I'll be my own doctor, thank you very much

[WaikikiWaves]

Originally Posted by Medical Lab Guy

Those are not the only variables that one is talking about. It just proves my point that it is useless to make recommendations lacking clinical studies. There's variability of M proteins not only in this country but throughout the world. ARF is other countries is higher and differ in M proteins. M proteins alter phsyiology and outcomes.

There has been vaccine studies using M proteins. Antibody responses if one is talking about ASO antibodies is also variable. There's also over diagnosis based on simply stand alone titers. It is more optimal to see a rise in titer.

In either case until there are clinical studies showing outcomes then we can talk about that.

I doubt it has anything to do with M protein variability from regions but instead HLA gene variability among populations.

Also, generally it’s been understood that if you’re arguing that the medical intervention does X, then you’re the one to present clinical studies. Not the other way around.

[Medical Lab Guy]

Originally Posted by WaikikiWaves

I doubt it has anything to do with M protein variability from regions but instead HLA gene variability among populations.

Also, generally it’s been understood that if you’re arguing that the medical intervention does X, then you’re the one to present clinical studies. Not the other way around.

I posted a study involving ARF and the reduction with antibiotics. I that one argument that it does X.

Another example is with PSGN

"Over the past three decades, PSGN incidence has significantly dropped in developed countries; such as the United States, UK, Central Europe, and Japan. The reason for this progress is the use of antibiotic prophylaxis and the improvement of hygienic states. In these developed countries, PSGN has become more frequently seen in adult patients who suffer from chronic debilitating diseases.[6] "

That's another example of it doing X.

With regard to M protein in that same citation,

"Group A Streptococcus (GAS) has been subtyped depending on the surface M protein and opacity factor, which are known to be nephrogenic and can cause PSGN."

https://www.ncbi.nlm.nih.gov/books/NBK538255/

"In particular, the M protein molecule has been finely tuned to allow the streptococcus to persist in infected tissues while skillfully avoiding human immune cells. As the first molecule on S. pyogenes to be completely sequenced, it is considered the archetypical surface molecule for these organisms and other Gram-positive bacteria;"

The ability of S. pyogenes to persist in infected tissues can be primarily attributed to the cell surface M protein, a molecule that gives the streptococcus the ability to resist phagocytosis by polymorphonuclear leukocytes in the absence of type-specific antibodies.

The streptococcal M protein is now probably one of the best-defined molecules among the Gram-positive bacterial virulence determinants. Its structure, function, immunochemistry, and method of antigenic variation are unique among known virulence molecules, and may serve as a model for certain microbial systems.

Resistance to a group A streptococcal infection is directly related to the presence of type-specific antibodies to the M molecule (Lancefield, 1959; Lancefield, 1962). Since there are >200 different serotypes of M protein (i.e., M6, M12, M18, M24, and so on), an individual may become infected by more than one group A streptococcal type during a lifetime.

https://www.ncbi.nlm.nih.gov/books/NBK333431/

Pathogenesis of ARF,

Molecular mimicry

"There are a number of lines of evidence that suggest molecular mimicry plays a role in the development of carditis by stimulating both humoral and cellular cross-reactive immune responses (Cunningham, 2000; Guilherme, Kalil, & Cunningham, 2006; Cunningham, et al., 1992). The alpha-helical protein structures found in M protein and N-acetyl-beta-D-glucosamine (the carbohydrate antigen of S. pyogenes) share epitopes with myosin, and antibodies against both of these antigens cross-react against human tissues."

All of the above is speculative but what isn't is the reduction of incidence when given antibiotics. Thus it became the standard of care because of it. If the virulence factor changed or environmental factors have changed implying that antibiotics are no longer needed than one does a study comparing the present standard of care vs the proposed standard of care of not using antibiotics and then one sees what happens.

The proposed mechanisms don't need to be proved only the outcomes.

You can not simply stop using antibiotics without outcome studies being done to see what happens.

[WaikikiWaves]

Originally Posted by Medical Lab Guy

I posted a study involving ARF and the reduction with antibiotics. I that one argument that it does X.

Technically a review of 10 studies, only 3 of which included placebos.

Of those 3 included, only 1 dealt with reduction of ARF (the other's were measuring antibody titers and symptoms).

So I had a look at this one, just for fun: https://www.nejm.org/doi/full/10.105...95409162511203

Go to table 6.

There were 2 cases of ARF reported in the control, none in higher or lower doses of dbed.

But what is interesting is that 5 cases of "possible" ARF (or reaction to medication) were reported in the higher dose of dbed arm, 1 in the lower dose of dbed arm, and 0 in the control.

Since the study was not blinded (from the point of the PI), I have to say it's not convincing. Why were so many possible ARF in the treatment groups (6) vs 0 in the controls? Were all of these reaction to medication or were these some cases of ARF?

Ignoring that, 2 vs 0 is not a properly powered study.

If you want to hang your hat on this study, you can. But I don't. Simple as that.

Your statement here: All of the above is speculative but what isn't is the reduction of incidence when given antibiotics.

Is simply not correct, or put too strongly to say the least. The evidence base for antibiotics reducing these autoimmune mediated disorders is weak at best, and really inconclusive.

And to note, all 3 of these studies featured antibiotics delivered parenterally, not orally.