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  #1  
Old Thu Mar 1, 2012, 02:40 PM
Paul Paul is offline
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Recommended frequency of follow up bone marrow biopsies?

Hi all,

Haven't posted here in a while. No news is usually good news in that regard. My son, now 11 has been in full AA remission for about 6 years. In recent past, our medical follow up consisted of a yearly blood draw to run a complete blood count. The doctor is now indicating that they would like to do a yearly bone marrow biopsy going forward. The theory being that frequent biopsies would monitor for potential changes to leukemia or mds before it would show via a complete blood count. If someone needed a bone marrow transplant the hope would be that the earlier one knew that was going to be the course of action the better the possible outcome.

The last bone marrow biopsey occurred about 5 years ago. It's not the end of the world, but neither my son or I are eager to have him undergo a yearly biopsy. We try to give him as normal of a childhood as possible under the circumstances.

I'm curious, if anyone else out there in remission undergoes frequent biopsies. If so, what is the frequency? Thanks for any input.
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Paul
Son diagnosed 3/2006 with VSAA at age of 4 years old; No sibling match; received IST with CsA, counts reached normal level after about 6 months; Currently in remission.
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  #2  
Old Thu Mar 1, 2012, 03:55 PM
Marlene Marlene is offline
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My knee jerk reaction is NO to a yearly BMB. They are assuming your son will go on to develop some other type of blood disorder. What are they basing this on? I haven't kept up the stats on how many go on to develop MDS or Leukemia but I would think he has a better chance of an SAA relapse than the other two. And if that's the case, it's not treated until it's at the SAA stage and sometimes when it's moderate. A BMB is not the sole criteria , somehow, you can maintain normal peripheral blood counts with low cellularity. So they would never treat based on just low cellularity.

I think the risk out weighs the benefit. I think more frequent CBCs would be a better option. That's just my opinion.

So to answer your question. John is going on his 10 year anniversary this year. He's had only two BMB. Both were done before treatment. The first was inconclusive so he needed a second. He has not had any since. And he's in a partial, stable remission.
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Marlene, wife to John DX w/SAA April 2002, Stable partial remission; Treated with High Dose Cytoxan, Johns Hopkins, June 2002. Final phlebotomy 11/2016. As of January 2017, FE is 233, HGB 11.7, WBC 5.1/ANC 4.0, Plts 146K.

Last edited by Marlene : Thu Mar 1, 2012 at 05:51 PM.
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  #3  
Old Thu Mar 1, 2012, 04:16 PM
mscrzy1 mscrzy1 is offline
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No. I was in full remission for 15 years with no BMB's. I only did cbc's yearly. There really is no need for yearly BMB's because a BMB isn't going to determine anything at that point that a cbc won't help to indicate on its own. There is nothing to prove that your son will definitely develop into leukemia or MDS or even that he will have to deal with AA again. I would fear that doing yearly BMB's is suggesting to your son that he WILL get sick again, and I don't underestimate the power of suggestion and self fulfilling prophecy.
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Angie

36 yr. old, dx SAA in Jan 1996, treated with ATG in Mar. 1996, off cyclosporine Sept. 1996, last blood transfusion in Aug. 1997, slow decline in counts again November 2010, AA and current count decline thought to be caused by lupus, currently taking 400mg Plaquinil
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  #4  
Old Fri Mar 2, 2012, 08:32 PM
Hawaii Bill Hawaii Bill is offline
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hmm

I find their idea odd, too.

Seems like there must be SOMETHING that would make them want to do something so invasive without anything other than a old history of VSAA.
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Male, 56, dx Nov2006 VSAA (BMA:0%). Responded to ATG/CsA/Prednisone/Neupogen Dec 2006, but relapsed in June 2007. Counts are responding to using CsA 200mg bid alone since Jun 2008. Last PRBC tx: Jul 2008.
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  #5  
Old Sat Mar 3, 2012, 02:47 PM
Lisa V Lisa V is offline
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It's a good question, and one I have wrestled with too. You can read my concerns about it on this thread from 4 years ago:

http://forums.marrowforums.org/showthread.php?t=447

I still don't know how you can detect any early changes without doing a BMB, but I don't want to submit Ken to it either if there's no indication it's really necessary, and not likely to change his course of treatment. We talked to his doctor some more and he did have another one a few months after I wrote that, just to satisfy all of our curiosities about what was going on. There were no changes, so he hasn't had one since then.
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-Lisa, husband Ken age 60 dx SAA 7/04, dx hypo MDS 1/06 w/finding of trisomy 8; 2 ATGs, partial remission, still using cyclosporine
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  #6  
Old Sun Mar 4, 2012, 11:25 PM
Greg H Greg H is offline
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Paul,

This is going to sound like a broken record, but I can't see the benefit of annual BMBs in the absence of clinical symptoms.

Imagine that his CBC is fine, they do a BMB, and they find dysplasia in one or more cell lines (the hallmark of MDS). What's the next step? If that dysplasia isn't affecting his counts, is it MDS? Maybe, maybe not.

Even if his counts started to slide and he had dysplasia, I'm not sure a transplant would be the first line therapy.

We know how to look at bone marrow and see that dysplastic forms are present. We know how to look at chromosomes and see that some are broken. What we do not know is exactly what those things mean in every single case.

I can't imagine treating someone who has normal counts. So, I can't see the value of a BMB unless the counts are abnormal.

Take care!

Greg
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Greg, 59, dx MDS RCMD Int-1 03/10, 8+ & Dup1(q21q31). NIH Campath 11/2010. Non-responder. Tiny telomeres. TERT mutation. Danazol at NIH 12/11. TX independent 7/12. Pancreatitis 4/15. 15% blasts 4/16. DX RAEB-2. Beginning Vidaza to prep for MUD STC. Check out my blog at www.greghankins.com
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  #7  
Old Mon Mar 5, 2012, 11:49 AM
cheri cheri is offline
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Pardon my cynicism, but remember, doctors and hospitals are businesses!
They will often encourage unnecessary testing to increase revenue. I think I saw a bill of $10,000 for an in office, unsedated BMB! In the past, I have been a victim unnecessary testing, and it infuriated me when I realized it.

Bone marrow biopsies are a useful tool, but having had some that were innaccurate due to meds I was on at the time, is not the final answer on any given day.

I am at the point where having another BMB will not change my course of action/treatment, so why take the risk?

I agree with the others to wait until there are indicators that make a BMB necessary to determine treatment...

In the meantime, go to the movies instead!!!!
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Cheri Age 54; dx Oct 2009 AML, induction chemo only;dx MDS July 2010,- PRBC transfusion dependent; Results BMB 8/4/11--- 6-8% blasts; Danazol 100 mg 3xday; quit Exjade/ GI distress; platelets holding 40's; Fluctuation in blasts in blood--Neupogen 3-4xweek; off Revlimid again! Procrit weekly
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  #8  
Old Mon Mar 5, 2012, 02:38 PM
Paul Paul is offline
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Thank you all for your helpful responses!
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Son diagnosed 3/2006 with VSAA at age of 4 years old; No sibling match; received IST with CsA, counts reached normal level after about 6 months; Currently in remission.
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  #9  
Old Tue Mar 6, 2012, 02:35 PM
Karenish Karenish is offline
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how many bmb's?

I have been following this thread with interest. Was diagnosed with saa jan last year having had a bmb.....then....6 months after rabbit atg consultant took another bmb to see if my marrow was improving at all....showed tiny improvement so we waited... counts now hovering around...8.5 for hb (could do better lol) plates 30 (although they dropped this week as I have a horrid cold) whites 4 and neuts 1.97......Katie my consultants secretary phoned me the other day to say doc had man flu so couldn't make our appointment, but he is after another bmb. My question I feel should be, why? what is this bmb going to show him, if my marrow is slowly improving he is not going to find anything else out is he? or perhaps my learned friends know different? over to you guys, before I give Doc grief for asking the question in the first place! xx
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  #10  
Old Tue Mar 6, 2012, 02:46 PM
Greg H Greg H is offline
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Hi Karenish!

I'm not going to weigh in on this one because I am too ignorant of AA, but I want to piggyback on your question, so the learned folk who reply can answer this related one as well:

What are the key things that docs look for in and AA patients bone marrow results?

Is it mostly that we want to see an increase in cellularity? (I know we don't want to see dysplasia or cytogenetic irregularities, since those would get us heading toward MDS.) If we're just looking for an increase in cellularity, then, as Karenish asks, do we really learn anything if the CBC is showing slow but steady improvement?

Take care!

Greg
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Greg, 59, dx MDS RCMD Int-1 03/10, 8+ & Dup1(q21q31). NIH Campath 11/2010. Non-responder. Tiny telomeres. TERT mutation. Danazol at NIH 12/11. TX independent 7/12. Pancreatitis 4/15. 15% blasts 4/16. DX RAEB-2. Beginning Vidaza to prep for MUD STC. Check out my blog at www.greghankins.com
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  #11  
Old Tue Mar 6, 2012, 04:01 PM
Marlene Marlene is offline
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I think it's mainly to see if there are any abnormalities. It's possible they mis-diagnosed the SAA in the first place or they want to see if maybe it's progressed to MDS/AML. But the second, post ATG BMB would have shown that. I guess you can make an argument to do a BMB before retreating to make sure you are still dealing with SAA.

SAA is a diagnosis of exclusion. Well....you don't X, Y or Z. Your counts are low and you have little marrow. Must be SAA. That's my simple view of this disease.

Cellularity alone is not a good indicator of when to treat. There have people with good cellularity but continued with low counts. While others with low cellularity, seem to maintain normal counts.

I think it's a very valid question to ask your doctor why he wants to do another. You are in a watch and wait scenario. Your current options are to continue to wait, retreat with ATG or another immunosuppressant, or a BMT.

My guess is that your doctor thinks he need to move forward with something and needs a BMB to help him figure out your next steps.

But since John did not have ATG, I may be over simplifying things. So hopefully, others with ATG experience can address this also.
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Marlene, wife to John DX w/SAA April 2002, Stable partial remission; Treated with High Dose Cytoxan, Johns Hopkins, June 2002. Final phlebotomy 11/2016. As of January 2017, FE is 233, HGB 11.7, WBC 5.1/ANC 4.0, Plts 146K.
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  #12  
Old Fri Mar 9, 2012, 11:51 PM
Lisa V Lisa V is offline
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I agree with everything Marlene has said, and I'm not sure I have much to add to that. Yes, they're looking at cellularity as an indicator which way things are going, but if there is a discrepancy between that and periferal blood counts, I'm not sure what conclusion they draw from that.

In our case, the main concern has been about any further cytogenetic mutations, and what is going on with the one he already has. They didn't spot the trisomy 8 until his 3rd BMB, which was after his first ATG, but that doesn't necessarily mean it wasn't there all along. I'd really like to know if it was, and if it could have been what triggered the autoimmune response in the first place, or if it arose secondary to IST. To my mind, that could conceivably make a difference in his treatment plan, but since we don't know, we just have to play it by ear. What we do know is that the next 3 BMBs showed no increase in clone size, so that was enough to ease some concerns. If there had been a change, I'm sure we'd still be doing them regularly, but for now, we're just relying on his CBCs.
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-Lisa, husband Ken age 60 dx SAA 7/04, dx hypo MDS 1/06 w/finding of trisomy 8; 2 ATGs, partial remission, still using cyclosporine
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  #13  
Old Sat Mar 10, 2012, 12:10 PM
Greg H Greg H is offline
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Lisa,

Very interesting question about the Trisomy 8. My first BMB, which included Karotype but no FISH, found no Trisomy 8. A couple of months later, my second BMB included FISH, and that found 5% Trisomy 8, which still didn't show up in the karotype. Six months later, the Karotype showed Trisomy 8 (15%, I think), and, over the course of a year, that percentage went as high as 85% before disappearing in my most recent BMB.

The work that Elaine Sloand did at NIH on Trisomy 8 showed that the body can create a subpopulation of T-cells aimed at Trisomy 8, but also seemed to show that Trisomy 8 cells can continue to generate viable blood cells.

It's a great mystery: the bone marrow.

Take care!

Greg
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Greg, 59, dx MDS RCMD Int-1 03/10, 8+ & Dup1(q21q31). NIH Campath 11/2010. Non-responder. Tiny telomeres. TERT mutation. Danazol at NIH 12/11. TX independent 7/12. Pancreatitis 4/15. 15% blasts 4/16. DX RAEB-2. Beginning Vidaza to prep for MUD STC. Check out my blog at www.greghankins.com
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  #14  
Old Sat Mar 10, 2012, 01:57 PM
Lisa V Lisa V is offline
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Quote:
Originally Posted by Greg H View Post

The work that Elaine Sloand did at NIH on Trisomy 8 showed that the body can create a subpopulation of T-cells aimed at Trisomy 8, but also seemed to show that Trisomy 8 cells can continue to generate viable blood cells.
Greg, do you have a link or a source for Dr. Sloand's research? I'd like to read that.

I'm encouraged to hear that your clone seems to have disappeared after increasing so much. Ken's doc said it could potentially diminish, but once we found it, it seemed to remain pretty stable at 25%. Since there seems to be a link between trisomy 8 and cyclosporine dependancy, it would be nice to see it disappear, but I guess a certain percentage of AAers remain cyclo dependant with or without that mutation.

My thought was that if the trisomy is what triggered the initial immune attack, couldn't an autologous transplant simply remove the clone and give him back his own marrow? I know someone with AML who had an auto transplant, and his recovery has been so much better than most of the allogenic BMT accounts I've read. Without knowing whether it was the cause or an aftereffect, however, it would be kind of a longshot.
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-Lisa, husband Ken age 60 dx SAA 7/04, dx hypo MDS 1/06 w/finding of trisomy 8; 2 ATGs, partial remission, still using cyclosporine
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  #15  
Old Sat Mar 10, 2012, 10:04 PM
Greg H Greg H is offline
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Hey Lisa!

Here's the article, from 2005 in Blood:

http://bloodjournal.hematologylibrary.org/content/106/3/841.full

It's pretty think stuff, but the basic point -- that MDSers with Trisomy 8 do develop a subpopulation of T-Cells primed to attack Trisomy 8 cells -- is pretty clear.

I asked Dr. Matt Olnes, who worked closely with Dr. Sloand, whether they felt this T-cell phenomenon was confined to Trisomy 8, and he said "No." They just picked that particular abnormality because it is relatively common in MDS and because it tied into their work on immunosuppression in MDS. But Olnes said they believed that other chromosomal abnormalities likely also spawned their own subpopulation of auto-immune T-cells.

I don't know what to think about the autologous idea. Wouldn't any set of stem cells drawn from a patient with a chromosomal abnormality be likely to have a certain percentage of cells with the abnormality? So you'd just be transplanting back in the same problem you're trying to get rid of?

Take care!

Greg
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Greg, 59, dx MDS RCMD Int-1 03/10, 8+ & Dup1(q21q31). NIH Campath 11/2010. Non-responder. Tiny telomeres. TERT mutation. Danazol at NIH 12/11. TX independent 7/12. Pancreatitis 4/15. 15% blasts 4/16. DX RAEB-2. Beginning Vidaza to prep for MUD STC. Check out my blog at www.greghankins.com
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  #16  
Old Mon Mar 12, 2012, 02:10 AM
Lisa V Lisa V is offline
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Thanks Greg! Most of the methodology was over my head, but skipping straight to the conclusions was helpful. It answered some of my questions but raised a lot more.

One thing that was interesting is that their criteria for complete hematological remission contained no mention of cellularity. So that brings us back to the question of what conclusions might be drawn from monitoring cellularity in the absence of any chromosomal abnormalities. I'm with the others here in not seeing a clear benefit.

Re: autologous transplant: maybe I have it wrong, but isn't the purpose of using that approach with clonal disorders to remove the clone and then reinfuse the "good" part? AA in and of itself is not a clonal disorder so there'd be nothing to remove, but wouldn't a trisomy 8 or other mutation qualify as a clone? Or would it be too difficult to identify and remove? My understanding of the process is admittedly pretty limited.
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-Lisa, husband Ken age 60 dx SAA 7/04, dx hypo MDS 1/06 w/finding of trisomy 8; 2 ATGs, partial remission, still using cyclosporine
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  #17  
Old Mon Mar 12, 2012, 01:47 PM
Greg H Greg H is offline
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Hey Lisa!

I'm not that smart about autologous transplant; I need to read up on it. My impression is that it's mainly used in Lymphoma and Myeloma, but I'm not sure why those and not other ailments.

It's also my impression that there is no reliable way to get rid of the clone in the collected sample of stem cells. I know attempts have been made to "purge" the collected stem cells of the bad clone cells, but I don't think that has been particularly successful to date.

If it worked, on the other hand, it would be a fantastic idea, since the GVHD would be pretty much nil.

Take care!

Greg
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Greg, 59, dx MDS RCMD Int-1 03/10, 8+ & Dup1(q21q31). NIH Campath 11/2010. Non-responder. Tiny telomeres. TERT mutation. Danazol at NIH 12/11. TX independent 7/12. Pancreatitis 4/15. 15% blasts 4/16. DX RAEB-2. Beginning Vidaza to prep for MUD STC. Check out my blog at www.greghankins.com
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