The buspirone challenge test clearly distinguishes ME/CFS patients from healthy controls: why is it not being developed and deployed?

[forestglip]

I'm not sure how useful a diagnostic lab test would be unless and until it can help guide treatment decisions.

Maybe this was too dismissive. I could see how there could be value if a person with ME/CFS could get a prolactin response test and their doctor could see something clearly abnormal. I'm thinking in terms of doctors, family, and insurance/disability being more willing to accept that something is wrong that does require limiting exertion.

I'm not sure if it could possibly be counterproductive for the people for whom it gives a false negative result. Would a doctor see that and say "well ME/CFS is a biological disease with a biomarker, and you don't have the marker, so it's likely you're fine to go back to work"?

But anyway, I think the more important thing is trying to use it to help identify treatments, which will provide a lot more value in the long run.

 

[hotblack]

I’m also concerned about the negative impacts on severely affected patients of evoking this response. You don’t want a test that triggers worsening symptoms and it seems like this does for at least some, even if temporarily. It just doesn’t sound like a viable diagnostic test to me. More a research tool.

But anyway, I think the more important thing is trying to use it to help identify treatments, which will provide a lot more value in the long run.

That does sound like it could be useful.

 

[V.R.T.]

Maybe this was too dismissive. I could see how there could be value if a person with ME/CFS could get a prolactin response test and their doctor could see something clearly abnormal. I'm thinking in terms of doctors, family, and insurance/disability being more willing to accept that something is wrong that does require limiting exertion.

I'm not sure if it could possibly be counterproductive for the people for whom it gives a false negative result. Would a doctor see that and say "well ME/CFS is a biological disease with a biomarker, and you don't have the marker, so it's likely you're fine to go back to work"?

But anyway, I think the more important thing is trying to use it to help identify treatments, which will provide a lot more value in the long run.

Just for clarity, how specifically do you envisage this finding helping to identify treatments? Helping to pinpoint the mechinism and also as a marker for clinical response if it does change with severity, as you say in your previous post?

If the former I'm wondering if there is a post in this thread that explains how we could use this test and others like it to figure out what's causing MECFS.

Asking from interest not skepticism

 

[forestglip]

Just for clarity, how specifically do you envisage this finding helping to identify treatments? Helping to pinpoint the mechinism and also as a marker for clinical response if it does change with severity, as you say in your previous post?

Yeah, mainly the mechanism thing. If it's a real finding, then we have a specific starting point for research, and can then start testing many things related to it: Do other drugs have similar effects? Is there anything abnormal about the pituitary or hypothalamus on imaging? Are any genes upregulated in the prolactin-secreting cells?

If any of the above results in identifying another abnormality, then we have another clue to help think of other things to test. If, for example, the estrogen receptor is upregulated in the pituitary, then we could test if the same receptor is upregulated in other parts of the brain.

And we iterate on that and consider those findings together with other ME/CFS findings until one of the things that makes sense to test next is a specific treatment that we might expect to work when considering all the previous clues.

If the former I'm wondering if there is a post in this thread that explains how we could use this test and others like it to figure out what's causing MECFS.

I'm not sure if there's a post, but I don't really consider it much different from something like a causal gene identified in a genetic study. It's a clue, and we try to figure out why it's abnormal or what kind of treatment might help by connecting it with other research.

 

[ScoutB]

I'm thinking in terms of doctors, family, and insurance/disability being more willing to accept that something is wrong that does require limiting exertion.

Yeah it could be very interesting depending on how it plays out. My sense is having a lab test that captures 80% of patients is often enough to make the disease 'real' to doctors and they feel more comfortable diagnosing people who fit the profile well even if they have a negative test (in cases where it makes sense). Perhaps this also comes from the clinical experience of using the test allowing them to 'learn' what the disease looks like more deeply. So if we're lucky a test could have benefits even for those with a negative result.

The other possible outcome I see is that it could reduce the emphasis on clinical tests that really don't seem well grounded. I've had regular family doctors (i.e. not alternative health folks) raise the idea of testing for MCAS and POTS when I describe my symptoms. It's clear this is stuff they've heard about through the grapevine and they are just trying to find something 'medical' (where a lab test feels 'medical') to offer. And patients of course want a positive test due to the cultural pressures we talk about all day on here (disbelief, illness not being seen as legitimate unless in falls into an accepted category, etc). If a prolactin test could meet some of that need I bet we'd see less focus on tests that don't work. And maybe, as a result, more patient (and research) focus on things that seem more strongly associated with ME/CFS.

 

[Jonathan Edwards]

My guess is that if the prolactin response proves reproducible and that there is not more than about 30% overlap with normals further use is likely to reveal that it correlates with various clinical aspects, like time since onset, presence of major pain, OI, or other features. With time it is likely that it would prove to be of additional prognostic value, beyond the virtues mentioned above. And ultimately diagnosis is all about refining prognosis. For RA, the rheumatoid factor test is not diagnostic but it has some extra prognostic value. We talk of seronegative and seropositive RA. It might turn out to be useful to talk of Buspirone positive and negative ME/CFS.

 

[SugarSquared]

My guess is that if the prolactin response proves reproducible and that there is not more than about 30% overlap with normals further use is likely to reveal that it correlates with various clinical aspects, like time since onset, presence of major pain, OI, or other features. With time it is likely that it would prove to be of additional prognostic value, beyond the virtues mentioned above. And ultimately diagnosis is all about refining prognosis. For RA, the rheumatoid factor test is not diagnostic but it has some extra prognostic value. We talk of seronegative and seropositive RA. It might turn out to be useful to talk of Buspirone positive and negative ME/CFS.

I think this is the more realistic version, and it also can leave room for the fact that ME/CFS is not the only illness that has an exaggerated prolactin response to buspirone. Migraine has more literature about this than ME/CFS. So, what I could imagine is that this test would exist alongside a symptom questionnaire that can distinguish ME/CFS and similar conditions. Hopefully there can be some other biological marker that can confirm an ME/CFS diagnosis, like an MRI or a genetic test if anything proves to be specific enough. The prolactin response cannot be a biomarker on its own.