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Use of atorvastatin as an anti-inflammatory treatment in Crohn's disease.

Grip, Olof LU ; Janciauskiene, Sabina LU and Bredberg, Anders LU (2008) In British Journal of Pharmacology 155. p.1085-1092
Abstract
Background and purpose:Experimental and clinical investigations have revealed that statins can downregulate both acute and chronic inflammatory processes. Whether statins express anti-inflammatory activities in the treatment of Crohn's disease is unknown.Experimental approach:Ten patients were given 80 mg atorvastatin once daily for 13 weeks and then followed up for 8 weeks after the treatment. The anti-inflammatory effects of statin were assessed by measuring levels of plasma C-reactive protein (CRP), soluble (s) CD14, tumour necrosis factor (TNF)-alpha, sTNFRI and II, CCL2 and 8 and the mucosal inflammation by faecal calprotectin. Circulating monocytes were subgrouped and their chemokine receptor expression of CCR2 and CX(3)CR1 were... (More)
Background and purpose:Experimental and clinical investigations have revealed that statins can downregulate both acute and chronic inflammatory processes. Whether statins express anti-inflammatory activities in the treatment of Crohn's disease is unknown.Experimental approach:Ten patients were given 80 mg atorvastatin once daily for 13 weeks and then followed up for 8 weeks after the treatment. The anti-inflammatory effects of statin were assessed by measuring levels of plasma C-reactive protein (CRP), soluble (s) CD14, tumour necrosis factor (TNF)-alpha, sTNFRI and II, CCL2 and 8 and the mucosal inflammation by faecal calprotectin. Circulating monocytes were subgrouped and their chemokine receptor expression of CCR2 and CX(3)CR1 were analysed.Key results:In 8 of 10 patients, atorvastatin treatment reduced CRP (P=0.008) and sTNFRII (P=0.064). A slight decrease in plasma levels of sCD14, TNF-alpha and sTNFRI was observed in 7/10 patients and faecal calprotectin was reduced in 8/10 patients. We also observed that the treatment diminished expression of CCR2 and CX(3)CR1 on monocyte populations (P=0.014). At the follow-up visit, 8 weeks after the atorvastatin treatment was terminated, CRP levels had returned to those seen before the treatment.Conclusions and implications:Our findings imply that atorvastatin therapy reduces inflammation in patients with Crohn's disease and, therefore, encourage further investigations of statin-mediated protective effects in inflammatory bowel diseases.British Journal of Pharmacology advance online publication, 22 September 2008; doi:10.1038/bjp.2008.369. (Less)
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author
organization
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type
Contribution to journal
publication status
published
subject
in
British Journal of Pharmacology
volume
155
pages
1085 - 1092
publisher
The British Pharmacological Society
external identifiers
  • WOS:000261220700015
  • PMID:18806816
  • Scopus:56749161704
ISSN
1476-5381
DOI
10.1038/bjp.2008.369
language
English
LU publication?
yes
id
fc3e671c-ff2c-4aec-b8bc-627ae4c0fc5b (old id 1242784)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/18806816?dopt=Abstract
date added to LUP
2008-10-03 16:16:20
date last changed
2017-01-01 07:42:42
@article{fc3e671c-ff2c-4aec-b8bc-627ae4c0fc5b,
  abstract     = {Background and purpose:Experimental and clinical investigations have revealed that statins can downregulate both acute and chronic inflammatory processes. Whether statins express anti-inflammatory activities in the treatment of Crohn's disease is unknown.Experimental approach:Ten patients were given 80 mg atorvastatin once daily for 13 weeks and then followed up for 8 weeks after the treatment. The anti-inflammatory effects of statin were assessed by measuring levels of plasma C-reactive protein (CRP), soluble (s) CD14, tumour necrosis factor (TNF)-alpha, sTNFRI and II, CCL2 and 8 and the mucosal inflammation by faecal calprotectin. Circulating monocytes were subgrouped and their chemokine receptor expression of CCR2 and CX(3)CR1 were analysed.Key results:In 8 of 10 patients, atorvastatin treatment reduced CRP (P=0.008) and sTNFRII (P=0.064). A slight decrease in plasma levels of sCD14, TNF-alpha and sTNFRI was observed in 7/10 patients and faecal calprotectin was reduced in 8/10 patients. We also observed that the treatment diminished expression of CCR2 and CX(3)CR1 on monocyte populations (P=0.014). At the follow-up visit, 8 weeks after the atorvastatin treatment was terminated, CRP levels had returned to those seen before the treatment.Conclusions and implications:Our findings imply that atorvastatin therapy reduces inflammation in patients with Crohn's disease and, therefore, encourage further investigations of statin-mediated protective effects in inflammatory bowel diseases.British Journal of Pharmacology advance online publication, 22 September 2008; doi:10.1038/bjp.2008.369.},
  author       = {Grip, Olof and Janciauskiene, Sabina and Bredberg, Anders},
  issn         = {1476-5381},
  language     = {eng},
  pages        = {1085--1092},
  publisher    = {The British Pharmacological Society},
  series       = {British Journal of Pharmacology},
  title        = {Use of atorvastatin as an anti-inflammatory treatment in Crohn's disease.},
  url          = {http://dx.doi.org/10.1038/bjp.2008.369},
  volume       = {155},
  year         = {2008},
}