Who will respond?

Hi All,
Here is an abstract about assessing mechanisms of treatment effects in ITP patients. The study investigated the immature platelet fraction. Nonresponders to thrombopoietic agents like Nplate and Promacta had not increased absolute immature platelet fraction. One of the authors - James B. Bussel – is a big shot in this field.
bloodjournal.hematologylibrary.org/content/117/21/5723.abstract
Kind regards
Birgitta-A

Wow - that's really interesting! Break-through stuff!

can we get a reprint in english - twas greek to me! :laugh:

Same here. Must be a Male thing. :lol: :lol:

SteveC wrote: can we get a reprint in english - twas greek to me! :laugh:

Does this help?

The IPF or Immature Platelet Fraction is the percentage of new platelets we have.
The A-IPF or Mean Absolute IPF is the actual number of new platelets we have.
So a high percentage of an ITP person's platelets will be new although there actually won't be an awful lot of them so the actual number will be quite low.

By seeing how these figures change in a patient with treatment, we can see how the different treatments work.

Perhaps this is a little more clear:

This study investigated the immature platelet fraction in assessing treatment effects in ITP. Immature platelet fraction was measured on a special autoanalyzer. The mean absolute immature platelet fraction was lower for ITP patients than for healthy controls whereas immature platelet fraction percentage was greater.

All 5 patients with a platelet response to Eltrombopag, but none responding to a special antibody (CD16) found on the surface of several blood cells, had corresponding absolute immature platelet fraction responses.

Seven of 7 patients responding to RhoD immuneglobulin and 6 of 8 responding to intravenous immunoglobulin did not have corresponding increases in absolute immature platelet fraction, but 2 with intravenous immunoglobulin and 1 with intravenous immunoglobulin anti-D did.

This supports inhibition of platelet destruction as the primary mechanism of intravenous anti-D and intravenous immunoglobulin , although intravenous immunoglobulin may also enhance thrombopoiesis.

Plasma glycocalicin, released during platelet destruction, normalized as glycocalicin index, was higher in ITP patients than controls.

There was an inverse correlation between glycocalicin index and absolute immature platelet fraction in ITP patients, demonstrating the relationship between platelet production and destruction.

Nonresponders to thrombopoietic agents had increased megakaryocytes but not increased absolute immature platelet fraction, suggesting that antibodies blocked platelet release.

In conclusion, absolute immature platelet fraction measures real-time thrombopoiesis, providing insight into mechanisms of treatment effect.

Kind regards
Birgitta-A

Thanks guys. I used to be good at interpreting, just didn't get to it.

Thanks Ann & Birgitta-A, you improved it from Greek to English with an accent. Translation: If I really really concentrate I sort of understand - just don't test me on it! But it seems with this analysis the really smart R&D MD's can evaluate the effectiveness of all these Rx's I can't pronounce. But since this just allows better real time analysis of effectiveness, it doesn't seem to offer any insight to the base cause, nor does it by itself indicate who will respond or not to a particular treatment. Thus seems only useful to the researchers as they test and evaluate more quantitatively drug effectiveness. Now I'm going to take two aspirin (whoops, make that tylenol, and try to rid myself of a headache. :laugh:

Hi Steve,
As far as I understand they should be able to see if a patient has increased absolute immature platelet fraction or not. According to this study responders to thrombopoietic agents should have increased absolute immature platelet fraction.
Kind regards
Birgitta-A