[Note: Intestinal permeability – “leaky gut” – is when irritation or damage of the intestinal lining, as from bacterial overgrowth, causes loosening of junctions between the cells, allowing the escape of molecules that would not normally be allowed to pass through to the bloodstream (pathogens, undigested food, toxins) and triggering an immune system response that can cause inflammation in the body. Dr. Kenny De Meirleir's recent reports, for example, point to problems with the intestinal lining in the majority of ME/CFS patients he sees
Objectives: The pain intensity of patients with FM has recently been reported to be correlated with the degree of small intestinal bacterial overgrowth (SIBO). SIBO is often associated with an increased intestinal permeability (IP). Increased IP, if shown in FM, may have pathogenetic relevance because it leads to the exposure of immune cells to luminal antigens and consequent immune modulation.
It is currently unknown whether IP is altered in FM. We therefore examined the IP in a group of patients with primary FM and in two control groups - healthy volunteers and patients with an unrelated chronic pain syndrome, complex regional pain syndrome (CRPS).
We hypothesized that patients with FM, but not volunteers or those patients with CRPS, would have altered IP.
Methods: Both gastroduodenal and small IP were assessed using an established three-sugar test, where urinary disaccharide excretion reflecting intestinal uptake was measured using HPLC.
Results: Forty patients with primary FM, 57 age- and sex-matched volunteers and 17 patients with CRPS were enrolled in this study.
In the FM group, 13 patients had raised gastroduodenal permeability and 15 patients had raised small intestinal permeability,
But only 1 volunteer had increased gastroduodenal permeability (P < 0.0001, chi-square test for the three groups).
The IP values were significantly increased in the patient groups (P < 0.0003 for all comparisons, one-way analysis of variance).
Conclusions: The IPs in primary FM and, unexpectedly, CRPS are increased.
This study should stimulate further research to determine the implication of altered IP in the disease pathophysiology of FM and CRPS.
Source: Rheumatology (Oxford). June 7, 2008. [Epub ahead of print] PMID: 18540025, by Goebel A, Buhner S, Schedel R, Lochs H, Sprotte G. Pain Management Centre, University Hospital Wuerzburg, Wuerzburg; Department for Gastroenterology, Hepatology and Endocrinology, Charite Universitatsmedizin, Berlin, Germany. [E-mail: