Anyone see this article?? Platelets could possibly be formed in lungs?!

Hey check out this article and see what you think!

www.sciencealert.com/an-unexpected-new-lung-function-has-been-discovered-and-it-could-disrupt-decades-of-scientific-thought

Stunning discovery! It is amazing how much conventional wisdom eventually gets overturned.
It will be interesting to see what the implications might be for ITP.

It will indeed Rob

I'd like to see more info. It will take time for me to wrap my head around this.

Poseymint was just saying in another thread that her counts shot way up after having (lung) Bronchitis. I think that was the first time I've ever heard about someone's counts going up after being sick.

Hal, I was thinking along the same lines, that perhaps respiratory infections might cause spikes, while other infections might cause drops in counts, or vice versa. Pure conjecture, though.
Ellen recently had a spike in counts with a sinus infection, fwiw.

Don't thrombopoietin Receptors exist on Megakaryocytes? Wouldn't thrombopoietin therefore combine with thrombopoietin Receptors in the lung?

I've wondered about how the immune system could start producing antibodies to Thrombopoietin (TPO). Once one realizes that TPO normally attaches to platelets, then it can be seen that the immune system consuming old platelets, with TPO attached to them, makes it possible.

And then there are thrombopoietin Receptor antibodies. How could the immune system generate antibodies if these Receptors are located in bone? Now we see that Receptors are / can be located in the lung. That is making more sense. Still, seems to be a mystery about how Receptor antibodies occur to me. The immune system consuming old Megakaryocytes running through the circulatory system ? ?

This is an interesting read

www.ncbi.nlm.nih.gov/pmc/articles/PMC2789970/

mrsb, it would be interesting to see that 2009 study redone. Redone taking into account ITP production problems exist as either TPO antibodies, or, TPO Receptor antibodies. Some ideas presented seemed to be erroneously coerced from the presumption that only TPO antibodies exist.

Take a look at the first reference in the study: "Amgen, Inc.; 2008. ODAC Meeting Briefing Document". It appears to be a summary of all of Amgen's data on NPlate at the time, especial data on the drug's trial with FDA monitoring. Wow, pretty comprehensive. One item that caught my eye was Table One on page 24. Nice summary of many treatments - by the numbers.

In what I read, no one in the FDA trial developed antibodies to NPlate itself. Regardless, from the stories here on PSDA, this does seem to happen with regularity.

Another interesting and ironic item is described at the bottom of page 42. During the trial, exactly one (of 42?) placebo/control group patient went into remission. Apparently the placebo group could take other ITP drugs like steroids, Azathioprine, or Danazol. The person that went into remission was taking Danazol.