CA19-9 going up and back pain at night - recurrence?

omus,

As mm noted, above, I too would note that restarting chemo is essential at this point. I'm not a medical professional, but every thread I've read indicates continued, maintenance chemo is essential - for as long as you can tolerate it - in whichever of the two varieties works. Pancan cells must be killed and any gap in chemo allows them to grow and spread.

@mayoconnectuser1, does "two varieties" (in your sentence "maintenance chemo is essential – for as long as you can tolerate it – in whichever of the two varieties works.") refer to IV chemo vs oral chemo?

Or is it referring to the two primary regimens (Folfirinox vs Gem/Abraxane)? Or, is it referring to something else? (If yes, then what?) Thanks and best wishes.

Please forgive me I'm repeating myself once too often here, but for readers who may not have seen the older threads:

1) The promise of ctDNA tests for presence/recurrence seems to be less than advertised for pancreatic cancer (PDAC in particular). My PA told me if Signatera is positive I almost definitely have cancer. If Signatera is negative, I might still have cancer. Two negative Signateras and one negative Grail/Galleri shortly before my recurrence was identified on MRI (and hinted at by my rising CA19-9) demonstrate there is something sneaky about PDAC cells that evades these tests. Likewise, the post-recurrence spread obvious on imaging while Signatera continues to report "0.00" ... (Fine print on the report indicates cancer may be present below detectable threshold. One cell is all it takes... 🙁 )

2) CA19-9 is not the holy grail, but one indicator that can be combined with others to add confidence to a conclusion. It's cheap and easy and should be done frequently pre-op and post-op so you know your own normal and have a "low noise" data set to help detect trends.

3) https://pubmed.ncbi.nlm.nih.gov/34751822/
It's only one paper, but recent, and says:

"During the last twenty years, it has been well established
that all surgical approaches to pancreatic cancer need to be
supplemented by adjuvant therapy."

and

"it remains clear that resectable pan-
creatic cancer patients should not be treated with a neoadju-
vant therapy outside clinical studies"

The paper does also have some blanket statements I disagree with, and I acknowledge that I don't have the medical training to judge the paper's accuracy. The authors do cite references for most of these statements, but I think some come across as more broadly applicable than they're meant to. I also acknowledge that I can't remove confirmation bias from my interpretation of scientific papers, given my own experience and outcome.

< rant deleted about the mythical median patient>

Summary: Err on the side of caution. Your life depends on it!!!

I'm going to be offline for a few days (I think), and just wanted to elaborate a little more on my thought process behind the previous posts, with the repeated disclosure that I have no medical training.

If @mmatunis was a patient with no history of cancer but did have the increasing CA19-9 results described, I would not be advocating for chemo this early, but I would encourage a deeper, quicker investigation into all the possible causes with an eye toward "worst first." That is, benign is fine, and benign causes can be investigated more leisurely. But if the worst possible cause is indeed cancer, increase the frequency of imaging, CA19-9 testing, and ctDNA regardless, because delay could prove catastrophic. And with that said, most of the benign causes listed earlier can be detected with basic blood tests and/or imaging.

However, with @mmatunis' history of recent cancer, and recently much lower CA19-9 levels, I would assume the worst and work backward from there. It's entirely possible there is inflammation underlying the rise, but it's also possible to have inflammation (or other benign causes) AND cancer. You wouldn't want to treat just inflammation and overlook the cancer. An anti-inflammatory might actually reduce any CA19-9 elevation caused by inflammation, but a decrease in that number might also mask an increase truly due to recurrent cancer and delay treatment. [My very first signs of cancer were elevated liver enzymes associated w/ bile duct blockage. Liver ultrasound was inconclusive, and dietary change plus elimination of Tylenol brought the enzyme levels down temporarily, delaying my initial diagnosis by a couple weeks.] On the other hand, while treating @mmatunis with Folfirinox might drive CA19-9 down (especially with a prior good response to it), I think it would likely be due to killing cancer cells. If it did mask inflammation or another cause, that would theoretically be a more benign issue that could be treated with less urgency.

Finally, from the basic logic perspective, if you miss the window of opportunity to kill cancer or confine it to another surgically resectable/radiatable area, you're probably going to be on chemo the rest of your life with the same side effects (neuropathy, risk of organ damage, etc) AND have metastatic cancer on top of that. It's not a great analogy, but starting chemo now on the assumption of disease could be viewed as "adjuvant therapy started a good bit later than usual." 😉 I would personally rather go through that for a while and deal with organ damage than go through it for a lifetime and deal with cancer.

I hate to sound like Chicken Little ('The sky is falling!"), but @mmatunis' case sounds too much like my own which went from negative biopsy and negative ctDNA to metastatic stage-4 while we waited 6 weeks for confirmation. Immediate surgery (Whipple revision or total pancreatectomy) might have avoided that outcome. It could have been difficult to justify at the time because of the negative biopsy, even though the primary tumor was visible at the original surgery site on MRI. However, I already had a chemo port that could have been put to use immediately, and that might have made a difference in stopping the spread. Adjuvant therapy for Whipple normally begins about 2 months after surgery. Starting me on chemo when my recurrence first showed up on MRI would have been at the 4.5-month mark after surgery, and while not conventional, would not have seemed unreasonable to me.

Doctors sometimes take offense at what appears to be "questioning the science," but they also sometimes need to be gently reminded that they're treating an individual patient, not a median statistic.

I can't speak to any of this surgery/recurrence stuff, since I don't qualify for surgery. However, I noted your comment re trying to get a PET scan. I had an oncologist appointment today, and as part of that I asked whether it was worth getting a PET scan to determine the extent of abdominal mets. My thinking was that if we could determine that the chemo had killed the abdominal mets, maybe radiation on the main tumor would now be appropriate. He said that a PET scan can't pick up anything smaller than 1.5cm diameter, and by the time a met was that large, it would have shown up on the CT scan I had Wednesday, and it would likely make my CA 19-9 increase. That would seem to jibe with what your surgeon said.

I think the statement about neoadjuvant studies is saying patients should not be treated with chemo more than the number of sessions than has shown to prove successful, like 8 sessions, or whatever that number is as obviously the tumor could possibly grow in size if for some reason the chemo didn't work.

Thank you so much for your posts at such an elevated content level! They are so helpful and I wish you well in your journey - cause that's what it is I believe.

Sorry, it was a very general comment on my part - I should have been more specific.

I was referring to F and G/A - my only background on oral is that which is administered with radiation following initial chemo.

Hi, What was your experience with the oral chemo?

I misread something you wrote, so I've deleted my reply.

I hope your next test results are good.