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Intestinal Disorders & Joint Pain


Arthritis of the spine and limbs can affect to up to 30 percent of people who have inflammatory conditions of the intestines:  inflammatory bowel disease. 

Lower-grade intestinal inflammation, sometimes called sublinical inflammation, can occur in up to 60 percent of people with inflammatory arthritis.  This makes the gut an important considerations as you wrestle with how to improve your joint health.  It is also important to understand the possible involvement of the gut, because anti-inflammatory drugs can significantly worsen intestinal health, which sets up a viscious cycle of ever worsening gut health and joint health.

[Meier, C, Plevy, S. Therapy insight: how the gut talks to the joints--inflammatory bowel disease and the spondyloarthropathies. Nat Clin Pract Rheumatol 2007;3(11):667-74.]

 

Gut Bacteria and Healthy Joints

The human gut is home to some 1000 species of bacteria.  There are now studies showing that disruption of this population of gut bacteria may contribute to a situation that favors joint inflammation.

Ann Rheum Dis. 2006 Oct;65(10):1293-300. Epub 2006 Feb 13.
Altered gut transcriptome in spondyloarthropathy.

Laukens D, Peeters H, Cruyssen BV, Boonefaes T, Elewaut D, De Keyser F, Mielants H, Cuvelier C, Veys EM, Knecht K, Van Hummelen P, Remaut E, Steidler L, De Vos M, Rottiers P.

Department for Molecular Biomedical Research, Flanders Interuniversity Institute for Biotechnology, Ghent, Belgium. debby.laukens@dmbr.Ugent.be

BACKGROUND: Intestinal inflammation is a common feature of spondyloarthropathy (SpA) and Crohn's disease. Inflammation is manifested clinically in Crohn's disease and subclinically in SpA. However, a fraction of patients with SpA develops overt Crohn's disease. AIMS: To investigate whether subclinical gut lesions in patients with SpA are associated with transcriptome changes comparable to those seen in Crohn's disease and to examine global gene expression in non-inflamed colon biopsy specimens and screen patients for differentially expressed genes. METHODS: Macroarray analysis was used as an initial genomewide screen for selecting a comprehensive set of genes relevant to Crohn's disease and SpA. This led to the identification of 2625 expressed sequence tags that are differentially expressed in the colon of patients with Crohn's disease or SpA. These clones, with appropriate controls (6779 in total), were used to construct a glass-based microarray, which was then used to analyse colon biopsy specimens from 15 patients with SpA, 11 patients with Crohn's disease and 10 controls. RESULTS: 95 genes were identified as differentially expressed in patients with SpA having a history of subclinical chronic gut inflammation and also in patients with Crohn's disease. Principal component analysis of this filtered set of genes successfully distinguished colon biopsy specimens from the three groups studied. Patients with SpA having subclinical chronic gut inflammation cluster together and are more related to those with Crohn's disease. CONCLUSION: The transcriptome in the intestine of patients with SpA differs from that of controls. Moreover, these gene changes are comparable to those seen in patients with Crohn's disease, confirming initial clinical observations. On the basis of these findings, new (genetic) markers for detection of early Crohn's disease in patients with SpA can be considered.

 

 

  
 
 
 
 
 

 

 

 

 

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