Evidence of Clinical Pathology Abnormalities in People with ME/CFS from an Analytic Cross-Section (2019) Nacul et al.

John Mac

John Mac

Senior Member (Voting Rights)
Abstract
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating disease presenting with extreme fatigue, post-exertional malaise, and other symptoms.

In the absence of a diagnostic biomarker, ME/CFS is diagnosed clinically, although laboratory tests are routinely used to exclude alternative diagnoses.

In this analytical cross-sectional study, we aimed to explore potential haematological and biochemical markers for ME/CFS, and disease severity.

We reviewed laboratory test results from 272 people with ME/CFS and 136 healthy controls participating in the UK ME/CFS Biobank (UKMEB).

After corrections for multiple comparisons, most results were within the normal range, but people with severe ME/CFS presented with lower median values (p< 0.001) of serum creatine kinase (CK; median = 54 U/L), compared to healthy controls (HCs; median = 101.5 U/L) and non-severe ME/CFS (median = 84 U/L).

The differences in CK concentrations persisted after adjusting for sex, age, body mass index, muscle mass, disease duration, and activity levels (odds ratio (OR) for being a severe case = 0.05 (95% confidence interval (CI) = 0.02–0.15) compared to controls, and OR = 0.16 (95% CI = 0.07–0.40), compared to mild cases).

This is the first report that serum CK concentrations are markedly reduced in severe ME/CFS, and these results suggest that serum CK merits further investigation as a biomarker for severe ME/CFS.
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https://www.mdpi.com/2075-4418/9/2/41
 
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Interesting but a bit difficult to interpret. Creatine kinase mirrors activity to a significant extent. Going to a disco could double it. A level of 50 is very normal, just at the lower end. Pathology is associated with raised levels and not low levels by and large.
 
One thing maybe to think about is that CK might be a useful indicator of recovery of regular activity. It would be much simpler than actometry and could give a guide to activity over a recent period rather as glycated Haemoglobin gives a guide to average recent blood glucose levels.

It might not matter whether the CK was a byproduct of activity or an index of a restoration of muscle health as such. Either way it would be an objective measure of the muscle being more regularly usable.
 
My CK has been intermittently elevated for about 14 years now and it appears it could be related to MCAS. Anyone else had elevated CK?

Musculoskeletal

Clinical myositis, often diffusely migratory (fibromyalgia is a common pre-existing diagnosis), subclinical myositis (i.e., asymptomatic elevated creatine kinase not otherwise explained), arthritis (typically migratory), joint laxity/hypermobility, osteoporosis/osteopenia, osteosclerosis, sometimes mixed osteoporosis/osteopenia/ osteosclerosis; MCAS-driven musculoskeletal pain not uncommonly is poorly responsive to NSAIDs and narcotics
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https://www.clinicaltherapeutics.com/article/S0149-2918(15)00074-0/pdf

I need to have a muscle biopsy done but my doctor won't do it until my vitamin d levels are back in range because it can skew the results but I don't tolerate vitamin d so that's not gonna happen.
 
Jonathan Edwards said:
One thing maybe to think about is that CK might be a useful indicator of recovery of regular activity. It would be much simpler than actometry and could give a guide to activity over a recent period rather as glycated Haemoglobin gives a guide to average recent blood glucose levels.

It might not matter whether the CK was a byproduct of activity or an index of a restoration of muscle health as such. Either way it would be an objective measure of the muscle being more regularly usable.
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That's a good idea.
 
Jonathan Edwards said:
One thing maybe to think about is that CK might be a useful indicator of recovery of regular activity. It would be much simpler than actometry and could give a guide to activity over a recent period rather as glycated Haemoglobin gives a guide to average recent blood glucose levels.

It might not matter whether the CK was a byproduct of activity or an index of a restoration of muscle health as such. Either way it would be an objective measure of the muscle being more regularly usable.
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Interesting. I also wonder if people with mild/moderate ME might not show much discrepancy, given my wife, for instance, can actually do quite a lot, compared to so many people here. But of course if that is true, then that itself might prove some useful discriminator for severity?
 
Jonathan Edwards said:
One thing maybe to think about is that CK might be a useful indicator of recovery of regular activity. It would be much simpler than actometry and could give a guide to activity over a recent period rather as glycated Haemoglobin gives a guide to average recent blood glucose levels.
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I'm a bit puzzled, as it seems to suggest in the abstract that they took account of activity levels and still found the difference in CK levels in severe patients.

The differences in CK concentrations persisted after adjusting for sex, age, body mass index, muscle mass, disease duration, and activity levels (odds ratio (OR) for being a severe case = 0.05 (95% confidence interval (CI) = 0.02–0.15) compared to controls, and OR = 0.16 (95% CI = 0.07–0.40), compared to mild cases).
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my bolding
 
When I had my first episode of extreme burning I was tested for CK and the levels were elevated. One test doesn't mean anything really but Rheumatologist thought it was important, so I was referred to a Neurophysiologist who performed electromyography and nerve conduction study, all normal, but he said that small fiber neuropathy couldn't be ruled out by the tests.
 
Trish said:
I'm a bit puzzled, as it seems to suggest in the abstract that they took account of activity levels and still found the difference in CK levels in severe patients.
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I’m not sure they did a very good job of ‘adjusting for’ activity levels which were based on subjective reporting:

Activity levels were estimated from answers to specific questions on the bespoke participant questionnaire: participants were asked to put their perceived activity levels over the 7 days preceding the blood draw into one of five categories, ranging from “not active at all” to “very active”.
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I can imagine for example that the activity level of a healthy control answering “not active at all” would likely be vastly greater than a severe ME patient who put themselves in the same category.
 
Snowflake said:
I’m not sure they did a very good job of ‘adjusting for’ activity levels which were based on subjective reporting
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They did pick up on this in the paper:

The low concentrations of serum CK found in people with ME/CFS suggests an abnormality in energy metabolism, which have been reported by distinct authors (e.g., references [28–32]) and could explain the intolerance to exertion commonly reported by patients, and consequent reduction in activity levels [2]. An alternative or additional explanation is that the lower serum CK resulted, at least partially, from physical inactivity. Nevertheless, the persistent significant association between lower serum CK and disease severity in the multivariate model that controls for activity suggests that these results cannot be fully explained by reduced physical activity, but that there are other factors involved. To explore further a potential confounding role of activity levels, we compared median serum values of CK in different strata of activity category. The values were reduced in severely affected cases in all strata Nevertheless, the potential for residual confounding is still present, and Diagnostics 2019, 9, 41 10 of 16 differential misclassification on activity levels, with over-estimation of activity in severe ME/CFS cases, remains a possible (and at least partial) explanation, for the difference in the levels of CK observed.
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My bolding.

I’m unsure why they say it remains only a possible ‘partial’ explanation and why this couldn’t potentially provide a full explanation for the differences in CK levels?
 
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Also interesting, from the paper:

Some researchers have previously reported intriguing findings on serum CK in PWME. For example, two studies with 30 and 33 individuals, compared the CK serum concentration of ME/CFS patients (diagnosed by the CDC-1994 criteria [3]) with those of healthy controls before and after exercise, in order to evaluate physical capacity [34,35]. The mean CK in PWME was lower, though not significantly, than in controls, and did not increase with exertion in those with ME/CFS (as seen in healthy individuals). The results suggests that lack of acute physical effort was not the main factor determining CK levels in PWME [34,35]. Another study on PWME found higher serum CK in participants with enterovirus-specific RNA detected in muscle by biopsy, than in those with no evidence of enteroviral infections. That study suggested that a sub-group of PWME might have muscle damage secondary to enterovirus infection, but unfortunately, the authors did not specify the concentrations of CK in the group of patients with lower values [36].
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