Spironolactone as a treatment for CFS in patients with positive Epstein Barr virus serology, 2020, Campo and Taylor

What is ‘positive serology’ means? IgM+ (Suggestive of active infection) or IgG positive? early Antigen +?

 

An endocrinologist here trialled Spironolactone on his ME/CFS patients in the late 1990s. An old friend from uni happened to be a colleague of his and wrote me a prescription for it. I tried it for 6 months and noticed no effect (I'd had an EBV onset about 8-9 months earlier).

It's strange how all these old treatments from the 90s (eg, niacin) are suddenly making a comeback.

 

Whole new group of punters who haven't experienced enough to know that 'simple' fixes don't work.

No matter how many monks from far away were 'involved' in producing them.

IMO it should be illegal, but it seems a lot of this old marketing led 'research' is actually being promoted/paid for by the authorities. Just so they can say ' we are doing something, look at how much money we're spending'.

 

I don't know what viral infection I had at onset, but it wasn't considered important by ME doctor.

I continue to have reactivations of EBV and HHV6 and would consider taking a medication to shorten the duration? I don't understand how that would 'help' or treat CFS though?

 

I had a quick look through a local ME/CFS group because the use of spironolactone rang a few bells. The main author is a specialist at Noosa hospital in Queensland. The person that had seen him said he was very considerate.

Regarding the justification for using spironolactone, he had referred them to this paper: Spironolactone blocks Epstein–Barr virus production by inhibiting EBV SM protein function

Edit: link fixed

 

Link doesn't work.

This is a corrected version

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4822607/

However, in common with @Mij I fail to see how this would help anyone unless the hypothesis is that ME is directly caused, and maintained, by EBV was correct.

Which, as far as I know, has been pretty conclusively refuted over the years.

 

Goodness knows what the Royal Australian College of Physicians are doing publishing this.
It hasn't even been checked for grammar.

Edit: I see it may be just a poster. But it is still not good enough to present at a meeting.

 

I was aware of it. I was sent the abstract in June. I don’t know anything about their method, but I agree with the concerns raised here.

 

This seems to be the same thing republished.

SPIRONOLACTONE OFF-LABEL THERAPEUTIC BENEFIT IN ME/CFS

Background

In The RACP Congress 2020 we presented an abstract which demonstrated the results of patients treated with spironolactone for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) with Epstein Bar (EBV) positive serology. Spironolactone has an antivirus effect against EBV by inhibiting the EBV SM protein function (1). Patients with positive EBV serology and ME/CFS may be carriers of a chronic latent infection. As reported by multiple authors in previous research ME/CFS is a neuro-inflammation. When investigating patients with magnetic resonance spectroscopy it was described widespread metabolite abnormalities in ME/CFS. Areas of increased temperature include right insula and thalamus, putamen, frontal cortex, and cerebellum. The areas of neuro-inflammation are in the microglia and the microglia cells are macrophage of the central nervous system, these macrophages are indistinguishable from bone marrow derived macrophages. Emerging research indicates that Angiotensin Converting Enzyme 2 receptors (ACE2) may be responsible for protective effect of microglia (2). Spironolactone increase the ACE2 receptors activity (3).

Population and Method
21 patients (17 females) with positive serology for EBV infection and ME/CFS were included All the patients were treated with ascorbic acid oral 50 mg/Kg. They have supplementation with Cholecalciferol 1000 Units/day, Vitamin B12 intramuscular 1 mg every 4 weeks, Thiamine 100 mg a day and Folic acid 5 mg a day. Patients were educated about benefit and adverse effects of spironolactone before treatment then starting dose was 12.5mg a day increased to 25 mg a day after the first follow up.

Patients used the pedometer as management strategy for every day activity. The target has been to limit the physical activity to avoid exercise triggering fatigue crisis.

Patients were follow up in outpatient clinic and GP clinic.

Results
21 Patients 17 were Females age 54.2 +11, four Males 63.7+5. Five patients presented intolerance to spironolactone. 16 tolerated the dose of 25 mg a day. Five of these patients had no more CFS and all the rest improved in fatigue and general symptoms.

Improvement in cognitive skills was the early manifestation of spironolactone benefit. Patients reported to be less brain foggy, more alert and they found it easier to focus when doing normal every day activities. They also were less irritable by noise and light and described themselves to be able to do multi task again. Later, after six weeks, they improved their tolerance to walking exercise.

Conclusion
Patients with ME/CFS improve their cognitive skills when treated with spironolactone.

Spironolactone increased macrophage ACE2 receptors activity and in the microglia this effect may represent a reduction of neuro-inflammation.


Open access, https://onlinelibrary.wiley.com/doi/10.1111/imj.1_15291