Hi...I recently had a muscle biopsy at Stanford that showed inflammatory myopathy and type II fiber atrophy. I will be going back to NIH March 3 for part 2 of the study. NIH is going to look at the slides from Stanford but they may decide to do another biopsy too because their procedures are different. The good news is that we have ruled out inclusion body myositis, which is untreatable. The doc at Stanford suggested IVIG for the inflammatory myopathy.
Do you have the reference to the study of muscle atrophy in ME patients?
Thanks.
Hi
@viggster . Great news about the NIH including biopsies. I also have a couple of questions when you get a chance I would be most grateful if you could reply.
@Gingergrrl you might also be interested in the information I share in this post.
As well as the type II atrophy my biopsy also revealed myositis but it was only in one fascicle so the report did not make any conclusions on this. I am wondering if you could give more details on what inflammatory myopathy was shown and how they ruled out the inclusion myositis (and I assume polymyositis) as I have been finding it difficult to get info on that finding... At the end of my hospital stay the overseeing doctor also suggested the possibility of IVIG trial but since the myositis was only in one fascicle and they haven't found any auto-antibodies so far I haven't been able to get any progress with doctors regarding this.
Also my other consistent finding is high ferritin and low transferrin which my doctor attributes to an inflammatory process-- have you had your iron panel tested and if so would you share your results?
The reference for the type II fibre atrophy is:
Mitochondrial abnormalities in the postviral fatigue syndrome* W. M. H. Behan1, I. A. R. More1, and P. O. Behan2
My doctor and I have since been researching as to why type II rather than I atrophy might be part of ME or at least a subset. The following is a good article which explains these possibilities and points towards malnutrition/inflammation (one key to share with relevant people is that disuse causes more type I atrophy so the type II findings aren't caused by disuse):
Mechanisms for fiber-type specificity of skeletal muscle atrophy.
Wang Y1,
Pessin JE.
Additionally, I experience chest and breathing weakness (I can't pass a Spirometry test) and cant talk much of the time. This paper on respiratory muscles explains that each fast twitch (type II) exertion uses 3-4 times the ATP of a slow twitch (type I) exertion so my hypothesis is this might contribute to why type II fibre atrophies in ME/CFS or whatever subset of disease causes type II muscle atrophy and potentially inflammation:
Respiratory Muscle Fibres: Specialisation and Plasticity Polla, Bottinelli, Regianni
For your information
@Gingergrrl I would describe my muscle weakness as a burning weakness with discomfort but not particularly painful that can affect different areas of the body more or less so at different times usually the worst being upper legs and chest but currently it is also bad in my arms/hands.