4 aut
710	2	a Karolinska Institutetb Institutionen för odontologi4 org
773	0	t Rheumatologyd : Oxford University Press (OUP)g 52:4, s. 733-742q 52:4<733-742x 1462-0324x 1462-0332
856	4	u https://academic.oup.com/rheumatology/article-pdf/52/4/733/5085295/kes369.pdf
856	4 8	u https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-82922
856	4 8	u https://doi.org/10.1093/rheumatology/kes369
856	4 8	u https://gup.ub.gu.se/publication/170664
856	4 8	u http://kipublications.ki.se/Default.aspx?queryparsed=id:126459716

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