International ME/CFS and FM Awareness Day Is On May 12, 2018
Thomas Hennessy, Jr., selected May 12th to be our international awareness day back in 1992. He knew that May 12th had also been the birthday of Florence Nightingale. She was the English army nurse who helped to found the Red Cross as well as the first school of nursing in the world.
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C-Reactive Protein Response in Patients With Post-Treatment Lyme vs ME/CFS

Discussion in 'Latest ME/CFS Research' started by Murph, May 10, 2018.

  1. Murph

    Murph :)

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    C-Reactive Protein Response in Patients With Post-Treatment Lyme Disease Symptoms Versus Those With Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

    Melanie Uhde,1 Alyssa Indart,1 Brian A. Fallon,2 Gary P. Wormser,3 Adriana R. Marques,4 Suzanne D. Vernon,5 and Armin Alaedini1

    Departments of 1Medicine and 2Psychiatry, Columbia University Medical Center, New York, and 3Division of Infectious Diseases, Department of Medicine, New York Medical College, Valhalla; 4Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland; and 5Bateman Horne Center, Salt Lake City, Utah


    To the Editor—There is substantial overlap in symptoms, including fatigue, muscle and joint pain, and cognitive and memory deficits, between post-treatment Lyme disease syndrome (PTLDS) and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) [1]. Increasing evidence suggests a role for immunologic and inflammatory pathways in both PTLDS and ME/CFS [2–4]. However, in part owing to their etiologic complexity and the lack of established biomarkers, our understanding of the pathways involved and potential mechanistic differences between the 2 conditions is very limited.

    In a 2016 study published in Clinical Infectious Diseases, Uhde et al [5] examined the concentrations of acute-phase response proteins, including C-reactive protein (CRP), in individuals with PTLDS. CRP is a highly sensitive marker of infection and inflammation that binds a variety of ligands present on the surface of pathogens or exposed during autologous cell stress or death, exerting its effect through opsonin deposition and activation of the complement path- way, in addition to direct interaction with phagocytic cells [6]. We found that the circulating levels of CRP, as well as the frequency of concentrations >3 mg/ mL (generally considered to represent some degree of inflammation [7]) to be significantly higher in the PTLDS cohort than in a control group of subjects who had a history of Lyme disease but with- out persistent symptoms (both P < .001). The data provided evidence for increased expression of an objective marker of inflammation in PTLDS but suggested a mechanism of activation distinct from that in active infection, as previously dis- cussed [5].

    Using the same methods [5] in a new study, we screened plasma samples from 131 patients with ME/CFS (89 female; mean age [standard deviation], 50.0 [11.4] years; mean body mass index (BMI), 26.0 [5.5]) and 86 healthy controls (68 female; mean age, 50.0 [12.8] years; mean BMI, 26.5 [6.8]), provided by the SolveCFS BioBank [8]. Patients with ME/ CFS met the criteria of Fukuda et al [9] and the Canadian criteria [10] for this condition [9, 10].

    Screening questionnaires were used to evaluate the general health of the unaffected controls and to con rm that they did not meet ME/CFS case definition criteria. The ME/CFS and control sample sizes provided >95% power, with an α value <.05, to detect the same increase in CRP response as in the patients with PTLDS [5]. Group differences were assessed by the analysis of covariance, using the general linear model, to account for the potential confounding effect of age, sex, and BMI. is study was approved by the Institutional Review Board of Columbia University.

    In contrast to data from patients with PTLDS [5], we did not fi nd a statistically significant difference in the circulating levels of CRP (Figure 1) or the frequency of CRP levels >3 mg/L (33 of 131 [25.2%] vs 22 of 86 [25.6%], respectively) between patients with ME/CFS and controls.


    These data provide evidence for the likely existence of distinct in inflammatory mechanisms in ME/CFS versus PTLDS, which may be driven in part by the potentially more heterogeneous etiology of ME/CFS symptoms in comparison with PTLDS. e absence of a significantly enhanced CRP response in ME/CFS, despite published data suggesting activation of various in ammatory pathways, war- rants further examination.

    (Figure 1. C-reactive protein (CRP) concentrations in the cohorts of patients with myalgic encephalomy- elitis/chronic fatigue syndrome (ME/CFS) and healthy controls (HCs). The difference between the 2 groups was not statistically signi cant (P = .55). Horizontal red bars represent the mean for each group.)
     
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  2. hamsterman

    hamsterman Senior Member

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    Glad they are doing this type of study. And this strengthens the argument that post-treatment Lyme disease IS CFS/ME. And that it fits into the subsets setup by the landmark Younger study:
    https://www.healthrising.org/blog/2017/07/15/immune-subsets-chronic-fatigue-syndrome-younger/
    Which found C-reactive protein (CRP) levels are tracking with fatigue specifically with Infection triggered ME/CFS.

    I think it's important we understand the subsets and the inflammatory responses, but also acknowledge that these are all different sides of the same coin.
     
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  3. Runner5

    Runner5 Senior Member

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    Yeah....but a lot of the US isn't home to Lyme disease, nor is most of the world....
     
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  4. Murph

    Murph :)

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    I really can't draw the same conclusion as you. They found that ME/CFS had similar levels of c-reactive protein to controls, and different to the people with post-treatment lyme disease.

    And they say the inflammatory mechanisms are "distinct" i.e. different.
     
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  5. mariovitali

    mariovitali Senior Member

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    Yep, this is what i understand too. However there are many overlaping symptoms. Although a simplistic thought, it may be possible that in both cases we have the same main mechanism as a root cause (e.g Liver functioning disruption) which then manifests in two different ways.

    Recall that the latest work by Hanson (although the sample was small) suggested the existence of several signs related to impaired Hepatic function.

    We also know that for some patients, Lyme Disease may affect Liver function :


    https://www.mayoclinic.org/diseases-conditions/lyme-disease/symptoms-causes/syc-20374651
     
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  6. Simon

    Simon

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    That’s been a pretty consistent finding over the years. Whatever is going on in ME/CFS is more subtle than simply CRP-related information. E.g. the T cell clonal expansion found by /Mark Davis (still to be published)
     
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  7. adambeyoncelowe

    adambeyoncelowe

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    My understanding is that ME, Lyme, FM and GWI all have overlap. It could be something metabolic, such as a dauer state or enzyme metabolising problems. It could be something more central, such as sensory gating issues or CNS disturbance.

    This study seems to confirm that. Ron and the OMF team seem to imply the issue of subgroups may have been overstated. Perhaps, then, it's just a matter of people being misdiagnosed with one thing when they have another, similar but distinct thing, rather than a multitude of subtypes.

    Hyde finds aerotoxic syndrome patients indistinguishable from those ill from enteroviruses. Maybe the idea of subgroups will dissipate once Ron publishes his findings.
     
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  8. Runner5

    Runner5 Senior Member

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    Do people with ME / CFS have a wonky C-Reactive Protein result? I thought C-Reactive Protein was for autoimmune diseases. Mine was normal. (I'm not being critical, just curious - that doesn't always translate to writing on the Internet as it's difficult to convey tone...)
     
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  9. Murph

    Murph :)

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    The data in this study say no. We look normal on CRP.
     
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  10. Runner5

    Runner5 Senior Member

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    Murph likes this.
  11. adambeyoncelowe

    adambeyoncelowe

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    Agreed. CRP is usually normal for us, and ESR is normally low.
     
  12. mariovitali

    mariovitali Senior Member

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    @Murph

    I wonder how hs-CRP (hs=High Sensitivity) would look like instead of CRP.
     
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