Increased risks of cancer and autoimmune disease among the first-degree relatives of patients with ME/CFS, 2022, Moslehi et al

Further to this, the following thread was tweeted by Dr Gurdasani (clinical epidemiologist and beacon of wisdom in the Covid/Long Covid space). Here she describes her experience of UC.

I don't think this is going off-topic. My question would be: do we think UC is a potential co-morbid disease to ME, with a common predisposition (autoimmune or as Jo clarifies above autoinflammatory); or is UC actually more commonly associated with ME, but ME isn't diagnosed as such, as ME symptoms are put down to the known UC with its clear history and established biomarkers?

Selected quotes from the thread —

 

I think UC has symptoms that sound very like ME, but the key thing about the cycles of symptoms in ME is that they do not seem to relate to any identifiable inflammatory disease.

Although feeling fatigued after sitting on a chair with UC might be post-exertional and a similar malaise to ME I think there is more to the concept of PEM than that.

We come back to the fact that lists of symptoms are not what diagnoses are based on. Diagnoses are based on careful analysis of the temporal course and detail of symptoms in the context of known aggravating or relieving factors.

I am not sure we have any reason to think UC and ME are connected other than by chance?

 

Do you think the female to male sex bias seen in both ME and the majority of autoimmune diseases is suggestive of autoimmune involvement in ME?

As for PEM I'd love to hear if there have been any studies looking at how it manifests in different people. As it stands I don't feel satisfied there is a consensus about how this symptom really manifests. I've heard people describe a clear relationship between an overexertion, a delay, and a deterioration. For others like myself - how i feel in 6 months seems to depend on an aggregate of how much i exert myself on many occasions up to that point. Her description of UC post exertion feels more relatable in my case than the 24-48 delay type.

 

A few people in that Twitter thread talking about being misdiagnosed with ME and then later receiving a diagnosis of lupus or Sjogren's, which makes me wonder how common that may be. If you had a significant number of people who had an autoimmune disease misdiagnosed as ME, then maybe the high rates of autoimmune disease in relatives of those with ME could be explained by some of the people with ME actually having an autoimmune disease (and thus perhaps being more likely to have relatives with an autoimmune disease). It would be interesting to know which autoimmune diseases this study found in relatives.

 

Not particularly, the pattern of incidence with age is not similar to autoimmune disease in general.
Some autoimmune diseases have odd age incidence profiles like lupus and MS but even there the pattern is different. The data for ME may be biased but that is taking it at face value.

 

It is likely that a small proportion of people diagnosed with ME in fact have an autoimmune disease. But equally, people often get given diagnoses like Sjögren's syndrome on very dubious grounds by overenthusiastic rheumatologists.

The main issue for a study like this for me is that associations looked for in clinic cohorts or internet cohorts are very likely to be biased towards the positive. The only real way to get a meaningful answer is to have a population based cohort.

 

article
COVID-19 May Be a Trigger for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

https://www.albany.edu/sph/news/202...gic-encephalomyelitischronic-fatigue-syndrome

 

I agree.

The p-values are good here, but the small sample size makes me concerned about reliability.

 

This is my experience. I had severe symptoms for 4 years (including severe PEM at times) that were eventually diagnosed as ME/CFS after tons of other stuff was ruled out. I had SO MANY blood tests, scans, etc. But finally after 4 years I developed new symptoms that were unique and specific to a very rare autoimmune disease called Relapsing Polychondritis. There is no biomarker for this condition so until I developed the hallmark symptoms there was no way to know I had it. I was also diagnosed with the UCTD (also no biomarker for this AI disease) at the same time. Starting on daily Prednisone, Hydroxychloroquine and Leflunomide was life changing for me. I am still affected enough that I continue to not be able to work but my quality of life and functionality is MUCH improved from where it was before.