Association between C-reactive protein and chronic fatigue syndrome: a meta-analysis, 2017, Wang et al

Andy

Retired committee member
For what its worth.
Abstract: Chronic fatigue syndrome (CFS) is an agnogenic disease, which has recently been linked to inflammation. Several studies have found an association between inflammatory factors such as C-reactive protein (CRP) and CFS. However, these studies have shown inconsistent results.

PubMed, Embase, and CBM (Chinese Biomedical Literature Database) were searched for relevant studies published as of August 2016. A total of 8 studies were included in the meta-analysis and trial sequential analyses (TSA). Meta-analysis revealed a mean difference (MD) of 0.39 μg/mL (95% CI: 0.15-0.64) in CRP levels between the CFS patients and healthy controls. Subgroup analysis revealed that CRP levels were not elevated in teenagers [MD 0.10 μg/mL (95% CI: -0.04-0.24)]. There was a statistically significant between-group difference with respect to CRP levels between adult European population [MD 1.58 μg/mL (95% CI: 0.88-2.27)] and adult American population [MD 0.34 μg/mL (95% CI: 0.16-0.51)]. TSA results showed that the trial sequential monitoring boundary (TSBM) was crossed only in the group of European adults, while the group of European teenagers did not cross TSBM and the traditional futility boundary. The group of American adults crossed the traditional boundary, but not TSBM.

These findings suggest that baseline CRP levels are greater in CFS patients with the exception of European teenage patients, which could provide insights into the causality of CFS. However, considering the sample size, further studies with larger sample size and more robust design are needed to validate the association between CRP and CFS.
PDF download, http://www.ijcem.com/files/ijcem0053166.pdf
 
These results are pretty consistent, imo. When they isolated those studies that used high sensitivity CRP assays, every single one showed a trend towards higher CRP in the ME patients vs. controls.

The difference is pretty tiny, which suggests that it might be driven by a subset of patients.

One potential problem is that its unclear just from the paper whether all studies controlled for BMI. This is a pretty strong predictor of CRP levels so you need to control for that.

But if you think its great new biomedical evidence validating the existence of ME, then think again. An association has also been shown between CRP and depression (independently of BMI), and the psychosocial people believe that its the bad thoughts causing the inflammation.

We need to be prepared for when the BPS crowd start to get with the inflammation trend (which they will, its only a matter of time)
 
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