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

Sure, the ideal test would actually measure some biological parameter which is at the core of ME/CFS pathophysiology, and hopefully a parameter unique to ME/CFS. Though as we are not currently sure what the core pathophysiology of ME/CFS is, that makes it difficult to develop such a test.

 

Are you kidding?
People have been misdiagnosed with more things instead of ME then we could shake a stick at.
I bet if anyone collected a list it would be Yuge!

 

Yes, the lists of symptomatically similar diseases to ME/CFS are quite long, but I have not seen any lists that contain dyspepsia or social anxiety (= anxiety about how other people judge or evaluate you).

 

[Patient] has social anxiety hence you want to avoid future situations so your brain tells you your tired as a way to avoid them.
The fact it happens in other situations that involve physical activity means you need a lifetime of Freudian "therapy"
Or it just might mean [Patient] has hysteria and this was the trigger...

Framing complex problems in similar terms to these is not at all rare. I got lucky that i had a doctor who at his retirement and years of testing to no avail told me i don't know whats wrong with you instead of your obviously neurotic...

 

I think so too. It's unfortunate that there are two alternative theories to explain the mechanism of the buspirone-stimulated prolactin release, so although we know that there is exaggerated release in ME/CFS, we cannot be sure of the mechanism.

The original theory is that there may be an increased sensitivity or up-regulation of the serotonin receptors in the hypothalamus in ME/CFS, and so when buspirone — a serotonin 5-HT1A agonist — is given to ME/CFS patients, it produces a larger than normal stimulation in the hypothalamus. If true, this assumed increased hypothalamic serotonin receptor sensitivity might shine some light on the HPA-axis dysfunction in ME/CFS.

The alternative theory proposed by Sharpe et al is that the increased prolactin response to buspirone in ME/CFS might reflect changes in the dopamine system, as buspirone is also a dopamine D2 receptor antagonist, and these D2 receptors are also involved in prolactin secretion. That may also shine some light on the HPA-axis dysfunction, but a dopaminergic rather than serotonergic light.

 

For any marker to be used as a diagnostic test it needs to have very high sensitivity and specificity, demonstrated by replication studies comparing to other illnesses as well as healthy controls. As far as I know, no numbers of sensitivity/specificity have been published for the buspirone challenge, so it's use as a test is speculative at best.

My personal opinion is that it will have poor sensitivity/specificity, but I'm willing to be proven wrong.

 

CBT for dyspepsia?

 

The Richardson study on 30 ME/CFS patients and 30 controls gives some information on this:

The ratio here refers to the person's buspirone-stimulated blood prolactin level, divided by the mean buspirone-stimulated prolactin level of the healthy controls. Judging by Figure 2 in the study the mean level of the controls is 400 mIU/L, meaning the threshold level for ME/CFS diagnosis would be 2.5 x 400 = 1000 mIU/L = 47 ng/mL (conversion to different units of measurement given here).

So it looks like in this small-scale study at least, the buspirone challenge test sensitivity and specificity are both 87% if you set the threshold for positive diagnosis at a ratio of 2.5.

As a reminder: Sensitivity is the proportion of people with disease who have a positive test result. Specificity is the proportion of people without disease who have a negative test result.

It's possible one might be able to improve this sensitivity and specificity even further if you also take into account the time-to-peak data that was measured in the Sharpe study (this study found not only higher prolactin peaks in ME/CFS patients after buspirone stimulation, but also a faster time-to-peak).

 

Seconded!

 

I came across this UK finger prick home blood test for prolactin levels for £39, which means you could test yourself.

The only thing is that I understand finger prick home blood tests are not that accurate, as finger prick blood samples are too small. But the same test also has an option to supply the blood by normal venipuncture (for an additional charge), which will have the normal accuracy.

 

You assume wrongly. It is a serious idea.

In the UK it is legal to import any non-controlled prescription medication for personal use, so you don't need to involve your doctor if he is unwilling.

 

@Hip I get that your enthusiastic about this but this is not a smart thing to play with especially when something like the Canadian Consensus Criteria work quite well. Not to mention Dr Leonard Jason's high specificity questionnaires which i would love to see verified since he claims they work well even in early stages of mild ME.
If this is about smashing the PACErs it won't work because they have no interest in facts, as we see in politics reality means nothing to ideologues. To them its about belief and anything that contradicts their beliefs will be dismissed. Sophistry is a well sharpened sword in todays world.

 

87% is very poor for a cherry picked/post-hoc threshold.

 

Yes, the CCC do work quite well, but we have all seen the cases of patients who were misdiagnosed with ME/CFS for years when they actually had a much more treatable illness.

I remember one patient on Phoenix Rising who though she had ME/CFS, but it eventually turned out to be growth hormone deficiency, and GH treatment fixed all her symptoms. More recently a patient on Health Rising, who for 10 years thought he had ME/CFS, later realized it was CIRS (biotoxin illness), and again the right treatment got him back to near full health in just 5 months. And another recent patient on PR, who it turns out had craniocervical instability causing all the symptoms of ME/CFS including PEM, once he got the correct diagnosis and had surgery, that fixed all his symptoms.

These patients probably met the CCC, but did not have ME/CFS, and wasted years chasing the wrong disease and the wrong treatments.

So there is a need for a ME/CFS blood test, and I am wondering why this one, which is cheap and simple, was not further developed.

Maybe, but since research seems to have stopped on the buspirone challenge test, so we will never know what sensitivity and specificity might be possible.

 

I've known of people with ME to have been diagnosed with general anxiety disorder, social anxiety and agoraphobia. There is also the problem that it is hard to separate social anxiety from agoraphobia, and sometimes it is both. I would not be surprised if a feeling of not having the backing of the medical system, or past mistreatment can contribute to them being co-morbid in ME patients.

When the fear avoidance model is used as an explanation for ME, illnesses with fear avoidance can look like ME and vice versa. It's no co-incidence that the behavioural treatments are very very similar, including CBT and GET.

 

I will not argue that having a disease thats diagnosed by exclusion will lead to misdiagnosis because it will which is what i hate about conclusion by exclusion. But we do not know whether or not those other patients met the CCC. That said i don't think this is the test that is going to weed out all other diseases. I would consider the nanoeedle to be a better candidate though it even needs to be validated (and the molecule causing the signal identified).

 

It's also important to remember that Sharpe's patients fulfilled CFS criteria but also criteria for neurasthenia. I'm not sure what the latter means, or whether it affects those results (e.g., by selecting for patients with obvious nervous/anxious symptoms which might skew the response).