Tough Stuff Part 4, the last part for now

Maybe I am trying to read the tea leaves and what I am looking into is a mug with leftover coffee grains.

Not sure this makes all any sense. Last glance backward to put it all together for the future plan.

I developed ITP the first time when I had a significant tumor load. When the combination of cyclosporine A (CsA), an killer immunosuppressive drug, mostly used to prevent transplant rejection, and occasionally to calm down an over zealous immune system, and rituximab, a monoclonal antibody, Vitamin R, used for everything from CLL to rheumatoid arthritis and ITP, worked their magic and sent my platelets skyward, my celebration had just begun. The combo offered a surprise bonus no-one expected when it had a profound anti-leukemic effect, shrinking all my palpable nodes, and reducing the CLL in my marrow from 90% to 3%. Went on to transplant and the rest is history.

I am focusing on the ITP here. These two drugs work well on ITP for people who don't have leukemia, so it is completely logical, but far from certain, that the reduction of my tumor load was not the issue in controlling my ITP.

Here's where it gets tricky. True, my ITP was gone when my tumor burden was only 3%, but it was also gone when it had climbed to 25% after 4 months off the R, though still on CsA.

I was on CsA and IVig until just before the transplant.

With the heavy conditioning chemo (FCR) for the transplant, my tumor burden dropped even more, to MRD negative in the marrow with shrunken gut nodes. Eventually, the CLL creeped back, slowly and last August, when my platelets started to fall again, a bone marrow biopsy showed it had snuck back like a terrorist cells in the Swat valley, claiming 2.8% of the niches of my marrow. The nodes were growing slowly too.

So here's the way I see the relationship between my CLL and my ITP. A weakness of this analysis is that it only assesses the bone marrow and not the nodes, and the nodes have always taken the lead in my CLL dance.

1 year of CLL growth = no ITP

High tumor load (90%) = 1st episode of ITP

Reduced load (3%) = ITP controlled w CsA+R

Increased load (25%) = ITP still controlled w CsA and IVIG

Greatly reduced load (MRD-) = ITP still controlled post transplant & heavy FCR

Slight increase (2.8%) =ITP back gentler & controlled sorta with IVIG

The relationship is hardly lock stepped. Immune dysfunction does increase with the time with the disease, so the ITP may recur with less and less CLL induced immune chaos.

Dr Hamblin says if steroids fail, I should move to control the underlying disease that drives it. My concern is that I need to get a MRD neg,. remission, (and possibly shrink all the nodes, including the more provocative ones in the gut) to control the ITP. I worry that a simple PR ( partial remission) or even an old school CR (complete remission) will not accomplish the mission.

R+HDMP gives me an over 90% chance of a response , but the odds of a CR are much lower. and the odds of a CR, MRD negative without adding campath are even smaller.

Will that solve my ITP? A dear friend developed ITP after R+HDMP did a great job on her blood, nodes and marrow. She developed ITP, like me, with a very low tumor burden too.

The effects that are caused by all these drugs on the CD200+ and Tregs and who knows what else that play a vital role in self tolerance and thus prevention of ITP is beyond my understanding. I think it is fair to worry that not only might R+HDMP not get me over the finish line to MRD negative and thus control of the ITP, but could make matters worse.

Might it make my platelets situation critical and refractory again? Not likely.

Might it make things more difficult to move to the next more myelo-suppressive step? Quite possibly.

It still might be worth the risk to avoid the more toxic path of FRC and transplant, but I need to prepare for the Sabbath, and lay my burdens down for next 25 hours.