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


METHODS
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.


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
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.
Grip
O
O
Division of Gastroenterology and Hepatology, Department of Clinical Sciences Malmö, Lund University, University Hospital MAS, Malmö, Sweden. olof.grip@med.lu.se
Janciauskiene
S
S
Bredberg
A
A
D000328:Adult; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D000069059:Atorvastatin; D002097:C-Reactive Protein / Q000187:drug effects / Q000378:metabolism; D000073883:CX3C Chemokine Receptor 1; D018932:Chemokine CCL2 / Q000187:drug effects / Q000378:metabolism; D054412:Chemokine CCL8 / Q000187:drug effects / Q000378:metabolism; D003424:Crohn Disease / Q000188:drug therapy* / Q000503:physiopathology; D005260:Female; D005500:Follow-Up Studies; D005786:Gene Expression Regulation / Q000187:drug effects; D006538:Heptanoic Acids / Q000494:pharmacology*; D006801:Humans; D039841:Leukocyte L1 Antigen Complex / Q000187:drug effects / Q000378:metabolism; D018950:Lipopolysaccharide Receptors / Q000097:blood / Q000187:drug effects; D008297:Male; D009000:Monocytes / Q000187:drug effects / Q000378:metabolism; D011758:Pyrroles / Q000494:pharmacology*; D054390:Receptors, CCR2 / Q000187:drug effects / Q000378:metabolism; D019707:Receptors, Chemokine / Q000187:drug effects / Q000378:metabolism; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000187:drug effects / Q000378:metabolism; D047889:Receptors, Tumor Necrosis Factor, Type II / Q000187:drug effects / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000187:drug effects / Q000378:metabolism; D055815:Young Adult
D000893:Anti-Inflammatory Agents; C515334:CCR2 protein, human; D000073883:CX3C Chemokine Receptor 1; C095235:CX3CR1 protein, human; D018932:Chemokine CCL2; D054412:Chemokine CCL8; D006538:Heptanoic Acids; D039841:Leukocyte L1 Antigen Complex; D018950:Lipopolysaccharide Receptors; D011758:Pyrroles; D054390:Receptors, CCR2; D019707:Receptors, Chemokine; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D000069059:Atorvastatin