Thousands could have Lyme disease without knowing

[Daffodil]

I'd like to see someone perform a study on treating a group of chronic Lyme disease patients displaying ME/CFS symptoms with rituximab; if these patients had the same clinical response as regular ME/CFS patients get from rituximab, it would suggest that Lyme ME/CFS is the same as or very similar to regular ME/CFS.

I am not sure that would prove anything because many or most? autoimmune diseases respond to rituximab already.

however, there are those who think that all autoimmune disease is caused by intracellular bacteria ....

 

[Hip]

I am not sure that would prove anything because many or most? autoimmune diseases respond to rituximab already.

however, there are those who think that all autoimmune disease is caused by intracellular bacteria ....

If Lyme could be cured by rituximab, it would suggest that Lyme disease is an autoimmune condition. Not only that, but if it worked, it would provide a very valuable treatment option for Lyme patients.

It's quite conceivable that intracellular infections might cause autoimmune disease, but that would not negate the benefits of rituximab, if it worked for Lyme. In Lyme, you may not be able to kill off all the intracellular infection (because we don't have powerful enough antibiotics), but if you can halt the autoimmunity that may be caused by that intracellular infection, by means of rituximab, you may be able to cure Lyme disease anyway, even with the bacteria still present.

 

[dadouv47]

I'd like to see someone perform a study on treating a group of chronic Lyme disease patients displaying ME/CFS symptoms with rituximab; if these patients had the same clinical response as regular ME/CFS patients get from rituximab, it would suggest that Lyme ME/CFS is the same as or very similar to regular ME/CFS.

Or you do the exact opposite study and give some LDI to CFS/ME patients, which is IMHO more promising/reliable right now for patients with Chronic Lyme.

 

[Hip]

Or you do the exact opposite study and give some LDI to CFS/ME patients, which is IMHO more promising/reliable right now for patients with Chronic Lyme.

Has LDI cured any Lyme or ME/CFS patients (ie, complete remission with no symptoms), in the same way that rituximab cures around one third of ME/CFS patients, and significantly improves the health of another third?

 

[dadouv47]

Has LDI cured any Lyme or ME/CFS patients (ie, complete remission with no symptoms), in the same way that rituximab cures around one third of ME/CFS patients, and significantly improves the health of another third?

I'm not an LDI expert ( neither rituximab) but it's helping a lot of Lyme patients in a big way.

Are your 66% cure/huge improvements with rituximab for ME/CFS accurated ? Sounds a lot...

 

[Hip]

Are your 66% cure/huge improvements with rituximab for ME/CFS accurated ? Sounds a lot...

That's what Kolibri and the OMI are saying: see this post.

 

[Hip]

I'm not an LDI expert ( neither rituximab) but it's helping a lot of Lyme patients in a big way.

Do you know if there have been any published studies on LDI for Lyme or ME/CFS, or even just reports from reputable doctors?

 

[duncan]

@Hip, I cannot help but wonder what impact rituximab might have in people with a Borrelial infection. It might be an interesting dilemma for those of us that have both ME/CFS and tbd diagnoses. I actually have a fervernt hope to have to embrace that dilemma one day.

I am pretty sure we discussed this earlier, like a year or so ago.

 

[Hip]

@Hip, I cannot help but wonder what impact rituximab might have in people with a Borrelial infection.

Yes, I am not about safety; you do very occasionally get fatal viral infections after rituximab. I am just wondering why, as far as I am aware, no researchers or Lyme doctors are looking at this.

Here is a story of one patient with Borrelia who was treated with rituximab.

 

[duncan]

Here is a story of one patient with Borrelia who was treated with rituximab

Good find. I wonder if we can speculate that the rituximab triggered the relapse...? I do not think they supply enough insight in that abstract.


I have the impression that Lyme doctors and ME/CFS doctors, although aware of each other because they share orphaned disease specialties, do not cross over into each others' territories too often.

I am just wondering why, as far as I am aware, no researchers or Lyme doctors are looking at this.

I was pleasantly surprised, though, that one day I was discussing ME/CFS with my Lyme doctor, and New York City came up, and he volunteered he knew about Susan Levine.

Lyme doctors are in a tough spot - they are constantly under scrutiny in some countries. So they may have an understandable reluctance to venture further out on a limb with treatments not earmarked even peripherally for Lyme.

 

[Hip]

I wonder if we can speculate that the rituximab triggered the relapse...? I do not think they supply enough insight in that abstract.

In the full paper, it says she had rituximab treatment from April 2009 to November 2009.

Then around one year later in September 2010, she had sudden onset of severe shooting pains in her back and both legs, followed by progressive deafness, nausea, vertigo, a headache and 5 kg loss of weight.

The authors think it almost certainly was due to Borrelia, because:

In contrast, B burgdorferi PCR on CSF, which is known to have a sensitivity of only 10–50%, demonstrated the presence of B burgdorferi DNA in CSF, which was confirmed in a consecutive CSF sample 2 weeks later. This, combined with the fact that the patient's complaints disappeared upon treatment with ceftriaxon, strongly supports the diagnosis of Lyme neuroborreliosis.

The outcome was good:

With a diagnosis of seronegative Lyme neuroborreliosis, our patient was treated with ceftriaxone once daily 2000 mg intravenously for 3 weeks.

During these 3 weeks she improved dramatically, which further strengthened the diagnosis. She gained weight, the complaints of headache and vertigo disappeared and her hearing loss slowly improved. Paired serology on blood and CSF 7 weeks later still revealed no antibodies against B burgdorferi.

One-and-a-half years later, a routine MRI of the myelum showed no evidence for relapse of the lymphoma and the hearing ability had completely returned. During neurological follow-up the patient reported a slight unsteadiness of gait, which was attributed to residual postinfectious complications. The rituximab maintenance therapy had been discontinued during her hospital admission, but despite the slow repopulation of B-lymphocyte subsets, 1.5 years after her initial presentation, there were still no antibodies against B burgdorferi (figure 3).

 

[duncan]

I just want to point out as a side bar -although it certainly ties back into the subject of this thread - how lucky this woman in the case provided by @Hip was.

She was seronegative for Borreila. So neither the ELISA nor the WB picked it up. I am assuming they would have checked her AI in her CSF and that also appears, if they did it, to have been negative.

So they throw the PCR at her CSF fully knowing the odds were vastly against the PCR working, cuz it just doesn't on CSF very often...

And BAM! they get a hit. This woman had neuroborreliosis and the majority of conventional tests failed her, and the only one which helped, on paper, SHOULDN'T have, at least not statistically.

So any body who thinks the 2 tier tests promoted by the US and the NHS and others are virtually foolproof - well, here is another anecdotal proof they ain't.

 

[Hip]

So they throw the PCR at her CSF fully knowing the odds were vastly against the PCR working, cuz it just doesn't on CSF very often...

Don't forget though that she had been immunosuppressed due to rituximab, so presumably that would have allowed the Borrelia to proliferate more, increasing the chances of a successful PCR detection.

 

[Marky90]

what is wrong with the armin lab test?

They`re based on the premise that what they`re testing for is a biomarker, and that has not been proved.

 

[Daffodil]

They`re based on the premise that what they`re testing for is a biomarker, and that has not been proved.

oh

 

[Marky90]

oh

At least that is my conclusion after reading up on it, and there are also conflicts of interest in the research. Maybe @Jonathan Edwards has a better overview.

 

[Daffodil]

@Marky90 i'm too foggy to understand anyway lol

 

[Daffodil]

if i had a chronic infection, i am not sure i would want to take ritximab.

where does it say that 1/3rd of patients are cured ? i thought it almost always comes back in several months

@Hip if you really want to halt autoimmunity, you would probably have to halt HERV or something...not kill off B cells

just my 2 cents whicn arent worth much cuz my brain is mush lol

 

[AndyPR]

if i had a chronic infection, i am not sure i would want to take ritximab.

where does it say that 1/3rd of patients are cured ? i thought it almost always comes back in several months

@Hip if you really want to halt autoimmunity, you would probably have to halt HERV or something...not kill off B cells

just my 2 cents whicn arent worth much cuz my brain is mush lol

From the Stage 2 Rituximab trial - http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0129898

Clinically significant responses were seen in 18 out of 28 patients (64%) receiving rituximab maintenance treatment. For these 18 patients, the mean response durations within the 156 weeks study period were 105 weeks in 14 major responders, and 69 weeks in four moderate responders. At end of follow-up (36 months), 11 out of 18 [39% of all patients, 61% of responding patients] responding patients were still in ongoing clinical remission.

I added the percentages in square brackets in the quote.

 

[Daffodil]

thanks @AndyPR