MCP-1 is Increased in Patients with CFS and FM, whilst several other immune markers are significantly lower than healthy controls, 2020, Groven et al

[Kalliope]

Elsevier - Brain, Behaviour, & Immunity - Health
MCP-1 is Increased in Patients with CFS and FM, whilst several other immune markers are significantly lower than healthy controls - Nina Groven, Egil Andreas Fors, Astrid Kamilla Stunes, Solveig Klæbo Reitan

Abstract
The role of the immune system in the pathogenesis of Fibromyalgia (FM) and Chronic fatigue syndrome (CFS) is not clear. We have previously reported increased levels of C-reactive protein (CRP) in these patient groups compared to healthy controls and wanted to further explore the levels of circulating immune markers in these populations.

The population consisted of three groups, 58 patients with FM, 49 with CFS and 54 healthy controls. All participants were females aged 18–60. Patients were recruited from a specialised university hospital clinic and controls were recruited by advertisement among the staff and students at the hospital and university. Plasma levels of Interferon (IFN)-γ, Interleukin (IL)-1β, IL-1ra, IL-4, IL-6, IL-8, IL-10, IL-17, Interferon gamma-induced protein (IP)-10, Monocyte Chemoattractant Protein (MCP)-1, Transforming Growth Factor (TGF)-β1, TGF-β2, TGF-β3 and Tumour Necrosis Factor (TNF)-α were analysed by multiplex. Differences between the three groups CFS, FM and controls, were analysed by Kruskal Wallis tests.

MCP-1 was significantly increased in both patient groups compared to healthy controls. IL-1β, Il-4, IL-6, TNF-α, TGF-β1, TGF-β2, TGF-β3, IL-10 and IL17 all were significantly lower in the patient groups than healthy controls. IFN-γ was significantly lower in the FM group. For IL-8, IL-10 and IL-1ra there were no significant difference when controlled for multiple testing.

In conclusion, in our material MCP-1 seems to be increased in patients both with CFS and with FM, while several other immune markers are significantly lower in patients than controls.

 

[Kalliope]

At least one of the co authors, Egil A. Fors, is a strong defender of the biopsychosomatic approach to ME.

Nina Groven, Egil A. Fors and Solveig Klæbo Reitan published the study "Patients with Fibromyalgia and Chronic Fatigue Syndrome show increased hsCRP compared to healthy controls" last year (discussed here).

 

[Andy]

ACR is Fibromyalgia criteria.

All patients were assessed by using the 1990 ACR (Wolfe et al., 1990) and the 1994 Fukuda criteria (Fukuda et al., 1994) as both were still used as diagnostic tools in the clinic during the recruitment period. FM patients (n = 58) were eligible if they fulfilled the 1990 ACR criteria (Wolfe et al., 1990). CFS patients (n = 49) were eligible if they fulfilled the Fukuda diagnostic criteria (Fukuda, Straus et al. 1994). Exclusion criteria were in accordance with diagnostic criteria including known inflammatory diseases.

Shame that they didn't retrospectively run the participants through any other criteria.

From the Limitations section (my bolding).

The diagnostic groups FM and CFS are purely clinically based and with no objective paraclinical measures, and the recruitment of patients from a university specialist clinic only may not be representative for a patient population cohort. However, the patients were referred to this clinic from general practitioners in the primary health care, and we have used strict diagnostic criteria by a specially trained group of specialists in a specialised chronic fatigue and pain centre and this reduces this possible limitation as much as possible. The control group consisted of mainly hospital and university staff, which may not in all aspects represent the general population.

Fukuda strict!

 

[wigglethemouse]

It always puzzles me why they don't show a scatter plot of the results to help with visualisation of the data. They claim a significance of P<0.001 but the standard deviation is pretty high, meaning there is a lot of overlap of the data points between the groups. A picture would give a better idea how significant the overlap was or not ..........

I remember a talk given by Montoya where he said that for Cytokine analysis, patient and control samples had to be mixed within the same centrifuge and processed at the same time, to remove processing variations. He, and others I've listened to, have said the same equipment should be used for all samples in the study, to remove equipment variation. This paper does not go into that level of detail.

Unfortunately Cytokine studies seem pretty unrepeatable by others as reported in Michael Van Elzakker's paper. So take with a pinch of salt.