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Does successful Rituximab treatment also resolve POTS & hypoglycaemia?

Kenny Banya

Senior Member
Messages
356
Location
Australia
Wondering how these physical symptoms are considered 'resolved'

Postural Orthostatic Tachycardia Syndrome might be resolved because with more activity the heart's 'standard' pulse pressure increases? Hence no need to increase pulse rate.
Then again, if it is brain (brain stem?) signalling to the heart regarding pulse pressure, how does increased immunity affect brain signalling.
Then there's hypoglycaemia - maybe the change in cells from Rituximab allow the cells to process glucose better. Maybe the ADP cycle is fixed.
Questions, questions....
 

halcyon

Senior Member
Messages
2,482
What the two have in common would be beta adrenergic receptors not working properly. As recent research has shown, there might be autoantibodies that are blocking activation of these receptors in POTS patients. So rituximab might improve both things by depleting the B cells that are producing the autoantibodies that are blocking beta adrenergic receptor function in the body.
 

Diwi9

Administrator
Messages
1,780
Location
USA
What the two have in common would be beta adrenergic receptors not working properly. As recent research has shown, there might be autoantibodies that are blocking activation of these receptors in POTS patients. So rituximab might improve both things by depleting the B cells that are producing the autoantibodies that are blocking beta adrenergic receptor function in the body.
This is why you, @halcyon, are one of PR's rockstars. One day all of this data is going to congeal and make sense to me...cannot wait for the day when there is a textbook describing ME/CFS based on biological research.
 

Kenny Banya

Senior Member
Messages
356
Location
Australia
What the two have in common would be beta adrenergic receptors not working properly. As recent research has shown, there might be autoantibodies that are blocking activation of these receptors in POTS patients. So rituximab might improve both things by depleting the B cells that are producing the autoantibodies that are blocking beta adrenergic receptor function in the body.
Do you have any references about the potential connection between Rituximab & beta adrenergic receptors (BAR)?
Or any links on drugs that have affected BAR?
 

halcyon

Senior Member
Messages
2,482
Do you have any references about the potential connection between Rituximab & beta adrenergic receptors (BAR)?
This came up in the Charite study. It's not a direct connection. Rituximab has no direct effect on adrenergic receptors as far as I know.
Antibodies against β2, M3 and M4 receptors were significantly elevated in CFS patients compared to controls. In contrast, levels of antibodies against α adrenergic, dopamine, serotonin, angiotensin, and endothelin receptors were not different between patients and controls. A high correlation was found between levels of autoantibodies and elevated IgG1-3 subclasses, but not with IgG4. Further patients with high β2 antibodies had significantly more frequently activated HLA-DR+ T cells and more frequently thyreoperoxidase and anti-nuclear antibodies. In patients receiving rituximab maintenance treatment achieving prolonged B-cell depletion, elevated β2 and M4 receptor autoantibodies significantly declined in clinical responder, but not in non-responder. We provide evidence that 29.5% of patients with CFS had elevated antibodies against one or more M acetylcholine and β adrenergic receptors which are potential biomarkers for response to B-cell depleting therapy.
 

Kenny Banya

Senior Member
Messages
356
Location
Australia
This came up in the Charite study. It's not a direct connection. Rituximab has no direct effect on adrenergic receptors as far as I know.
Thanks. Have now read it.
I guess what it is saying is in the current trial, 30% have responded to Rituximab treatment (at least based on autoantibody decline) and this has resulted in the correct function of neuronal signals (transmitters reaching receptors) for the heart to pump at an adequate pressure.