It's been a while since I've read about the different western blot bands and CD57 on this forum. It's like a cascade of memories. Very cool.
Yep. Definitions come by the dozen in Lymeworld. It's very political. I always advise new Lyme patients to hone up on the history of the Lyme struggle. (I realize you're not new to Lyme.) Without appreciating how we got here, it's almost like approaching treatment in a vacuum.
Which symptoms? ME/CFS? Yes, I pace. I suffer from bad insomnia, so I take sleep meds. Levo for my thyroid.
That's a tough position to be in.
I have a good sarc specialist. He is by no means certain re Lyme but there is the broader issue of latent infection which has, perhaps, a better audience among sarc specialists than in many medical circles. Basically very good sense as e.g. you really do not want to "encourage" histoplasmosis which is a granuloma causing fungus, with steroids. Do that and you can further the infection, produce granulomas which wilt cause confusion with sarc granulomas and also not know which non specific symptom comes from what. Anyway for the moment I am on watch and wait and deal with thing as they arise. My whole history since at least 1985 throws up question after question.That's a tough position to be in.
Please feel free to ask questions. No, I only refer to the German words as they clearly associate chronicity with borrelia albeit often neuro- (though not always) Just shows the fatuity of the rejectionist position. My story is as told in the longer post. It's about plausibility relative to other explanations and the wisdom of empirical medicine and, in a case of sarcoid, the absolute necessity of taking possibility of chronic infection seriously. There is no safe space for casual "chronic lyme does not exist" in cases such as my own. The plausibility lies in the low CD56 in 2003 (this can occur in sarc but alongside normal wbc a chronic infection is more likely) WB 2005 albeit IgM, blots resolved after abx , continuing CD47 deficiency resolving after more abx 2025-2018, and the 2 Il2 Elispot IL2s 2015 2024. Against are all the doubts that can be cast on each "proof" but it is not certain either way and the criticisms can be so "cook book of anti Lyme advocacy" that I simply have contempt for them (but not for more refined criticism). I have develped neuromuscular symptoms from covid (myoclonus, fasciculation, formication) so that need not have been lyme and fatigue and a form of PEM do not prove Lyme either but alongside tendon probs, neurosensory deafness and joint issues , the diagnosis does not become less likely. Basically the non negotiable is be caution and that certinlay includes accommodating the possibility of latency. And minocycline has benefitted me (though anti-inflammatory and broad spectrum ab properties might have helped in the presence of sarcoid alone or sarcoid promoted by another bacterium.
The question still remans as to what the illness is.
This forum seeks scientific rigour. That is what it is about. fair play. The problem is that the very nature of the diagnosis - by criteria - is essentially anecdote, patients' stories. Anything that has helped me incl. for sarc has been anecdotal (except the odd herbal has some scientific papers), the science around Lyme is disputed but then everything around ME has been disputed over the years and prob DeCode ME is the most accepted science, though implications are far from certain or agreed. One thing we do agree on here is that we have "Real stories of Non-imaginary illness" Is there a book in that?
It may do, but the alternatve to overdiagnosis (which has numerous definitions or rather somewhat casual descriptions) is often fatuous assessment which may gets its own "non medicalising" clinical label. Beyond that an approach which is based on seeking not to medicalise is hardly likely to promote objective diagnostic practice. There are problems a either way. i do not wish to go back to the "routine bloods OK. nowt wrong" school of "thought".
But the pathway to your type of symptoms may be different according to underlyng pathology. There may be overlaps in pathway and clinical treatment of PEM may be similar but there may be key differences. One question would be "what sets the energy limit in the first place?" Whether the processes occurring in PEM t are common regardless of condition is another fair question. People with metabolic myopathies like Pompe's will report PEM which is partially relieved by treatment but does not go away. They get wahcked and recover slowly, Sarc, lupus. All the same story. Different conditions but a similar PEM picture. How do we draw the line? I reckon probably matters in common but maybe key differences too. And 2 day CPET , once used as proof of PEM but not abnormal in many cases of PEM. Do 2n day CPET abnormal folk have sth different which needs special help? Might theri PEM be distinct?
I have seen a few diligent doctors, but I've never met one who is diligent enough. They all bring their own biases to the game. It is encumbent on the patient to be diligent enough.